Table of Contents

1. Internal Medicine A. Dennatology .......................................................................................................................... 1 B. Diabetes Mellitus .................................................................................................................... 16 C. Infectious Disease

1. Work-up ........................................................................................................................... 23 2. Osteomyelitis ................................................................................................................... 31 3. Septic Arthritis ................................................................................................................. 34 4. mv .................................................................................................................................. 47

D. Neurology .............................................................................................................................. 49 E. Oncology

1. Bone Tumors .................................................................................................................... 58 2. Soft Tissue Tumors .......................................................................................................... 67

F. Peripheral Vascular Disease 1. Deep Venous Thrombosis and Pulmonary Embolism ..................................................... 69 2. Arterial Disease ................................................................................................................ 71

G. Radiology 1. MRI .................................................................................................................................. 74 2. Bone Scans ....................................................................................................................... 79 3. CT .................................................................................................................................... 83

H. Rheumatic Diseases 1. Gout and CPPD ................................................................................................................ 83 2. Charcot Disease ............................................................................................................... 89 3. Lyme Diesease ................................................................................................................. 92 4. Rheumatoid Arthritis ....................................................................................................... 94 5. Osteoarthritis .................................................................................................................... 100 6. Paget's Disease of Bone ................................................................................................... 101 7. Seronegative Spondyloarthropathies (General) .............................................................. .1 03

2. Pharmacology A. Antibiotics .............................................................................................................................. 114 B. Antifungals ............................................................................................................................. 120 C. Local Anesthetics ................................................................................................................... 126 D. Steroids .................................................................................................................................. 128 E. General Medications

1. SedativeslHypnotics ......................................................................................................... 133 2. Antipruritics ..................................................................................................................... 134 3. Antiemetics ...................................................................................................................... 13 5 4. Laxatives .......................................................................................................................... 136 5. Antidiarrheals ................................................................................................................... 13 7

F. Analgesics 1. Narcotics .......................................................................................................................... 138 2. NSAIDS .............................. , ............................................................................................ 142

G. Tables and Fonnulas .............................................................................................................. 151

3. Perioperative Management A. Hospital Charting ................................................ '" ........................ '" ..................................... 159 B. Perioperative Complications .................................................................................................. 163 C. Anemias ................................................................................................................................. 167 D. Blood Transfusions ......................................................................... ; ...................................... 169 E. Pre-and Post -Operati ve Management .................................................................................... 171

4. Principles of Surgery A. Regional Nerve Blocks .......................................................................................................... 180 B. Bone Healing ......................................................................................................................... 183 C. Wound Healing ...................................................................................................................... 189 D. Principles and Techniques of Fixation ................................................................................... 192 E. Biodegradable Fixation .......................................................................................................... 202 F. Suture Materials ..................................................................................................................... 203

5. Forefoot Surgery A. Accessory Bones .................................................................................................................... 209 B. Ossification of Bones ............................................................................................................. 211 C. Digital Surgery

1. Anatomy ........................................................................................................................... 211 2. Nail Surgery ..................................................................................................................... 213 3. Hammertoes/ClawtoeslFloating Toes/Overlapping Fifth Toes ....................................... 217 4. Polydactyly ...................................................................................................................... 221 5. Predislocation Syndrome (Lesser MTPJ Instability) ....................................................... 223

D. Lesser Metatarsal Surgery 1. Brachymetatarsia .............................................................................................................. 224 2. Lesser Metatarsal Surgery ................................................................................................ 226 3. Tailor's Bunion ................................................................................................................. 228 4. Joint Implants ................................................................................................................... 230

E. Amputations ........................................................................................................................... 233 F. Intermetatarsal Neuroma ........................................................................................................ 235 G. First Ray Surgery

1. Anatomy of the First Ray .................................................................................................. 239 2. Radiology of the First Ray ................................................................................................ 241 3. Surgery of the First Ray

a. Soft Tissue Procedures ............................................................................................... 245 b. Proximal Phalangeal Osteotomies ............................................................................. 246 c. Distal Metatarsal Osteotomies ................................................................................... 246 d. Proximal Metatarsal Osteotomies .............................................................................. 249 e. Joint Destructive Procedures ...................................................................................... 251 f. Hallux LimituslRigidus .............................................................................................. 258 g. Hallux Varus .............................................................................................................. 262

6. Rearfoot and Ankle Surgery A. Bone Grafting ......................................................................................................................... 264 B. Inferior Calcaneal Spur and Plantar Fasciitis ........................................................................ .266 C. Endoscopic Plantar Fasciotomy ............................................................................................. 268 D. Metatarsal-Cuneiform Exostosis/Haglund's Deformity ......................................................... 269 E. Equinus .................................................................................................................................. 272 F. Flatfoot ................................................................................................................................... 274 G. Cavus Deformity .................................................................................................................... 279 H. Tarsal Tunnel Syndrome ........................................................................................................ 282 I. Triple Arthrodesis .................................................................................................................. 283 J. Tendon Transfers ................................................................................................................... 284 K. Ankle Surgery

1. Medial Ankle Instability .................................................................................................. 287 2. Lateral Ankle Instability .................................................................................................. 287 3. Dislocating Peroneal Tendons ......................................................................................... 289 4. Arthroscopy ...................................................................................................................... 290 5. Ankle Fusions .................................................................................................................. 292

7. Plastic Surgery A. Wound Healing ....................................................................................... : .............................. 294 B. Split Thickness Skin Grafts ................................................................................................... 295 C. Skin Flaps .............................................................................................................................. 298 D. Skin Plasties ........................................................................................................................... 299

8. Pediatrics A. Metatarsus Adductus .............................................................................................................. 302 B. Clubfoot ................................................................................................................................. 31 0 C. Calcaneovalgus ...................................................................................................................... 315 D. Vertical Talus ......................................................................................................................... 317 E. Torsional Abnormalities ........................................................................................................ 320

9. Emergency Medicine A. Anaphylaxis ........................................................................................................................... 325 B. Chest Pain .............................................................................................................................. 326 C. Electrocardiogram .................................................................................................................. 327 D. Comatose Patient ................................................................................................................... 329 E. Shock ...................................................................................................................................... 330

10. Trauma A. General Fracture Management. .............................................................................................. 333 B. Digital and Sesamoidal Fractures .......................................................................................... 336 C. Metatarsal Fractures ............................................................................................................... 337 D. Fifth Metatarsal Base Fractures ............................................................................................. 338 E. Midfoot Fractures

1. LisFranc's Fractures ......................................................................................................... 340

10. Rearfoot Fractures (Contined) F. Rearfoot Fractures

1. CuneifonnlCuboidlNavicular Fractures .......................................................................... .342 2. Talar Fractures ....................................................................... , ......................................... 343 3. Calcaneal Fractures ................................................................... , ...................................... 347

G. Syndesmosis Sprains .............................................................................................................. 351 H. Ankle Fractures ...................................................................................................................... 353 I. Tibial Plafond Fractures (Pilon Fractures) ............................................................................ .356 1. Physeal Fractures ................................................................................................................... 357 K. Open Fractures ....................................................................................................................... 362 L. General Trauma

1. Avascular Necrosis .......................................................................................................... 364 2. Compartment Syndrome .................................................................................................. 364 3. Osteochndritides .............................................................................................................. 366

M. Gunshot Wounds .................................................................................................................... 367 N. Soft Tissue Trauma

1. General Guidelines ........................................................................................................... 368 2. Chronic Regional Pain Syndrome .................................................................................... 370 3. Nerve Injury ..................................................................................................................... 370

O. Tendon and Ligament Trauma 1. Achilles Tendon Ruptures ................................................................................................. 374 2. Ligamentours Ankle Injuries ........................................................................................... 375

P. Vascular Trauma .................................................................................................................... 377 Q. Nail Bed Injuries .................................................................................................................... 377 R. Puncture Wounds ................................................................................................................... 378 S. Bite Wounds ........................................................................................................................... 379 T. Burns ...................................................................................................................................... 379 U. Cold Injuries ........................................................................................................................... 380

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DERMATOLOGY

I. SKIN LAYERS A Epidermis

1. Stratum Corneum: horny, keratin layer 2. Stratum Granulosum: granular layer 3. Stratum Lucidum: seen with thick horny layer (palms & soles) 4. spiny layer

tUIllCti<m as macrophage of the epidermis and process contact antigens 5. Stratum Genninativum: basal cell layer

I ,.... only cell of the epidermis capable of division. They divide an ... ~ ~·DlI .... Total turnover time is 28 days (14 days of migration and 14 . = melanin which is t:mnsferred to keratinocytes. Melanin protects

. skin from UV radiation. In whites, found mostly in basal cell layer. In blacks, found throughout the epidermis.

Langerhans cell

Keratinocyte

Melanocyte

. 6 ... . -. ••• .:. I •

Layers of the Epidermis

B. Dermal-Epidermal Junction (Basement Membrnne Zone) 1. Lamina Lucida 2. Lamina Densa 3. Sublamina Densa

C. Dermis

..

Stratum malpighii

1. Papillary Dermis: immediately beneath epidermis. Thin haphazardly arranged collagen fibers, abundant ground substance. and delicate elastic fibers.

2. Reticular Dermis: extends to the subcutaneous fat. Coarse elastic fibers and thick collagen bundles arranged mostly parallel to skin surface.

1

.. .. .

. . l~

.. ~.

II. SKIN STRUCTURES A Hair Follicle: hair growth proceeds through distinct phases

Anagen~ prolonged gro\\-1h CatageD.: short lived interphase T eIogen: final resting phase

Diagramatic Anatomy ofa Hair Follicle

Phases ofthe growth cycle of a hair

• growing hair ;". ....... ..',

iS~~ )!-,l ... Y(~! .. ,_~

CATAGEN ANAGEN

Cells of hair bulb produce hair shaft which is completely keratinized and has no living cells. Hair color is due to the amount and type of melanin.

B. Eccrme:6laoos: found in highest concentration on palms, soles, and axillae. Secretory coil located in dermis transmits sweat directly to skin surface for cooling of body.

2

C. ;~: found primarily in axillae and anogenital ~gions and serves as a scent gland. De1lVed from hair germ and opens directly into pilosebaceous follicle lather than skin surface. Become active at puberty.

D. SebaceOOsGIaDds: found on all body parts except palms and soles. Produces oil (sebum) that is einlm~~ ~ hm,r follicle. This lubricates and protects the hair and skin.

E. AIreCtOresPilorUm: smooth muscle attached to the base of the hair follicle. Contract in response to cold or fright "Goose Bumps".

nerve

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DERMIS

reticular

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" -Diagramatic cross section of the skin and panniculus

m. SKIN LESIONS

A ~~~bed change in color of normal skin without elevation or depression < lern in diameter. (Freckle)

2. Patch: similar to macule but > I em. 3. Papule: circumscribed solid elevation, I ern in diameter. 4. Wheal: an edematous papule. 5. Nodule: similar to papule but > 1 cm 6. Tumor: similar to nodule but > 2 cm 7. Plagye: an elevation above the skin with a plateau-like surface. 8. Vesicle: elevated lesion < I em, containing clear fluid 9. Bulla: similar to vesicle but> 1 em. 10. Pustule: similar to vesicle but filled with neutrophils and dead bacteria Fluid is white or yellow

(pus).

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Macula Papule Nodule Pustule

Vesicle Bulla Tumor Wheal

B. Secondary Lesions 1. Scale: an excess of horny material on the skin. 2. Crust: scab consisting of dried blood, serum. or pus. 3. Erosion: scooped out and shallow break. No damage to the dermis. 4. Fissure: linear form of an erosion. 5. IDeer: deep lesion involving the dermis. 1. Eschar: darlc colored, hard to remove crust on ulcer.

Secondary Lesions

Scale Crust Excoriation Fissure

Erosion Ulcer Scar

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C. , ~ The rim is different from the center. 2. Linear: long, thin lesion or smaller lesions in a long, thin line. 3. Target or Iris: concentric rings like an archers taIget. 4. Imbricated: target lesions with normal skin between the abnormal zones. Very rare. 5. Serpiginous: snake-like. Partially circular and undulating 6. Geographic: outline of a continent on a map. . 7. Vegetating: lesion bas a surface that grows outward in uneven, fleshy tufts that feel soft. 8. Venucous: wart-like. Tufts ofprottuding lesion are hyperlreratotic, not soft. 9. Zosteriform: conforming to the distribution of a nerve root 10. PolYCYclic or Circinate: annular lesions grow together; parts of their circles form larger lesion. 11. Grouped: several similar lesions located in close proximity surrounded by a large area of normal

skin.

D.:'· ~~: ~~ The folloWing aspects should be included in every description: 1. Size 2. Color 3. Consistency: soft, medium, :firm. 4. Configuration: shape or outline of lesion. 5. Margination: sharp or diffuse. 6. Surface ChaIacteristics: smooth or rough.

IV. BACTERIAL INFECTIONS OF THE SKIN A: Iriiiietimi' .

1 t ·A SUperficial skin infection due to s. pyogenes & s. aureus, alone or together. Especially common in children in hot, humid climates.

2. Small. thin-walled vesicles or pustules on an erythematous base rupture to form characteristic yellow-brown (honey-colored) crusts. Removal of the crusts reveal a superficial. moist base. Lesions do not ulcerate.

3. Commonly found on the face and extremities. 4. Involved areas may be pruritic. Regional lymph node involvement is common but other

systemic manifestations areI3fe. 5. Treatme~ t~aotibiotiCS (Mupirocin, Bacitracin. Neomycin)

. ~~OliCs(Dicloxicillin, Clindamycin)

B. Ecthyma 1. A superficial skin infection caused by Group A Strep. And or S. aureus. 2. Begins as vesicles or bullae that rupture to form crusts. Removal of crust reveals an ulceration.

Heals with scarring. 3. Lesions are typically erythematous. circular. and multiple. Most commonly involve the lower

e",'tremities. 4. \freatDtent: pml3i1tibiotics (Dj.cloxacillin)

- <~." ! •..•• '., .,' • : ... ~ •.

c. !En$meJa!rand,€elliiJitist ...., .......

1. When a Strep. infection spreads into the'di:DDal;~,*erysipe!~occurs and when it ,. involves the deeperdermis·and subcUtanOOUSrat,.cellulitis'occurs:~'

2. S. Pyogenes releases enzymes to facilitate rapid spre3<iofthe infection through tissue planes and prevent abscess formation.'~ .erytheIna; and~ develop. The enzymes also produce systemic manifestations (fever,:~y~ confusion; and hypotension).

3. PredisposiIlg factors: edema, ilii~pe&S:-pievioosiii:Unato SkID- burns, surgery, or radiation. 4. Most common sites are the face and lower extremities. 5. Erysipelas unlike cellulitis has a shaIply demarcated and elevated border. 6. Both needle aspiration and skin biopsy of the lesion usually fail to yield organisms.

5

7. Causative agents: Usually Strep. S. aureus- around abscess or open wound H. influenzae- facial cellulitis in young children (6-36 months). P. multocida - cat and dog bites. P. aeruginosa & other gram (-) organisms- common in immunocompromised hosts.

8. Treatment: Mild- Ora} antibiotics Severe- Intravenous antibiotics

Signs and sytnptoms JJJaY worsen after therapy is initiated because the antimicrobial rapidly kills the bacteria causing the release of potent enzymes.

D. Furuncles and Carbuncles 1. A'ftiiU:riCltS is an infection of the hair follicle that produces an inflammatory nodule with a pustule

centeilliiough which the hair emerges. 2. A carbunG!~affects several adjacent hair follicles and begins as a nodule which enlarges to create

an inflamnlatory mass that discharges pus from multiple follicular orifices. They occur ..E!'edominantly on the back of the neck and is more common in diabetics.

3. (5. au.~is the most common cause of both. ~. Treatment: Small furuncles- moist heat to promote drainage.

Carbuncles & Large furuncles- I&D

E. Folliculitis 1. Inflammation at the opening of the hair follicle. Pathogenesis involves occlusion of the follicular

ostium. 2. Skin lesions are erythematous papules or pustules surrounding the individual hairs most

commonly on the scalp and extremities. 3. Predisposing factors: chemicals, trauma, tight clothing, excessive sweating, occlusive dressings,

<f0lon~ed immersion in water. 4. :allrilllibis the most common cause. P. aeruginosa is common with inadequate disinfection of

swi11lI1liD.g pools. hot tubs, and whirlpools. 5. A-eatment: Systemic antibiotics.

F. Erythrasma 1. ASiiPerficial infection., usually asymptomatic involving intertriginous areas (groin, axillae, toe

webs). Scaling, fissuring, and maceration of toe weDs (particularly the fourth). 2. Causative organism is Corynebacterium minutissimum (gram positive bacilli). This organism

produces porphyrins so all lesions fluoresce with a ~ or pink "coral" CQ!~~ with a Wood's lamp. 3. In other areas the lesions are scaly, brown or red, sharply demarcatedpatcnes. 4. Treatment: Wash with soapand~

Whitfield's ointm~ or topical miconazole ti!Fiit:p~tj~iotid EfYtbromyciil

G. Necrotizing Fasciitis (Hemolytic Streptococcus Gangrene) 1. A fulminating infection of thcf super:fici3larid~faSCia:. Thrombosis of subcutaneous vessels

occur with gangrene of underlying tissues, 2. Disorder ~f()lIo\VS a cut3neous injuiy (puncture wound or laceration) and most commonly

: involves th~extrem1ties. 3. Early in course, affected area becomes red, ho(aDd·edematoUs. Between.days 2 and 4, skin"

assumes a bl~,mJ:~~; Blisters may be present. Process advances to areas of frank cutaneous gangrene with eventual sloughing.

4. Radiographs usually reveal ~~softtissues. ~ 5. S. pyogenes lllone~beethecaDse; but more commonly a mixture of aerobic and anaerobic ~~, ._" .. ,

6. Treatment Immediate I&D Intravenous antibiotics

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V. CUTANEOUS SIGNS OF BACfERIAL INFECTION A. Bacterial Endocarditis

1. An infection of native or prosthetic cardiac valves most commonly due to various Strep. & Staph. 2. Infection causes vegetations of fibrin, platelets, blood cells, and organisms to form on the valve.

These vegetations can break off and obstruct small and medium sized vessels. 3. Most patients have a fever and a heart murmur. 4. Four skin signs can occur:

a. Petechiae: small reddish-brown, nonbalancing macules or slightly raised papules most commonly found on the extremities and mucous membranes. Develops in 10-20010 of the cases.

b. Splinter Hemorrhages: 1-3mm brown.. red, or black linear discolorations beneath the nail plate. Occurience is 20%.

c. Osler's Nodes: red or pwple painful nodules on pads of fingers and toes. Present in IO%. d Janeway's Lesions: nontender, erythematous macules on palms and soles. Occurrence is

15%.

B. Disseminated Gonococcal Infection I. N. gonofihea is transmitted by seA"Ual activity. Disseminated disease occurs when gonococci

enter the bloodstream usually from an asymptomatic location (urethra, pharynx, rectum). 2. Clinical features:

a. Arthralgias: usually involving several joints (wrists, hands, knees). Septic arthritis can occur. b. Tenosynovitis: pain, swelling, and erythema along tendon sheaths. Pain on movements. c. Skin Lesions: begin as tiny red papules or petechiae and become vesicular and pustular with a

gray necrotic center on an erythematous base. Usually located on extremities. Occurrence is 50-70%. Will usually clear in 4 days but new lesions may appear.

3. Treatment: Ceftriaxone

C. Staphvlococcal Scalded Skin Syndrome 1. Infection or mucous membrane colonization with toxin producing S. aureus which causes the

skin to cleave at the granular cell layer. 2. Fever and irritability precede a generalized macular eruption which progresses to diffuse

erythema Vesicles and bullae then develop followed by skin separation. Skin sloughs leaving a moist, red base that quickly dries.

3 . Vesicular fluid is usually sterile. Nikolsky's sign, shearing of normal epidermis in response to lateral pressure is present.

4. Occurs mostly in children < 5 years old 5. Treatment: Systemic antibiotics

POSSIble drainage of abscesses Possible intravenous fluids

VI. VIRAL VESICULAR DISEASES A Herpes Simplex

1. Charncterized by small, grouped vesicles on a red base. 2. Lesions are painful, self-limited, and usually recurrent Recurrences average 2 a year. 3. Although the lesions can occur anywhere, HSV -1 is most often associated with oral-labial lesions

and HSV-2 with genital lesions. 4. Fever blisters and cold sores are the most common presentation of reactivated HSV infection.

Lesions occur at the oral mucocutaneous border and outer portion of the lips. The vesicles progress to ulcerated areas that heal without scars.

5. Lesions usually crust ",ithin 4-5 days and completely disappear within 10 days. Vtral shedding ends when lesions have crusted.

6. PrimaIy infection results most often from direct contact with another infected person. 7. Factors that initiate reactivation: UV radiation, fever, emotional stress, fatigue, trauma,

menstruation. and pregnancy. 8. HSV's contain a linear double stranded DNA molecule.

7

9. Treatment: Acyclovir Palliative Care: analgesics, antipruritics

B. Varicella (Chickenpox) 1. Highly contagious disease caused by primary infection with varicella-zoster virus, a member of

the herpes family. 2. Experienced by most children, usually in the spring. 3. Characterized by 2 or 3 successive crops of widespread pruritic, small, clear vesicles with pink

halos on the scalp, face, mouth, and trunk. 4. Lesions begin as macules and progress through papules, vesicles, and pustules that crust and heal

usually without scarring. Distinctive feature is that in one area of the body all of the stages of a lesion can be seen.

5. Incubation is about 14 days. Constitutional signs (fever, chills, myalgias, and arthralgias) may precede the rash by 1-3 days. Crusting of the lesion usually occurs by day 6 with complete healing in 1-3 weeks.

6. Disease is acquired by direct contact \\'ith lesions or inhalation of infected airborne droplets. 7. Treatment: Isolation

Antipruritics and antipyretics (Nonsalicylate- aspirin can cause Reye' s Syndrome) Topical antibiotic ointment

C. Herpes Zoster (Shingles) 1. Characterized by painful, small, grouped vesicles occurring on an inflamed base and usually

localized to 1 or 2 dermatomes without crossing the midline. 2. Vesicles tend to enlarge and become pustular in 3-4 days then erode and crust in 7-10 days.

Patient is contagious until vesicles form crust. Scarring is common. 3. Rash is usually preceded by a prodrome of fever, malaise, headache, and localized pain and

parasthesias lasting 1-4 days. Lymphadenopathy is also common. 4 . Varicella results from primary infection and herpes-zoster represents reactivation of the latent

virus. 5. Treatment: Usually self-limiting and treatment is unnecessary

Acyclovir Topical Zostrix (Capsaicin) to reduce pain

D. Hand-Foot-And-Mouth Disease 1. A relatively benign, highly contagious, self-limiting disorder usually seen in infants and young

children. 2. Acquired by direct contact and caused most commonly by coxsackie virus A16 or enterovirus 71. 3. After an incubation of 1-3 days, 2-8mm bright, red macules appear on the tongue, hard palate,

and buccal mucosa. These lesions develop into thin-walled gray vesicles surrounded by a red halo. Healing takes 7-10 days.

4. Cutaneous lesions on the sides and dorsum of the hands, feet, fingers, and toes occur after the oral lesions. Initially, these lesions appear as red papules with small, thin, gray vesicles appearing in the center. They are usually oval or linear and run parallel to skin lines and usually resolve in 10-14 days.

5. Sore throat and mouth, anorexia, malaise, and fever are also common. 6. Treatment: Symptomatic therapy- disease is usually self-limiting.

VII. VIRAL WARTS (VERRUCAE) Warts are benign growths caused by papilloma viruses of the papovavirus group. They are slow­

growing, DNA-containing viruses that replicate in the nucleus of cells. They can occur on all areas of the body and are very common on the foot. Warts are housed in the epidermis. Upon debridement, pinpoint bleeding occurs because the vessels in the dermal papillae are cut. Remember, the dermal papillae have finger-like projections that interlock with the epidermis.

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A Verruca Vulgaris 1. Most common form of wart. 2. Seen on fingers, bands, and knees most commonly in children. 3. Firm nodule extnbiting vegetations with thrombosed capillaIy loops. These are the warts blood

supply and are pathognomonic for warts (looks like black dots on the skin).

B. VenucaFlantaris 1. Trauma at pressure sites on plantar surface of the foot allows penetIation by wart virus. 2. Hyperkeratotic plaque with thrombosed capillaries form (may not be noticeable until

debridement). 3. Tender on lateral compression.

c. Mosaic Warts 1. Very large, diffuse group ofwarts with ill-defined boundaries. May look similar to a callous. 2. No pinpoint bleeding upon debridement because the dermal papillae are not pushed superficially.

Lesion has a more horizontal than vertical arrangement.

D. Histology of Warts 1. Large vacuolated "swiss cheese effect" of warty plug. 2. Pyknotic nuclei: small, shrunken cells. 3. Basophilic inclusion bodies surrounded by a peri-nuclear halo.

E. TreaunentofWarts l. Acid Therapy

a. Best conservative approach. b. SOOAl Monochloracetic acid (Monocete) is best for sharply cimnnscribed warts. c. 60% Salicylic acid can also be used alone or in combination with the monochloracetic acid. d For the mosaic warts, it is better to use the monochlomcetic acid because it doesn't spread out

upon weigbtbearing and destroy surrounding good skin, like the salicylic acid paste does. e. Treatment takes about 6 weeks, has a success rate of 75-800/0, and is often painful.

2. Surgical Excision: must be down to the level of the superficial fascia. 3. Ctyotherapy (Freezing): very painful and not vety effective. 4. Laser Surgery

F. Molluscum Contagiosum 1. An epidermal DNA poxvirus which resides in the kemtinocyte. The virus multiplies and forms

globules of viml proteins (molluscum or Henderson-Patterson bodies). 2. Historically, the disease was recognized as a highly contagious childhood condition. More

recently, it has become a sexually transmitted disease. 3. Incubation period avemges 4-8 weeks. 4. Individual warts occur as asymptomatic smooth-surfaced, flesh-colored, hemi-spherical papules

seveml millimeters in diameter. In 250/0, these lesions are surrounded by a flat, erythematous halo. This centml umbilication is pathognomonic.

5. In children, face, extremities, and sometimes trunk are involved. Lesions spontaneously involute over seveml months. Total course is about 2 years.

6. In adults, inner thighs, pubis, and genetalia are usually involved Resolution is quicker than in children.

VIII. DERMATOPHYTES AND SUPERFICIAL FUNGI Dermatophytes are capable of colonizing or infecting kemtinized tissue such as hair, nails, and

stIatum corneum. Infections are caused by members of the genem Microsporum, Trichophyton, and Epidermophytes. A KOH prepamtion can be performed in order to identify the species by culture.

A Tinea Pedis (Athlete's Foot) 1. T. mentagrophytes, T. rubrum, and E. floccosum are the main causative agents.

9

2. Itching and foul odor are the most common symptoms. 3. Four classifications:

a. Chronic Interdigital: characterized by maceration and dermatitis in the toe webs. Skin is white with a foul odor.

b. Chronic Papulosquamous Hyperkeratotic: characterized by fine, dry, white scales that may be patchy or cover the foot in a moccasin-like distribution. Usually occurs bilaterally and is associated with T. rubrum

c. Vesicular or Subacute: characterized by tense vesicles and bullae containing a serous fluid. Usually associated with T. mentagrophytes and is the form most responsible for an id reaction on other parts of the body.

d. Acute Ulcerative: a rapid spread of an eczematoid vesiculopustular process. Secondary bacterial infection can occur and the vesicular fluid turns purulent. Can involve large areas of the foot and can appear with cellulitis,. lymphangitis, and lymphadenitis.

4. Treatment: Appropriate hygiene- avoid going barefoot, wash and dry feet daily.

B. Tinea Capitis

Topical imidazole agents (usually for 2-4 weeks) -Clotrimazole (Lotrimin) -Miconazole (Micatin) -Econazole (Spectazole) -Ketoconazole (Nizoral) -Sulconazole (Exelderm) -Oxiconazole (Oxistat)

1. Scalp ringworm caused by T. tonsurallS. 2. Non-inflammatory type is characterized by multiple scaly lesions and areas of broken hair.

e. Tinea Barbae 1. Commonly referred to as barber's itch and is most often seen in farm workers in contact nith

animals. 2. The superficial form appears with scaling, erythema, and broken hair associated with T. rubrum

and T. violaceum. 3. In deeper form&. perifollicular pustules, crusting, and exudates are seen associated with T.

verrucosum and T. mentagrophytes. D. Tinea Faciale

I. Presents as erythematous, scaling, pruritic lesions on the face and neck 2. Causative organisms are T. rubrum, T. mentagroph}1eS, and M. canis.

E. Tinea Corporis 1. Characterized by 1 or more circular, sharply circumscribed, slightly erythematous, dry, scaly

patches 'with progressive central clearing on the trunk and limbs. 2. T. rubrum, and T. mentagrophytes are most commonly involved 3. Majocchi's granuloma consists of perifollicular and granulomatous, slightly elevated nodules

occurring on the lower leg. F. Tinea Cruris

1. Commonly known as "jock itch". 2. Appears as well demarcated, scaling, circinate lesions with erythematous raised borders involving

the groin and intertriginous areas. 3. T. rubrum, T. mentagrophytes, and E. floccosum are most common

G. Tinea Versicolor 1. Characterized by finely scaling, guttate or nummular patches occurring on the upper trunk and

extending onto the neck and arms. 2. Caused by dimorphic yeast, Pityrosporum orbiculare.

H. Tinea Manum 1. Clinical presentation ranges from mild, asymptomatic scaling to discrete vesiculopustular plaques

and patches . 2. Involvement of one hand and both feet is common and unexplainable. 3. T. rubrumis most common.

L Tinea Nigra

10

1. A superficial infection of the stratum corneum caused by Exophiala wernecki. Usually found in tropical and subtropical areas.

2. An asymptomatic, nonscaling, dark brown to black lesion on the palms, soles, and fingers.

IX. SUBCUTANEOUS AND DEEP FUNGAL INFECTIONS A Mycetoma <Madura Foot)

1. An infection caused by a wide variety of agents (bacteria and fungi found in soil and plants) resulting in an indolent condition consisting of a triad of tumefaction, draining sinuses, and grains (microcolonies of organisms).

2. Infection begins as an initial implantation that forms a locally invasive indolent tumor-like mass. The mass slowly enlarges and sinus tracts form, and edema and induration lead to scarring into a wooden fimmess in parts of the tissue. New nodules fonn and more sinus tracts develop and destruction of the tissue and bone occur.

3. Treatment: 1&D of abscess and surgical debridement Antimicrobial therapy depending on the causative organism

X. PAPULOSQUAMOUS DISEASES A Psoriasis

1. A chronic, inflammatory rash with increased and rapid epidennal proliferation resulting in accumulation of stratum corneum.

2. Classic lesion is well-circumscribed , erythematous plaque with a dry, silvery scale appearing on extensor surfaces of the limbs. Lesions are bilateral and symmetrical in distribution.

3. Lesion exhibits the Koebner phenomenon which means replication of skin in an area of pressure due to scratching.

4. Removal of the scales results in pinpoint bleeding known as the Auspitz' sign. 5. Nails are involved in 50010 of the cases and present with pitted depressions and onycholysis. 6. Different types include: plaque, guttate, erythrodermic, pustular, and arthritic. 7. Histopathology: Epidermis- hyperkeratosis and acanthosis with elongated rete ridges. Also see

Munroe's abscesses (a collection ofneutrophils in the stratum corneum).

Dermis- capillary proliferation with perivascular inflammation. 8. Treatment: Lubricants

Tars Anthralin (hydrocarbon ointment) Topical corticosteroids Phototherapy- Ultraviolet B (UVB) radiation Oral psoralen plus ultraviolet A (pUV A)

Psoralen is a drug derived from plants which when activated by long wave UV light is phototoxic and melanogenic. The UV light causes binding of the psoralen to DNA thus inhibiting DNA production; therefore, inhibiting cellular production.

Systemic therapy- methotrexate, retinoids, cyclosporin, hydroxyurea vitamin D3 B. Reiter's

I. A seronegative asymmetric arthropathy. Syndrome consists of conjunctivitis, urethritis, and arthritis.

2. Disease has a strong male preponderance (9:1) and most patients have an HLA-B27 haplotype. 3. Classic lesion is termed keratoderma blenorrhagicum. Very similar to pustular psoriasis on the

palmer and plantar skin but lesions of Reiter's have a tbicklayer of keratin overlying the pustules. 4. Penis may also be involved with moist, red plaques. 5. Treatment: NSAlD's

Immunosuppressive agents

11

C. Lichen Planus 1. An inflammatory dermatitis of unknown etiology that is primarily papular in origin. 2. Violaceous, polygonal, flaHopped, pruritic papules displaying a lace-like pattern of white lines

on their surfaces (Wickham's striae). 3. Lesions appear on flexor surfaces of the wrists and foreanns, lumbar area, penis, ankles, anterior

aspects of the legs, and dorsum of the hands. Lesions display the Koebner phenomenon. 4. Mucous membranes are affected in over 50%. 5. Nails are involved in about 1O%. Most common changes are thinning and longitudinal ridging of

the nail plate and onycholysis. 6. Variants include: annular, linear, hypertrophic, atrophic, bullous, ulcerative or erosive, lupus

erythematous overlap, pemphigoides, and planopilaris or follicular. 7. Histopathology: Epidermis- hyperkeratosis "With degeneration of the basal ceUlayer. Damaged

cells release melanin. Acanthosis resulting in a "sawtooth" appearance. Clusters of eosinophilic bodies result from keratinocyte degeneration and are seen along the epidermal-dermal junction.

Dermis- band-like lymphOCytic infiltrate in upper dermis. 8 Treatment: Oral, intralesional, and topical corticosteroids

Antihistamines Phototherapy Systemic retinoid therapy Dapsone

D. Pitvriasis Rosea 1. Acute, self-limiting, inflammatory disease of unknown but suspected viral etiology affecting

children and young adults with the highest incidence in the winter. 2. Lesions are found to oval, eI}1hematous papules and plaques with an inncr collarette of scale.

The center usually shows some clearing. 3. First cutaneous manifestation is a "herald patch" usually on the trunk that begins as a small

erythematous papule and rapidly a round to oval patch 2-10 cm in diameter. Lesions are distributed along lines of cleavage on the trunk and proximal extremities to produce a "Christmas tree" pattern.

4. Treatment: Topical corticosteroids Ultraviolet light

E. Pityriasis Rubra Pilaris 1. Characterized by hyperkeratotic follicular papules, salmon colored scaly plaques, and palmer-

plantar keratoderma. 2. Striking feature is "island sparing" - normal appearing skin within sheets of erythema. 3. Lesions usually appear first on the upper half of the body, often in the scalp, and spread caudally. 4. Plantar lesions can extend up the sides of the feet to produce a sharply demarcated "keratodermic

sanda!". Fissuring is common. 5. Treatment: Topical steroids, emollients, andkeratolytics

Systemic retinoids Methotrexate Oral Vitamin A

XI. ECZEMATOUS DISEASES Eczema is a Greek word meaning "boiling over". We use it as a general term. The hallmark of all of the eczemas is the presence of itching. All conditions can appear in the acute, subacute, or chronic phases. Treatment of eczema of unknown etiology is usually topical corticosteroids.

A. Atopic Dermatitis 1. A genetic disorder sometimes associated with ast:hJ:na, allergic rhinitis, or hay fever. 2. Frequently immunoglobulin E is increased in the serum. 3. Skin disease usually starts in infancy and many children experience resolution after 2-6 years.

12

4. 3 phases are: infantile, childhood, and adolescent or adult 5. Sites commonly affected are: face, scalp, diaper areas and buttocks, hands, antecubital and

popliteal fossae. 6. Aggravating factors: extreme temperature changes, sweating, bacteria, soaps, and detergents.

B. Contact Dermatitis 1. Allergic Contact Dermatitis

a. A cell-mediated, type IV, delayed immunologic reaction. b. 2 phases: First is sensitization in which the patient becomes allergic to the chemical. The

second occurs with continued or repeat exposure to the allergen. c. Eruptions usually appear as itchy feet, generally of a chronic nature secondary to shoegear

breaking down and putting the feet into contact with various components of the shoes. Dorsum of the foot is the most common area.

d 2 common allergens in shoes are mercaptobenzothiazole and tetramethylthiuratll, which are used in rubber adhesives. Phenolic resins, leather tanning agents, and formaldehyde have also been identified as allergens.

e. A diagnosis can be confirmed with a patch test by cutting out a small sample of the shoe and placing it on the patients back. A shoe contact dermatitis kit is also available.

2. Irritant Contact Dermatitis a. Represents 80% of contact dermatoses and results from non-immunologic physical or

chemical damage to the skin. b. Skin reactions may be acute, as with exposure to acids. or chronic, due to repeated damage

from a weaker agent.

C. Seborrheic Dermatitis 1. Usually occurs at 20-40 years of age and persists for life. 2. Occurs in hairy areas and clinically consists of mild erythema covered with a greasy scale. 3. Most common forms:

a. Scalp seborrhea can mimic psoriasis but is less scaly, more diffuse, and more easily managed b. Facial seborrhea appears with a mild erythema and greasy scale· in the paranasal area. c. Truncal seborrhea occurs as small circinate or petaloid patches in the central chest. d Flexmal seborrhea occurs in the axillae, groin, and inframammary areas and is similar to the

scalp lesions. 4. Patients can have 1 or several forms simultaneously. 5. Etiology is unknown but evidence favors Pityrosporum ovale. 6. Treatment: Keratolytic shampoos- Zinc pyrithione (Sebulon, Danex, Head and Shoulders)

Selenium sulfide suspension (Selsun Blue) Salcylic acid and sulfur (Sebulex)

Topical steroids Tar preparations Antifungals (Ketaconazole)

D. Stasis Dermatitis 1. Characterized by erythema, dependent edema, and hemosiderin pigmentation of the distal lower

legs, particularly medially. 2. Most commonly occurs as a consequence of phlebitis or varicose veins, which lead to venous

insufficiency, venous hypertension, and eventually stasis dermatitis. 3. Stasis ulcers are a complication of uncontrolled disease. 4. Treatment: Control the venous insufficiency- support stockings, elevation, diuretics

E. Dvshydrosis (pompholyx) 1. A non-inflammatory, idiopathic, recurrent vesicular eruption on the palms and soles.

13

2. ChaIacterized by symmetrical, tense, deep-seated, pruritic, burning vesicles, 1-5 mm in diameter, on the sides of the digits and the volar aspects of the palms and soles. Vesicles may coalesce to form bullae or evolve into sterile pustules that dry and shrink or rupture.

3. The cause is unknown but the patient is usually a type A personality; thus a psychogenic basis is a possibility. Disorder is exacerbated with stress.

4. Treatment: Usually responds very poorly to all therapy other than systemic steroids Topical corticosteroids and antihistamines Cool water soaks

XII. CUTANEOUS DRUG REACTIONS A. En1hema Multiforme

1. Syndrome characterized clinically by acute, self-limited, but often recurrent episodes and by symmetrically distributed round, fixed skin lesions.

2. Primary lesion is a round, erythematous papule. Over hours to days the papules evolve in several different patterns.

3. Lesions may enlarge and coalesce to produce, small plaques or may evolve with concentric zones to reveal target lesions. Outer zone of target lesion is erythematous and central portion is white, yellow, or gray.

4. In 25%, the lesions are limited to the oral cavity. 5. Treatment: Topical corticosteroids

Antihistamines

B. En1hema Multiforme Major (Stevens-Johnson Syndrome) 1. Usually follows a 1-14 day prodrome offever, malaise, cough, sore throat, arthralgia, and

myalgia. 2. Inflammatory bullous lesions suddenly appear on the mucous membranes which are

characteristically covered by hemorrhagic crusts. 3. Bilateral purulent conjunctivitis appears. Nares, pharynx, larynx, and lower respiratory tract can

be involved. 4. Skin involvement varies from urticarial to target or bullous lesions. 5. Complications include: blindness, renal failure, pneumonia, scarring of the skin, and nail loss. 6. Treatment: Large doses of systemic steroids

Mortality of patients not treated is 5-15%

C. Erythema Nodosum 1. Most often presents with the sudden onset of ill-defined, tender, erythematous nodnles or plaques

distributed symmetrically over the anterior lower legs. 2. Initially lesions are red, slightly elevated, and 1-5 em in diameter with diffuse borders. Nodnles

evolve through color changes of a bruise from red to blue to yellow with a green tint 3. Nodules may last between 1-2 weeks and usually resolve without scarring. Entire episode

subsides over a 3-6 week period. 4. Fever, malaise, and arthralgias may precede lesions. 5. Females are affected more than males (9:1).

6. Etiologic factors include: infectious agents, sarcoidosis, inflammatory bowel disease, and drugs such as sulfonamides and oral contraceptives.

7. Treatment: NSAID's Oral potassium iodide Steroids are not that effective

XIII. GRANULOMATOUS DISEASES A. Necrobiosis Liooidica Diabeticorum

1. ChaIacterized by several, sharply but irregularly demarcated patches, usually on the shins.

14

2. Indmated patches appear yellowish in center and violaceous at the periphery. 3. About 75% are females and about 213 have diabetes mellitus. 4. Histopathology: Degeneration or necrobiosis of collagen with polymorphic cellular infiltrates

composed of lymphoid cells, fibroblasts, and histiocytes.

5. Treatment: Topical corticosteroids Intralesional steroid injection

B. Gnmuloma Annulare 1. A benign, usually self-limiting disorder of unknown etiology. 2. Occurs predominantly in children and young adults. Affects women more commonly than men 3. 4 clinical types: localized, generalized, perforating, and subcutaneous (deep).

4. Localized is the most common and presents with a limited number of asymptomatic, flesh­colored to red-purple, 1-5 mm. dermal papules, often arranged in an arciform or annular pattern.

5. Lesions found most commonly on the hands and feet. Involvement of the arms, legs, trunk, and face may also occur.

6. Histopathology: Focal degeneration of collagen with an intlammatoty infiltrate and fibrosis within the

dermis. 7. Treatment: Spontaneous resolution occurs in 50% within 2 years.

XlV. NAIL DISORDERS A Psoriasis: subungual keratosis, nail pitting, onycholysis, discoloration (oil spots). B. Lichen Planus: longitudinal grooving and ridging, shedding of nail plate and atrophy of nail bed,

ptetygium formation, subungual hyperpigmentation

C. Darier's Disease: longitudinal subungual red and white streaks, distal wedge-shaped subungual keratoses.

D. Alopecia Areata: pitted (stripped) nails. E. Onycholysis: separation of nail plate from nail bed- psoriasis, hypothyroidism, hyperthyroidism,

pregnancy, moniliasis, tetracyclines, artificial nails.

F. Clubbing: biliary cinhosis, chronic respiratory illnesses, congenital heart defects, familial (Increase in

Lovibond's angle > 180 degreesJ. G. Sooon Nails (Koilonychia): faulty iron metabolism, familial, inflammatoty skin diseases, idiopathic. H. Onychogryphosis: hypertrophy and curvature- trawna or circulatoty disorder. I. AnOnychia: Stevens-Johnson syndrome, epidermolysis bullosa, absence of nails. J. Beau's Lines: transverse furrows- systemic illness, trawna. K. Onychoschizia: splitting of distal nail plate into layers, dehydration of nail plate. L. Half and Half Nails: proximal white, distal red- renal disease. M. Muehrcke's Lines: narrow, white, transverse bands occurring in pairs- hypoalbuminemia. N. Mee's Lines: white transverse lines, single or multiple- arsenic poisoning. o. Onychorrhexis: brightness with breakage of nail. P. Terry's Syndrome: distal 1-2 mm normal pink color, proximal end has white appearance- cirrhosis. Q. Racquet Nails: inherited disorder. R Median Nail Dystrophy: inverted fir tree- trauma. S. Leukonychia: white discoloration of nail plate, bed, or matrix. T. Yellow Nail Syndrome: pulmonaty disease and lymphedema.

15

DIABETES MELLITUS

Pathogenesis

Group of disorders characterized by glucose intolerance. Insulin produced by beta cells in the pancreas decreases blood glucose by inhtbiting glycogen breakdown and facilitates entry of glucose into the tissues. When tissues fail to use glucose, hyperglycemia results. Diabetes affects 2-5% of the population in the U.S.

Types a. Type 1 (IDDM) Insulin dependent diabetes was formerly called juvenile-onset diabetes but

now is referred to as type I because it is not restricted to the juvenile age group. It is characterized by abrupt onset, polyuria, polydipsia, polyphagia, and often rapid weight loss.

b. Type 11 (NIDDM) Non-insulin dependent diabetes was referred to as adult onset. Symptoms are often less pronounced than type 1. Patients with NIDDM present with thirst, pruritus and fatigue. Obesity is present in 60-90% of these patients.

c. Secondary 1. Pancreatic disease: hemochromatosis, pancreatic deficiency, pancreatectomy 2. Hormonal: Cushing's syndrome, acromegaly, pheochromocytoma 3. Drug-induced: thiazides, diuretics, steroids, phenytoin 4. Genetic syndromes: lipodystrophy, myotonic dystrophy, ataxia, telangiectasia

d. Impaired glucose tolerance (lGT) , also known as chemical, latent, borderline,or subclinical e. Gestational: glucose intolerance with onset during pregnancy

Distinguishing Features of DM

Features age onset prevalence Ketosis weight complication genetics:HLA monozygotic twins 100% islet cell antibody insulin secretion hyperinsulinism insulin treatment required insulin resistance defect

Diagnosis

IDDM <30 .2-.3% common nonnaI frequent yes 40-50010

yes severe deficiency

always

occasional:poor control excess antibody

a. Classic symptoms: polydipsia, polyphagia, polyuria

NIDDM >30 2-4% rare obese (80%) frequent no Concord near

no moderate to

usually not

usual: receptor

b. Hypergylcemia: fasting plasma glucose level greater than l40mgldl on more than one occasion

c. Oral glucose tolerance test: 75g glucose dose dissolved in 300ml water after overnight fast; plasma glucose above 200mgldl at both 2 hrs and at least one other time between zero and 2 hrs.

d Hemoglobin Alc: (gylcosylated hemoglobin) Concentration in normal individuals 3-6%; patients with DM have two-to threefold elevation. Is a rough reflection of the mean level of circulating glucose for the previous 2 to 3 months (life of RBC-120 days).

16

Treatment a. Diet : is the cornerstone of treatment Objectives include providing nutrition with a balance of

protein, fat and carbohydrates and to normalize weight b. Oral Hypogylcemics: Sulfonylureas are recommended for patients with symptomatic NIDDM

who cannot be controlled by diet alone and in whom an addition of insulin is impractical or unacceptable. (For a detailed discussion see pbarmacology section.)

c. Insulin : Used primarily for the type I (lDDM) diabetic who is hypoinsulinemic and prone to ketosis. Also can be provided for type II diabetic who is not compliant with diet.(see pharmacology section for details)

Complications A Acute:

I.Ketoacidosis: precipitating factors- infection. omission of insulin. new onset diabetes a. chamc. by pH <7.2 .hyperglycemia, hyperventilation. inc. anion gap. hyponatremia,

hyperkalemia, inc. BUNtCr ketones in blood and urine b. absolute insulin deficiency leads to inc. lypolysis, inc. fatty acids in the blood and ketosis c. Dx.:polyuria, polydypsia, nausea, vomiting. abdpain, dehydration,. altered mental status,

acetone halitosis d. Tx:

-fluids to restore intravascular volume with monitoring of cardiac and renal function -bicarbonate ifDKA associated with shock/coma, arterial pH of <7.1, severe hyperkalemia -K replacement (monitor ECG to ensure no hyperkalemia) -insulin, monitor electrolytes -phosphate (insulin inc. cellular uptake of phosphate and dec. plasma levels)

2.Hyperosmolar Nonketotic Hyperglycemic Coma a. glucose>600mgldl without ketosis-see in type II more common b. Signs: lethargy ,confusion. seizures, coma, dehydration. hypertension, polyuria, polydypsia c. Tx: fluid replacement, insulin, electrolytes( esp. K + and phosphate)

3.Infection: at increased risk due to triopathy A) neuropathy, B) vascular insufficiency,and C) immunopathy

a. immune status decreased due to granulocyte depletion and defective phagocyte ingestion b. nephropathy can compromise antibiosis c. Infections can include epidermophytosis, ascending un pyelonephritis, septicemia and

gas infections d (see section on diabetic foot infections for details)

4.Hypoglycemia-plasma glucose <50mgldl

B. Chronic:

a. due to I )IDDM -imbalance btw.insulin and glucose,2)reactive-insulin secretion vs. absorption of food 3)insulin overproduction-pancreatic tumor or alcohol ingestion

b. Dx.: Whipple's triad-I)risk of hypoglycemia,2)BS 40mgldl or less3)immediate recurrence following admin. of glucose

c. Tx.: related to cause(ie insulinoma-surgery) adjustment of dosage and patient education d somogyi phenomenon: hypoglycemia results in rebound hyperglycemia-may be due to

excess secretion of counterreguJatory hormones(glucagon and epinephrine)

I.Atherosclerosis a. Possibly due to oxidation of LDL b. macroangiopathy- plaque occluding larger vessels(Ml, HfN, CV A) c. microangioapathy-increase basement membrane thickening(neuropathy, nephropathy,

retinopathy) d. high incidence of lower extremity disease-ant tib. Post.tib and peronael arteries usually

affected(see PVD section) 2.Retinopathy

a. increased capillary permeability b. microaneurysms c. hemorrhages d retinal detachment

17

3.Nephropathy a.Diffuse:

1. widening of glomerular basement membrane 2. mesangial cell thickening

b.Nodular: 1. accumulation of PAS-positive material at the glomerular tufts(Kimmelsteil-Wilson

lesion) 2. hylanization of afferent glomerular arterioles

c.Tx: 1. strict control of blood sugar 2. control HTN 3. decrease protein in diet

4.Neuropathy Anatomic Classification structure signs/symptoms

nerve root pain,dermatome sensory loss

mixed nerve vascular pain, weakness, sen. loss, reflex change

nerve terminal sen loss(stocking-glove) absent reflex mild weakness,

nerve tenninal(muscle) anterior thigh pain with weakness

sympathetic ganglion postural hypotension, impotence,gastrophy, anhydrosis,arhtropathy

a. Pathogenic mechanisms

disorder

radiculopathy

mononeuropathy

polyneuropathy

amyotrophy

autonomic neuropathy

etiology

probably vascular

probably

metabolic

unknown

unknown

1. sorbitol pathway-schwann cell hyperosmolality due to sorbitol excess, swelling, and destruction

2. occlusion ofvasa nervorum 3. decreased nerve myoinositol 4. decreased nerve conduction 5. altered myelin synthesis and deficient repair 6. motor and sensory neuropathy 7. autonomic disorders 8. neurotrophic factors:nerve growth factors

2. Treatment: 1. antidepressants-amitriptyline 10-25mg qd, nortriptyline 300mg tid 2. anticonvulsant~apine

3. topical-<:apsaicin 4. analgesics/sedatives

18

Diabetic Charcot Foot: a. pathophysiology:

1 newopathy: loss of pain perception. proprioception and sympathetic activity 2.trauma: increased weight bearing promotes joint degenerntion and subluxation

b. stages: l.development: destructive phase. joint laxity, subluxation.osteochondral fragmentation 2.colescence: absorption of debris and fusion of larger fragments to adjacent bone 3.reconstruction: revascularization and remodeling of bone and fragments

c. clinical features: vascular neuropathic

bounding pulse erythema swelling warmth

absent/diminished pain proprioception vibrntion

deep tendon reflexes d. treatment:

I. casting/immobilization 2. accommodative foot gear 3. reconstructive surgery

Diabetic Foot Ulcers:

skeletal

rocker bottom deformity medial tarsal subluxation

digital subluxation crepitus hypermobility

I. abnormal pressure distribution secondary to newopathy -accentuated by faulty biomechanicslbone distortion -poorly fitted shoes

2. secondary to cuts or puncture wounds from foreign bodies 3. high infection rnte often with multiple organisms 4. prevention is cornerstone of tx.

-adequate shoe gear -proper hygiene -control of blood sugar -firequentinspection

Diabetes and Surgery:

1. good metabolic balance prior to surgery -normal vital signs/electrolytes -blood glucose btw. 100 and 200 mgtdl -renal and hepatic status -preopEKG

cutaneous

ulcer hyperkeratosis infection

hyperhydrosis

2. prefernble to admit patient to hospital the day before surgery to adjust insulin dose 3. glucose measurements several hrs before and after surgery

Management during Minor Procedures I. those patients undergoing local anesthesia 2. will be given oral nutrition immediately postop. 3. no change in diet, oral hypogycemic or insulin regimen 4. monitor glucose 1 hour before and 1 hour after surgery

Management during Major Procedures l.Preop. eval

-type I vs type II -type of therapy (diet, oral , insulin)

19

Pharmacology:

-diabetic control -evaluate for any systemic complications -admit to hospital a day prior to surgery or 2-3 days if poor control -preop labs (ECG, UA, Chemistry, CBC, glycolsylated hemoglobin) -schedule early in day-better equilibrium btw insulin dose and caloric intake -if diet controlled and stable, fasting blood glucose on the morning of surgery -if oral hypogycemics, discontinue the morning before the day of surgery -if on insulin and controlled «250mgfdl), give liz the usual dose on morning of surgery

2. Intraoperative and Postoperative Management a. Important considerations

-blood glucose should be between lOO-200mgfdl -frequent intraop glucose testing to avoid iatrogenic hypoglycemia

b. Methods of management preop start IV with l000ml5% dextrose (D5W) \\'ith 40mEqIL ofKCL run at lOOmllhr (need to dec. rate in pts. with CHF or renal failure) administer liz of usual morning insulin,glucose test immediately after surgery continue IV fluids at 80m11hr, monitor blood every 4 to 6 hr with appropriate regular insulin coverage

-or-low dose continuous regular insulin IV solution consist of 100 U of regular insulin added to 500 ml of .5% normal saline solution

Glucose level: following surgery, hydration status and glucose most important info. diet controlled, glucose <300mgfdl can manage on diet alone 12 to 24 hrs after surgery oral hypogycemics, if glucose under control, can start oral agent the day following surgery taking insulin, requires frequent (every 4 hrs for the first 12 postop hrs) glucose testing- insulin given only if patients glucose values> 300mgfdl -only regular insulin is to be used at intervals of 4 to 6 hrs.

Insulin: a source- beef, pork, human admin. - is a protein structure usually given subcutaneously adverse IX. - mainly sx. of hypoglycemia

-tachycardia <anfusion -vertigo -diaphoresis

b. preparations: 1. Rapid acting -crystalline zinc or regular-can give subq or IV -semilente-only given subq 2.Intennediate -isophane or NPH(neutral protamine hagedom)-only subq

20

3. Prolonged Protamine zinc-max effect in 24hr ultralente-given with semilente to form lente an intermediate acting form

4.Humalog 70/30

Oral Hypoglycemics: used in patients with NIDDM mechanism: -stimulate insulin release from beta cells

-reduce serum glucagon levels -increase binding of insulin to target tissues

adverse rx.: -GI disturbances -hypoglycemia -pruritus -nausea -anemia

drug interactions: 1. Displace from plasma proteins -clofibrate

-phenylbutazone -salicylates -sulfonamides

2. reduce hepatic metabolism -dicumarol -chloramphenicol -monoamine oxidase inhibitors -phenylbutazone

3. decrease urinary excretion -allopurinol -probenecid -salicylates -sulfonamides

Biguanide: (metformin) classification: antihypergylcemic NOT hypoglycemic mechanism: -decrease intestinal glucose absorption

-increased periphernl glucose uptake -iner. Insulin-mediated glucose uptake -decreased hepatic glucose production

advantage: -gylcemic control without weight gain (which occurs "With insulin and hypogylcemic agents)

-reduces total serum cholesterol -inereases HDL -decreases trigylcerides

adverse rx: most serious is lactic acidosis risk factors (contraindications)

-renal insufficiency -hepatic disease -severe cardiovascular disease -severe pulmoDary disease temporary discontinue;

-IV contrast medium -infection -surgery, trauma -acute MI, angina

21

-stroke -dehydration -severe GI illness

Drug rx: oral sulfonylureaslinsulin alcohol-iner lactic acidosis cimetidine-iner metformin levels nifedipine cationic drugs (ranitidine,triamterine, trimethoprim) nephrotoxic drugs aggressive use of diuretics

Dose: 500mg tablets BID Rezulin (Troglitazone) -Troglitazone is a thiazolidinedione antidiabetic agent that lowers blood glucose by improving target cell response to insulin -Troglitazone decreases hepatic glucose output and inereases insulin-dependent glucose disposal in skeletal muscle. Its mechanism of action is thought to involve binding to nuclear receptors Peroxisome Proliferator Activated Receptor (PP AR) that regulate the trans...'Tiption of a number of insulin responsive genes critical for the control of glucose and lipid metabolism. -Rezulin is indicated to improve glycemic control in patients with type 2 diabetes mellitus as an acljunct to diet and exercise in combination with (not substituted for): • A sulfonylurea drug for patients who are not adequately controlled with a

sulfonylurea alone or, • A sulfonylurea drug together with metformin for patients who are not

adequately controlled with the combination of a sulfonylurea and metformin or,

• Insulin in patients who are not adequately controlled with insulin alone. -Contraindications

-Severe idiosyncratic hepatocellular injury has been reported during marketed use , Rezulin therapy should not be initiated if the patient exhibits clinical evidence of active liver disease or increased serum transaminase levels (AL T> 1.5 times the upper limit of normal)

-Thus, dose adjustment in patients with renal dysfunction is not necessary -Rezulin is not indicated as initial therapy in patients with type 2 diabetes. -Rezulin is available in 200, 300 and 400 mg tablets as follows -Rezulin should be taken with a meal.

Combination Therapy

• Sulfonylureas • Metformin • Insulin

22

Infection Work-Up

Def'mition: Invasion of the body by hannful organisms (pathogens) such as bacteria, fungi, and viruses with an initiation of an inflammatory response by the host.

Infectious Dose: Minimal number of viral particles necessary to establish a disease state: I X 106 • This allows for differentiation between colonization and infection.

Key: Diagnose an infectious process quickly and accurately. Diagnosis is made by clinical exam, NOT by ancillary tests. Make diagnosis then implement a proactive treatment plan.

Goals: To establish a treatment plan, work to answer 2 questions: A Is hospitalization required? Outpatient versus in-patient therapy. Oral antIbiotics versus IV antIbiotics B. Is surgical intervention warranted?

Bedside debridement versus OR I&D

I. History (Subjective): A Chief Complaint B. History of Present Illness C. NLDOCAT

1. Any previous ulceration or infection? 2. Any recent antibiotic usage? 3. Trauma? 4. Last meal? 5. Check shoegear for foreign body or signs of irritation. 6. Constitutional signs & symptoms: fever (highest temp & when?), chills, night sweats,

rigors (violent shaking), nausea, vomiting, loss of appetite, dianhea, weight loss, general malaise/fatigue, myalgias.

History of.. .. (begin to think empirically):

negative

Post-op IV line sepsis Implant Scratching

Puncture Wound Pseudomonas

Diabetic Infection IV Drug Abuse Water Related

volnificans,

Fever

Dog/Cat Bites Human Bites

Staph. aureus Staph. epidermidis Staph. epidermidis Tinea info with secondary bacterial info = gram

Cellulitis = Staph & Strep Osteomyelitis =

Polymicrobial MRSA, MRSE, Pseudomonas Pseudomonas, Aeromonas hydrophilia Vibrio

Mycobacterium marinum Pasteurella multicida Eikenella corrodens

Body temperature is regulated by the hypothalamic thermoregulator), center in response to various stimuli. The stimuli affecting the hypothalamus are endogenous pyrogens secreted by leukocytes and Kupfer cells. Other stimuli are bacterial endotoxins, phagocytosis, and certain immune reactions. The endogenous pyrogen then increases the set point and temperature is raised Two signs of increased set point are chills and shivering. Gram negative bacteria tend to cause more of an intense fever. Gram positive bacteria tend to evoke a profound inflammatory response, which releases endogenous pyrogens. It is believed that a certain threshold of endogenous pyrogens is necessary for fever to occur. It is for this reason we may not see fevers with early localized infections.

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General Guide to Post-Op Temperature Elevations

107 Anesthetic Hyperthermia 106 lOS Blood Transfusion Reactions 104 Closed Abscesses 103 AtelectasislPneumonitislDrug ReactionslLiver Disease 102 Wound Infection 101 Draining Abscess 100 Benign Post-op FeverlPost-anesthesia Overshoot 99 98 Usual Range ofNonnal 97 96 Post-op Hypothermia

II. Past Medical Histon': A. Diabetes: What type and for how long? Last BG? Classic triad (neuropathy, nephropathy,

retinopathy). B. Cardiovascular: CABG (how many bypasses and when?), H1N, Murmurs, MVP, MI (last one),

phlebitis. C. LungILiverlRenal disease.

III. Medications: Note dosages and frequencies. If on antibiotics: how long and why? IV. Allergies: Penicillin, Local anesthetics, Iodine/Shellfish. Note type of reaction. V. Past Surgical History: List all surgeries, dates, & physicians and/or hospital. Get medical records

on recent lower extremity surgeries. VI. Social History:

A. Cigarettes, Alcohol, IV Drugs (how long & how much?). B. Occupation: Is patient on feet at work. C. HIV risk factors.

vn. Family History: A. Are parents still alive? If not, what was cause of death. B. Person to contact in case of emergency.

VIII. Re~iew of Systems: A. HEENT: headaches, glaucoma. retinopathy, eye or ear infections, sinusitis, sore throat, stiff neck B. CVS: HTN, MI, CHF, MVP, murmur, angina, dyspnea, phlebitis, claudication C. Resp: COPD, asthma, bronchitis, recent cough or cold, TB, pneumonia D. GI: ulcers, GERD's, diarrhea, constipation (last bowel movement), hepatitis E. GU: urgency, frequency, nocturia, hematuria, retention, incontinence, UTI, renal stones, SID's F. MS: Muscle or joint pain, arthritis (type & how long?). Is patient ambulatory? Any assistive

devices? G. Neuro: CV AfTIA, seizures, vertigo, syncope, paralysis, NM disorder, peripheral neuropathy

IX. Physical Examination (Objective): A. Geneml appearance of patient:

Does patient look sick? Are they diaphoretic, flushed, disheveled, poor attitude? B. Vital Signs: Preliminary way to detennine the amount of stress the infection has placed upon

patient. 1. Temperature: Note Tmax in past 24 hours & Tpres 2. Blood Pressure: May decrease during infection. 3. Pulse: May increase during infection. 4. Respiratory Rate: may increase during infection. S. Finger Stick Blood Glucose in Diabetics: Usually elevated during infection.

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Septic Patient: Elevated temperature, bypotensive, tacbycardic. tacbypnic. C. Bacteremia:

L Definition: simple presence of bacteria in the blood stream that have clinical manifestations. 2. Significance: method by which infections can be spread to distant foci.

D. Septicemia: 1. Definition: clinical state in which in addition to bacteremia there are fever, cbills, & other

clinical symptoms. 2. Significance: represents failnre of the body to localize infection.

E. Don't limit exam to the lower extremity: 1. Look for other sources of infection:

a. Eyes, ears, nose, throat b. Respiratory Tract c. SBE d Phlebitis, IV line sepsis e. Gastrointestinal Tract f. Genitourinary Tract g. Skin: decubs or ulcerations on other parts of body.

X. Lower Extremity Examination: A. Vascular Status:

1. Pulses: a. If non-palpable then check with Doppler. If non-audible or weak with Doppler, get non­

invasive arterial studies (pYR.'s).

b. ABI < 0.45 is inadequate for healing in diabetics. At least 30mmHg needed to heal digital wounds.

c. May need arteriogram and vascular surgery consult for possible bypass. d Question for ischemic rest pain/relief of pain with dependency of limb

2. Capillary Refill: Also check color and temperature of digits. B. Neurological Status:

1. Check all sensory, motor, & reflex functions. 2. Determine level & duration of neuropathy ifpresent

a. Use Semmes-Weinstein monofilameDts. Comes in 3 sizes. If patient cannot feel the 5.07 size, protective threshold is lost.

e. Ortbopedic Status: 1. Note all boney prominences. 2. Note foot type and deformities. 3. Previous amputations? 4. Pain \\<ith range of motion of affected joint versus tenderness upon palpation.

D. Dennatologic Status: 1. Assess for the 5 CARDINAL SIGNS OF INFLAMMATION:

a. Dolor - Pain This is the most indicative sign. Even neuropathic patients will have pain. b. Rubor - Redness c. Calor - Heat d. Tumor - Swelling e. Functio Lasea - Loss of Function

At the site of inflammation, blood vessels dilate and there is an increase in blood flow to the area causing RUBOR & CALOR Then there is extravasation of phagocytes and fluid into the perivascular space resulting in TUMOR This edema causes stretching of the cutaneous nerve fibers and the patient experiences DOLOR which causes FUNCTIO LASEA Always uote Intensity of tbe signs of inflammation & compare to the contralateral limb.

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2. Wound Evaluation: a. Location - digits, interspaces, boney prominences, plantar space. b. Size - always measure after debridement c. Base - granular, fibrotic, fatty, necrotic, macerated d. Depth - Does wound probe to bone or track up tendon sheaths or fascial planes? Is bone or

tendon exposed?

Wagner Classification of Diabetic, Neuropathic, & Vascular Foot Lesions o - No open lesions, may have keratosis. I - Full thickness ulceration that does not go beyond skin. 2 - Beyond full thickness of skin. Tendon or joint capsule may be exposed. 3 - Ulceration open to bone. Osteomyelitis is present. 4 - Wet or dry gangrene with or without cellulitis localized to the forefoot. 5 - Gangrene to extensive portion offoot or whole foot. Foot salvage is not possible. c. Drainage - serous, serosanguinous, hemorrhagic, liquefactive, purulence. f Odor - foul odor indicative of anaerobes, fruity odor indicative of pseudomonas. g. Margins of Wound - viable, nonviable, necrotic, undermined, irregular border, punched-out,

keratotic, hyperpigmented indurated, macerated h. Surrounding Tissue

1. Erythema versus Cellulitis (outline borders with marker to monitor regression or progression).

Erythema - abnormal redness of the skin due to capillary congestion such as inflammation. CeUuIitis - an acute spreading infection of the skin and connective tissue. More wide-spread than erythema and boundaries are not clearly demarcated (Most common organisms associated with cellulitis are Group A Strep & Staph aureus.) 2. Edema - as edema decreases, you will see an increase in skin lines. 3. Lymphadenopathy - check for lumps in groin & behind knee. 4. Lymphangiitis - "blood poisoning". Red streaks up legs along lymphatic channels. Infection is drained from the body via lymphatics. Lymph nodes can become swollen during this process due to excess bacteria & increase in pressure from the edema. If lymph nodes become overwhelmed, lymph drainage can be blocked and red streaks can occur (#1 org. is grp. A Strep) Bacteria can also seed the blood via l}rophatics and cause a bacteremia which can lead to a septicemia.

XL Medical Imaging: A Conventional Radiographs:

1. Always order even with soft tissue infectious. Need baseline radiographs. 2. Examine for:

a. Soft tissue swelling. b. Gas in soft tissues. (May also be able to feel crepitation in skin clinically.) c. Foreign Body. d Trauma e. Osteomyelitis:

• Periosteal reaction. • Lytic changes with sclerotic border.

• Cortical breaking. • Osseous destruction. • Sequestrum, involucrum, cloaca, Brodie's abscess (chronic changes).

3. Lag time can be 10-14 days.

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The following medical imaging modalities should only be used as an adjunct to therapy. They should only be used if the results would alter a treatment pJan or benefit the patient. They should never be relied upon to make a diagnosis. Diagnosis is made by CLINICAL EXAM. Please see the section on Radiology of Infection for complete discussion of each.

B. Nuclear Scinitigraphy (See radiology section). C. CT Scan. (See radiology section). D. MRI. (See radiology section).

XII. Laboratory Evaluation: FIRST LINE TESTS SECOND LINE TESTS 1. CBC with diff I. ESRlCRP 2. Chemistry Panel 2. Blood Cultures

a. BUN 3. Urinalysis b. Creatinine 4. Urine Culture c. Glucose

TESTS FOR SURGERY 1. Pf,PTT 2. LFT's,. TFT's 3.CXR 4.EKG

First line tests should be performed upon initial presentation of patient to aid in diagnosis & establish appropriate treatment protocol. Second line tests can be performed after initial presentation. They may help monitor patients progress or help rule-out other sources of infection. Tests for surgery should be performed initially only if patient needs to go to the OR immediately. (Do not order if they are not medically indicated) Please see section on "Pre & Postop Management: Hospital Charting" for normal lab values.

A. Complete Blood Count (CEC): 1. Hemoglobin (Hgb). 2. Hematocrit (Hct). 3. Platelets (pIts). 4. White Blood Cells (WBC): Usually> 10,000 for infection (Leukocytosis). a. Differential:

Granulocytes (Contain granules in cytosol) Neutrophils:

Polymorphonuclear (PMN) cells Band cells

Basophils Eosinophils

Agranulocvtes Monocytes Lymphocytes

• PMN's: Mature neutrophil. Initial killer cell, actively phagocytic. Contains lysozymes & lactoferrin. Half-life is 6 hours but functions last for 1-2 days. Maturation tinie is 14 days.

• Band cells: Immature neutrophil Nucleus is elongated & twisted It is less deformable & less motile; therefore, less effective in phagocytosis & killing. Increases during acute infection (Left Shift).

• Basophils: Contain heparin, histamine, & other substances to contract smooth muscle & increase permeability of blood vessels.

• Eosinophils: Function unknown. Increased in (NAACP): Neoplasms,. Allergens, Addisons, Collagen vascular diseases, Parasites • Monocytes: Second line of phagocytic response (replaces neutrophil within 24 hours).

Activated into macrophage at inflammatory site. A Macrophage is an aggressive phagocytic, bactericidal, & long-lived cell. It processes antigen & delivers them to lymphocytes for specific antibody production.

• Lymphocytes: Possess cellular mediators for immunity. B cells are produced from bone marrow & produce specific antibody. T cells are produced from thymus & produce specific sensitized lymphocytes.

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Laboratory diagnosis of infection: Leukocytosis (increase WBC's) with a shift to the left (increase band cells).

During acute infection, the body tries to fight the infection by increasing the number of WEC' s, specifically neutrophils. Unfortunately, the neutrophils do not have time to mature before they are needed to try to "kill" the infection and band cells are produced.

B. Chemistry Panel: 1. BUN: Measures hydration state. Less specific for renal function. BUNICr may be elevated in

dehydrated state. Follow levels closely 2. Creatinine: Best hematologic index of renal function. Use to measure creatinine clearance for

proper antibiotic dosages. 3. Glucose: Stress of infection may cause an increase & may complicate wound healing. 4. Electrolytes: Na, K Cl, CCh.

C. Second Line Tests: 1. Erythrocyte Sedimentation Rate (ESR):

a. Detennined by measuring the distance in mm a column of erythrocytes falls in 1 hour. b. NON-SPECIFIC: inflammation, infection, malignancy, renal disease, connective tissue

disease, age. c. Use as a baseline to monitor effectiveness. Draw every 5-7 days.

2. C-Reactive Protein: Similar to ESR but more difficult to perform & more expensive. 3. Urinalysis: (+) leukocytes & nitrates (probable UTI). If there are an increase in the squamous

epithelial cells, the sample was probably contaminated (need to repeat test). Check urine culture to detennine specific organism(s).

4. Blood Cultures: a. Used to diagnose bacteremia; however, most bacteremias are intermittent & a (+) culture

can be difficult to obtain. b. Take as soon as possible after the onset ofa fever (usually 101). c. Need 2-3 cultures at least 20 minutes apart & from different sites. This increases the

chances of catching the organism. d Must utilize aspetic technique to avoid skin contaminants.

DECISION MAKING

#1 Does tbe patient need to be admitted? • Outpatient versus Inpatient therapy. • Oral antIbiotics versus IV antIbiotics.

1. Outpatient Therapy: a. Localized signs of infection with no systemic manifestations. b. Benign medical history (patient is not immunocompromised). c. Can be sent home on oral antibiotics.

2. Inpatient Therapy: a. Extension of infection. b. Systemic manifestations. c. Need IV antibiotics. d Require surgical intervention. e. Immunocompromised host.

• Diabetes • Peripheral Vascular Disease (vascular surgery consult)

• HIV • Cancer • Rheumatoid Arthritis • Steroid Therapy • Elderly

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Jmmunocompromised patients may not be able to elicit an inflammatory response & the infection may look benign. The typical redness, rn-elling. & heat may not be present but this does not mean that the infection is localized. Their immune system cannot fight the infection as effectively as a healthy patient: therefore, what may look benign can tum into a rapidly progressing & fatal infection. Caution should be used with these patients and hospitalization even for localized infections should be considered

#2 Is surgical intervention necessary? • Bedside debridement versus OR I&D

1. Bedside Debridement: a. Localized infection. b. Neuropathic patients. c. Better evaluation of the wound

2. Operating Room Incision & Drainage: a. Unknown extent of infection. b. Wound probes to bone or bone is exposed c. Wound tracks up fascial planes or tendon sheaths. d Abscess. e. Gas in soft tissues: Needs immediate I&D.

XIII. Treatment: A Systemic Therapy (Antibiotics):

1. Oral versus IV. 2. Choose according to clinical scenario:

a. Diabetes: polymicrobial b. Cellulitis: Group A Strep, Staph aureus c. Gas: clostridium d Foul odor: anaerobes e. Fruity odor: pseudomonas f. Jnterspaces: gram ( -) g. Golden purulence: Staph aureus

3. Start broad & narrow spectrum pending culture results & sensitivities. Good options for intial therapy are Ancef7Flagyl or BactrimlFlagyl or Unasyn (will vary depeding of hospital micro. resistance profile)

4. Obtain cultures before starting antibiotics. May get negative cultures if patient is already on antlbiotics.

5. Calculate Creatinine clearance prior to dosing Abx B. Local Therapy (Wound Care):

1. Incision & Drainage: a. Use general anesthesia or spinal if extent of infection is unknown. Infection may track

up leg beyond the boundaries of a local block. b. Don't use a tourniquet Need to differentiate healthy, bleeding tissue from necrotic

tissue. If a tourniquet is used, drop it before final debridement to ensure adequate debridement.

c. Plan all incisions. Final goal is wound closure. d Debridement (Remember the 3 D's: debridement, drainage, decompression):

• Do not separate tissue planes. Initial incision should be down to bone. • Resect all infected, necrotic soft tissue and bone. • Careful handling of skin edges, especially in patients with PVD.

e. Cultures: • Soft tissue swabs: gram stain, aerobic, anaerobic, fungal, acid-fast. • Bone: obtain pieces for culture & biopsy. • Request sensitivities on all cultures

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f. Irrigation: • Need high power for lavage. Pulse lavage apparatus or 60cc syringe with an 18

gauge blunt tip needle. The high power and pressure facilitates debridement. • lrrigant solution is irrelevant, usually use normal saline. • Adding antibiotics to irrigant solution offers no benefit.

g. Wound should be packed open: • Use plain Nu Gauze packing on smaller wounds & 4X4 gauzes or Kerlix on larger

wounds. • Perform daily dressing changes on wound & monitor for signs of healing. • When all signs of infection have been irradicated wound can be closed, usually 3-4

days after initial 1&D.

2. Daily Wound Care (Bedside): a. Irrigation. b. Local debridement. c. Packing. d. Wet to Dry Dressings:

1. Absorbs fluid exudates. 2. Facilitates debridement upon removal. 3. Solutions:

• Saline: isotonic, drying. • Betadine: drying, antimicrobial, can be caustic to tissues. • Dilute Betadine: less drying & less caustic to tissues. • Dakins (hypocblorate, usually 114%): antimicrobial, promotes granulation

tissue. • Acetic Acid (usually WYO): antimicrobial, good for pseudomonas.

e. Monitor for healthy tissue. Final goal is wound closure. f. Biologic & Synthetic Membrane Dressing:

I. Not used often, but if desire to use, granulation tissue must be present. 2. Materials:

• Porcine skin graft. • Amniotic membrane. • Epiguard: A synthetic membrane with 2 layers. The inner layer is made of

polyurethane. Granulation tissue grows into & attaches to this layer. The outer layer is composed of teflon. This layer is breathable and bacteria impermeable.

g. Elevate limb. This encourages venous & lymphatic drainage to reduce edema & improve local blood flow. Patients with compromised circulation should have legs level in bed, not elevated

3. Wound Closure: a. Primary Closure: never use unless all necrotic tissue is excised & no signs of infection

exist. b. Delayed Primary Closure:

• Usually 3-4 days after initial 1&D. • Excise all necrotic, non-viable tissue. • Obtain bleeding skin edges. • Irrigation.

• Culture. • Suture: Avoid closure of deep tissues. Utilize non-reactive materials (Nylon,

Prolene). c. Secondary Intention: for large wounds that cannot be reapproximated d. Skin Grafts (Apligraft}

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·Patients with severe PVD require lower extremity bypass surgery or angioplasty prior to closure

Osteomyelitis

I. Definitions: A. Hematogenous Osteomyelitis: Usually occurs in children & is primarily a medically treated disease.

When it occurs in adults, it is usually a smgically treated disease. Now increasing incidnce in the elderly >50 yrs -Primarily long bones LE and the hwnerus -Vertebrea in 1he elderly -So Aureus, S1rep in neoneates Lew and Waldvogel, NElM' 336: 1997

-GNRs in elderly, immlDlocompromised patients -Pseudomonas in IVDAs and long tenn indwelling urinary ca1hetcrs

B. Contiguous Osteomyelitis(direct extension): Direct infection of bone from and exogenous source or spread of infection from a near by infected focus. -Prothesis, implants, open fractw'es primary concerns con

C. Osteomyelitis in a patient with vascular impairment: These patients have difficulty mounting an inflammatory response. They also have poor delivery of antIbiotic to the infection site. -vascularity needs to be addressed to insme adequet healing

D. Acute Osteomyelitis: Suppurative infection accompanied by edema, vascular congestim, & small vessel thrombosis.

E. Chronic Osteomyelitis: Nidus of infected dead bone or scar tissue, an ischemic soft tissue envelope, & a refractory clinical course.

F. Sequestrum: Piece of necrotic tissue, usually bone, that has become separated from smrolDlding heal1hy tissue.

G. Involucrum: The sheath of new bone that forms around a sequestrwn. H. Brodie's Abscess: A chrmic abscess of bone surrolDlded by dense fibrous tissue and sclerotic bone.

II. Classification: Waldvogel

Hematogenous Osteomyelitis Contiguous Focus Osteomyelitis Osteomyelitis associated with Vascular Disease Chrmic Osteomyelitis

III. Clinical Evaluation: (Please see infection work-up.)

IV. Imaging Modalities: A. Radiographs:

Oemy-Mader Anatomic Stage

1. Medullary Osteomyelitis 2. Superficial Osteomyelitis 3. Localized Osteomyelitis 4. Diffuse Osteomyelitis

Physiologic Stage A. NormalHost B. Systemically Compromised

Host (BS) Locally Compromised Host (BL) C. Treatment is worse than the

Disease

l. Need 30-50% resorption to detect osseous changes on x-ray. This can take 10-14 days. 2. Always take x-rays for an infection. Can act as a baseline & monitor the regression or

progression of the infectious process. 3. Signs (In order by which appears first):

• Soft tissue swelling. • Periosteal reaction (thickening or elevatim). • Focal osteopenia.

B. Please refer to Radiology of Infection for bone scans, MRI. & CT.

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v. Diagnosis: A. Bone biopsy:

1. Definitive diagnosis. 2. Bone culture & microscopic examination of bone. 3. Utilize imaging modalities to determine best area to take biopsy.

B. Hematogenous Osteomyelitis may be diagnosed with positive blood cultures with a positive bone scan.

VI. Treatment: A. Primary Goals:

1. Adequate drainage. 2. Thorough debridement. 3. Obliteration of deadspace. 4. Antimicrobial coverage.

B. Primary Surgical: 1. Debridement of all nonviable & marginally viable tissue. 2. Antibiotic Polymethylmethacrylate Impregnated Beads (PMMA):

a. Indications for use: • Deadspace maintenance followed by bone grafting, bone fusion, or primary closure. • Debridement & closure. • Combined debridement & internal fixation procedure. • Systemic disease which contraindicates adequate systemic levels of organ toxic

antibiotics, such as aminoglycosides. b. Gentamycin is the traditional antibiotic used with PMMA beads because it is not heat labile

and the curing process of the PMMA is an exothermic process. Other antibiotics may be used; however, the antibiotic must be added in the dough phase of the PMMA. This prevents the heat degradation of the antibiotic. Antibiotics that have been used include:

• Gentamycin • Cephalosporins- Cefazolin, Moxalactam, Cefotaxime

• Tobramycin • Vancomycin • Ticarcillin

c. Procedure: • Mix & construct the beads on a wire and place in the wound. • Close the wound over the beads. • Leave the beads in for about 2-4 weeks.

d. Mechanism • Immediate ans sustained release of antibiotic in the local area • Release of antibiotic declines exponentially with time

3. Ingress-Egress Systems: a. Closed suction irrigation. A closed system in which continual flushing of the wound is

accomplished through inflow tubing (ingress) & outflow tubing (egress). There are many problems with this system, such as contamination of the outflow tubing (usually pseudomonas).

4. Bypass Surgery: (Consult vascular surgery for options.)

C. Secondary Surgical- Reconstructive: 1. Papineau bone graft: This technique is for filling bone defects. SmaIl cancellous chips are

packed into bone deficits when the wound is granular. This graft is given time to take then various closures can be used.

2. Bone Fusion: Used after resection when infections are near articular surfaces. 3. Delayed primary closure. 4. Tissue transfer/Skin grafting. 5. Bead therapy, bone grafting, & closure.

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VII. Follow-Up: A. Goal is to prevent rectnTence. B. Antibiotics:

1. Customarily 6-8 weeks following last surgery or since initial clinical resolution of infection when no surgery has been performed.

2. The word "cure" is inappropriate. It is possible for an area to activate for up to 20 years. 3. Follow-up intervals:

• First 6 months: every month. • 6 months-I year: every 3 months. • 1 year-2 years: every 5 months.

Local Antibiotics/Antibiotic Beads

The implantable admixture of antibiotic to any of several carriers for the purpose of localizing increased antibiotic concentrations at specific target tissue sites.

Selected antibiotic should meet the following criteria: A. H2O soluble B. nontoxic to tissue C. bactericidal (preferably) D. available in powder form E. heat stable if used with PMMA

Carriers may be: A. biological

1. cancellous bone graft 2. demineralized bone matrix 3. Ca ++ hydroxyapatite

B. biologically inert 1. polymethyl methacrylate (PMMA) 2. plaster of paris

* commercially prepared antibiotic carriers are available in Europe, and are expected to be available in the United States after further investigation of possible toxicities

Miclau et al compared the elution oftobramycin from various carriers, and found: A. cancellous bone graft eluted 70% of its antibiotic within the first 24 hours of implantation, and

had non-measureable levels at 14 days B. demineralized bone matrix released 45% of its antibiotic within the first 24 hours of

implantation, and had non-measurable levels at 14 days C. plaster of paris eluted 17% of its antibiotic in the first 24 hours after implantation, with

measurable levels of antibiotic up to 21 days post-implantation D. PMMA eluted 7% of its antibiotic within the first 24 hours of implantation, with trace amounts

measurable up to 14 days post-implantation

PMMA, the most commonly used carrier for implantable antibiosis, usually comes in half-packs (20 g) or full-packs (40-60 g); consists of

A. monomer (liquid) B. polymer (powder) * the monomer and polymer are mixed together (an exothennic reaction) with the antibiotic

powder ootil a doughy consistency is achieved, at which time small beads are fashioned and placed on 26 or 28 gauge wire like pearls on a necklace. The hardened beads are then implanted into a dead space in which high local levels of antibiotic are desired, typically within an area of debrided osteomyelitic bone or the space previously occupied by osteomyelitic bone after resection. (N.B. no one wearing contacts should be in the surgical suite during preparation of the beads, as offensive vapors have been linked to morbidity with those individuals)

33

Suggested Ratio of Antibiotic:PMMA

Antibiotic Amount of Antibiotic AmountofPMMA

Cefazolin 4-8 g 40-60 g

Cefotaxime 4-8 g 40-60 g

Nafcillin 4-8 g 40-60 g

Tobramycin 5-10 g 40-60 g

Vancomycin 4-8 g 40-60 g

Ticarcillin 6-13 g 40-60 g

Clindamycin 4-8 g 40-60g

Diffusion (Elution) of Antibiotic from PMMA depends on: A. type of cement used (Palacos vs. Simplex vs. CMW) B. coefficient of diffusion for each antibiotic C. concentration of antibiotic within the bead D. size/surface area/roughness of the bead E. amount of fluid that moves past the bead

Bead Properties A. smaller beads = more surface area to total volume, leading to increased elution rates B. higher concentrations of antibiotic within a bead leads to increased pore size and roughness,

each leading to increased rates of elution C. Ciemy proposed a ratio of 1:5 when adding antibiotic powder to the PMMA powder; e.g. for

every 109 of powdered PMMA polymer, add 2 g powdered antibiotic, stating that any higher ratio would prevent proper hardening of the PMMA

D. most studies conducted with 1-2 g antibiotic to 40-60 g PMMA in literature

Complications with Antibiotic-Impregnated PMMA Beads: very few A. if the cement is used for fixation, mechanical strength is compromised with greater than 1 ()O/O

antibiotic content (not an issue with beads) B. care should be used in patients with renal disease, though local antibiotic concentrations 10-50

times greater than the toxic serum levels can be achieved without the serum ever absorbing enough to achieve those toxic levels

C. no allergic reactions have been reported to date in the literature

Disadvantages A. second procedure required for bead removal, typically after 10-14 days

SEPTIC ARTHRITIS

Infectious arthritis stands apart from other rhemnatic disocders because cure rather than mere control is possible. Whether oc not this goal can be achieved depends upoo the type of ocganisrn, promptness in initiating therapy, medical status of the individual, and prioc status of the involved joint Almost any pathogen may affect articular cartilage and periarticular tissues. A multitude ofbacteria, viruses, mycobacteria, and fimgi have been associated with arthritis.

MECHANISMS OF SEPI'IC ARTHRITIS

I. DIRECT JOINT INVASION BY THE MICROBE : pathogens may invade the joint directly and produce on-going inflammation and destruction. Examples include direct joint innoculation (puncture wound) oc hematogenous spread.

2. JOINTS MAY BE AFFECTED INDIRECIL Y AS A RESULT OF:

34

A the resulting immune response of the affected host For example, in Hepatitis-B arthritis circulating imnnme complexes appear to mediate the polyarthritis that accompanies the prodromal stage of this infection.

B. miaobial debris that may persist in the joint and perpetuate an inflammatory respoose. even after the organism is no longer in the joint. This appears true in some cases of gonnococca1 arthritis in which an on­going synovitis is associated with sterile joint fluid that is non-inflammatory, so called " post-infectious sterile arthritis."

c. unknown mechanisms. This applies to almost all of the reactive arlhritides, such as those associated with gastrointestinal infections with some of the enteric gram negative organisms (Shigella sp., Yersinia sp.).

ACUTE BACI'ERIAL ARTHRITIS

PREDISPOSING FACTORS AND ASSOCIATED CONDITIONS

1. Rhewnatoid arthritis

possible mechanism for association damaged joint is a good nidus for infection compromised defenses from medications defective phagocytosis (?)

important clinical features usually due to Staph. aureus treatment results often poor

2. Crystal-induced arthritis

possible mechanism for association synovial fluid acidosis may promote crystal deposition enzymatic" strip-mining" of cartilage

important clinical features identification of crystals in the joint does not rule out septic arthritis

3. Severe osteoarthritis, Charcot joints, Hemarthroses

possible mechanism for association • joint disorganization, chronic synovitis, and bloody effusions all provide nidus for bacteria

important clinical features • always send bloody joint fluid for culture

4. Chronic systemic disease (SLE, sickle cell anemia, cancer, etc.)

possible mechanism for association • impaired generalized defenses due to chronic illness, phagocytic deficiencies, and medications

important clinical features • often due to Staph aureus or gram negative bacilli • consider Salmonella sp. in patients with sickle cell

35

ACUTE BACTERIAL ARTHRITIS

PREDISPOSING FACTORS AND ASSOCIATED CONDmONS

I. Rheumatoid arthritis

possible mechanism for association damaged joint is a good nidus for infection compromised defenses from medications defective phagocy10sis (?)

important clinical features usually due to Staph. aureus treatment results often poor

2. Crystal-induced arthritis

possible mechanism for association synovial fluid acidosis may promote crystal deposition enzymatic" strip-ruining" of cartilage

important clinical features identification of crystals in the joint does not rule out septic arthritis

3. Severe osteoarthritis, ChaIrot joints, Hemarthroses

possible mechanism for association • joint disorgmization, chronic synovitis, and bloody effusions all provide nidus for bacteria

important clinical features • always send bloody joint fluid for culture

4. Chronic systemic disease (SLE, sickle cell anemia, cancer, etc.)

possible mechanism for association • impaired generalized defenses due to chronic illness, phagocytic deficiencies. and medications

important clinical features • often due to Staph aureus or gram negative bacilli • consider Salmonella sp. in JB1ients with sickle cell

PATHOGENESIS

Acute bacterial arthritis occurs most often by hematogenous dissemination from a primary source of infection. However, joint sepsis may also result from the extension of an adjacent soft tissue infection or adjoining osteomyelitis.

Three stages of cartilage destruction have been described:

36

1. Initial events include liberation of lysosomal enzymes from PMN's and synovial lining cells resulting in the loss of proteoglycan from cartilage. If the infectious process is resolved early, a restomtion of proteoglycan matrix may be achieved and chondrocyte damage avoided.

2. Dming the second stage, increased mechanical stress and inadequate nutrition result in chondrocyte damage.

3. In the last stage, enzymes released from PMN's and synovial lining cells with the altered joint mtrlJanics gradually destroy the collagen network.

CLINICAL FEATURES

Septic arthritis usually affects one joint, but may involve two or more joints. The involved joint is geneI3lly red, hot, swollen and acutely painful. There is also extreme pain and limitation with range of motion. The knee followed by the hip and ankle are the most commonly involved joints in non-gonococcal septic arthritis.

Systemic features include fever ( may be low gtade ), chills and rigors. A careful physical exam may reveal an infectious focus involving any site, but the usual sowces include the skin, nasopharynx, sinuses, lungs, cervix, and the rectum.

JOINT DISTRIBUTION %OFCASES

JOINT ADULTS ClllLDREN

knee 55 40 hip 11 28 ankle 8 14 shoulder 8 4 wrist 7 3 elbow 6 11 others 5 3

LABORATORY TESTS

Peripheral leukocytosis occurs in the majority of patients with acute bacterial arthritis. An elevated ESR is also genetally found.

Patients suspected of having septic arthritis should have blood cultures and cultures of regions that may be the primary SOUICe of infection ( physical examination will help to determine areas that may need to be cultured ). Blood cultures may be positive in up to 75% of patients.

A diagnosis of septic arthritis is established by gram stain and a positive synovial fluid culture. A typical joint infection demonstI3tes a purulent effusion with a synmial fluid white count greater than 50,000 cellsIcmm and more than 9()01o PMN's. Gram stain and culture are obligatory if septic arthritis is suspected.

INCIDENCE OF ORGANISMS IN ACUTE BACTERIAL ARTHRITIS IN ADULTS

Gram-positive cocci

Gram-negative cocci ( N. gonorrhoeae )

Gram-negative bacilli

TREATMENT

45%

50%

5%

1. Treatment should begin immediately after the suspicion and/or confirmation of the diagnosis.

37

2. Antibiotics are chosen primarily on the basis of the synovial fluid gram stain and are acljusted based on the culture results. 3. Oosed needle aspiration should be performed at least once daily to drain the affected joint. 4. Open surgical drainage is indicated if there is a lack of response to therapy ( joint fluid cultures remain persistently positive or patients remain febrile after 3-4 days of antIbiotic therapy ); Some studies espouse immediate open surgical drainage. S. The infectedjoint should be kept at rest to prevent mechanical stress; generally using a splint will provide adequate immobilization and reduce pain and trauma 6. As joint symptoms resolve, passive range of motion exercises should be started to avoid joint contractures. 7. Weightbearing should be deferred until inflammation has completely resolved

SYNOVIAL FLUID EXAMINATION (IMPORTANT POINTS)

Cultures are nearly 100010 positive in non-gonococcal bacterial arthritis, but only 2S-S0% positive in gonococcal arthritis.

Gram stain smears are approximately 7S% positive with gram positive cocci, SO% with gram negative bacilli, and less than 25% in gonococcal arthritis.

1be leukocyte and differential leukocyte counts are generally greater than SO,OOO cellslcmm and greater than 80% PMN's, but these results can also occur with noninfectious inflammatory arthritis.

Synovial fluid glucose is less than 50% fasting, simultaneous serum glucose but may not be present and may be seen with Rheumatoid arthritis.

RADIOGRAPIDC TESTING

Radiographic examination of affected joints may reveal only soft tissue swelling early in the course of the disease. Juxta-articular osteopenia appears about 7-10 days after the onset of joint infection. If the joint infection is not eradicated, progressive joint space narrowing may develop. Late radiographic findings include joint subluxation and eventual joint destruction.

Radioisotope scanning may be helpful in localizing sites of infection, however the findings are non-specific and radionuclide imaging generally has little role in the initial evaluation of acute septic arthritis.

RADIOGRAPIDC-PATHOLOGIC CORRELATION

PATHOLOGIC ABNORMALITY

edema and hypertrophy of soft tissue

synovial membrane with fluid production

hyperemia

inflammatory pannus with chondral destruction

pannus destruction of bone fibrous or bony ankylosis

CHaDHOODSEYnCAR~TIS

BACIERIA (# OF CASES) < 2 YRS 2-6YRS >6YRS

RADIOGRAPmC ABNORMALI1Y

joint effusion,

swelling

osteoporosis

joint space loss

marginal and central erosions bony ankylosis

TOTAL

38

S. aureus 49 36 81 166(34%) H influenza 154 19 1 174(36%) Streptococci 27 23 24 74(15%) Gram neg. 24 9 6 39 (SOlo) bacilli S. pneumoniae 23 4 3 30(6%)

482

From series by Fink and Nelson. Speiser et al, PeltoJa and Vahvaven, Borella et el., and Samilson et a1.

39

INODENCE OF ORGANISMS IN CHILDHOOD SEPTIC ARTHRITIS

Gram-positive cocci 70%

Gram-negative cocci 5%

Gram-negative bacilli <15%

H. influenza 10%

GONOCOCCALAR~ (DISSEMINATED GONOCOCCAL INFECTION)

Gonococcal arthritis is the most common form of acute bacterial arthritis. Joint involvement occurs during dissemination of the gonococcal infection from a primary source of infection.

CLINICAL MANIFESTATIONS

The organism initially infects mucosal cell surfaces. Typically the primary infection involves the reproductive or~ but may involve the pharynx or rectum.

Disseminated gonococcal infections occur in approximately 1-3% of all primary infections. Dissemination seems to occur more commonly in females, generally around the time of menstruation. *** An important note is that patients with complement deficiencies are at an increased risk of gonococcal bacteremia.

Most patients with disseminated gonococcal infections are less than 40 years of age and relate a history of promiscuity and unprotected sexual intercourse. Again the primary sites of infection are the urethra in males, cervix: in females, auf the rectum and phaIyn.x in both sexes.

Patients disseminated disease may have systemic findings that include fever, chills, and malaise. A migratort polyarthritis is the most common initial joint manifestation, and subsequent findings may localize to one or more joints. Any joint may be involved

Peri-articular pain and swelling are common, and tenosynovitis is found in a significant number of patients. Typical skin lesions are a frequent manifestation, generally beginning as smaI1 erythematous macules, which may develop into pustular lesions characterized by a grey, necrotic center with a hemhorragic base.

LABORATORY TESTS

Peripheral leukocyte counts may be normal or moderately elevated Synovial fluid analysis reveals an inflammatory fluid with a variable number of white cells ranging from a few thousand to several hundred thousand per cubic millimeter. Joint fluid cultures are positive in less than half of all patients even under ideal conditions.

DIAGNOSIS

Disseminated infection should be suspected in young, sexually active [patients who develop an acute migratory polyarthritis, tenosynovitis, and/or a characteristic rash. Primary source and joint cultures along with synovial fluid analysis should be performed

40

TREATMENT

1. Antlbiotics : Ceftriaxone ( Rocephin ) IM/IV or ~QxDne(~ox)rvor

Cefotaxime ( C1afman ) IV then, Cefuroxime axetil ( Ceftin ) po or Amoxici1IinlclavuJanate ( Augmentin ) po or Ciprofioxacin ( Cipro ) po

Parenteral antiobiotics are generally contimJed for 24-48 hours until symptoms begin to resolve, and then patients are switched to enteral antibiotics to complete a 7-10 day course of therapy.

2. Joint aspiration

3. Joint immobilization

VIRAL ARTHRlTIS

Viral arthritis often begins with non-spec.ific symptoms such as ma1aise and fatigue, headache, neck. stiffness, sore throat, and nausea and vomiting. Joint involvement is generally polyarticular, and the arthritis is usually short-lived and rnrely results in joint damage. Laboratory tests are non-specifi.c. The following are some of the most conunon causes of viIal arthritis :

1. Hepati.tis-B - joint manifestations may be seen in 10-30010 of patients . The arthritis is generally self-limiting. 2. Rubel1a - may occur in natural rubella infection or after immunization ",ith the live attenuated "irus. 3. Parvovirus B 19 4. HlY related arthropathy

FUNGAL ARTHRITIS

A wide variety of fungi may cause joint infection, which may arise either from direct extension from a focus of osteomyelitis or by hematogenous dissemination. The arthritis is usually monolpau.ciarti.cular, most often in large weighfuearing joints, and generally follows a chronic or indolent course. Synovial fluid analysis and allture are variable, often providing little to no diagnostic value. Fungi that may be associated with infectious arthritis may be grouped as superficial or deep organsims. Although normal hosts may develop fungal arthritis, there is usually some predisposing factor that increases susceptIbility to infection. The diagnosis can be made by synovial fiuid culture or synovial tissue biopsy.

SUPERFICIAL Sporothrix schenckii Candida albicans Actinomyces israelii " Maduromycoses"

DEEP Aspergillus fumigatus Histoplasma capsuIatum Cryptococcus neoformans Coccidioides immuns, Blastomyces dermatitidis

MYCOBACTERIAL BONE AND JOINT INFECTIONS

Extrapulmonary tuberculosis occurs in approximately 1-2.6% of patients with tuberculosis.

It is generally believed that skeletal TB is caused by dissemination of bacilli by hematogenous spread or lymphatic drainage:from another area of lB. TB arthritis most frequently involves weightbearingjoints and is usually monoarticular. A positive tuberculin skin test is obtained in most patients, and in about 50010 a previous personal or family history is present.

S)'U.ovial pathology reveals a chronic granulomatous reaction with giant, Langhan-type cellular infiltration. Acid-f3st staining of the synovium or surrounding tissue may reveal the organisms.

41

Radiographically the affected joint may reveal only soft tissue swelling or more advanced changes with destruction of peri-articular bone, narrowing of the space, and osteoporosis. Chest X-ray abnonnalities of past or present 1B may be present in 50010 of patients.

ARTHROCENTESIS AND SYNOVIAL FLUID ANALYSIS

Synovial fluid is an invaluable source of diagnostic information. One of the most important reasons to perfonn synovial fluid analysis is to rule out bacterial infection in severely inflamed joints. There is no other sufficiently reliable way to differentiate septic arthritis from acute crystal-induced arthritis. Arthrocentesis may be therapeutic as well as diagnostic. For tense effusions in which the intra-articular pressure is higa removal of the fluid will relieve symptoms and at least theoretically decrease joint damage.

TECHNIQUE

1. The joint should be moved through its I31lge of motion to resuspend its contents. 2. Anatomic landmarks defining the joint surface should be identified and may be outlined with a pen or

marker. 3. The specific area of the joint to be aspirated is identified and may be marked with the retracted portion of a

ball point pen. 4. The skin should be cleansed of obvious dirt with soap and water. 5. The skin can be infiltrated with a local anesthetic. 6. A brief scrub with a betadine solution followed by an alcohol swab should provide adequate protection. 7. Do not touch the skin at the aspiration site after cleansing! 8. It is a mistake to select a small needle with the intention of sparing the patient pain. VIscous material flows

with great difficulty, if at all, through needles smaller than 20 gauge. 9. Stretch the skin slightly, penetrate the skin, aspirate gently, and advance the needle slowly until fluid

appears in the syringe. 10. After removal of the needle, apply gentle compression at the puncture site for several minutes. Then apply

a band-id or light dressing.

C. COMPLICATIONS OF ARTHROCENfESIS 1. Iatrogenic infection of a previously sterile joint (it has been estimated that infection occurs in less than 1 in 10,000 instances of diagnostic arthrocentesis ).

2. Bleeding at the puncture site and presumably within the joint; in anticoagulated patients who develop acute arthritis, anticoagulation itself is not a contraindication to arthrocentesis.

3. Possible injury to cartilage by the needle.

4. Occasionally patients may experience a vasovagal ( syncopll ) episode during or after the procedure.

SYNOVIAL FLUID ANALYSIS

I. GROSS EXAMINATION

1. VOLUME : can serve as one measure of the severity of a process, but low volume does not mean the absence of an important intIa-articular rrocess.

2. VISCOSITY : fluid of normal viscosity holds together and stretches approximately one inch before separating. Low viscosity fluid drops from a syringe like water. VIscosity is generally decreased in intlannnatory joint fluids.

42

3. COLOR AND CLARITY: if newspJpef print cannot be read through the fluid, it generally suggests an inflammatory process. The plastic of some syringes makes fluids appear falsely cloudy, so examine the fluid in a glass container (ie. test tube ). NoIIDal and noninflammatory joint fluids are a transparent straw or yellow color depending on the amount of albumin or bilirubin present.

II. MICROSCOPIC EXAMINATION

1. WET MOUNT: Useful for identification of cells, cartilage 1iagments, lipid droplets, cytoplasmic inclusions, and some crystals. Sickled red cells may be seen in effusions of patients with sickle oeIl disease.

2. CRYSTAL ANALYSIS: A polarizing light microscope provides the gold standaId for crystal identification. Monosodium urate crystals of gout are needle shaped or long with blunt ends, and display a strong

negative birefringence. CPPD crystals display a weak positive birefringence. The number of crystals associated with human disease is increasing and includes calcium oxalate associated with renal failure, crystals of protein in dysproteinemic states, cholesterol crystals in chronic inflammatory diseases, and apatites.

3. GRAM'S STAIN: Useful iftbere is any suspicion of joint infection. Based on gram stain finding:; bacteria can classified into broad groups to allow empirical therapy. The following steps are used in preparing a slide:

A flame the smear B. add crystal violet C. Gram's iodine D. wash with 95% alcohol E. safranin

4. OIlIER STAINS:

Prussian blue: stain for iron that may show iron in synovial lining cells in pigmented viUonodular synovitis or hemochromatosis.

Ziel-Nielson : may be helpful in evaluating poSSible tuberculosis.

Congo red : amyloid deposits show an apple-green birefringence on polarized light examination.

Alizarin red S : a calcium stain used for apatite crystals.

ID. SPECIAL LABORATORY JESTS

1. CULTURES: if joint infection is suspected the fluid should be sent for culture and sensitivity. The following type of cultures can be sent: aerobic, anaerobic, gonococcaL fungal, and tuberculosis.

2. MUCIN CLOf lEST: several drops of syno"ial fluid are added to about 20 mI. of 5% acetic acid in a small beaker allowing one minute for a clot to form A " good clot " from notmal or osteoarthritis fluid forms a finn mass that does not fragment on shaking. A n poor clot" like that from many inflammatory fluids fragments easily and forms flakes, shreds, and cloudiness in the surrounding fluid " Good mucin clot " generally reflects the normal integrity of hyaluronate.

43

3. LEUKOCYIE COUNT AND DIFFERENTIAL: will provide infonnation about the level of joint inflammation.

4. GLUCOSE: synovial fluid glucose concentration is normally slightly less than that of blood glucose. A very low level of glucose in the synovial fluid suggests joint infection Occasional effusions in Rheumatoid arthritis have a S)'novial fluid level ofless than half that ofblood

RHEUMATIC DISEASES CHARACTERIZED BY SYNOVIAL FLUID ANALYSIS

NONINFLAMMATORY Osteoarthritis Trauma Osteochondritis dessicans Neuropathic arthropathy Sickle cell disease Osteochondromatosis Hypertrophic osteoarthropathy Ochronosis Hemochromatosis Acromegaly Amyloidosis

HEMORRHAGIC Trauma with or without fracture Postsurgical Pigmented villonodular S}novitis Synovioma Neuropathic arthropathy Hemangioma Coagulation disorders

Hemophilia von Wtllebrand's disease Therapeutic anticoagulation

Sickle cell disease Thrombocytopenia Ehlers-Danlos syndrome Scurvy

CLASSIF1CATION OF SYNOVIAL EFFUSIONS

EXAM NORMAL NONINFLAMM

color straw strawlyellow

WBC(mm3) <200 200-2,000

PMN(%) <25 <25

culture (-) (-)

mucin finn firm clot

INFLAMMATORY Rheumatoid disease Reiter's syndrome Psoriatic arthritis Ankylosing spondylitis Ulcerative colitis Acute crystal synovitis Systemic lupus erythematosus VIral or fungal infections

SEPTIC Bacterial infections

INFLAMM.

yellow

2,000-75,000

>50

(-) often(+)

friable

SEPTIC

variable

>100,000

>75

friable

44

Tuberculosis of Bones and Joints Amer Thoracic AssI.>cAmer J Resp and Clin Care Med, 149:

INlRODUCTION 1. The prevalence of tuberculosis bas been rising since 1986, with moIbidity increasing 14% from

1985 to 1993. 2. Urban areas of developed countries are more likely to encounter patients who have tuberculosis 3. Factors that contribute to increased rate include:

a. suppression of the immune system b. development of drug-resistant strains of Mycobacterium c. aging population d inaeased number of health-care workers who are exposed to the disease

4. mv remains the leading known risk: for the reactivation of latent tuberculosis infection 5. Spinal tuberculosis has existed for at least 5000 years 6. Pott noted the association between tuberculosis involvement of the thoracic spine and paraplegia 7. The sanitarium setting, in the era before antitubercular drugs, was considered to be successful

treatment in that era, still bad a 60% mortality rate within six years after discharge from the sanitorium

THREE RELATED ORGANISMS 1. Mycobacterium tuberculosis - most common 2. Mycobacterium africanum - found outside Northwestern Africa 3. Mycobacterium bovis - found in areas not utilizing milk pasteurization

MYCOBACTERIUM TUBERCULOSIS 4hin rod, with round ends, nonmotile, without capsule, resists decolorization with strong mineral acids and alcohol; hence, is considered an acid-alcohol-fast or acid-fast bacillus. -grows only on enriched medium containing egg and potato base or serum (albumin) base -visible colonies appear at around 2 to 4 weeks, secondary to o~1'gen tension. Increased oxygen tension, as in the lung, allows the organism to grow freely.

INCIDENCE -one-thiId of the global population is infected with Mycobacterium tuberculosis -M. tuberculosis is the cause of 3 million deaths per year -ten million persons are presently infected, and 9()0" of new activated cases come from this infected pool of individuals -in non-Hispanic white people, the median age at diagnosis is 61 years -among the American minority, the median age of diagnosis is 39 years -one-thiId of patents with tuberculosis who are also infected with mv will have extrapulmonary disease, with or without a pulmonary component

SITE OF INFECTION -Tuberculosis has been reported in alI bones of the body -In the U.S., the spine is involved 5OO" of the time

Thoracic spine 50% Cervical spine 25% Pott's Disease- TB of the vertebra Lumbar spine 25%

-other reported areas are less common, pelvis 12% hip & femur loo" knee & tibia 10% nbs 7% ankle or shoulder 2% elbow or wrist 2% multiple sites 3%

-extrapulmonary tuberculosis is more common in children than in adults -most common extrapulmonary involvement in children is the superficial lymph nodes(scrofula)

45

DIAGNOSIS OF MUSCULOSKELETAL TUBERCULOSIS CLINICAL 1. Localized pain 2. Associated fever 3. weight loss 4. truncal rigidity 5. muscle spasm 6. neurological signs 7. cold abscess (swelling without inflammation) - strongly suggestive of TB osteomyelitis

o Tubercular skeletal lesions demands further evaluation of other organ involvement, i.e. lungs, intestinal tract and kidneys. One-third of patients with bone or joint 1B have a history of pulmonaty involvement

PLAIN RADIOORAPHS 1. NO SPECIFIC RADIOORAPIDC FINDINGS 2. osteopenia 3. soft-tissue swelling 4. minimal periosteal reaction 5. narrowing of joint space 6. cysts in bone adjacent to joint 7. enlargement of the epiphysis in children 8. subchondral erosions 9. new-bone formation

BONE SCANS - not terribly helpful

SKIN TESTS ~Koch discovered the material tuberculin that was the antigenic component of Mycobacterium tuberculosis. This was later precipitated out to reveal the purified protein derivative (PPD)

~Interpretation of the PPD test depends on exposure to M tuberculosis, immunosuppresion of the host and Pfe'rious exposure to bacille Calmette-Guerin (bCG).

~at least 20% of debilitated or malnourished patients who have extensive disease have a false­negative skin test ~mv infected patients with concomitant 1B are prone to be anergic and will therefore provide a negative skin-testing.

01HER TESTS 1. ESR - neither specific nor completely reliable 2. ELISA (enzyme-linked immunosorbent assay) - reported sensitivity of 60 - 800/0., but these

tests may be negative for patients who have advanced disease. 3. Chromatography-not widely available 4. Nucleic Acid Probes-not widely available 5. Polymerase Chain Reactions-not widely available

Crn.,TURE ~ultimate diagnosis depends on recognition of Mycobacrerium tuberculosis on either histologic study or culture or both.

BIOPSY ~Biopsy and possible operative treatment are reserved for patients who fail to respond to adequate chemotherapy, who have substantial neurological impainnent(as in rn infected vertebrae), or in whom either resistant strains or other disease entities are suspected.

46

TREATMENT 1. If patient is suspected of having tuberculosis, that patient must be placed in an isolation

room 2. operative intervention should be delayed until the patient is no longer infectious 3. Medical treatment

a. contact Center for Disease Control for most recent guidelines b. consult an infectious~ specialist

4. Antibiosis a. minimum of three dru~ to which the organism is susceptible b. at least one of these dru~ must be bactericidal c. Possible antibiotic selection includes, but is not limited to,

Isoniazid 3-5 mg/kglday Pyridoxine 10 mg QD Rifampin 10 mg/kglday Pyrazinamide 20-25 mg/kglday Ethambutol 15-25 mglkglday StreptomycinlS-20 mglkglday

5. Optimum duration of treatment, 6-9 months for patients with pulmonary involvement alone. Patents with extrapulmonary tuberculosis require 12-18 months of treatment

MANAGEMENT of HIV L Definition: a human retrovirus that infects lymphocytes and other cells bearing the CD4 surface marker. Infection leads to lymphopenia, CD4lymphocyte deficiency and dysfunction, impaired cell-mediated immune response, and polyclonal B-cell activation with impaired B-cell response to new antigens.

1. AIDS: characterized by opportunistic infections and unusual malignancies

II. Standard of Care 1. Document CD4 count every 3-4 months as long as CD4>50. Do not need to follow CD4 count<50.

Viral load testing every 3-4 months.

2. All HIV -infected patients should have the following regardless of CD4 count: A PPD/anergy panel

1. IfPPD is (+) give INH for I year. 2. Anergy panel-Checks the ability to host an immune system response. Want it red and

raised. B. RPRlFfA: IfRPR is reactive, get an LP. C. Pneumococcal vaccine: Get every 3-5 years. D. Influenzal shot: Get every year. This is controversial. E. Hepatitis screen and heptavax series if HBV serology is negative. F. Cervial pap smear for all women eveyr 6-12 months. G. Toxoplasma titer.

3. CD4 of 500 begin combination antiretroviral therapy using: A AZT 200mg TID + a second reverse transcriptase inhibitor +/- a protease inhibitor.

1. AZT: can cause megaloblastic anemia, neutropenia, GI effects, anxiety, dark blue nails. B. Other nucleoside reverse transcriptase inhibitors include:

1. DOl: can cause pancreatitis, peripheral neuropathy. 2. DOC: can cause month ulcers, peripheral neuropathy. 3. D4T 4. 3TC: has the least amount of side effects.

C. Protease inhibitors: (saquinavir, indenovir, nalfinC\ic, ritonavir, amprenovir) 1. Decrease ~iralload markedly and prolong life. 2. Be selective with patient: Have to be compliant with medication. If doses are missed

resistance can form

47

D. Nonnucleoside ribonuclease reverse transcriptase inhibitors: 1. viramine 2. delavadine 3. efavirenz

4. CD4,200 begin PCP (Pneumocystis carinii pneumonia) prophylaxis: A. PCP prophylaxis should be started regradless of CD4 count if patient has oropharyngeal candidiasis

(thrush), fevers, weight loss/wasting syndrome. B. PCP prophylaxis drug therapy:

l. Bactrim I DS on Mon., Wed, and Fri. This is the drug of choice. Can cause rash, fever, neutropenia, GI effects, liver dysfunciton.

2. Dapsone: Second drug of choice. Must check for G6PD-can cause hemolytic anemia. May also use dapsone plus pyrimethamine.

3. Aerosolized pentamidine: Third drug of choice. Can still get PCP in upper lobes. Can cause cardiomyopathy, damage to retina. Can also give monthly IV pentamidine.

C. To diagnose PCP: 1. WH wil be increased 2. If gallium scan is (=) possible PCP, if (-) definitely NOT PCP. 3. Get ABG, ifp02<75, start tapering doses of steroids (ie, prednisone 40mg BID x 5 days,

40 mg QD x 5 days, 20 mg QD x 5 days). 4. Bronchoscopy.

D. PCP tretment: 1. Bactrim 2. Pentamidine: Second drug of choice. Must correct for renal insufficiency. Can cause

pancreatitis, life-threatening hypoglycemia and hypertension.

5. CD4<75 begin MAC (Mycobacterium avium complex) prophylaxis: A. Rifabutin: Drug of choice for prophylaxis. Can cause GI effects and hepatotoxicity. Second line

choices include clarithromycin or azithromycin. B. Can cause bone marrow suppression and pancytopenia Need to check AFB in blood. May also be

found in respiratory or GI tract. C. Treatment for MAC is for life. Usually clarithromycin + one other drug (ethambutol, clofazimine,

ciprofloxacin, rifabutin). 6. CMV (cytomegalovirus):

A Retinits: Most common place it presents. Usually patient is at end stage disease. Treat for life. B. May be found in bone marrow, liver, urine, blood. C. Treatment (There is no prophylaxis available):

1. Ganciclovir. Can cause bone marrow suppression and neutropenia. Oral fonn can be used for CMV colitis.

2. Foscamet: Assocaited with renal failure and electrolyte abnormalities. May have some anti-retroviral properties.

D. Recurrences occur frequently and require reinstitntion of high dose induction therapy. E. +Note-CMV, MAC, lymphoma all can present with fever, bone marrow suppression, pmcytopenia,

and an increase in LFT's. 7. Kaposis

A Can be found in skin, mouth, GI tract, liver (can cause biliary obatruction), lung (these bleed easily- prognosis very poor).

B. Treatment is chemotherapy. Intralesion interferon can be injected for skin lesion. 8. TB

A. Rise with increase in my. With this see an increase in extra-pulmonary TB. B. If patient has been incarcerated, homeless, or lived in a shelter, should be tested for TB. C. Treatment for patients with HIV and 'IB should be for one year.

9. Peripheral neuropathy: A About 50% ofHIV patients will have this. B. Treatment:

1. Elavil: as much as their blood pressure can tolerate.

48

I I I

2. MoIpbine. 3. Mexilitine.

10. Other possible infections: A Toxoplasmic encepablitis: Prevention-do not eat raw meat, wash all vegetables, stay away from

cats. Prophylaxis is Bactrim or dapsone plus pyrimethamine. B. Cryptosporidosis: Found in contaminated drinking water. No available prophylaxis. C. Cryptococcus: Avoid sites contaminated with pigeon droppings. Treatment is fluconazole. D. Coccidiomycosis: F01D1d in soil, fanns. Preferred treatment is fluconazole. "Alternate drugs

include itraconazole, ketaconazole, amphotericin B. E. Histoplasmosis: F01D1d in chicken coops. caves, bini roosting sites. Treatment is fluconazole. F. Candidiasis: F01D1d on mucosal smfaces and skin. Treatment is an oral azole (fluconazole).

Can also use topical nystatin or clotrimazo1e. Herpes Simplex: Treatment is acyclovir until lesions have resolved. Can use IV

foscamet for strains resistant to acyclovir. H. Varicella-Zoster: Effectiveness of acyclovir is questionable. 1. Human Papillomavirus: May need biopsy of cervix. 1. Bacillary angiometosis: Looks similar to Kaposis. Treatment is erythromycin. K. Seborrheic Dermatitis.

NEUROLOGY

Nemologic disonlers may lead to various lower extremity manifestations including cavus deformities, equinus, pes planus, spasticity, paralysis, gait abnormalities and diminished sensation

1 DIAGNOSTIC WORKUP:

l.History of illness - Should be obtained from all available sources. - Utilize a problem oriented fonnat i.e.NLDOCAT.

a. Patient b. Family/Guardian

if patient is a child, ascertain pregnancy course delivery, APGAR score, developmental milestones.

c. Other healtbc.are professionals 2.Past medical history 3.Past surgical history 4.Cunent medications 5.Family history 6.Social history - occupation, EtOH, illicit drugs, SID'slHIV

II. PHYSICAL EXAM -a complete neurologic exam should be performed. Neurology consultation is highly recommended.

1. Mental status check - obtained by obseIvation and. during history taking. - Assess general appearance, level of consciousness, orientation, affect, cognition.

49

2. CI3Dial nerves I. Olfactory- sense of smell II. Optic- visual acuity and fields

aanopsia- loss in 1 eye b. bi-temporal hemianopsia- loss temporal fields c.homonymous hemianopsia-loss complete field,L or R (see Fig. 1)

ill. Occulomotor »> IV. Trochlear »»» extraocular eye motions VI. Abducens »> V. Trigeminal- Motor- muscles of mastication

- Sensory- entire face via 3 divisions VII. Facial- Motor- muscles offacial ex-pression

- Sensory- anterior 213 tongue VII. VestIbulocochlear - hearing IX. Glossopharyngeal - sensory posterior 1/3 tongue X Vagus -uvula midline, normal voice, gag response Xl Spinal accessory - Motor sternocleidomastoid and trapezius XII. Hypoglossal - motor tongue

3. Motor exam - evaluate symmetry, function and muscle tone

a Lower extremity

Tl2-L3 - Iliopsoas L2-4 - Adductors, Quadriceps lA - Tibialis anterior L5 - Abductors, EBL, EDL, EDB S I - Gluteus maximus, PL, PB, TP, Gastrosoleus S2-3 - Instrinsics

b. Upper extremity

C5 -Deltoid C5-6 -Biceps C6 - Wrist extensors C7 - Triceps, Wrist flexors, Finger extensors C8 - Finger flexors, C8-Tl - Hand intrinsics

c. Manual muscle test grading

5 - Normal - Complete ROM ag;rinst gravity with full resistance 4 - Good - Complete ROM ~ gravity with some resistance 3 - Fair - Complete ROM against gravity 2 - Poor - Complete ROM with gmity eliminated I - Trace - Evidence of slight contractility. No ROM o -Zero - No evidence of contractility

50

4. Sensation - determine if sensory loss is localized to a single dermatome or stocking-glove distribution

a Posterior colwnns -Vibratory -2-point discrimination -Position sense

't h. OO'erjor spinotha1am.ic -Light touch

\t" c. 8!ternl spinotha1am.ic '1 -Pain and tempeIature

5. Reflexes

a Deep tendon U - Patellar tendon Sl - Achilles tendon C5 - Biceps tendon C6 - Brachimadialis tendon C7 - Triceps tendon

Grading ofDTR's

-!{) - absent + I - hypoactive +2 -normal

+3 -hyperactive +4 - pathologically brisk: / clonus

51

b. Pathological reflexes - assesses UMN dysfunction

Babinski - not present - plantarflexion of toes - Present - dorsiflexion of halllLX and fanning of lesser toes.

6. Cerebellar tests

a.Rhomberg b. Rebound c. Rapidly alternating movements d Heel to shin e. Tandem walking (heel to toe)

7. Orthopedic lower extremity exam

a. assess deformities present - mild, moderate, or severe - flexible or rigid - location - rearfoot, midfoot, forefoot or combination of deformities - compensatory mechanisms present - evaluate weightbearing and non-weightbearing - gait analysis

-sensory ataxic - demyelinating peripheral neuropathies, spinocerebellar degeneration, Vit Bl2 deficiency, M.S. -steppage - peripheral or spinal motor nerve lesions, polio, CMf, progressive muscular atrophy

-myopathic - Muscular dystrophy and other myopathies -<:erebellar ataxic - cerebellar lesions -extrapyramidal- PaIkinson's -spastic - CV A, tumor, tramna, corticospinal lesion, M.S., c.P. -apractic - Alzheimer's, normal pressure hydrocephalus -hysterical

8. Labs and Special Studies

may include CPK, aldolase, EMGlNCV, muscle and nerve biopsies, lumbar puncture, cr scan, MRI, X-rays and other procedures.

ill. Differentiation on Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) dysfunction

Voluntary control Tone Reflex arc Pathologic reflexes Atrophy

UMN LMN lost lost splStic flaccid present absent present not present little or none significant

52

I I I

N. Neurologic Diseases affecting the lower extremities

1. Caws Foot - 75% of patients with a pes cavus deformity will have an underlying neurologic problem (Brewerton et al.) Congenital causes:

CHARCOT-MARJE-TOOm DISEASE (Peroneal muscular atrophy) -most common neuromuscular disorder resulting in cavus foot. Symmetric hereditary motor and sensory nemopathy that is progressive. -3 modes of inheritance l. Autosomal dominant- affects 30/100,000 and is slowly progressive 2. X-linked recessive- affects 3.61100,000 and is more severe, onset during

adolescence 3. Autosomal recessive- affects 1.41100,000, is rapidly progressive and severely

disabling females> males 3-5:1. Seen primarily in Ca)!casians deformities- caws, caVOvarus, equinocavoV311lS due to overpowering of muscles. Rigid or Flexible

CHARCOT-MARJE-room DISEASE (cont) PL> TA produces a plantarflexed medial column TP> PB produces a rearfoot varus

-Contracture of plantar fascia increases cavus -FDL > EDL and intrinsics leads to clawtoes

generalized LE atrophy leads to the development of "stork leg" or "inverted champagne bottle" deformity.

-present with high steppage or marionette gait -progressive atrophy of distal UE leads to "monkey fist" or "skeleton hand" deformity. -Diminished sensation in stocking-glove distnbution -NCVare delayed by awroximately 50010 -Diagnosis based on positive family history and clinical findings. Recently available is a blood test to diagnose the Type I autosomal dominant form.

DEJERINE-SOTTAS DISEAE (Hypertrophic interstitial polyneuropathy) -autosomal recessive -progressive disease with onset in childhood to early adulthood. ~ weakness and sensory loss of primarily the lower extremities. -peripheral nerves are enlarged and frequently palpable due to "onion bulb" fonnation of the nerves -nerve biopsy reveals concentric proliferation of Schwann cells around an area of demyelination.

FREIDRICH'S ATAXIA -recessively inherited disease -idiopathic degeneration of the posterior and lateral colmnns of the spinal cord -onset in late childhood and early adolescence, rapidly disabling. -weakness oflower extremities, anterior and lateral compartments. Later upper extremity weakness, primarily ulnar nerve distribution. -stocking-glove sensory loss. -cerebellar involvement with incoordination, nystagmus, dysarthric speech, ataxia. -no lab abnonnality is diagnostic however, sensory action potentials are absent or markedly decreased NCV remain nonna! or decrease slightly with disease progression.

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ROUSSY-LEVY SYNDROME -autosomal dominant inherited disease -slowly progressive -common findings include resting tremor, clwnsy gait, atrophy of the distal LE's and UE's, abnormal equilibrium, and absent D1R's.

REFSUM'S DISEASE (Heredopathia atactia polyneuritiformis) -autosomal recessive, hypertrophic sensory-motor polyneuropathy -metabolic neuropathy caused by a disturbance in lipid metabolism which leads to an accumulation of phytanic acid -males = females -periods of acute exacerbations -retinitis pigmentosa, ataxia, ichthyosis, deafness, distal extremity weakness with gait distwbances, diminished D1R's. -sennn phytanic acid levels are >50010 above normal.

SPINAL DYSRAPHISM

CEREBRAL PALSY

-failure of mesoderm and neuroectoderm to fuse and form the neural tube -Types:

1. Spina bifida-Iack of closure of vertebral arches, primarily lumbar

2. Spina bifida occulta- not accompanied by protrusion of meningeal or spinal

elements

3. Spina bifida cystica- protrusion of meninges

4. Meningoradiculocele- protrusion of meninges and nerve roots

5. Meningomyelocele- protrusion of meninges and spinal cord.

-leg weakness with feet in equinovarus position -(timinished D1R, sensmy loss feet and saddle area -may be associated with hydrocephalus -associated with congenital abnormalities and mental retardation

-caused by static brain lesion acquired in utero, during delivery or months after birth. -commonly due to trauma, asphyxia or premature birth -irreversible, non-progressive brain deformity -classification:

-Spastic (65%) 1. Spastic diplegia- BIL LE spasticity- scissoring gait, variable mental

impairment 2. Spastic quadriplegia- severe BIL UE and LE spasticity, severe

intellectual impairment 3. Spastic hemiplegia- unilateral spastic hemiparesis, less severe mental

impairment -Athetoid (20%) -Ataxic -Rigid -Tremor -Atonic

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-treatment ofCP -Physical therapy -Surgical intervention-release contractures -Muscle relaxants

MUSCULAR DYSTROPHY -familial disoIders that lead to degeneration of muscle fibers, due to enzymatic defect

-Types: L Docbenne' Pseudohypertrophic - most common sex-linked inherited myopathy, diagnosed during early childhood due to slow motor development SOOIo show pseudohypemophy of ca1f musculature due to fill deposition which can be seen on biopsy. Girdle weakness leads to the classic

"Gower's sign" utilized when going from the floor to standing. Ankle equinus and equinovarus deformities are common. Progressive and the n»gority of pdients are wheelchair bound by age 20. Elevated CPK levels are noted

2. Becker MD. - similar pattern of muscle weakness as Duchenne however, less aggressive. Patients with Becker MD. often walk to approximately age 35 and have longer life spans. 3. Facioscapulohumeral MD. - mildly progressive, affects faciaI and shoulder muscles with weakness and atrophy. Lower extremity weakness usually oca:as 20-30 years later. 4. Myotonic MD. - multisystemic disorder, onset I3Dges from birth to 50 years of age. Presents with tonic JIWSCle spasms. Often a foot drop develops. 5. Limb giIdle MD. - diagnosis of exclusion, has inconsistent features. Initial }ESeDtation of shoulder and pelvic giIdle weakness and atrophy.

SYRINGOMYELIA -progressive disorder, onset usually 2nd-3rd decade -characterized by muscle atrophy, dissociated anesthesia, pamparesis with neurotrophic changes including neurogenic osteoarthropathy (Charcot), loss ofD1R ~ by a tubular dilatation in the spinal cord most commonly in the cervical -diagnosis easily made with MRI or cr

2. Peripheral neuropathy ( COMMON CAUSES) -Hereditary

-CMT -Dejerine-Souas ~Refsum's disease -Amyloidosis

-Acquired -Diabetic -Myeloma -Guillain-Barre' -Malignancy -Uremia -CtyOglobulinemia -HlV

-Tangier's disease -Fabry's disease -Abetalipoproteinemia -Freidrich's ataxia

-Hypothyroidism -Sarcoidosis -Alcoholic -Collagen-vascular -Acromegaly -VitaminB

55

-Toxic (ie drugs, chemicals) <hloramphenicol -isoniazid -nitrofurantoin -DaJEone ~spIatin

-metronidazole -hydralazine -phenytoin -lead -cyanide -thallium -zerit

-Infectious -leprosy -diphtheria -IHV

-Entrapment -aupal and tarsal tunnel

3. Various neurologic disease

1. PARKINSON'S DISEASE

-lithium -pyridoxine -disulfuram -ethionamide -vincristine -gold -amiodarone -colchicine -arsenic -mercwy -trichloroethylene -ddI

-herpes zoster -Lyme disease

-progressive disorder, characterized by ~1opJasmic eosinophilic inclusious in the neurons of the substantia nigra. <haracterized by rigidity, resting tremor, bradJkinesia, loss of postural reflexes, festinating gait Dementia occurs in 50010 of patients. -males=females, onset 40-60 years of age -multiple drugs utilized in treatment including levodopl, caIbidopl, amantadine, bromocriptine. pergolide. Physical therapy helpful to improve function.

2. MULTIPLE SCLEROSIS -chronic CNS disease of unknown origin ~rized by inflammatory demyelinating plaques in white matter of eNS. Infiltration oflymphocytes, plasma cells and macrophages. -ooset at around 30, 2: 1 female:male -course is relapsing and remitting -optic neuritis is most common presenting SJDlPI:om -LE affected> UE often with SJmIicity and futigue -cerebellar involvement with ataxia, scanning dysarthria and intention tremor -autonomic symptoms- incontinence, impotence and orthostatic hypotension. -often see peISOnaIity changes, memory loss, dementia and emotional lability. -MRI diagnostic in >90% of cases -mean survivalawrox. 25yrs and is improving -avoid physical and emotional stress, infections and prolonged exrposure to extremes of temperature.

3. CEREBRAL VASCULAR ACCIDENT -rapid onset of a nemologic deficit involving a vascular territory of the brain and lasting for greater than 24 hams. < 24 hours considered a transient ischemic attack (TIA). -most often due to thrombosis or embolic event as well as hemorrhage from aneurysm or A V malformation.

56

I t

I I I I I I I I I I I I I I

-presentation varies with the vessel involved and portion of the brain infarcted. -cr scan diagnostically helpful -Genemlly, early flaccid paralysis followed by increasing spasticity and development of synergistic patterns. -Physical therapy and orthotic fabrication can improve functional ability

4. EPILEPSY -characterized by abnonnal, recurrent, excessive discharges from neurons. -50010 have no 1lIJ.<b-lying neurologic disorder -other etiologies include EtOH withdrawaL head trauma, hypoglycemia, meningitis, encepbalitis -most seizures last 30-90 seconds -Classification

l.Focal (Partiallocal)- originate from a localized portion of the brain -Simple focal

-motor- focal motor with march Jacksonian -sensory- somatosensory, visual,auditory, gustatory -autonomic- epigastric sensation, pallor,sweating, flushing, piloerection, pupillary dilatation -psychic- dysphasia., affective, cognitive, illusions. hallucinations.

-Complex focal -simple focal followed by impairment of consciousness -impaired consciousness at onset sometimes with automations.

-Any focal seizure may evolve to a secondary generalized seizure.

2.Generalized - no focal component,therefore no prodrome, aura or focal motor or sensory symptoms. -Absence (petit Mal)

-impairment of consciousness only, may show mild clonic,atonic,tonic component.

-Myoclonic seizures -Tonic -Tonic-Clonic (Grand mal) -Atonia (astatic) seizures

3.Unclassified

-Status epilepticus -condition in which patient has a series seizures \\'ithout total recovery of consciousness. Most common cause in compliance with seizure medications.

-AnticonvuIsants (ie. phenytoin, carbamazepine) are most commonly utilized. Need to

obtain therapeutic blood levels.

5. MYASTHENIA GRAVIS -Acetylcholine (Ach) receptor antibodies destroy the receptor sites on the postsynaptic membrane. Results in miniature end plate potentials that are reduced in size and number. -Due to an autoimmunoplthy -Ha1.lma1k is exercise induced fatigue that is resolved with rest. -Often get double vision and ptosis, difficulty with che,viog. Only involves skeletal muscle. -Ach receptor antibody found in the serum of>90%

57

-Tensilon (edrophonium) is helpful diagnostically. -EMG shows classic changes of decrement -5% of patients have an associated thymoma which is most easily diagnosed with CT scan. -Treatments include long term anticholinesterase meds or disease modifying drugs such as Immuran. Also plasmaphoresis has been found to be effective.

MG (cont) -*** Eaton-Lambert syndrome is similar to myasthenia gra"is however, it involves a defect in neuromuscular transmission due to a decreased number of Ach packets released at the presynaptic terminal. - use certain meds such as aminoglycosides and tetracycline with caution

6. GUllLAIN-BARRE' SYNDROME (Acute idiopathic polyneuritis) -immunologically mediated demyelinating polyneuropathy -affects all ages and se"{es -bimodal peaks of occurrence- 15-35 yrs and 50-75yrs -usually preceded by a viral or mycoplasma infection. surgery, immunization or in patients with systemic lupus erythematosis (SLE) and lymphomas. <haracterized by rapidly progressing symmetrical motor weakness in a distal to proximal fashion. Can lead to severe respiratory paralysis and occasionally cranial nerve involvement <auses stocking-glove paresthesias -decreased or absent DTR's -may cause autonomic dysfunction including-brndycardia/tachycardia, hypotension/hypertension. -diagnosis-lumbar puncture reveals elevated CSF protein and the presence of a fe.v mononuclear leukocytes. -EMG reveals decreased NCV and prolonged latencies -functional recovery occurs usually 2-4 weeks

BONE TUMORS

I ccmr H:M. F1nous IIYSPt.4S fit ~~~ ---ua

1 J-~--

i ~------ ---------~~-1

~IMtr CEL{.1UMCIt aUlD; oI1Eli'f'Sn'5EIl

=:....!i:l--_-AIULJ~ .,.,. ICII'"

58

CIassification: Histologically based on the cell or tissue type from which the lesion originates. Osseous, Cartilaginous and Fibrous are the origin of most primaIy benign and malignant neoplasms in bone.

Diagnosis: Subjective symptoms(NLDOCAT) Past medical history Clinical evaluation of objective signs

Radiogrnphic evaluation: Helps to determine the rate and aggressiveness of the bone tumor

1. Pattern ofbone deslruction: a) Geographic -least aggressive, well defined b) Moth eaten -more aggressive, less defined c) Permeative - highly aggressive

2. Sclerotic border: -slowly growing lesions are associated with reactive sclerosis of the surrounding bone -sclerosis can be of variable thickness and partially or completely surround the lesion

3. Cortical involvement: -bone cortex serves as a barrier to Iateral expansion of the tumor -nonaggressive medullary lesions may cause little change in the endosteal surfuce, however, some benign lesions such as aneurysmal bone cysts can expand rnpidly

-aggressive lesions cause endosteal erosion and can penetrate the corte.x in more than one pJace

4. Periosteal reaction: 1. Continuous

a. Cortex destroyed smooth shell· - due to expansile pressure benign lesions (giant cell, enchondroma, fibrous dysplasia) lobulated shell - due to ,'31iation of growth rate ridged shell - AKA "soap bubble" due to slowing rate of prolifemtion (non-ossifying fibroma, enchondroma)

b. Cortex present solid - implies slow growth rate, can be seen in osteoid osteoma, enchondroma and eosinophilic granuloma undulating - variant of solid, seen with periostitis, hypertrophic osteoartbropath lamellar - may be single or onion skin in appearance parallel or spiculated "hair on end" -often associated with malignancy (Ewing's sarcoma)

2. Interrupted a Buttress

solid appearing wedge ofbone, forms at margins of slowly enlarging lesion( chondromyxoid fibroma, malignant change oflong-standing benign lesion)

b. Codman Triangle suggests aggressive malignant lesion seen in

59

osteosarcoma and chondrosarcoma c. Lamellated Reaction

onion skin appearance can be seen in malignant (osteosarcoma) and benign lesions (eosinophilic granuloma)

3. Complex Sunburst pattern, highly suggestive of osteosarcoma

5. Size and Shape: In general, malignant tumors are larger than benign tumors, often >6Cm Elongated lesions in which the greatest lesional diameter is 1.5 times the least diameter may be indicative of Ewing's sarcoma, histiocytic lymphoma, chondrosarcoma and angiosarcoma.

6. Soft tissue involvement: If lesion leads to cortical breakthrough than it is aggressive

7. Skeletal location oflesion: Tumors may predominate in areas of red, or hematopoietic, marrow. These include metastatic disease, plasma cell myeloma, Ewing's sarcoma and histiocytic lymphoma. The tendency for these tumors to involve appendicular and axial skeleton in the young and only the axial skeleton in aged is related to the changing distnbution of red marrow. Some tumors are more prevalent in areas of rapid bone growth such as distal femur and proximal ubia. Tibia: increased incidence of adamantinoma, nonossifying fibroma and chondromyxoid fibroma, osteosarcoma, osteoid osteoma, Giant cell tumor Fibula: non-ossifying fibroma, aneurysmal bone cyst, Ewing's sarcoma, lipoma Foot chondromyxoid fibroma, aneurysmal bone cyst, chondroblastoma, osteoid osteoma, osteoblastoma, enchondroma, lipoma

8. Location oflesion in bone: (Fig.!) Transverse plane: Central .......... Solitary bone cyst, enchondroma Eccentric ........ Aneurysmal bone cyst, giant cell tumor, osteosarcoma, chondrosarcoma, fibrosarcoma, chondromyxoid fibroma Cortical ......... Non ossifying fibroma, osteoid osteoma lID..1acorticallParosteal .... Osteochondroma, juxtacortical chondromas, parosteal osteosarcoma

Longitudinal plane: Epiphysis ........ Chondroblastoma Metaphysis. ...... Osteosarcoma Diaphysis ........ Ewing's sarcoma, retinaculum cell sarcoma, multiple myeloma and

metastases Physeal .......... Giant cell tumor MetalDiapbyseal..Unicameral bone cyst, enchondroma

9. Trabeculation: -may reflect residual trabeculation displaced by tumor or new bone formation due to the tumor Pattern delicate, thin coarse, thick lobulated delicate, horizontally oriented striated, radiating

Tumor Giant Cell tumor Chondromyxoid fibroma

non ossifying fibroma aneurysmal bone cyst

hemangioma

60

10. Matrix Pattern:

Size

~ tumors produce matrix that calcifies or ossifies Cartilage tumors: -calcific circles (rings) -<hIe to endochondral bone formation .

-flocculent -fleck-like (stippled)

11. Patient age: (Fig.2) ~ 1. 1 year

2. 1 year to 10 yrs.

3. 10 years to 20 yrs.

4. 10 years to 30 yrs.

5. Skeletally immature ~ 6. Skeletally mature to

5Oyrs.

7. 30 years to 60 yrs.

8. 50 years to 80 yrs.

Lesion Melaslatic neuroblastoma

Ewing's sarcoma

Aneurysmal bone cyst

Osteosarcoma

ChondrobJastoma Lesion

Giant aill tumor

ChondrosaIcoma PrimaIy lymphoma Malignant fibrous histiocytoma FibrosaIooma

Multiple myeloma Metastasis

Benign versus Malignant Bone Lesions Benign Small

Malignant Large

Soft tissue mass Periosteal reaction Margins

None Large Rare Common Sclerotic None

Zone of transition Trabeculation Cortical destruction Overall~

Other diagnostic tests include: -Bone scans

Narrow Wide Yes Rare Geographic

provides insight on multiple sites of involvement Increased upIake of the nucleotide in bone reflects the hypermetabolic osteoblastic activity

-Computerized tomography

No Usual Permeative or Moth-eaten

helps to detennine more precisely the location and extent of involvement of the tumor -Magnetic resonance imaging

also helps to detennine the location and extent of involvement of the tumor, however, better in assessing the soft tissues and tumor characteristics.

-Laborntory studies Alkaline phosphatase(blood and urine) Complete blood count Chest x rny

61

-Biopsy

age and gender specific studies may include serum protein electrophoresis(SPEP) urine protein electrophoresis(upEP) prostate specific antigen(pSA) thyroid function tests(1Frs) liver function test (LFf) carcinoembryonic antigen(CEA)

lncisional: cutting into the lesion to remove a sample for pathology evaluation -required for malignant bone lesions -carries risk of spreading lesion by lymphatic or blood seeding

-complications are minimized with careful incision planning, strict hemostasis, minimal dissection, avoidance of neurovascular structures and tight wound closure

Excisional: removal of entire lesion (done for benign tumors)

Common Tumors of the Distal Leg and Foot:

BENIGN TUMORS: 1. Osteoid osteoma

-benign osteoblastic lesion clmacterized by a well demarcated core(nidus)of usually less than 1 cm. and a distinctive surrounding zone of reactive bone formation.

-age: 10-25 years (rare>30 years) males>females -location: femur 32% tIbia 24% . foot 11% -presentation: point tenderness over the lesion, nocturnal pain, local soft tissue swelling in

the foot, the lesion usually appears at the junction of the anterior mid-third of the talus or OS calcis, salicylates may completely relieve symptoms by prostaglandin

inlubition -radiographic foatures: lesion is located most commonly in the cortex. The lesion has a radiolucent nidus with a striking thickening of adjacent cortical bone and periosteal new bone formation. -pathologic foatures: lesion is clmacterized by varying degrees of osteoid and highly

vascular supporting osseous tissue. -treatment: excision of the nidus and surrounding bone

2. OsteobIastoma -benign, rapidly growing tumor that is histologically similar to osteoid osteoma Characterized by the absence of any reactive perifocal bone formation. -age: 20-30 years of age (9()01o are <30 years of age)2: 1 males:females -location: diaphyseal and metaphyseal in the foot the tumor occurs most commonly in the dorsal aspect of the anterior portion of the talus -presentation: dull, aching, localized pain. Not noetumal pain. Pain is not relieved by salicylates. Localized swelling -radiographic foatures: lesions are weIl circumscnbed, radi~ lucent and usually expansive with occasionally a thin shelf of reactive bone. -pathologic foatures: tumor is hemonbagic, gritty and friable. Large lesions may show central softening and cystic degenerntion -treatment: cmettage and packing of the defect

3. Enchondroma -benign hyaline cartilage grol\1h that develops within the medullary cavity of a single bone

-age: usually manifest during 3rd or 4th decade; equal distribution between the sexes -location: metaphyseal to diaphyseal- most occur in the small

62

\J

~

'lj

J

J J J

tubJlar bones in the foot, seen in metatarsals and pba1anges -presentation: lesions develops slowly and gradually and is well established before clinical symptom Often painless swelling is the fust manifestation. Painful lesions without trauma sbould arouse suspicion that a malignant ttansformation is occurring. -radiographic features: lesions are well ciIcumscribed with distinct ares of Iarefuction-the lesion may show speckled calcification -pathologic features: hyaline cartilage with scattered calcification -treatment: curettage ** The syndrome of multiple enchondromas is known as OIlier's disease. If also associated with soft tissue hemangiomas, the disoIder is known as MafIbcci's syndrome.

4. Osteochondroma -beDign, slow growing mushroom shaped hyaline cartilage capped lesions. Classically arise from a growth plate in long bones, growth ceases with skeletal maturity -age: 2nd decade, 2: I male:female -location: metaphyseal to diaphyseal- exostosis points away from adjacent joint -commooly seen in the distal femur and proximal tibia -presentation: often an incidental finding on x my most commonly a painless, slow growing lesion - pain may becaused by impingement of smrounding anatomic structures. -radiographic features: shaIply peduncu1ated or sessile tumor at the level of the metaphysis that points away :from the nemby joint -pathologic features: cortex and periosteum of the tumor are continuous with underlying bone. Hyaline cartilage is usually 2-3 mm thick and this diffentiates an oste<K;hondroma from a subungual exostosis which has a fibrocartilage cap. ' -treatment: excision **less than 1% give rise to chondrosarcoma

5. Non-ossifying fibroma age: 1st and 2nd decade location: cortically based metaphyseal lytic lesion, eccentrically located-most common in distal femur and proximal tlbia presentation: usually asymptomatic unless associated with a pathologic fracture 'with accompanying pain. swelling and'disability. radiographic features: Lesion ,is an active and proliferating frum of fibrous cortical defect seen in infimts and childrenLucent, eccentric lesions that may be loculated, with a sclerotic rim pathologic features: dense col1agen. giant cells and lipid filled histiocytes treatment: curettage

6. Chondromyxoid fibroma rare, benign tumor composed of chondroid, fibrous and myxoid tissues age: 2nd to 3rd decades, male>females location: occur in the metaphyses oflong bones offoot - 16% presentation: usually complain oflocalized, dull, achy pain possibly swelling and tenderness radiographic features: lucent tumor, usually>5cm. with well-defined sclerotic borders pathologic features: nodules of poorly fonned hyaline cartilage and myxoid tissue delineated by fibrous septae treatment: curettage

7. Aneurysmal bone cyst

primary tumor like lesion which initates an A V fistula and thereby creates, via hemo­dynamic forces, a secondary reactive bone lesion age: most occur in patients under 30 years of age, equal se..x distnbution

63

location: may affect any bone - foot-8% presentation: mild to moderate pain as the lesion develops, patient may limp radiographic features: small lytic lesion seen early later, areas resembling Codman's triangle may develop, at the blowout stage the bone may appear expanded with no shell around the lesion. Late lesions as a result of fibrous septae and bony spicules appear loculated. **angiography may help to define the vascular malformation treatment: curettage and packing with bone chips

8. Simple bone Cyst (Unicameral bone cyst) -fluid containing solitary unilocular cyst -age: 80-90% <20 years old, 2: 1 males:females -location: metaphyseal region of long tubular bones in juxtaposition to the epiphyseal plate -presentation: indistinct discomfort makes the cysts presence known. In 50%, pathologic fracture is the cause of diagnosis -radiographic features: from its principle metaphyseal location, the cyst extends into the diaphysis. Characteristically, they occupy a central location, its length is greater than its width. The overlying cortex is eggshell thin but always intact. ***fallen fragment sign-radiologic finding describing a free fragment of cortical bone fallen by gravity in the fluidcontaining cyst. -pathologic features: serous usually bloody tinged fluid is expelled upon opening. Cavity is unicystic with a whitish, thin glistening lining. -treatment: curettage and packing with bone chips

9. Giant cell tumor -uncommon, locally aggressive tumor so named because it contains multinucleated, osteo­clast type giant cells. -age: arise during 3rd to 5th decades -location: adults: involve both epiphysis and metaphysis (adolescents: confined proximally by the growth plate and are limited to the metaphysis-most arise about the knee)

-presentation: location of the tumor near ends of bones causes arthritis type symptoms-occasionally pathologic fracture is presenting concern. Swelling, intermittent pain and limited range of motion also can be seen. -radiographic features: large, lytic "soap bubble" lesions which are eccentric may have a thin, perilesional sclerotic shell -pathologic features: large and red-brown and frequently undergo cystic degeneration.. Composed of uniform oval mono­nuclear cells which are the proliferating component of the tumor. Scattered within this background are giant cells having 100 or more nuclei. -treatment: curettage, recurrence rate is 4O-6()OIo

10. Fibrous dysplasia

-localized, progressive replacement of bone by a fibrous proliferation intermixed with

poorly formed, haphazardly arranged trabeculae of woven bone. -age: 2nd to 3rd decade most common -location:monostotic-involvement of single bone

polyostotic-involves more than one bone, can be seen with various endo-crinopathies

-presentation: symptoms depend on bone(s)involved and degree of involvement-pain and swelling may accompmy pathologic fracture.

-radiographic features: "ground glass" appearance with a well-defined sclerotic rim -central meta-diaphyseal in tubular bones -pathologic features: lesional tissue composed of curvilinear

64

trabeculae of woven bone surrounded by a modeIately cellular fibroblastic proliferation. -treatment excision or curettage in monostotic forntS.

11. Chondroblastoma age: 2nd decade, 2:1 male:female location: epiphyseal, eccentrically located - foot 10010 presentation: painful and due to location ·often lead to arthritis type symptoms with joint effusions and limited range of motion. radiographic features: well-defined geographic lucency that commonly bas spotty calcifications pathologic features: composed of sheets of compact polyhedral chondroblasts with well defined cytoplasmic borders treatment curettage

MAliGNANT TUMORS

1. Osteosarcoma -ggressive mesenchymal tumor in which neoplastic cells produce bone matrix age: most common in persons <20 years old, 2: 1 male:female location: 80-90% arise in the medullary cavity of the metaphyseal ends of long bones but any bone can be involved. presentation: pain, local tenderness and swelling - sudden fracture is sometimes the presenting syndrome - at time of diagnosis 20% of patients have demonstrable lung metastases radiographic features: large destructive, mixed lytic and blastic mass with penneative margins. Periosteal reaction = Codman's triangle treatment chemotherapy and irradiation to debulk lesion followed by resection/amputation.

2. Chondrosarcoma second most common matrix-producing tumor of bone behind osteosarcoma common feature is the prodnction of neoplastic cartilage- often asymptomatic age: most commonly seen in 40-60 year age group, 1.5: 1 male:female location: commonly arise in the central portions of the skeleton, pelvis and shoulder girdle, proximal femur. presentation: painful, progressively enlarging masses radiographic features: localized area of bone destruction punctuated by mottled densities from calcification or ossification. patholOgiC features: conventional chondrosarcomas are composed of malignant hyaline cartilage. Myxoid variants are viscous and gelatinous-spotty calcifications are typically present. treatment: amputation

3. Fibrosarcoma rare collagen-producing metastatic neoplasm age: can occur at any age, however, most common in 2nd -4ti1 decade, equal sex distribution location: arise in metaphysis oflong bones and pelvic flat bones - most common in femur presentation: enlarging painful masses which may be palpable and tender often present with pathologic fracture radiographic features: permeative and lytic lesion that often eJ\.1ends into the soft tissue­slight sclerosis at margins of tumor patholOgiC features: composed of malignant fibroblasts arranged in herringbone pattern treatment: amputation

65

4. Ewing's SarcQma _ uncommon primary small round cell tumor that exhibits a

primitive neural phenotype age: 10-15 years old, male>female, blacks rarely afilicted location: arises in the diaphysis oflong tubular bones especially the femur presentation: painful enlarging mass. Affected site is frequently tender, warm and swollen. Pathologic fractures may occur radiographic features: affected bones may demonstrate non-specific "onion skinning" and lytic lesions patholOgiC features: composed of sheets of uniform small. round cells that are slightly larger than lymphocytes whichappear clear due to increased glycogen content. treatment: chemotherapy and surgical resection with or without radiation

5. Multiple Myeloma most common malignant bone tumor age: 40-70 years old males>females location: multiple sites, metaphysis of long bones, spine, skulL and pelvis presentation: fever, malaise, weight loss, fatigue, anemia,thrombocytopenia and renal failure. Pain in one or more bones that increases with weightbearing- monoclonal gammopathy on SPEP. Proteinuria due to renal damage and characteristic Bence-Jones Protein. radiographic features: Yaooue radiolucent. oval lesions

METASTATIC TUMORS -pathways of spread include:

1. direct extension 2. lymphatic and 3. intraspinal seeding

carcinomas of the breast, prostate, lung, kidney, and thyroid are most common sources skeletal metastases are typically multifocal, however, carcinomas of the kidney and thyroid may produce solitary lesions. most metastases induce a mixed lytic and blastic reaction in lytic lesions, the metastatic cells secrete substances such as prostaglandins, interleukins, and parathyroid hormone related protein that stimulates osteoclastic bone resorption. Carcinomas of the kidney, lung, GI and melanoma produce this type of bone destruction. metastases that produce a sclerotic response stimulate osteoblastic bone formation Prostatic adenocarcinomas typically produce this type of response .

• ;Fi~ ... ~a··"""'IIc.r.a.&.iJuulNk~ Sn1iA".. ........ II: ... ..

AB . n..o5 ....... - ....... _ir,...,.... .......... II,..Doa_I$.5 .. ID ...... ~."'m. 0.-.. .. _ Clto_d_~~_ ... lib..:.....~_

til ... , ............. .

66

Benign verses Malignant Benign

- Resemble derivative tissue - Automous growth rate - Local invasion rare - Low recurrence rate - Small - Cystic/fluid-filled - Movable

Evaluation

Soft-Tissue Masses

Malignant - Sarcoma· - Aggressive - Rapid destructive growth - Recurrence/metastasis -Large - Solid - Fixed

- Visually inspect the lesion for edema, color, overlying skin, location and transillumination.

- Palpate for size, consistency, mobility and tenderness/pain.

MRI - Benign verses Malignant Benign Malignant

- Well-defined margins - Poorly defined margins - Homogeneous signal intensity - Heterogeneous signal - No N-V or bone involved - N-V or bone involvement

Biopsy Definition: Removal and examination of tissue, cells and fluid from the living body.

Types of Biopsy: 1. Closed - obtain tissue percutaneously with a needle

- fine needle - done with 25-gauge needle to aspirate mass - core needle - done with cannulated needle with inner trocar * Closed biopsies are easy to perform and indicated for local recurrence

or infection. However, they oftentimes result in insufficient tissue retrieval and diagnostic inaccuracy.

2. Open - tissue is obtained through a surgical incision - excisional - removal of entire mass

- done for small subcuataneous, obviously benign lesions - incisional - removal of a portion of mass leaving main mass in situ

- performed for suspected malignant masses Incisional Placement:

longitudinal on extremities length short as possible over midportion of mass

67

Common Benign Tumors

Ganglion Cyst well circumscribed, soft, cystic mass usually in dorsal foot or ankle close relationto tnndon sheath or joint aspirate for definitive diagnosis - straw colored fluid treatment - marginal local excision

Plantar Fibroma

Lipoma

subcutaneous thickening of plantar fascia usually affects medial and central bands bilateral 10-15% treatment - wide local excision recurrence common

most common benign tumor subcutaneous, soft, movable mass 2 types:

- superficial - well-circumscribed, static - deep - no margin

treatment - marginal excision Neurofibroma

tumor of spindle cell origin fusiform expansion of nerve solitary or multiple cutaneoud or deep multiple associated with von Recklinghausens disease treatment - excise cutaneous, very difficult to excise deep without nerve

destruction Neurolemoma

tumor of peripheral nerve sheath discrete, tender nodule usually affects major nerve treatment - blunt marginal excision

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DEEP VENOUS THROMBOSIS AND PULMONARY EMBOLISM

I. Definitions A OVT - blood clots which usually form in the deep venous system of the lower extremity B. PE - a detached thrombus, usually from the deep veins in the leg (95%), which trav.el to and lodges in the

arteries of the lung

II. Promoting Factors - Vm:how's Triad 1. stasis 2. abnormalities of the vessel wall or damage to the wall 3. "hypen:oagulability"

ill. Pathogenesis I Pathophysiology Promoting Factors (Vm:how's Triad.)

White Thrombus - nidus ofpIatelets

Red Thrombus ---->Fibrinolysis --->Resolution (fibrin thrombus) or

Organization PulmonaIy Embolus

-red thrombus - develops rapidly (minutes) and is very unstable at first (1t takes 7-10 days to stabilize.) -fibrinolysis - the process by which fibrin is degraded -organization - a 7-10 day process during which the thrombus stabilizes resulting in vessel narrowing

N. Conditions associated with risk of thrombosis 1. post partum 5. lower extremity traumaIfracture 2. ventricular failure 6. chronic deep venous insufficiency 3. polonged bedrest 7. using estrogen/oral contrnceptive 4. C3Icinoma 8. recent pelvic or lower extremity

surgery

v. Diagnosis AOVT

1. Classical - pain, heat, swelling in the affected limb 2. PE - presents as the first sign in 70"/0 of prtients with OVI 3. Homan's Test - dorsiflexion of the foot elicits calfpain 4. PIatt's Sign - compression of calf canses pain

B. PE 1. sudden onset 2. "classic" triad (only experienced in 14% of patients)

a dyspnea b. chest pain c. hemoptysis (tachycardia is actually more common)

3. 85% of prtients with fatal PE have some warning sign such as prior embolic event or symptomatic venous disease

VI. Diagnostic Tests for OVI A Non-invasive Tests

1. Impedance Plethysmography - a rapid test to evaluate for OVT proximal to the thigh 2. Doppler Technique - an operator dependent technique which demonstrates OVI by lack of venous compression

69

3. Radiofibrinogen - a very sensitive test for the diagnosis of thrombosis in the calYes

B. Invasive Tests 1. Contrast venography

Vll. Diagnostic Tests for PE A Blood Gas - Pa02 < 80% mm Hg; PaC02 < or = to normal B. Chest X-ray - 50% are normal (may see a hemidiaphragm, atelectasis, density, pulmonary wedge) C. EKG - Tachycardia D. Ventilation-Perfusion Scan (V/Q Scan) - a mismatch demonstrating an area of ventilation but no

perfusion suggests PE 1. Perfusion Scan - Inject technetium 99 labeled human serum albumin 2. Ventilation Scan - Inhalation of xenon 133

E. Pulmonary Angiography 1. Definitive diagnosis thus indicated when VlQ scan is inconclusive 2. Diagnostic signs are: intraluminal filling defect, an abrupt vessel cutoff, or loss of side branches

F. Catheterization of the right side of the heart and measure the pulmonary artery and right ventricular diastolic pressure (increased pulmonary resistance)

VIII. Prophylaxis A Subcutaneous Heparin

1. Pre-op - 5,000 u SQ 2 hours before surgery 2. Maintenance - 5,000 u SQ q 8-12 hours 3. Compression stockings 4. Intermittent pneumatic compression devices 5. Early ambulation or range of motion

B. Aspirin 1. 325mgpo qd (baby ASA81 mgpoqd)

IX Treatment A Anticoagulation

1. Intravenous Heparin a. Loading dose - 10,000 - 15,000 u b. Maintenance via IV drip, start with 1,000 u /hr

(mix 25,000 u in 250cc ofD5 112 NSS) c. Monitor PIT daily - titrate hepnin to maintain 1.5 - 2 times patient control d Protamine sulfate reverses heparin (Ratio: 1 mgprotamine sulfate per 100 u heparin)

• caution should be used there are many possible side affects of protamine and due to baparin's short half life (112 -2 hours)

Note: Weight Based Pneumogram ofHepnin Dosage (variations exist) Bolus 80 u/kg Heparin IV \\'ith a maintenance rate of 18 u/kglhr, check PIT in 6 hours, then if:

PIT <35

and 36 -45 46-70 71-90 >90

BOLUS CHANGE RATE 80 u/kg (lean weight) increase 4 u/kglhr

40 u/kg increase 2 u/kg/hr ---take no action --­

decrease 2 u/kglhr hold heparin 1 hour and decrease 3 u/kgIhr

Need to heme check stools prior to

during initiation of anticoagulation

70

2. Coumadin (warfarin) a. Onset of action is delayed (peak effect 3-5 days) b. Started after heparin is therapeutic c. Dosage 2.5-15 mgfday d Titrate dosage to 1.5-2.0 times control e. Vitamin K reverses Coumadin

3. Lovenox

A Venous interruption operations - intracaval wnbrella balloon or wire filter placed in the inferior vena cava below the renal veins

B. Thrombolytic therapy - Urokinase or streptokinase to dissolve clot (must be initiated within 24-48 hours)

C. Pulmonary Embolectomy

x Differential Diagnosis for DVf A Ce1lulits B. Computmetn syndrome C. Venous stasis

XLMisce1laneous

A Fat Embolism 1. Usually occurs with large fractures of the lower extremity (from bone marrow fat) 2. Three organ systems with symptoms: Pulmonary (hypoxia), Cerebral (confusion), Cutaneous (petechiae) 3. Treatment -largely supportive

- N fluids, respiratory support, fracture care, steroids, and hypertonic glucose and insulin

B. Superficial Thrombophlebitis 1. Presents as a palp1ble cord along the distribution of a vein with erythema, edema, and pain locally. 2. Treatment - supportive consisting oflocal heal elevation and rest. Antiinflammatory agents may be

given.

D. Emboli secondary to endocarditis 1. Most common cause of endocarditis is Strep. Vrridans 2. IVDA- Staph. Aureus

Peripheral Vascular Disease

I. Arterial Disease: Definitions: Arteriosclerosis: generic term for a group of vascular diseases which cause thickening and inelasticity of arteries, decreasing the blood supply to the tissues. Atherosclerosis: diminished size of vessel lumen due to the formation of fibrofatty plaques along the intimal surface of the artery. Acute arterial occlusion: arterial embolic event usually derived from the heart (atrial fibrillation, MI, valvular disease, PICA, CABG) which cause occlusion of small end arteries with ischemia to corresponding tissues. Monckeberg's medial calcific sclerosis: calcification of the media of the artery. Does not decrease the vessel lumen but does falsely elevate ABJ's.

71

Major Risk Factors: -Diabetes Mellitus -Hypercholesterolemia -Hypertension -Smoking

Clinical Presentation: -Acute arterial occlusion

Pain Pallor Pulselessness Paresthesias Paralysis

-Chronic arterial occlusive disease

• Intermittant claudication

Minor Risk Factors: -Obesity -Stress -Age -Genetic predisposition -Decreased exercise

location related to level of obstruction, calf most common complain of cramping brought on by a certain amount of exercise symptoms are reproducible and relieved by rest

• RestPain nocturnal and diffuse in foot while l)iug with legs elevated legs placed in dependency for relief

• Ischemic ulceration / gangrene most advanced complication genernlly occur in distal portion of the foot ulcers look necrotic and do not bleed with debridement

Clinical Signs ofPVD: -Color: pallor, cyanosis, rubor on dependency -Temperature: decreased -Quality and Quantity of skin, nails and hair:

skin: shiny, scaly, atrophic nails: thickened, dystrophic hair: diminished

-Edema: may be increased due to continuous dependency

Vascular Examination -Pulses

palpate - femoral, popliteal, dorsalis pedis and posterior tibial arteries doppler

-Elevational pallor -elevate legs above heart for at least 30 seconds -evaluate color and grade 0 to 4 with +4 indicating marked pallor

-Venous filling time -after elevational pallor test have patient sit up quickly -measure time it takes to fill dorsal venous arch -NorrnallO-15 seconds, Significant disease 30-60 seconds -dependent rubor may follow 2-3 minutes later

Non-invasive vascular testing -Ankle mm index

-ankle systolic pressure / brachial systolic pressure -quick and reliable test, offers little information about anatomic level of occlusion

-Segmental limb pressures -systolic pressures measured with cuffs at groin, above knee, below knee, ankle and transmetatarsallevels -should note a gradual decrease of approx. 20mmHg down the ipselaterallirnb

72

-both limbs should be within 20rnmHg at similar levels -medial calcinosis results in falsely elevated pressures resulting in unreliable information

Indices 1.00- 0.9 0.89 - 0.7 0.69 - 0.5 0.49 - 0.3 0.29 - 0.0

-Segmental plethysmography

normal mild moderate impending gangrene distal necrosis

-air cuff technique (Raines) utilizes same cuffs as segmental pressure measurements -inflate cuffbelow DBP - allows small changes in extremity volume to be translated as a pressure change which is plotted versus time (PVR- pulse volume recording)

crest- rapid vessel expansion in systole normally <35%

dicrotic notch- due to elasic recoil amplitude- normally 8 -12 mm, decreased in arteriosclerois

-other plethysmography techniques impedence: measures volume changes by assessing differences in resistance between 2 electrodes mercury strain gauge: elastic tube filled with mercury is 'wrapped around extremity, as tube elongates \\'ith systolic expansion resistance changes. Photoplethysmography: sensor probe is placed on digit which contains infrared light and a sensor. The light reflected and absorbed by tissues is related to capillary bed volume.

Transcutaneous oxygen measurements assesses tissue metabolism as a function of perfusion < 20-30mmHg high correlation with dec. ability/inability to heal e}.1remity dependency increases TcP02 values

Stress testing / Exercise Response: ambulate on a treadmill at 100% gradient at 2MPH for 5 minutes at completion, perform ABI and repeat every 2 minutes until pre-exam level obtained, normal patients have no appreciable drop.

Magnetic Resonance Angiography: avoids use of ionizing radiation and need for contast media as in arteriography allows multiple imaging planes consider in pts. with renal failure Spin Echo (SE) -blood appears daIk ( low signal intensity) Gradient Echo (GRE) - blood appears bright (high signal intensity)

Arteriography: involves the injection of a organic iodine contrast medium in the arterial system which is then visualized with radiographs usually reserved for patients that may be candidates for bypass surgery contraindicated in patients with a iodine allergy need to stabilize Cr to <2.0 pts need to be Npo anticoagulation given after procedure (plavix)

73

Treatment: (Conservative) Exercise No tobacco Vasodilators Trental

Treatment: (Surgical) Balloon angioplasty - balloon catheter is fed into a localized area of stenosis and inflated to dilate the artery. Bypass surgery - utilizes either autogenous vein graft or synthetic arterial prosthesis (gortex) to circumvent areas of occlusion and improve distal circulation. Laser angioplasty - laser probe is passed percutaneously and then activaied at the site of occlusion / stenosis to recanalize the vessel. Atherectomy - utilizes a high speed rotational burr to ablate stenosis and improve flow.

II. VENOUS DISEASE: Superficial Thrombophlebitis:

-palpable cord along distribution of superficial vein \\'ith local eI)tbema, pain and edema -treatment consists of local warm compresses, elevation, rest and anti-inflammatory medications -discontinue heplock if on the involved e:x.1:remity

Deep Vein Thrombosis **see section on DVT**

MAGENTIC RESONANCE IMAGING GENERAL CONCEPTS AND PATHOLOGY

1. MRI Physics A Based on the hydrogen atom.

1. Hydrogen atom is made up of a single proton in its nucleus. 2. Hydrogen is abundant throughout our body. 3. Hydrogen has the highest gyromagnetic ratio known.

a. Precession is when a proton spins around its axis when placed in a magnetic field (Example­atop)

b. The frequency of this precession is determined by the Lormor Equation:

co =yXj3

co = Precessional (Larmor) Frequency y Gyro~eticRatio

f3 Strength of External Magnet

c. Since hydrogen bas the largest gyromagnetic ratio, it precesses at a higher frequency. B. Atoms \\'ith an odd number of protons and neutrons in their nucleus are small, rotating magnets that

align themselves in the direction of the magnetic field 1. Nuclei in a sample tissue are randomly oriented until a magnetic field is applied 2. Bulk Magnification Vector (M) is the sum of the magnetic moments of all of the hydrogen nuclei

in a sample tissue. C. A radio frequency is applied and potons are stimulated.

1. Resonance is a process where nuclei make transitions between low energy states (parallel to the magnetic field) and high energy states (anti-puallel).

2. A radiofrequency (RF) pulse induces transitions between energy states and tends to decrease the number of nuclei pointing to the main magnetic field

3. Before a 90° RF is induced: a. Protons are in a longitudinal, relaxed state parallel to the z axis.

74

b. Protons precess out of phase with one another.

_M~f_x.y J

e.

4. After a 900 RF is induced: a. Protons are excited and flip into the transverse xy plane. b. Protons precess in phase with one another.

D. After the temrination of the RF, the protons relax, radiowaves are emitted and an image is reconstructed onto the computer. The signal produced depends on the number of nuclei present and the time it takes for the nuclei to relax.

1. Tl Relaxation (Spin-Lattice Relaxation): a. Time it takes for nuclei to realign parallel (assmne a low energy state) to the magnetic field.

M must return to the z axis. b. Also called longitudinal relaxation. c. Reflects the chemical environment of the proton. Strength in which the nuclei are bound to

the chemical backbone (i.e. water, fat). 2. T2 Relaxation (Spin-Spin Relaxation):

a. An exponential decay of the xy component ofM back to O. b. Measures dephasing of the nuclei. c. Also called transverse relaxation. d Reflects the relationship of the proton to the smrounding nuclei.

II. Pulse Sequences A Spin Echo: Utilizes a 90° excitation pulse followed by a 1800 refocusing pulse. This is the most

common pulse sequence used.

Spin Echo

" 1ao-

Emm~ n~ ______________ __ 1E

~-~~-tR-----

DelQCfion ~-.-

1. TE crime to Echo): Time between a 90° excitation pulse and the production of a spin echo. 2. TR rome to Recovery): Time between 90° excitation pulses.

75

B. TI-Weighted Pulse Sequence: 1. Short TE (l5-3Omsec). 2. Short TR (200-600msec). 3. Main focus is on 1R As TR increases, the difference in signal intensity (SI) decreases. 1. T 1 is called the FA T image. Fat displays a high

S1. lOI'JGllUOINAL RE~T10N iT n 2. Used for normal AN4 TOMY.

nm,,(m) I".C!. 1.11. ""'''t .. m'"'I'~~I>D __ iI\'''''~

C. T2-Weigbted Pulse Sequence: ~.--,.

1. Long TE (60-8Omsec). 2. Long TR (2000msec). 3. Main focus is on TE. _1\.5 1E increases, the difference Ll1 SI increases.

4. T2 is called the r-VATER image. The following display a high S1: a. Fluid., edema, hematoma. • II: VQ"'-..I l1li1,....1 Ia..H... JI............",L'''-' .... ~II:..,I . .

b. Infection, inflammation. c. Tumor.

5. Used for PATHOLOGY.

D. Proton Densitv (Intermediate-Weighted Pulse Sequence): 1. Short TE (20-4Omsec). 2. Long TR (l500-2000msec). ttIl.l·1. -"'-.... IIJ'JI .... ~h .. u.r.-_

~~'*"-.rq ........ "'''''~ ............ 3. Has a high signal to noise ratio (SIN).

a. SIN is the ratio between the strength of the signal coming back from the nuclei and the intensity of the noise from the patient and the machine.

4. Good for delineating basic anatomv.

E. Fast Spin Echo: 1. Quicker than normal spin echo T2 sequence.

a. For each spin echo pulse sequence, multiple samples are used b. Instead of one data line per phase pulse, there are several sample echoes in the train of each

TR sequence. 2. Sacrifice slight resolution for speed.

a. An increase in speed results in a decrease in phase direction resolution. 3. Slight shift in contrast due to longer TR.

a. Typically use longer TR (4000-5000), but multi-echo train still makes it faster than normal T2.

F. STIR (Short Tl Inversion Recovery): I. A 1800 excitation pulse followed by a standard spin echo. 2. If Tl is very short the 900 pulse of the spin echo will occur at a time when the Moffat is near o.

a. Any tissue \\-ith a short Tl, such as fat, will be suppressed Not specific for fat 3. Tissues with longer Tl values \\-ill be non-zero.

a. Any tissue with a long Tl, such as water, will produce a high SI. 4. Useful for evaluating edema in high lipid regions, such as bone marrow.

a. Also useful in evaluating articular cartilage because the joint fluid is bright and the cartilage is darker.

76

5. When contmst agents that shorten Tl are used, such as gadolinium, the desired contmst enhancement may be suppressed.

"-lis

G. Fat Saturation: 1. Utilizes RF pulses prior to the spin echo sequence.

-,..,

2. RF pulse centered at the lipid resonant frequency will saturate lipid protons and rotate them into the xy plane.

a. Subsequent pulses rotate the lipid protons out of the xy plane and their resonance is inhibited. 3. Water protons are unaffected because there are differences in the resonant frequencies between

the lipid and water nuclei. 4. This technique is specific for fat, whereas, the STIR. technique is not. 5. Excellent technique to use with gadolinium to suppress high SI of fat.

H. Gradient Echo: 1. Starts with a RF pulse < 90°.

a. Protons are not completely rotated into the xy plane. b. Sufficient magnetization remains along the z axis which allows for short TR times. Shorter

TR times means shorter imaging times. 2. A short TR time does not allow the nuclei to completely dephase before the next RF is induced.

a. Common in tissues with long T2 relaxation. 3. Magnetization is "recycled". 4. Also called steady state magnetization. 5. Goodforjointimaging. 6. Bone marrow has a low SI.

I. Gadolinium: 1. Paramagnetic metal ion.

a. Chelated with DTP A to avoid side effects. b. Shortens Tl.

2. Good to use with fat saturation. 3. Two methods of use:

a. Intravenous: 1. Quickly distributed into intracellular fluid 2. Areas with increased vascularity, such as neoplasms and inflammation, enhance rapidly

and retain contmst longer. **Cellulitis and walls of abscesses will enhance but pus will not.

h. Intraarticular: I. Assess cartilage integrity, such as talar dome lesions.

III. Pathologv A. Bone Contusions (Bruises):

1. Trabecular microfracture with edema and hemorrhage. 2. Poorly defined, inhomogenous, low SI on T1. 3. High SI on T2 because of acute hemorrhage.

B. Stress Fractures: 1. Gradual and progressive resorption of lamellar bone and replacement of dense osteonal bone. 2. Characterized by local hyperemia, edema, and osteoclastic activity. 3. Tl- linear zone of decreased SI surrounded by less defined area oflower SI.

77

4. T2-Jinear zone continues to have decreased SI, but surrounding edema has a higher S1. 5. STIR- increase in SI because fatty bone marrow is suppressed 6. Callous forotation has an intermediate S1.

C. Neuropathic Osteoarthropathv: 1. Difficult to differentiate from osteomyelitis.

a. Marrow signal changes without involvement of the periosteum!cortex is not suggestive of osteomyelitis.

2. Tl- marked decrease in SI within medullary and cancellous bone. 3. T2- mild increase in SI (less than with osteomyelitis). 4. STIR- marked increase in S1.

D. Acute Osteomyelitis: 1. T 1- involvement of cortex/medullary bone shows slight areas of increased SI against background

of normally low SI cortex. 2. T2 and STIR- increased SI in the cortex/medullary portion of involved bone.

a. Reflects a decrease in the normal fat content and localized pus/edema. E. Chronic Osteomvelitis:

1. Sinus tracts- linear areas of increased SI on T2. 2. Foci may demonstrate the "rim sign".

a. Low SI area surrounded by an area of local, active disease. F. Soft Tissue Infections:

1. T2 and STIR sequences are preferred for detection of cellulitis and abscesses. a. Increased SI causing distortion of superficial soft tissues is seen in cellulitis. b. Well-marginated, homogenous, high SI collections are seen \\'ith abscesses. c. Gas contained within abscesses display low SI on all sequences.

G. Osteonecrosis (AYN>: 1. Hallmarlc is a reactive interface.

a. A distinct layer of inflammatory fibromesenchymal tissue between viable and infarcted bone. 2. Tl- well defined line of decreased S1.

a. Represents granulation replacement offat. 3. T2- decreased SI. 4. STIR and long T2- "double rim sign" (Mitchell & Kressel).

a. Inner margin- increase in S1. Represents granulation tissue. b. Outer margin- decrease in SI. Represents mineralization.

5. Staging System: a. Class A- characteristics similar to fat.

1. Tl- increase SI. 2. T2- intermediate SI.

b. Class B- reflects subacute hemorrhage with characteristics of blood. 1. Tl and T2- increase SI.

c. With increasing fluid development in necrotic tissue, SI on Tl decreases and SI on T2 increases.

d During the late stages when fibrosis and sclerosis take place, there is a decrease in SI on Tl andT2.

H. Osteochondral Lesions: 1. T 1- decreased SI within subchondral bone. 2. T2- SI may be increased 3. STIR - marlced increase in SI. 4. Gadolinium may be helpful. Will have a high SI on Tl.

1. Tendons: 1. Low SI on all sequences due to lower water content 2. T2 and STIR- optimizes the contrast between the dark tendon and the abnormal increase in water

content of the tendon 3. Classification ofPT Tendon Tears:

a. TJ!J!!U- incomplete, hypertrophy 4-5 times normal.

78

b. 'lYe!Ul- partial tears, longitudinal splitting. Tendon becomes attenuated and atrophic and assumes a long, ovoid configuration.

c. Tvpe Ill- complete tear, retraction of ends with obvious gap. Ends may hypertrophy. (Need. to distinguish from Type I.)

J. Soft Tissue Masses: 1. Most demonstrate low to intermediate SI on Tl and high SIon TI. 2. Certain benign lesions, such as lipoma, hemangioma, and ganglions reveal.cIwacteristic

morphology. K. Bone Tumors:

1. Most reveal low to intermediate SI on Tl and high SI on T2. 2. Lesions with high SIon Tl contain either fat or blood. 3. Very low SI seen on T2 images in cellular, densely fibrous lesions, and in lesions containing

bone. L. Septic Arthritis:

1. T2 and STIR- increased SI \\'ithin surrounding soft tissues as well as joint fluid is suggestive. 2. Need clinical correlation.

M. Metallic Artifact: 1. Two mechanisms:

a. Ferromagnetic objects have their own magnetic field They cannot be utilized in the MRI machine.

b. Most orthopedic implants are non-ferromagnetic. 1. Distorts RF uniformity. 2. Causes low SI adjacent to implant but no more than 1 cm away.

N. Magnetic Resonance Angiography: 1. Most of the experience is with extra-cranial carotid and intra-cranial circulation 2. Non-invasive technique. 3. Lower extremity indications:

a. PVD. b. DVf. c. Neoplasms. d Anatomic study preoperatively.

Radiology of Infection

I. Nuclear Medicine Studies: A Technetium - 99m:

1. Most commonly administered in the form ~c methylene diphosphonate (Tc-MDP) & hydroxymethylene diphosphonate (Tc-HMDP).

2. Binds directly to calcium hydroxyapatite to form soluble salts. Referred to as a "bone seeking" agent.

3. Isotope concentrates in active new bone formation due to osteoblastic activity related to bone injury.

4. Most widely used nuclear medicine study. 5. NON-SPECIFIC - Positive Scans For

Osteomyelitis Recent Surgery Neuropathic Osteoarthropathy Arthritis Bone Tumors RSD

Fracture Ischemic Necrosis of Bone

79

6. Half life = 6 homs. 7. Remains positive for ex1:ended periods in cases of osteomyelitis & post-osseous surgery because

of continued remodeling and osteogenesis. 8. Increased levels of isotope in the following sites in nonnaI bone:

• Cancellous bone> cortical bone • Metaphyseal bone • Periarticular regions, especially sacroiliac joints • Epiphyseal plates • Tips of the scapula • Petrous portion of the skull • Costochondral margin of the ribs

• Sternum 9. Extra-skeletal sites where the isotope occurs;

• Kidneys • Bladder • Nasopharynx • Oropharynx • Glandular tissue of the breasts • Lacrimal apparatus

10. Phases of Bone Scanning: a. Angiogram (Immediate, Earlv, 1st phase):

• After IV injection of the isotope, several images are taken 1-3 seconds apart as the isotope travels to the extremity.

• Displays arterial blood flow to the extremity. b. Blood Pool (2ad phase):

• Images are taken 2-5 minutes post IV injection. • Quantitatively describes "blood pool" occurring in the capillary beds & veins.

c. Delayed (3n1 phase): • Isotope seeks bone & demonstrates the amount of osteoblastic activity present • Images are taken 2-4 homs post IV injection. • Represents the bone uptake for repair or maintenance.

d. Fourth Phase: • Images taken 5-24 homs post IV injection. • The delay in the time post injection demonstrates more bone activity and less soft tissue

activity, • There is a decrease in the sensitivity because the half-life is 6 hours.

11. Interpretation: a. Evaluate all phases simultaneously. b. The angi~ & blood pool phases will be "hot" in both soft tissue and bone infections. c. Use the 3 or 4th phase bone scan to differentiate soft tissue infections from bone infections.

Blood Pool 4"'Phase Osteomyelitis focal uptake hot hot

CeUulitis diffuse uptake neg neg

Septic Arthritis diffuse uptake diffuse uptake diffuse uptake

B. Gallium -67 Citrate: 1. Localization in areas of acute inflammation & infection by binding mechanisms;

a Direct bacterial uptake by bacterial siderophore complex. b. Lactoferrin. a plasma protein released by leukocytes. c. Direct leukocyte labeling (only 6%).

2. Scan is taken 48-72 homs after injection of the isotope.

80

3. Like technetium, it is non-specific. It is not indicated for detection of osteomyelitis but sequential technetium - !¢hum scans can be used.

4. Returns to normal after infection and inflammation have resolved. 5. Positive scan may represent:

• Infection • Fractures

• Inflammation

• Epiphyseal plates

• Surgical trauma

• Neoplasms

• Gout

C. Sequential Technetium -Gallium Scan: 1. 4 hour technetium bone scan followed by a 48-72 hour !¢hum scan. 2. Increases the specificity for infection. 3. Positive sequential Tc - Ga scan if the gallium uptake is greater than the technetium uptake. 4. Normal scan if the gallium uptake is spatially congruent but is less than the technetium scan.

Technetium Gallium Acute Osteomvelitis + +

Septic Arthritis + +

Chronic Osteomyelitis +

Cellulitis +

D. Indium -111 Oxime: 1. WBC's are isolated from blood taken from the patient & labeled with indium -Ill. The tagged

cells are then reinjected back into the patient The scan is performed 24 hours later. 2. Highly sensitive & specific for acute soft tissue & osseous infections. 3. May not be effective in diagnosing chronic osteomyelitis because it is predominantly a

lymphocytic response & will not cause localization of indium labeled neutrophils. a. Acute & subacute osteomyelitis = neutrophil response = + scan. b. Chronic osteomyelitis = predominantly lymphocytic = neg scan.

4. Can be helpful in differentiating oSteomyelitis versus osteoarthrOpatllY. 5. Halflife = 67 hours. 6. Intetpretation:

a. (+) Scan - Presence of indium labeled WBC's - Higher uptake than surrounding bone

- Acute osteomyelitis b. (-) Scan - No localization of indium labeled WBC's

- Chronic osteomyelitis, osteoarthropathy 7. False positives may occur with:

a. Aseptic soft tissue and bone inflammation such as periostitis secondary to Charcot changes. b. Hyperemia & hypervascularity which may or may not be associated 'With inflanlmation

such as fractures, arthritis, inflammatory bone disease.

E. Technetium - 99m - HMPAO Leukocytic Scintigraphy: 1. Developed in order to have a tagged WBC study which is technically easier & with less radiation

than indium. This allows for more radioactive material to be used & increased anatomical contrast.

2. Tagging molecule = Hexylmethyl propylene amine oxime. 3. Performed by obtaining 50ml of whole blood and spinning off WBC's then taggingllabeling

them. 2ml of the preparation is then reinjected. The scan is performed 3 hours later.

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4. May show advantages over other nuclear medicine studies in diagnosis of early osteomyelitic changes; ho",-ever, it is non-specific and any area of inflammation will be hot

5. A negative scan can rule out a septic process with high precision (94%). 6. A positive scan may not discern septic from aseptic inflammation with sufficient accuracy.

Positive predictive value = 620/0. Note - a subtraction technique is available and may yield higher results.

II. Magnetic Resonance Imaging: Please refer to the MRI General Concepts & Pathology Section for basic principles. A Cellulitis:

1. Increase signal intensity (SI) on T2-weighted & STIR images. 2. Diffuse, infiltrative pattern throughout subcutaneous tissues. 3. On Tl-weighted images, a decrease in SI occurs due to the inflammatory process infiltrating

& replacing normal high SI for subcutaneous fat.

B. Abscesses: 1. Increase in SI on T2 & STIR images. 2. Localized,. well-demarcated, relatively homogeneous signal 3. Can add contrast agent, such as gadolinium, to improve contrast between normal tissue &

pathological lesions. 4. Note- If abscess is filled with necrotic tissue or purulence, instead of inflammatory fluid, the

SI decreases.

C. Osteomyelitis: 1. T2 preferred over STIR image for detection of osteomyelitis. 2. Increase SI on T2 & decrease SI on TI. 3. Detects changes in the medullary canal, cortex, and periosteum.

• Must have changes in both the medullary canal & cortex to be indicative of osteomyelitis.

D. Chronic Osteomyelitis: 1. Opposed to acute osteomyelitis, where the cortex & medullary canal are destroyed, they are

being remodeled in the chronic state. 2. Cortical changes are more extensive than the marrow & are low SI on T2. 3. Areas of active infection can still be seen as increase SI on T2 contrasted against lower SI on

thickened surrounding bone. This is known as the "rim sign". • The rim of low SI reflects fibrous tissue surrounding focal, active disease.

4. "Healed" osteomyelitis displays an increase in SI on T1. This represents the infiltration offat back into the marrow after resolution of the infection.

E. Septic Arthritis: 1. Joint fluid is best detected with T2 & STIR images. 2. To differentiate septic arthritis from non-infectious effusions, an increase of SI of surrounding

soft tissue must also be seen.

F. Advantages ofMRI: 1. More sensitive and specific for infection than other imaging modalities. 2. Assistance in pre-operative planning;

a. Helps localize infection & determine the proximal &distal boundaries. • Particularly helpful with long bones & the calcaneus. • Helps detennine necessary level of amputation or debridement.

3. Evaluate for other possible sources of infection: • Example: Patient with cellulitis not responding to current treatment protocol. Need

to rule out abscess or osteomyelitis. 4. Monitor infectious process:

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III. Computed Tomography (CD: A. Basic Principles:

1. Coronal and transverse plane images only. Sagittal plane images available via reconstruction on computer.

2. High-energy ionizing radiation. 3. Metallic implants will result in artifacts & distortion of images. 4. Windows vaJy density

Highest Density ................................................. Lowest Densitv Cortical Bone

Calcification Cancellous Bone

Nerve Tendon

Ligament

B. Clinical application of CT to evaluate infection:

Cartilage Fat

Air

1. Use of soft tissue ",indow can demonstrate abnormal soft tissue density which may represent suppuration. reactive granulation tissue, edema. or fibrosis.

2. Can be used to evaluate plantar compartments of the foot to diagnose plantar space infections. 3. Use of the bone window can demonstrate the osseous and articular alterations.

a. Early stages of osteomyelitis is noted as an increase in the density of the bone marrow.

GOUT

b. Can be used to establish the extent of the infection & help determine the approximate level of amputation or debridement.

Rheumatic Diseases

Gout is a metabolic disorder in which tissue deposition of monosodium urate crystals occurs from supersaturated e}l:tracellular fluids and results in one or more clinical manifestations which include gouty arthritis, tophi, gouty nephropathy, and uric acid calculi in the kidneys. *** Asymptomatic hyperuricemia in the absence of gout is not a disease state.

Gout is predominately a disease of adult men with a pt>ak incidence in the fifth decade. It is the most common cause of inflammatory arthritis in men over age 30. Gout rarely occurs in men before adolescence or women before menopause. Serum urate concentrations rise from normal childhood mean values of 3.5-4.0 mg/dl to adult levels during puberty in young men. In contrast urate levels remain rather constant in women until menopause. The discrepancy in serum urate levels between the sexes during the reproductive years appears to stem from the action of estrogens which promote renal excretion of unc acid Serum urate levels in women rise after cessation of the menses. The disease is widely distributed amongst many races.

PURINE BIOSYNTHESIS ( KEY STEPS )

1. RAW LIMITING SlEPS Mg2+

ribose-5-phosphate + AlP PRPP synthetase

>PRPP

PRPP + glutamine ;:::================================;> 5 phosphonbosvl-l-amine

I amidopbospboribosyl transferase I -

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2. SALVAGE PATHWAYS

Hypoxanthine + PRPP --------------> Inosinic Acid HGPRT

Gaunine + PRPP > Gaunylic Acid HGPRT

3. URIC ACID FORMATION

Hypoxanthine --------> Xanthine ------> Uric Acid Xanthine Oxidase Xanthine Oxidase

KEY Enzymes listed in bold print. PRPP = phosphoribosyl pjTophosphate HGPRT = Hypoxanthin~unine Phosphoribosyltransferase

PATHOGENESIS

1. Gout in humans arises from the species-·wide lack of the enzyme uricase which oxidizes uric acid to allantoin. 2. In humans uric acid is derived both from the ingestion offoods containing purines and endogenous synthesis of purine nucleotides. 3. Under steady state conditions renal excretion is the major route of uric acid disposal. The kidney accounts for approximately two-thirds of uric acid excretion Bacterial oxidation of urate excreted into the gut is the major mechanism of extra-renal disposal 4. Urinary uric acid excretion is the major a<ljustable mechanism for maintaining urate hemostasis. The capacity of extra-renal uric acid disposal is greatly limited in compnison to the kidney. 5. Increased uric acid production or djminjshed uric acid excretion by the kidney operating alone or in combination have been demonstrated to contribute substantially to the hyperuricemia of gout.

PATHOLOGY

1. Urate crystallizes as a monosodium salt in over-saturated joint tissue. 2. Decreased solubility of sodium urate at lower temperatures of peripheral structures such as toes and ears may explain why urate crystals deposit in these areas. 3. Histopathology of tophi reveals a chronic foreign body granuloma surrounding a core of monosodium urate. 4. The inflammatory reaction around the crystals consists mostly of mononuclear cells and giant cells. 5. Urate crystals appear to be directly able to initiate and sustain intense attacks of acute inflammation because of their capacity to stimulate the release of several inflammatory mediators.

STAGES OF GOUT

1. Asymptomatic Hyperuricemia 2. Acute Gouty Arthritis 3. Intercritical Gout 4. Chronic Tophaceous Gout

CLASSMCATIONS OF GOUT 1. PRIMARY: refers to those circumstances in which elevated serum urate levels or urate deposition appear to be consequences of inherent disorders of uric acid metabolism not associated with another acquired disorder and in which gout is a prominent feature of the clinical picture.

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2. SECONDARY: refers to those circumstances in which gout is a minor clinical feature secondary to any number of genetic or acquired processes.

3. URIC ACID OVERPRODUCTION: approximately 10010 of patients with hyperuricemia or gout excrete excessive quantities of uric acid into the urine. Overproduction of uric acid occurs with some frequency in a variety of acquired and genetic disorders cbaIacterized by excessive rntes of cell and nucleic acid turnover such as myeloproliferative and IymphoproJiferaitve disorders, hemolytic anemias, and psoriasis ( i.e. secondary gout ).

Uric acid ovetproduction can also occur secondary to inherited derangements in mechanisms of endogenous purine biosynthesis. In both partial deficiency of HGPRT and PRPP synthetase ovemctivity early onset gout and renal urate calculi constitute the usual clinical manifestations. Severe HGPRT deficiency is associated with spasticity, choreoathetosis, mental retardation, and compulsive self-mutilation (Lesch-Nyham Syndrome ) ( i.e. primary gout ).

4. URIC ACID UNDERSECRETION : the majority of ratients with hyperuricemia or gout ( up to 90 % ) show a relative deficit in the renal excretion of uric acid VntuaIly all plasma urate is filtered by the glomerulus, with greater than 95% of the filtered load undergoing proximal tubular resorption. Subsequent proximal tubular secretion contributes the mgor share of excreted uric acid A diminished tubular secretory rate may contribute to hyperuricemia, as well as increased tubu1ar reabsorption or diminished uric acid filtration.

CLINICAL FEATURES

1. Acute gouty arthritis is the most common early clinical manifestation. 2. The 1st MIP joint is involved most often and is affected at some point in 75% of patients. In approximately 10010 of patients there is never a recurrence, but up to 60% of patients experience a second attack in less than a year. 3. The ankle, tarsal area, and knee are also commonly affected. 4. The fust episode of acute gouty arthritis frequently begins abruptly in a single joint, often during the night, so that the patient awakens with dramatic, unexplained joint pain and swelling. 5. Affectedjoints are usually red, hot, swollen, and extremely tender. Diffuse erythema may be present which can be confused with cellulitis or thrombophlebitis. 6. Acute attacks of gouty arthritis may be associated with high grade fever and systemic symptoms which may be falsely interpreted as infection. 7. The most common sites for tophi are the base of the great toe, Achilles tendon, olecranon bursae, knees, wrists, and hands. 8. Approximately 10-20% of ratients with primary hypennicemia develop uric acid kidney stones. 9. Renal disease is the most common complication of gout except for the arthritis.

RADIOGRAPIDC FINDINGS

1. The earliest changes in gout are soft tissue swelling and joint effusions. 2. A lace pattern of erosion may be seen as an early change with a fine striated pattern of periosteal reaction along the cortex adjacent to a tophus. 3. Bony erosions tend to be round or oval with a sclerotic margin and have been described as " rat-bite erosions ", cyst-like, or " punched-out " erosions. 4. A feature distinguishing gout from other arthritides is the presence of destructive lesions in bone that are remote from the articular surface. 5. Many of the lesions are expmsile \\"ith overhanging margins ( Martel's sign ) that are displaced away from the axis of the bone. 6. Generally joint spaces are preseIVed until late in the course of the disease. 7. Ankylosis andjoint subluxation may occur in very advanced cases. 8. Tophi may be "isualized "ithin the soft tissues.

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LABORATORY FINDINGS

1. *** Demonstration of synovial fluid monosodium urate crystals is now generally considered mandatory for establishing the diagnosis of gout as an e..xplan.ation of acute arthritis. Monosodium mate crystals are needle­shaped and display a negative birefringence (bright yellow) when viewed under a polarizing light microscope parallel to the axis of slow vibration marked on the polarizing microscope. 2. Synovial fluid leukocytes are elevated ( 20,000-100,000 cells per cubic millimeter) with a predomination of neutrophils. 3. The value of serum uric acid levels in the diagnosis of acute gout is limited; levels can be normal at the time of an acute gouty attack. 4. The ESR ( erythrocy1e sedimentation rate) is generally elevated at the time of an acute gouty attack. 5. An elevated serum WBe count may also be seen with an acute attack.

TREATMENT

ACUTE GOUT

1. COLCHICINE: a potent inhibitor of inflammation, but also a very toxic drug. The mechanism of action appears to be interference with several steps of the inflammatory response in which neutrophils play a central role. Intracellular interference with the organization of labile fibrillar microtubular systems concerned with cell structure and movement may lead to micotubular disaggregation and to decreased neutrophil motility, chemotaxis, release of chemotactic factors, and lysosomal degranulation.

Dose: 1-2 mg IV over 2-5 minutes 0.5 mg po taken hourly until pain reduction, GI toxicity, or max. dose of 8 mg

It has been suggested that the prompt response of arthritis to colchicine is diagnostic of gout, but it should be noted that other arthropathies have been shown to respond to colchicine, and the response to colchicine may be variable if it is started 24 hours after an acute gouty attack.

ARTHROPATHIES WHICH MAY RESPOND TO COLCHICINE ADMINISTRATION

1. Gout 7. Sweet's Syndrome 2. Pseudogout 8. Serum Sickness 3. Familial Mediterranian Fever 9. Hydroxyapatite 4. Sarcoidosis 10. Erythema Nodosum 5. Behcet's Syndrome 11. Rheumatoid Arthritis 6. Amyloidosis

The oral administration of colchicine may cause gastrointestinal toxicity in up to goolo of patients. Nausea, vomiting, diarrhea, and cramping abdominal pain may be severe. The gradual use of small repeated doses is meant to minimize GI toxicity. The maximum dose should not exceed 8 milligrams over a 24 hour period

Avoidance of GI toxicity is one of the advantages of intravenous colchicine. With proper use the only anticipated side effects are thrombophlebitis if not properly diluted and skin sloughing if extravasated. Excessive intravenous dosages may produce bone marrow suppression, renal failure, myoplthy, disseminated intravascular coagulation, severe hypocalcemia, cardiopulmonary arrest, seizures, and death. The maximum daily dose should not exceed greater than 4 milligrams over a 24 hour period After intravenous therapy no more colchicine should be given for at least 7-10 days.

2. NSAIDS: are also potent inhibitors of inflammation. The mechanism of action appears to be inhibition of the enzyme cyc1ooxygenase. In general NSAIDS are started at the maximum daily dosages at the first sign of an acute gouty attack and grndually tapered and continued until the arthritis has resolved. Although less toxic than colchicine, NSAIDS may cause significant side effects involving the GI tract, kidneys, and hematologic

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systems. Among NSAIDS most physicians prefer indomethacin for acute gouty arthriIis. Other NSAIDS with proven efficacy include su)indac, naproxen, piroxicam, ketoprofen, tohnetin sodium. and meclofenamate sodium.

3. Corticosteroids: genernlly not recommen<krl for parenteral use in acute gouty arthritis because the effects are inconsistent and rebound attacks are frequent upon discontinuation. Intra-articular steroid injections are of benefit in cotYunction with colchicine or NSAIDS, or in pItients who are unable to take colchicine or NSAIDS due to various medical conditions.

4. Acrn : is produced by the pituitary gland and causes release of glucocorticoids from a nonna! functioning adrenal gland. Exogenous fonns can be administered with effects similar to corticosteroids.

CHRONIC GOUT

1. COLCIllCINE : generally given as 0.5~.6 mg by mouth two to three times daily as a prophylactic measure.

2. ALLOPURINOL : potent inhibitor of uric acid formation by blocking the action of the enzyme xanthine oxidase. Dosed as 300 mg po qdlbid

3. URICOSURICS ( PROBENICID, SULFINPYRAZONE ) : both increase uric acid excretion by the kidneys and effectively lower serum uric acid levels.

*** Allopurinol, probenicid, and sulfinpyrazone should not be started during an acute gouty attack. Rapid mobilization of uric acid and sudden changes in plasma mate levels may predispose an individual to an acute gouty attack.

4. CHANGElNDIET

SURGICAL PROPHYLAXIS To prevent perioperative acute gouty attacks colchicine 0.5-0.6 mg orally ti.d 3 days before and 3 days after surgery is recommended.

DIFFERENTIAL DIAGNOSIS OF PODAGRA

1. Gout 2. CPPD Disease 3. Rheumatoid Arthritis 4. Sarcoidosis 5. Sesamoiditis 6. Infection 7. Seroneg. Spondylo­

arthropIthies

8. Osteoarthritis 9. Type n U.poproteinemia 10. Calcium Hydro}.-yapat:ite 11. Calcium Oxalate 12. Paget's Disease 13. Calcific Tendonitis 14. Trauma

PATIENTS AT RISK AND PRECIPITATING FACTORS FOR GOUT

- male patient with 1st MIP joint arthritis and hyperuricemia - patients with a history of uric acid renal calculi - alcoholics - chronic renal insufficiency - post N contrast dye - post treatment for hematologic malignancy - stress, trauma, or surgery

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- medications

CONDmONS ASSOCIATED WITH GOUT AND HYPERURICEMlA

low dose salicylates diuretics TB medications warfarin nicotinic acid

- hemopoietic and neoplastic disease - hypertension .. ischelnic heart disease .. and hyperlipidemia - acute myocardial infurction - diabetes mellitus - chronic lead poisoning ( saturnine gout) - glycogen storage disease - sarcoidosis - psonasLS - chronic renal insufficiency - sickle cell anemia and other hemoglobinopathies - pernicions anemia and polycythemia vera - hyperparathyroidism - obesity - regular alcohol consumption -myxedema - toxemia of pregnancy - chronic berrylium disease - Down's syndrome

CALCIUM PYROPHOSPHATE DIHYDRATE CRYSTAL DEPOSmON DISEASE

CPPD crystal disease, also called pseudogout, is an inflammatory process wherein crystals are deposited in tendons, ligaments, articular capsules, synovium, and cartilage. The incidence of clinically symptomatic disease is about one-half that of classic gout. The male to female ratio is about 1.4:1. Radiologic studies show a steady increasing prevalence with age so that nearly 50010 of individuals have evidence of chondrocalcinosis ( radiographic appearence of calcified cartilage) by the ninth decade of life.

CLASSIF1CATION OF CPPD CRYSTAL DEPOSmON DISEASE 1. HEREDITARY 2. SPORADIC ( IDIOPATHIC) 3. ASSOCIA1ED WITI! METABOUC DISEASE

Hyperparathyroidism Hypothyroidism Hemochromatosis Hemosiderosis Hypomagnesemia Gout Amyloidosis

4. ASSOCIA1ED WITI! JOINT TRAUMA OR SURGERY

CLINICAL FEATURES 1. Acute psaIdogout is marked by inflammation in one or more joints lasting for several days or more. 2. These self-limited attacks can be as abrupt in onset and as severe as true acute gout, although the average attack is less prinful.

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-I

I

I

1

3. The knee is the site of almost one-half of all attacks, although involvement of nearly all joints, including the 1st MIP joint, has been noted. 4. Provocation by surgical stress, acute medical illnesses,. and tIauma can cause acute attacks of arthritis. 5. Due to both the inflammatory and degenerative features of CPPD crystal disease, it may simulate diseases such as rheumatoid arthritis,. ankylosing spondylitis,. and neuropathic osteoarthropathy.

RADIOGRAPmC FEATURES 1. The typical appearence of punctate and linear densities in articular hyaline or fibrocartilaginous tissues is diagnostically helpful. 2. Calcific deposits may also occur in articular capsule, ligaments, and tendons. 3. Subchondral bone cysts and hook-like osteophytes may be seen.

LABORATORY FINDINGS 1. *** The precise diagnosis of pseudogout is made by identification of CPPD crystals in joint fluid The crystals generally have a needle-shaped or rhomboid appearence and display positive birefringence when viewed under a polarizing light microscope. 2. Synovial fluid leukocytes may be elevated ( 1,000-50,000 cells per cubic millimeter) ,vith a predomination of neutrophils. 3. A systemic leukocytosis and elevated ESR may be present.

TREATMENT Unlike gout, there is no way to effectively remove CPPD crystals from the joint Acute attacks in large

joints can be treated by thorough aspiration alone or combined with injection of microcrystalline corticosteroids. NSAIDS are often very useful. Colchicine given inuavenously is effective, whereas the effectiveness of oral colchicine is less predictable. But both the number and duration of acute attacks can be reduced by colchicine. It is important to note that treatment of associated diseases does not result in resorption of intra-articualar CPPD crystal deposits.

NEUROPATHIC OSTEOARTHROPATHY

Without any appreciable e.xternal cause we may see, between one day and the next, the development of a general and often enormous tumefaction of a limb, most commonly without any pain whatever, or any febrile reaction. At the end of a few days the general tumefaction disappears, but a more or less considerable swelling of the joint remains,. owing to the formation of a hydrarthus: and sometimes to the accumulation of a liquid in the periarticular serous bursae also. On puncture being made, a transparent lemon-colored liquid has been frequently drawn from the joint.

One or two weeks after the invasion, sometimes much sooner, the existence of more or less marked cracking sounds may be noted, betraying the alteration of the articular surfaces which, at this period, is already profound The hydrarthus becomes quickly resolved, leaving after it an extreme mobility in the joint Hence consecutive luxations are frequently founcl, their production being largely aided by the wearing away of the heads of the bones which has taken place. I have several times observed a rapid wasting of the muscular masses of the limbs affected by the articular disorder ... Besides the wearing down of the articular surfaces ... you may notice the presence of foreign bodies, of all the customary accompaniments of arthritis deformans ... I am led to believe that .. they are all produced in an accidental manner, and to all appearances chiefly by the more or less energetic movements to which the patient sometimes continues to subject the affected limbs ...

J.M Charcot, 1868

I. DEFINITION neuropathic osteoarthropathy implies disease of nerves that leads to underlying bone and joint abnormalities first described by J.M Charcot in 1868

II. PATHOGENESIS Exact cause is still unknown, but both neurovascular and neurotraumatic theories exist and may both play a crucial role in the development of this disorder

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Neurovascular Theory ( French Theory ) : damage to trophic nerve centers with an alteration in the sympathetic control of blood flow to bones and joints leads to persistent hyperemia and active bone resorption

Neurotrnumatic Theory ( Gennan Theory) : An extreme progression of degenerative joint disease following loss of proprioception and protective pain sensation

Ill. CAUSES

Diabetes Mellitus Syringomyelia Tabes Dorsalis ( Lues) Excess ethyl alcohol Myelomeningocele Spinal cord injury Poliomyelitis CMf Disease Riley-Day Syndrome Spina Bifida Congenital Insensitivity Acrodystrophic neuropathy

Amyloidosis Leprosy Tuberculosis Uremia Pernicious anemia peripheral nerve injury Multiple Sclerosis Dejerine-Sottas Disease Tumor invading nerve Brain injury Intra-articular cortico­Phenylbutazone and indomethacin

*** Diabetes mellitus, Syringomyeli~ and Tabes Dorsalis are the three most common causes of Charcot Joints.

Specific diseases with a predilection for the lower extremity :

Diabetes Mellitus - tarsal, tarsometatarsal, and M1P joints Amyloid netlTOplthy - ankle, tarsal joints Myelomeningocele - ankle, tarsal joints Acrodystrophic ne\lfO}mhy - ankle, M1P joints Congenital insensitivtity to pain - ankle, tarsal joints

IV INCIDENCE OF CHARCOT JOINTS

** The most common cause of Charcot Joints is Diabetes Mellitus **

5-10% of JXl1ients with Diabetes Mellitus 10010 ofJXl1ients with Tabes Dorsalis 25% of JXl1ients with syringomyelia

V CLINICAL PRESENTATION

>red, hot, and swollenjoint(s) >defonned, unstablelbypermobile joint(s) >PAIN mayor may not be a feature owing to the degree, progression, and duration of the underlying illness, and when present is often mild considering the amount of joint distension and destruction that may be evident >variable neurologic exam with decreased sensation, atrophy of intrinsic muscles, and diminished patellar/Achilles reflexes >variable vascular exam, but generally pulses are easily palpable >spontaneous fractureldislocations

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>deformity possible in all three cardinal body planes, but especially common in the sagital plane ( rocker- bottom foot) >possible ulcerations over displaced/dislocated bony prominences

VI. RADIOGRAPHIC FINDINGS The two classic radiologic forms are atrophic and hypertrophic arthropathy. Atrophic arthropathy is encountered more commonly in the upper extremity, whereas hypertrophic arthropathy is encountered more commonly in the lower extremity. The underlying disease does not determine which foml predominates.

A'IROPIDC NEUROPATHIC OS1EOARTHROPATIIY

>extensive resorption of bone ends >osteoporosis is present, and destruction ofbone may lead to fracturesldislocations >no osteophytes, sclerosis, fiagmentation, or soft tissue debris is present >tapering of the distal aspect of the bones may be present, with a "mortar and pestle" or "pencil-in­cup " deformity

***a potential diagnostic problem which could be mistaken for cellulitis/osteomyelitis or an aggressive bone tumor

HYPER'IROPHIC NEUROPATHIC OS1EOAR11IROPATHY

>joint space narrowing with marked bony sclerosis >osteoporosis does not occur with this form >fractures and fiagmentation of the articular surfaces >a large amount of bony soft tissue debris forms and later fuses into a large, dense, well-organized

bony mass with an integral cortex

>periosteal new bone fomlation may occur >subluxation and dislocation proceed to destruction, malaligmnent of articular surfaces, and finally to total >disorganization of the joint, which appears as if it were pounded by a sledge-hammer

VII. STAGES OF DEVELOPMENT

Stage I : ACUTE or DEVELOPMENTAL joint laxity, subluxation, osteochondral fragmentation, and debris formation.

Stage II : COALESCENCE absorption of debris and fusion of bony fragments

Stage ill : RECONSTRUCTION remodelling and revascularization of bony fragments

*Stages are based on pathological finding'>. **Disease course is variable and progression may be very rapid

VII DIFFERENTIAI:DIAGNOSIS Acute septic arthritis Pigmented Villonodular Synovitis Osteomyelitis Synovial Chondromatosis and other tumors Apatite Crystal Deposition Disease Gout CPPD Crystal Deposition Disease Psoriatic Arthritis Osteonecrosis (Avascular Necrosis) Rheumatoid Arthritis

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IX. PATHOLOGY >multiple shards ( fragments) of bone and cartilage embedded in the deep layer of synovium are

characteristic findings in acutely resorbed joints, bone is replaced by highly vascular retinaculum

>bone is actively resorbed by osteoclasts >in acute stages S}novium is edematous, congested, and infiltrated with PMN's >noninOammatory and serosanginous or hemorrllagic effusions are ftequently described >bone and cartilage fragments as well as CPPD crystals can be identified in synovial fluid

X. 1REATMENT Conservative

>strict cessation of weightbearing >compression cast ( Jone's-type cast ) to control edema >cast immobilization for :fractures ( generally 8-12 weeks ) >gradual increase to :full weightbearing based on healing >long tenn accomadative foot wear (i.e. orthopedic shoes, custom molded shoes, AFO, PrE, CROW)

Surgical >should not be done during the acute phase >ulcer excision ( primary closure if possible; may require skin grafting ) >exostectomy >saucerization >digital stabilization >metatarsal head resection >Lisfranc arthrodesis >Triple and pantalar arthrodeses >amputation

LYME DISEASE

Lyme disease is a complex multisystem illness caused by the tick-borne spirochete Borrellia burgdorferi. The spirochete is transmitted primarily by certain ixodid ticks ( Ixodes dammini is the principal vector in the Northeastern andMidwestem U.S.; Ixodes pacificus is the vector in the West). The illness which closely mimics other rheumatic diseases usually occurs in stages "With remissions, exaceIbations, and different clinical manifestations at each stage. It was first recognized in 1975 in Lyme. Connecticut.

CLINICAL FEATURES

EARL Y DISEASE: After an incubation of 3-32 days, erythema ehronicum migrans occurs at the site of tick bite in about 80"10 of patients. Although the lesion can occur anywhere, the thigh, groin, and axi1.la are particulary common sites. The lesion is warm to the touch and is often prinless. Within several days after the onset of erythema chronicum migrans, 50% of patients develop multiple secondaIy lesions which may persist from 1 day to 14 monthes. These lesions are similiar in appearance to erythema chronicum migrans, but are usually smaller, migrate less, and lack indurated centers. Skin involvement is commonly accompanied by low grade fever and lympbadenoplthy.

IN1ERMEDIAlE DISEASE : GeneIally occurs approximately 1-6 monthes after the initial exposure. Neurologic abnormalities include meningitis, cranial neuritis, motor and sensory rndiculopathy, mononeuritis multiplex, alone or in various combinations. The most common cardiac abnormality is fluctuating degrees of atrioventricular block Less commonly peri- and myo- carditis may occur. The typical pattern of arthritis is one of migratory pain in joints, tendons, bursae, muscles, and bone.

LAlE DISEASE : <kcurs monthes to years after initial exposure. The most common form of chronic CNS involvement is a subtle encepbalopathy affecting memory, mood, or sleep. Most of these patients also have an axonal polyneuropathy manifested by either distal parasthesias or spinaVrndicular pain About 60% of untreated patients in the U.S. develop frank arthritis. The typical plttem of involvement is brie( intermittent attacks of monoarticular or oligoarticular arthritis in a few large joints, especially the knee.

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LABORATORY FEATURES

Serologic testing is currently the only pI3ClicalJaboratory aid in diagnosis. IgM antIDodies peak at approximately 3-6 weeks; IgG anb.bodies peak montbes to years after exposure. Direct blood, CSF, synovial fluid, and skin lesion cultures are rarely positive.

TREATMENT

EARLY ADULT Doxycycline 100 mg po bid Tetracycline 250 mg po qid Amoxicillin 500 mg po qid CIllIDREN Amoxicillin 50 tpg/lqifday in divided doses Etythromycin 30 mg/lqifday in divided doses

NEUROLOGIC ABNOMALITIES Ceftriaxone 2 gr/day N x 30 days Penicillin G 20 million unitslday in divided doses

ATRIOVENTRICULAR BWCK Intravenous anb.biotics Corticosteroids Cardiac monitoring

ARTHRITIS Oral antibiotics Intraarticular corticosteroids NSAIDS ? synovectomy if symptoms persist > 6-12 monthes

*** During the initial 24 hours after antibiotic therapy is started, 10-15% of prtients experience a Jarisch­Herxbeimer reaction characterized by high rever and worsening of symptoms.

STAGE

STAGE 1 : initial weeks of illness

STAGE 2 : weeks to monthes after stage 1

STAGE 3 : monthes to years after stage 1

LYME DISEASE: TIMETABLE OF A TRIPHASIC ILLNESS

SIGNS AND SYMPTOMS

constitutional symptoms erythema chronicum migrans

recurrent skin lesions neurologic manifestations

cardiac abnormalities

arthritis

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RHEUMATOID ARTHRITIS Rheumatoid arthritis is a systemic autoimmune disorder of unknown etiology. The major distinctive

feature is chronic, symmetric, and erosive synovitis of periphernl joints. The disease is known to affect multiple organ systems in addition to the joints. The average age of onset for adults is 40 years of age, but the disease may strike for the first time at any age. The disease tends to affect women slightly more commonly than men.

PAmOWGY Rheumatoid arthritis is a synovial disease with secondary pathologic changes taking place in the

synovial fluid cartilage, periarticular structures, and tendons. Although data are limited, the initial pathologic event appears to be activation and/or injury of the synovial microvascnlar endothelial cells which leads to edema in synovial tissue and effusions within the joint cavity. Synovitis is the initial lesion. As the disease progresses to chronic stages the synovium becomes massively hypertrophic and edematous. The formation of proliferative and invasive granulation tissue defined as pannus leads to periarticular bone and cartilage erosions and destruction. There is no known etiology.

CLINICAL FEATURES

SYMPTOMS

- The mode of presentation can be quite variable ( indolent, episodic, or progressive polyarthralgias ). - Monoarticular, oligoarticular, or polyarticular joint involvement may occur. - Constitutional symptoms such as malaise, fatigue, low-grade fever, anorexia,. and weight loss may occur. - Stiffness, Jmticularly after prolonged rest, is usually severe and lasts nearly 60 minutes or more.

SIGNS

ARTICULARMANlFESTATIONS

- joint swelling and periarticular tenderness - local 'warmth over affected joints - limitation of motion of affected joints - symm.etry of joint involvement - frequently affected joints include: MCPIMTP's, PIP's, wrists, knees, shoulders, hips, elbows, ankles, midtarsal joints, and cervical spine - tenosynovitis - deformities ( swan neck, boutonniere, hallux valgus, hammertoes, ankle valgus, fibular/ulnar deviation of digits ) - calcaneal erosions, plantar fusciitis, retrocalcaneal bursitis

EXTRA-ARTICULAR MANIFESTATIONS

1. Rheumatoid nodules : tend to <kvelop over pressure points. Rheumatoid nodules have chaIacteristic histopathologic findings when biopsy is perfonned A central zone of necrosis is surrounded by PJlisading histiocytes, fibroblasts, and DlOnocytes. The outer layer of inflammatory granu1ation tissue is composed of lymphocytes, histiocytes, and plasma cells 2. Pulmonary : the l~ are commonly affected by Rheumatoid arthritis. Cotnmmon complications include:

- pleurisy with or without effusions - diffuse interstitial lung disease - pulmonary rheumatoid nodules - Caplan's syndrome ( nodules with pneumoconiosis ) - pulmonary vasculitis and hypertension

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3. Vasculitis : the most common organ systems affected are the cutaneous. nervous, gast:rointestin and pu1monary systems. LeucocytocIastic angiitis. nail fold infim:ts. and splinter hemorrbages are examples of dermal vermlitis which may occur.

4. CardiovascuJar : a111ayers of the heart may be involved. Pericarditis is the most common clinical manifestation.

5. Hematologic: most patients with clinically active arthritis have anemia of chronic disease. Another hematologic manifestation is Felty's syndrome ( triad of neutropenia, sp1enomegaly, and Rheumatoid arthritis ).

6. Neurologic: multiple neurologic complications may develop in patients with Rheumatoid arthritis. - myelopathy caused by subluxation of cervical vertebrae - peripheral neuropIthies

entrapment ( i.e. tarsal tunnel syndrome ) peripheral sensory neuropathy sensorimotor neuropathy ( may be due to vasculitis )

- autonomic dysfunction ( palmarlplantar eJythema )

7. Ocular : the eyes are also commonly affected. - keratoconjunctivitis sicca ( dry eyes ) - episcleritis and scleritis

RADIOGRAPHIC FINDINGS

L Articular : articular manifestations ofRA tend to predominate in the small joints of the feet and wrists.

- soft tissue swelling which may be secondary to : periarticular edema joint effusions hyperplastic synovitis.

- subchondral osteoporosis ( osteoporosis of juxta-articular bone is one of the cardinal diagnostic criteria for RA). - marginal joint erosions ( erosions at the MIP joints most commonly occur at the plantar medial aspect of the

metatarsal heads.) - even joint space narrowing. - joint deformities and subluxations ( marked hallux valgus with fibular deviation oftoes 2,3,and 4 ). - arthritis mutiJans. - subluxation of the first and second cervical vertebrae. - late changes lead to bony ankylosis, frequently in the tarsal bones.

IL EXTRA-ARTICULAR

- resorption of the distal clavicle. - generalized osteoporosis ( associated with disease duration and severity, menopause, physical activity, and drugs such as corticosteroids, cyclosporin, and methotrexate ). - stress fractures of long bones. - Achilles' tendon thickening - erosions may be seen at the posterior and plantar aspects of the calcaneus, and well marginated plantar heel spurs are often present.

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ABNORMALITIES OF SYNOVIAL JOINTS IN RHEUMATOID ARTHRITIS

PATHOLOGIC

synovial inflammation and fluid production

hyperemia

pannus destruction of cartilage

pannus destruction of "unprotected" bone at margins of joints

RADIOLOGIC

soft tissue swelling and widening of joint spaces

osteoporosis

narrowing of joint space

marginal bony erosions

pannus destruction of subchondral bone

bony erosions and fonnation of sunchondral cysts

laxity of capsule, lig­aments, and muscular contraction/spasm

deformity, subluxation, dislocation, fracture, fragmentation, and sclerosis

THE AMERICAN RHEUMATISM ASSOCIATION 1987 REVISED CRITERIA FOR THE CLASSIFICATION OF RHEUMATOID ARTHRITIS

1. Morning stiffness : morning stiffness in and around the joints, lasting at least one hour before maximal improvement.

2. Arthritis of 3 or more joint areas : at least 3 joint areas have had soft tissue swelling or fluid observed by a physician. The 14 possible areas are right or left PIP, MCP, wrist, elbow, knee, ankle, and MIP joints.

3. Arthritis of band joints: at least one area swollen ( as defined above) in a wrist, MCP, or PIP joint

4. Symmetric arthritis : simultaneous involvement of the same joint areas ( as defined in 2 ) on both sides of the body

( bilateral involvement of PIP's, MCPs, or MTPs is acceptable without absolute symmetry ).

5. Rheumatoid nodules : subcutaneous nodules, over bony prominences, or extensor surfaces, or in juxtaarticular regions, observed by a physician.

6. Serum rheumatoid factor: demonstration of abnormal amounts of serum rheumatoid factor by any method for which the resuh has been positive in < 5% of normal control subjects.

7. Radiographic changes: radiographic changes typical of rheumatoid arthritis on posteroanterior hand and wrist radiographes, which must include erosions or unequivocal decalcification localized in or most marked acljacent to the involved joint ( osteoarthritis changes alone do not qualify ).

*** For classification pmposes, a patient shall be said to have rheumatoid arthritis if helshe has satisfied 4 of these 7 criteria. Criteria 1-4 must have been present for at least 6 weeks. Patients \\'ith 2 clinical diagnoses are not excluded Designation as classic, definite, or probable rheumatoid arthritis is not to be made.

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LABORATORY FINDINGS - elevated eI)'1:hrocyt:e sedimentation rate (ESR). - anemia of chronic disease. - inflammatory synovial fluid - elevated titers of rheumatoid factors in the serum of approximately 85% of patients with RA The Iheumatoid factors tend to correlate with severe and unremitting disease, nodules, and extIa-articular disease. The most common rheumatoid factor is IgM antibody to IgG antibody.

SELECTED DISEASES ASSOCIATED WITH ELEVATED SERUM RHEUMATOID FACTORS

1. SuhIcute Bacterial Endocarditis 7. Sarcoidosis 2. Leprosy 8. Liver disease 3. Pulmonary Interstitial Disease 9. Tuberculosis 4. Syphilis 10. Lyme disease 5. Rubella 11. C)10me~0,irus 6. Infectious Mononucleosis

DISEASES SEEN IN ASSOCIATION WITH RHEUMATOID ARTHRITIS

1. Sjogren's Syndrome 2. Amyloidosis 3. Felty's Syndrome - classically described as a triad but may include the following:

Rheumatoid arthritis, leukopenia, splenome~y, leg ulcers, lymphadenopathy, and thrombocytopenia.

TREATMENT

1. PHYSICAL MEDICINE (REHABILITATION)

Physical therapy : goals include improving muscle tone. preventing or correcting deformities, and maintaining joint mobility and function. Physical therapy is also very important during the perioperative setting.

Ckcupational therapy : goals include assisting patients in adapting to the activities of daily living ( ADL's), to the limitations of the disease, and supplying splints and assistive devices to aid in self care.

2: MEDICAL TREATMENT

Available medications can be considered in two groups: those that have the potential for symptomatic reliet: and those that have the potential to modify the disease.

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sYMPTOMATIC MEDICAL THERAPY:

Aspirin NSAIDS Glucocorticoids DMARDS ( Disease Modifying AntiRheumatic DrugS ) : ak.a SAARDS ( Slow Acting AntiRhewnatic DrugS) : Auronofin : oral gold preparation Parenteral gold salts Azothioprine ( Imuran ) : oral cytotoxic purine analog Hydroxychloroquine ( Plaquenil ) : oral antimalarial compound Methotrexate ( Rhemnatrex ) : folic acid antagonist Penicillamine: analog of the amino acid cysteine

3. SURGICAL TREATMENT

SOFT TISSUE SURGERY - synovectomyltenOS}novectomy - release of nerve entrapment - extiIpation of rheumatoid nodules - bursectomy - tendon balancing/relocation - release of joint contractures - manipulation of joints under general anesthesia

OSJEaI'OMY AR11IROPIAS1T +/­- resection - fuscial interposition - metallic hemiarthroplasty - plastic/silicone implant - total joint arthroplasty

AR11IRODESIS

4. SPECIFIC PROCEDURES FOR FOOT SURGERY

Modification of procedures of Hueter and Mayo: resection of the first metatarsal head Hoffman: resection of metatarsal heads 2,3,4,& 5 Keller: resection of the 00se of the first proximal phalanx Gocht: resection of the 00se of proximal phalanx 2,3,4,& 5 Clayton: resection of the base of proximal phalanx and head of metatarsal 1,2,3,4,& 5 Flint and Swertnam : amputation of the forefoot

5. INCISIONAL APPROACHES TO PANMETATARSAL HEAD RESECTION

Hoffman: transverse curved plantar incision just behind the web of the toes Fowler: resection of a plantar skin wedge Clayton: single dorsal transverse incision Larmon: three dorsal longitudinal incisions

- over the first metatarsal - between metatarsals two and three - between metatarsals four and five

Marmor: five dorsal longitudinal incisions centered over the MfP joints and extended onto the toes

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SURGICAL CONSIDERATIONS IN PATIENTS WITH RHEUMATOID ARTHRITIS

1. Perioperative corticosteroid supplementation: A patient who has received exogenous steroids within one year of smgery may develop sudden hypotension during surgical stress. The mechanism is based on suppresion of ACfH secretion. Chronic steroid therapy may be associated with adrenocortical atrophy and adrenal insufficiency. Several methods of SUAiementation can be employed.

Hydrocortisone sodium succinate 100 mg N preop ---------- 100 mgN q8Hrx24 Hr

Decrease by SOO" each day and resume oral medications

Solumedrol 40 mg 1M pm before smgery -----40 mg N during surgery

40 mg 1M night of surgery 20 mg 1M am and. pm POD # 1 20 mg 1M pm POD # 2 and. then resume preop routine

2. Aspirin or NSAID discontinuation: Aspirin and NSAIDS should be stopped at least 7 days prior to surgery in order to prevent bleeding complications. Aspirin irreversibly acetylates platelets interfering with platelet aggregation and. prolonging bleeding time. NSAID inhibition is reversible and. persists only 'while the drug is present. Preoperative laboratory evaluation should include a bleeding time, PT, PIT, serum creatinine. and IFf's for patients on long-term aspirin or NSAIDS.

3. Workup and prophylaxis of atlantoaDal subluxation: Atlantoaxial subluxation ( CI-C2 ) is present in ~" of patients with Ibeumatoid artluitis, and marked flexion of the neck during patient transport and anesthesia may cause severe neurologic disruption ( compression of C2 netVe root, posterior column dysfunction, or ultimately quadraparesis or quadraJmlegia ). Subaxial subluxation may be seen in up to 30% of patients with rheumatoid arthritis. Because there is a poor correlation between symptoms and. prthologic findings, it is advised to obtain lateral cervical spine X:rays in flexion and extension before undertaking general anesthesia on any patient with rheumatoid arthritis > 5 years duration Frequently a soft cervical collar or other form of cervical fixation is advised when these patients are being transported and. operated upon

4. Protection of skin : The skin tends to be vel)' thin in patients with rlleumatoid arthritis. The following recommendations can prevent untoward damage to the skin :

a Do not shave the skin because it can be easily damaged. by a sharp razor. The use of an electric-type I3Zor is safer.

b. The use of pJastic adherent drapes ( i.e. betadine impregnated. barriers, Op site) is contraiudicated. because the skin may be tom when the dIapes are removed..

c. Vigorous scrubbing of the skin is also contraindicated..

5. Increased risk of infection: Owing to immunologic defects in both humo:ral and cellular mechanisms of host defense, patients with rheumatoid arthritis have an increased susceptibility to infection The risk is also increased in patients treated with chronic corticosteroids. It is imperative that sterile technique is employed in performing invasive procedures such as insertion of peripheral/central venous access devices, during prolonged surgery, and duringjoint arthroplasty with implantation with artificial joints. The benefit of prophylactic antibiotics is v\lell recognized..

6. Delayed wound healing : Corticosteroids, penicillamine, and methotrexate may contribute to delayed wound healing. Anatomic dissection and gentle manipulation of the skin and soft tissues will help to enhance wound healing and decrease the risk of postoperative complications.

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7. Temporal-mandibular and cricoarytenoid abnormalities: 50-75% of patients "'ith rheumatoid arthritis have pathology of the 1MJ's. Two main areas of concern are 1)

limitation of mandibular opening that will prevent endotracheal intubation; 2) loss of upper pharyngeal airway space, which can result in complete airway obstruction with sedation or anesthesia. Difficult cases may require intubation for general anesthesia by a fiberoptic intubating bronchoscope.

Arthritis of the cricoarytenoid joints is seen in up to 25% of patients with rheumatoid arthritis. Arthritis produces progressive narrowing and fixation of the vocal cords thus compressing the airway. Following a long procedure with endotracheal intuOOtion, extubation must be performed with great caution, since swelling of the already compromised airnay may result in complete airn'ay obstruction in a patient who cannot be easily reintubated For this reason, a narrow diameter should be chosen when selecting an endotracheal tube.

5. DVT prophylaxis: Patients with rheumatoid arthritis may be at increased risk for developing a Dvr depending on their level of incapacitation. Mini-dose heparin could be started preoperatively on any patient undergoing surgery who may be bed ridden or incapacitated for an extended period of time postoperatively.

OSTEOARTHRITIS (DEGENERATIVE JOINT DISEASE)

-most common joint disease characterized by progressive loss of articular cartilage, appositional new bone formation in the subchondral trabeculae,. and formation of new cartilage and new bone at the joint margins. -the exact mechanisms by which primary osteoarthritis develops are unknown -secondary osteoarthritis is applied to the disease when it appears in response to some overt local or systemic pathology

PATHOLOGY

-in earlier stages the cartilage is thicker than normal. An increase in water content leads to swelling of cartilage and an increase in the net rate of proteoglycan synthesis. The increase in proteoglycan synthesis is an attempt at repair by the chondrocytes. -with disease progression the joint surface thins and proteoglycan synthesis diminishes. The integrity of the surface is lost and vertical clefts develop leading to exposed bone.

CLINICAL FEATURES

SYMPTOMS -pain early in the disease occurs after joint use, particularly after prolonged activity of the joint and is relieved by rest. -as the disease progresses pain occurs even at rest -stiffness, typically on arising and after periods of inacth·ity, is usually mild and lasts less than 15 minutes. -muscle spasm or pressure on nerves may result in more pain than the primary joint pain

SIGNS -asymmetric tenderness and pain onjoint range of motion -joint en1argement primarily due to bone proliferation, spurs, secondary chronic synovitis, or effusions. -pain on passive range of motion and crepitus

RADIOLOGIC FINDINGS

may appear normal in early stags uneven joint space narro",ing marginal osteophytes

subchondral sclerosis subchondral bone cysts possible joint mice(loose osseous bodies)

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LABORATORY FINDINGS -nonspecific -synovial fluid studies reveal minimal abnonnalities -lab studies other than rndiograpbs are helpful primarily in excluding other joint diseases

CLASSIFICATION

PRIMARY OSTEOARTHRITIS

- etiology is unknown; specific joints involved

HANDS: DIP Joints»>HebeIden's nodes PIP Joints>>>Bouchard's nodes 1st Carpo-metacaIpal joints

FEET: 1st Metatarsophalangeal joints KNEES HIPS SPINE

SECONDARY ARTIlRfTIS -applied to disease when it appears in response to some overt local or systemic pathology

1. trauma(post-traumatic joint malalignment) 2. metabolic or endocrine disorders

-ochronosis, hemochromatosis, acromegaly, Wilson's disease 3. crystal deposition disease 4. netIfOJXllhic osteoarthroJnthy (Charcot joints)

MANAGEMENT AND TREATMENT

i. GENERAL PRCXiRAM -pnient education -rest -physical therapy - heatlice, exercises, gait tI3ining -occupational therapy - splints, joint protection, assistive devices

2. DRUG TREATMENT -analgesics(aspirin, acetaminophen) -anti-inf1arnmatory agents(NSAIDS, intrn-articular corticosteroids)

3. SURGERY -correction of joint malalignment -<lebridement of loose osseous bodies and spurs -osteotomy to redistribute joint forces -arthrodesis -putial or total joint replacement

PAGET'S DISEASE OF BONE (OSTEITIS DEFORMANS)

Paget's disease of bone is a condition of unknown etiology that occurs in approximately 1-4% of the population over the age of 40. It was first described by Sir James Paget in 1877. It has variable clinical manifestations and most cases are asymptomatic. The disease is characterized by excessive and abnormal remodelling of bone. It is more common in males than females. Again the etiology is unknown. but most experimental evidence supports ............ " a slowly developing viral infection of osteoclasts ", as a cause.

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SKELETAL DISTRIBUTION

- predilection to involve the axial skeleton ( pelvis., sacnn:n,. spine. and skull ). - also involves the long lxmes such as the femur and tibia

( lesions of the fibula are rare). - location is similar to skeletal metastases; however the relative :frequency of tibial involvement, sparing of the upper limb, and infrequency of rib involvement are features of Paget's disease not shared by skeletal metastases. - bone involvement is polyostotic in most cases; may be initially or totally monostotic in 10-20% of cases. - involvement of the foot is relatively uncommon, with the calcaneus having the highest rate of involvement ( foot involvement is noted anywhere from 3-16.3% as noted by bone scanning ).

RADiOGRAPHIC FEATURES

- features can be explained by the underlying pathologic process STAGE I - osteolytic phase STAGE II - mixed pbase STAGE III - sclerotic pbase

- early stages may not be visualized on plain films depending on the amount of resorption, but bone scanning is very helpful in detecting early osseous involvement - late stages are usually well visualized on conventional radiographs. - long bones display the following features :

1. INCREASED cortical width 2. INCREASE in bone length 3. coursening of trabeculae 4. bony enlargement

LABORATORY FEATURES

- elevated serum alkaline phosphatase - increased urinary hydroxyproline

COMPLICATIONS

- osseous deformities ( bowing oflong bones., bony enlargement) - pathologic fractures - malignant transformation (fibro-, chondro-. osteosarcomas and Ewing's sarcoma) - osteomyelitis - crystal deposition - neurologic abnormalities secondary to osseous enlargement or fracture with subsequent nerve involvement - degenerative joint disease - high output cardiac failure and cardiomegaly secondary to marrow expansion and increased blood volume ( steal syndromes)

TREATMENT

- symptomatic with analgesics and appropriate bracing - calcitonin - disodium etidronate - mithramycin

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SERONEGA~SPONDYLOARTHROPATmmS The seronegative spondyl0artbr0pathies are an intetrelated group of multisystem inflammatory

disorders. As rheumatic disorders, they affect the spine, peripheral joints, periarticular structures, or all three, and they are variably associated with cbaracteristic extra-articu1ar manifestations. The Iatter include acute or chronic gastrointestinal or genitourinaIy inflanunation, sometimes due to bacterial infection; and, uncommonly lesions of the aortic root, cardiac conduction system, and pulmonary apices. Most but not all of these disorders show an increased prevalence among individuals who have inherited the Ill..A-B27 gene.

RECOGNIZED SERONEGATIVE SPONDYLOARTHROPATHIES

PAmOLOGY

1. Ankylosing Spondylitis 2. Reiter's Syndrome 3. Psoriatic Arthritis 4. Enteropathic Spondylitis ( Crobn's Disease and Ulcerative Colitis)

5. Reactive Arthritis

1. Sacroiliitis is the plthologic balJmaIk, and usually one of the earliest pathologic manifestations of ankylosing spondylitis. The initial lesion in the spine consists of inflammatmy granulation tissue at the junction of the intervertebral disc and the margin of the vertebIal bone. The outer annular fibers may eventually be :replaced by bone, fonning a syndesmophyte. Progression of this process leads to the bamboo spine observed radiographically. Similar axial plthology can occur in other spondyloartbropathies as wen. although with some difference.

2. The pathology of peripheral joint arthritis in ankylosing spondylitis can show synovial hyperplasia, lymphoid infiltration, and pannus formation. Similar synovial pathology can be seen in the other chronic spondyl0artbr0pathies, although Reiter's syndrome typically shows many more polymOlphonuclear cells in early disease.

3. Entbesitis., inflammation at sites of attachment of tendinous and ligamentous attachments to bone, is anOther pathologic hal1matk of the spondyloartbropathies. In ankylosing spondylitis it is especially common at sites localized around the spine and pelvis, where it may eventually undergo ossification. In the other spondyloarthropathies, it is more common at pmpheral sites such as the calcaneal attachment of the Achilles' tendon.

HLA-B27 ASSOCIATIONSAMONG THE SPONDYLOARTHROPATHIES

DISORDERS Ankylosing spondylitis ( with uveitis or aortitis )

Reactive arthritis and Reiter's syndrome ( with sacroiliitis or uveitis )

Inflammatory bowel disease ( \\'itb peripheral arthritis) not increased ( with spondylitis )

Psoriasis vulgaris ( \\'ith peripheral arthritis ) ( with spondylitis )

Normal caucasians

HLA-B27 FREQUENCY, 9()O/o

nearly 100%

not increased

50010

not increased not increased

500/0

~%

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REITER'S SYNDROME

Reiters's syndrome was first described by Hans Reiter in 1916. It is the most common cause of an inflammatory oligoartllroplthy in young males. It was traditionally stated that the male to female ratio was 20: 1. but realistically the ratio is closer to 5: 1. The classic triad in Reiter's S}'ndrome consists of non-gonococcal urethritis,. cotUWlctivitis, and arthritis. It has become clear tbat Reiter's syndrome develops in a genetically susceptible host following a genitourinary or gastrointestinal infection. It is grouped with the other seronegative spondyloarthropathies.

PAmOLOGY

The pathologic changes in the synovium are non-specific ( edema, vascular congestion. and infiltration with neutrophils, lymphocytes, and sparse plasma cells ). Osteolysis and periosteal new bone formation are other findings.

CLINICAL FEATURES

MUSCULOSKELEfAL

Arthritis typically begins one to three weeks after the inciting urethritis or diarrl1ea. Joint stiffness, myalgias. and low back pain are prominent early features. Typically only a few joints are involved in an as}'mmetric fashion ; the knees, ankles, small joints of the feel, and the wrists are most commonly affected. Joints are usually only moderately swollen but tender. stiff and limited in range of motion. Constitutional symptoms are usually mild and fever, if present, is usually low grade.

UROGENITAL TRACT

Men experience incn'2sed frequency of and burning during urination. Examination of the penis reveals meatal erythema and edema. and a clear mucoid drainage can be expressed. Prostatitis is common and has been reported in up to SOOIo of male patients. "Silent cystitis or cervicitis" without urethritis may be the only urogenital involvement in females which accounts the high male to female ratio that was once reported for Reiter's syndrome. Chlamydia t1uachomatis is a suspected pathogen for the development of Reiter's syndrome.

EYE

Up to 40% of patients demonstrate uni- or bilateral non-infectious conjuncthlitis which most often occurs early in the course of the disease. The conjuncti,,;tis is usually mild and transient.

MUCOUS MEMBRANES AND SKIN

There are two characteristic lesions associated with this syndrome. Balanitis Circinata : small sballow ulcers of the glans penis and urethIal meatus.

Keratoderma Blennorrbagicum : Hyperlreratotic skin lesions that begin as clear vesicles on erythematous bases and progress to macules, papules, and then to small keratotic nodules. Lesions ftequently involve the soles of the feet, but may involve the toes, palms, scrotum and scalp. The lesions are seen in approximately 12-14% of patients.

GASTROIN1ESTINAL lRACT

The precipitating episode of diarrhea is often mild and transient, but may be bloody and prolonged. Enteric infections by bacteria such as Shigella dysenteriae or fle.xneri, Salmonella enteritidis or t:yphimurinum. Yersinia enterolitica or pseudotuberculosis, and Campylobacter jejuni may p1ay crucial roles in the development of this syndrome.

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HEART

In 10010 of patients with severe and long standing disease, aortic regurgitation develops as a result of inflammation and scarring of the aortic valve and valvular cusps. Condnction defects sometimes occur early in the course of the disease, the most common being a prolonged P-R interval.

OTHER LESS COMMON FEATURES

1. IgA Glomerulonephritis 2. Renal Amyloidosis 3. Cranial and Peripheral Neuropathies 4. Thrombophlebiti 5.Pwpura 6. Livedo Reticularis

GENERAL RADIOGRAPmC FEATURES

1. SOFf TISSUE SWELLING Soft tissue swelling in the inteJpba1angeal joints of the toes and fingers may result in sausage-like deformities of entire digits. Latge effusions may be encountered in the knee and ankle joints.

2. OS1EOPQROSIS Regional or periarticular osteoporosis accompanies acute episodes of arthritis, but it is common to detect severe cartilaginous and osseous erosions without acljacent osteoporosis.

3. JOINT SPACE NARROWING Loss of the interosseous space is more frequent in the small articulations of the feet, bands, and wrists.

4. BONE EROSION The most frequent sites of osseous erosion are the small joints of the feet, hands, and wrists. Erosions initially appear at the joint margins and may later progress to involve the subchondral bone in the central portion of the articulation. The erosions tend to be indistinct in shape and outline.

5. BONE PROLIFERATION Bone proliferation is particularly chaIact:eristic of the seronegative spondyloarthropathies and is the most helpful tadiographic feature in distinguishing these conditions fron Rheumatoid arthritis. Bone proliferation may take several forms.

A Linear or fluffy periosteal proliferation may occur along metataIsa1s, metacmpals, pha1angeal shafts, or the malleoli of the ankles. Periostitis may occur without significant articular abnonnality. The periostitis is similiar to Hypertrophic Pulmonary Osteoarthropathy.

B. Periostitis may occur at the sites of tendon and ligament attachment to bone ( enthesitis ). C. Intra-articular bone formation may occur about sites of osseous erosion.

6. TENDINOUS CALCIFICATION AND OSSIFICATION These manifestations are frequent about the knee, at which site the findings can resemble Pelligrini-Stieda syndrone ( post-tmumatic calcification of the medial collateral ligament ).

SPECIFIC RADIOGRAPmC FEATURES

1. FOREFOOT The forefoot is affected in 40-55% of patients. Any joiny may be affected, although the 1st MIP and IP joints are especially vulnerable. At any location osteoporosis, joint space loss, marginal erosions, as well as periostitis of neighboring diaphyses of metatarsals and phalanges may occur. The sesamoid bones can demonstrate significant erosions and proliferation. Subluxation and defonnity of the MIP joints may be evident,. an

105

a~ that bas been.te~ed Launois's ~o~~. In these case~ the degree of articular mutilation may resemble that seen in Psonatlc and RheumatoId arthritls. or Neuropathic Osteoarthropathy.

2. CALCANEUS The calcaneus is affected in 25-50010 of patients. Bilateral changes are frequent. Retroca1caneal bursitis creates a radiodense shadow that obliterates the nonnallucent area between the postern-superior aspect of the calcaneus and the Achilles tendon. ill-defined erosions on the postero-superior and posterior surfaces of the calcaneus may be present. Posterior calcaneal spurs are rare with Reiter's syndrome, but common with ankylosing spondylitis, Rheumatoid arthritis, and Psoriatic arthritis. On the plantar surface of the bone osseous erosions, hyperostosis, and ill-defined spurs may develop.

3. M'KLE The ankle is affected in 30-500/0 of patients. Soft tissue swelling, large effusions, and fluffy or linear periostitis of the distal tibial and fibular diaphyses and metaphyses are common. Loss of joint space and articular erosions are much less common in the ankle joint.

·tKNEE The knee is affected in 25-40% of patients. The most common abnormality is a joint effusion, although osteoporosis, periostitis of the distal femur and proximal tlbia, and erosive changes can be detected

5. SACROILIAC JOINT The sacroiliac joints may be affected in 40-60% of patients. Bilateral symmetric or asymmetric changes are most commOlL

6. SPINE Although abnonnalities of the spine occur in Reiter's syndrome, their frequency and ex"tent are less than in classic ankylosing spondylitis and Psoriatic arthritis.

LABORATORY TESTS *** Most laboratory tests are very non-specific for Reiter's syndrome, and the diagnosis is based on clinical and radiographic findings.

1. Several lab tests reflect the presence of inflammation.

- Neutrophilic leukocytosis - Elevated erythrocyte sedimentation rate - Elevated C-reactive protein - Normocytic anemia - Synovial fluid is mild to moderately inflammatory and may show the presence of large macrophages that contain nuclear debris and engulfed neutrophils ( Reiter's cells ).

2. HLA-B27 is occasionally helpful.

3. New trends will be to document the presence of a specific infection from the genitourinary or gastrointestinal systems.

TREATMENT 1. NSAIDS 2. ROM I strengthening exercises of affected joints 3. Local corticosteroid injections 4. Topical corticosteroid and keratolytic agents 5. Su1fusa1azine 6. Immunosuppresive therapy ( methotrexate, azathioprine) 7. ? use oflong term antibiotics (investigational )

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PSORIATIC ARTHRITIS

Psoriatic artlnitis is an inflammatory arthropathy that OCCUIS in the range of 2-6% of pltients with psoriasis. The average age of onset is in the second decade and it OCCUIS more commonly in males. In most adult pltients a long history of skin disease is evident, although in a few individuals, the articular abnormalities coincide with or antedate the appearanre of skin lesions. Nail abnonnalities appear to corre1ate most closely with articular disease.

PATHOLOGY

Pathologic changes of psoriatic arthritis are basically similar to those of Iheumatoid arthritis, 00t there are also some pathologic chamcteristics of psoriatic artlnitis that are distinctive.

1. Synovial inflammation is encountered 00t the degree of cellular inflammation with lymphocytes and plasma cells is much less marlred than in rheumatoid artlnitis.

2. Inf1ammatory synovial tissue ( pannus ) is prominent only on the surfilce of cartilage, whereas in rheumatoid arthritis hyperplastic synovium is seen in both superficial and deep layers of the cartilage.

3. Bone proliferation is evident in peri-articular areas.

4. Fibrous ankylosis of the articulation may be noted as in rheumatoid arthritis, however in psoriatic arthritis bony ankylosis is also prominent.

CLINICAL FEATURES

- variable presentation with mono-, pauci-, or poly-articular distnbution. - virtually any articulation can be affected, although the small joints of the hands and feet are reportedly involved in 50-75% of patients with arthritis. - soft tissue swelling can be prominent - nail changes are generally apparent in the same digit in which there is significant distal IP joint articular abnormality. Nail changes include the following :

1. pitting 2. transverse ridges ( Beau's lines ) 3. subungual hyperkeratosis descnbed as a whitish, waxy, greasy debris which may cause onycholysis. 4. generalized discoloration and destruction of the entire nail 5. oil spot or droplet below the nail.

CHARACTERISTICS OF PSORIATIC ARTHRITIS

- involvement of synovial joints and entheses. - asymmetric distnbution is more common than symmetric distnbution. - involvement of the IP joints of the hands and feet. - sacroilitis and spondylitis with pru:avertebrnl ossification. - bone erosion with CKljacent bony proliferation. - destruction of phalangeal tufts.

107

GENERAL RADIOGRAPHIC FEATURES

SOFT TISSUE SWELLING - fusiform or symmetric soft tissue swelling about involved articulation. - " sausage-like" swelling of entire digits.

OSTEOPOROSIS - NOT a prominent feature. - lack of osteoporosis is a reliable sign in the differentiation of psoriatic arthritis from rheumatoid arthritis.

JOINT SPACE NARROWING AND WIDENING - articular space may be narrowed or ~idened - in small joints of the fingers and toes, severe destruction of marginal and subchondral bone can lead to significant widening of the articular space.

BONE EROSION - erosive abnonnalities are prominent - initially erosions predominate in marginal areas of the articulation, but as they progress central areas can also be affected - over a period of time it may appear as if the bones are being gnawed away or have been whittled by a pencil sharpener.

BONE PROLIFERATION - proliferation of bone is a striking featme and is recognized as a diagnostic sign. - irregular excrescences create a spiculated, frayed, or " paint-brush " appearence. - periosteal new bone formation and condensation of bone on the periosteal and endosteal surfaces of the cortex along with trabecu1ar thickening in the spongiosa can cause an entire phalange to appear radiodense ( ivory phalange - Bone proliferation occurs at sites at which tendons and ligaments insert on bones ( enthesopathies ).

TUFTAL RESORPTION - resorption of the tufts of the distal pha1anges of the hands and feet is characteristic of psoriatic arthritis. - the eroded bone may be smoothly tapered or irregular in outline. - the nail of the involved digit is almost always involved

SPECIFIC RADIOGRAPIDC FEATURES OF THE FOOT

FOREFOOT - bilateral asymmetric changes predominate in the IP and MfP joints and are characterized by marginal erosions, bone proliferation. alterations in joint spaces, and lack of osteoporosis. - extensive destruction of the IP joint of the great toe is more chamcteristic of psoriatic arthritis than any other disorder, although Reiter's syndrome and gout produce si.miliar but less marlred changes at this site. - osteolysis of phalangeal tufts, phalangeal and metatarsal shafts can be encountered (arthritis mutilans ).

CALCANEUS - erosion and proliferation of the posterior and inferior surface of the calcaneus may be present - retrocalcaneal bmsitis creates a radiodense area acljacent to the posterosuperior aspect of the bone. - the Achilles' tendon may be thickened and iIregular excrescences may develop at its site of attachment. - plantar heel spurs. - inferiorly erosions of the plantar surface frequently evoke extensive sclerosis of the surrounding bone. - occasionally the entire inferior surface of the calcaneus becomes ebumated.

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EXTRA-ARTICULAR FEATURES

SKIN : psoriatic skin lesions are macular or papu1ar with cbanK:teristic grey-white scales. Bleeding often occurs at sites of scale removal ( Auspitz sign ). Lesions take munerous shapes, but are most often round and located over extensor sur.taces.

EYE : eye jnflammatjon occms in 3O"AI of patients. F~ include COJYunctivitis,. . iritis,. episderitis,. anD keratocOnjunctivitis sicca.

HEART: aortic insufficiency has been reported

NEUROMUSCULAR: an associated myopathy has been ~

LABORATORY FINDINGS

- synovial fluid .from the joints is classically described as being lemon yellow. Synovial fluid analysis typically displays 2,000-15,000 WBCc per cubic millimeter with a predomination of neutrophils. Occasional massive effusions can have leukocyte counts in the l00,OOOImm3 :range. - abscence of rheumatoid :fuctor in most patients - mild anemia - elevated ESR ( erythrocyte sedimentation rate ). - occasionally elevated serum uric acid (related to celluJartunrover of psoriatic cutaneous lesions ). - HLA B27 is .frequently present.

TREATMENT

1. S~on of the skin dise$e may be important in helping to control the arthritis.

local application of ointments Goeckerman regimen PUV A therapy topical corticosteroids intm1esional corticosteroid injections

2. NSAIDS 3. Intm-articular corticosteroid iIijections 4. Methotrexate 5. ? Hydroxychloroquine 6. ? SulfuSalazine 7. Physical therapy 8. Surgery 9. Psycholgic support

Eoteropathic Arthritis

InflammatoI)' bowel disease is a general term that refers to both Crohn's disease and ulcerative colitis. Both of these diseases are chronic inflammatory processes of unknown origin with distinct intestinal distribution, histopathology and radiographic appemaDce. There is a direct causal relationship between the intestines and the joint disease. The arthritis may be peripheral, axial or both. The rheumatologic manifestations of these two disorders are similar but oot identical. Clinical signs of Crohn's disease usually begin in the 2nd-3rd decades and can occur anywhere between 15-60 years old in ulcerative colitis.

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CLINICAL MANIFESTATIONS

PERIPHERAL AR1HRITIS -periphemI articular manifestations occur in 10-200/0 of patients (more common in Crohn's disease) and equal male: female predilection -the etiology of the arthritis is unknown but the close association with the activity of the bowel disease activity suggests a common factor to both processes -one hypothesis implicates absorption of antigenic material through damaged intestinal mucosa and the development of a soluble antigen-antibody complex that enters the joint space to produce synovitis -also appears to be genetically-linked -periphemI arthritis usually indicates active bowel inflammation -however, the arthritic symptoms may begin before the bowel symptoms in Crohn' s disease as opposed to ulcerative colitis, which may occur within a few years after the appearance of bowel symptoms -typically, the arthritis is oligoarticular or monoarticular and affects large joints (most commonly the knees, ankles, shoulders or wrists) -joints of the lower extremity are affected more often then the upper extremity -asymmetric inflammation of the PIPJs of the toes is particularly suggestive ("sausage toes") - -the arthritis is frequently accompanied by fever, prinful omI ulcerations, uveitis or skin lesions (such as pyoderma gangrenosum in Crohn's disease and erythema nodosum in ulcerative colitis) -the more severe the bowel disease and extra-articular manifestation, the increased risk of periphernl arthritis -attacks of arthritis appear abruptly and reach a peak in 48-72 hours -these attacks are usually self-limited and resolve within sevemI weeks to several months -recurrences are common -Common sites ofperiphernl arthritis: knees (8-16%)

ankles (5-10%) shoulders (2-4%) wrists (1-2%)

-enthestopathies at the Achilles tendon and plantar fascia may also occur

EXTRASKELETAL MANIFESTATIONS

-Besides the associated bowel disease, the most common extraskeletal involvement is ocular inflammation (uveitis) which occurs in 100/0 of patients during the disease course -oral ulcerations, digital clubbing, hepatobiliary disease, kidney stones and amyloidosis all are seen in about 5% of patients -less common manifestations include pyoderma gangrenoSUlll, erythema nodosum, leg ulcers, thrombophlebitis and anal fistula formation

RADIOGRAPmC FEATURES

-Sacroiliitis with or without higher levels of spondylitis occurs in 10-15% of patients -this form of arthritis occurs independently of the active bowel inflammation -symptoms and radiographic changes are indistinguishable from ankylosing spondylitis -these changes include bilaternl sacroiliitis and thin, marginal, symmetric syndesmoph}1es (which may ultimately lead to bamboo spine) -the spondylitis occurs 2x as frequently in males than females and it may precede the bowel symptoms by several years -physical exam reveals sacroiliac joint tenderness and a decrease of lumbar spine range of motion and restriction of chest and spinal movement -radiographic evaluation of the periphernl arthritis usually shows soft tissue swelling and periarticular osteopenia -it is very uncommon to see evidence of osseous or cartilaginous destruction

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LABORATORY FINDINGS

-only 50% have a positive 1ll.,A-B27 ifhave spondylitis -there is no corre1ation between Ill..A-B27 and the peripheral arthritis or isolated sacroiliitis -increased SED late, mild anemia, leukocytosis and thrombocytosis -negative rheumatoid factor and ANA -synovial fluid analysis usually reveals inflammatory fluid with a leucocyte count between 10,000-50,OOO/mm3 with normal protein and glucose levels

TREATMENT -treatment of the bowel disease usually results in the disappearance of the extracolonic manifestations, including the arthritis -patient education -NSAIDs -physical therapy -corticosteroid injections (for symptomatic joints) -suJfasa1azine -methotrexate -systemic corticosteroids -bowel surgery/colectomy (resolves the peripheral arthritis but not the axial arthritis in ulcerative colitis but bas no beneficial effect in Crobn' s disease)

ANKYLOSING SPONDYLITIS

Ankylosing spondylitis is a chronic systemic inflammatory rheumatic disorder that primarily affects the axial skeleton, panwertebral soft tissues, spinal apophyseal joints. Sacroiliitis is the hallmaIk of joint involvement. The name is derived from the Greek roots ankylos meaning "bent" and spondylos meaning "spinal vertebrae." The disease is strongly associated with the Ill..A-B27 antigen. Clinical manifestations of the disease usually begin in late adolescense or early adulthood. Onset after age 40 is very uncommon. The disease bas both skeletal and extraskeletal manifestations and is three times more common in men than women.

CLINICAL MANIFESTATIONS

SKELEI'AL MANIFESTATIONS - the most common and cbaracteristic early complaint is chronic low reck pain of insidious onset, usually beginning in late adolescence or early adultbood. - the second common early symptom is reck stiffness, which is worse in the morning, and is eased by mild physical activity. - extra-articular or juxta-articular bony tenderness due to entbesitis may be an early feature of the disease and can be a major or presenting complaint in some patients. - involvement of peripberal joints, other than hips and shoulders, is inftequent in primary ankylosing spondylitis. - mild constitutional symptoms such as anorexia, malaise, or mild fever may occur in some patients in early stages of the disease. - physical signs may be quite minimal in early stages of the disease, however there is often some limitation of motion of the lumbar spine '\\ith associated spasm and soreness of the parnspinal muscles. - the Wright-Schober test is quite useful in detecting limitation of forward flexion of the lumbar spine. - involvement of costovertebral and costotransverse joints results in restriction of chest expansion ( nonnally no less than 1 inch in women and 1 112 inches in men ) and breathing that becomes primarily diaphragmatic. - direct pressure of the inflamed sacroiliac joints frequently causes pain. - back pain and stiffness generally diminish over the years but some degree of inflammatory pain persists. - contractures at hips and compensatory flexion of the knees favor the stooped over posture so that in advanced cases the patient appears to be doubled up. - sciatica-like pain may alternate from one side to another and is not significantly relieved by changes in position.

III

EX1RASKElEfAL MANIFESTATIONS

- the most common extraskeletal involvement is acute anterior uveitis ( acute iritis ) which occurs in 25-30% of patients at some time in the course of the disease. - cardiovascular involvement is rare and includes ascending aortitis, aortic valve incompetence, and conduction abnormalities. - lung parenchymal involvement is rare and is characterized by a slowly progressive fibrosis at the uwer lobes of the lungs. - neurologic involvement may occur most often related to spinal :fracture/dislocation, atlantoaxial sublu.~on, or cauda equina syndrome. Spontaneous anterior atlantoaxial subluxation is a well recognized complication occurring in about 2% of patients.

RADIOGRAPHIC FEATURES

1. Sacroiliac joint : Sacroiliitis is the hallmarlc of ankylosing spondylitis. Although an asymmetric or unilateral distnbution can be evident on initial radiographic ex.am, radiographic changes at later stages of the disease are almost invariably bilateral and asymmetrical in distribution.

2. Spine : Abnormalities of the spine can be seen in the discovertebral junction, apophyseal joints, costovertebral joints, posterior ligamentous attachments, and atlantoaxial articulations.

3. Ankle : Rarely, changes in the ankle.can be noted in ankylosing spondylitis. The changes resemble findings in other articulations. Periostitis is particularly characteristic in the distal medial tibia.

4. Forefoot and midfoot : Bilateral symmetric or asymmetric abnormalities of the feet, which can be evident in approximately 15% of patients with long standing ankylosing spondylitis, show a predilection for MfP and 1st tarsometatarsal joints, and for the IP joint of the great toe. Soft tissue swelling, diffuse joint space narrowing, erosions with adjacent bony proliferation predominately on the medial aspect of the metatarsal heads, periostitis of phalangeal and metatarsal shafts. and intra-articular bony ankylosis can be detected Subluxation at MfP joint articulations consisting of fibular deviation of the toes is less frequent and less severe than in rheumatoid arthritis.

5. Calcaneus : Although clinically manifest heel abnormalities are infrequent in ankylosing sponciylitits, radiographic changes of the calcaneus are common. Bilateral abnormalities predominate. Well defined plantar or posterior calcaneal spurs, or both, are a common manifestation, but are similar in appearance to those in a "normal" population. Retrocalcaneal swelling related to bursitis, posterior calcaneal erosion, and Achilles tendon thickening are also frequent Bony erosion and proliferation resulting in ill-defined spur formation at the site of ligamentous attachment to bone on the inferior surface of the calcaneus may occur. Periosteal proliferation along the entire undersurl'ace of the calcaneus is evident in a few patients.

LABORATORY FINDINGS

- there is no specific test for ankylosing spondylitis. - HLA-B27 has a 9()O/o sensitivity among Cancasians, but is an expensive test and should not be used for routine screening. - up to 75% of patients have an elevated erythrocyte sedimentation rate. - mild to moderate elevation of serum 19A is frequently observed - synovial fluid analysis is similar to Iheumatoid arthritis. - normocytic, hypochromic anemia may be seen.

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HLA-B27 ASSOCIATIONS

Spondyloarthropathies Balanitis, uveitis. etc. Colorectal cancer Asbestosis Chronic inflammatory bowel disease Lymphoblastic leukemia Secondary amyloidosis

TREATMENT

- patient education -NSAIDS - snJfasaJazine ( may be useful for peripheral arthritis ) - local corticosteroid injections - daily exeIcises - surgical intenrention

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PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY PHARMACOLOGY

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1--1.' 1"- 'R" "..-" (j' Ji, i-\.~. ,./-\ L .. ~_}

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ANTIBIOTICS

L Penicillins Mechanism of Action

-bactericidal - act on penicillin binding protein to inhibit cell wall synthesis

Classification of Penicillins

1. Natural Penicillins Penicillin G -1.2-40 million units 1M or N qd Penicillin V - 250-500 mg po qid

Spectrum of Activity - streptococci, nonpenicillinase staphylococci - non penicillinase producing gonococci - anaerobes (not Bacteroides)

2. Aminopenicillins Ampicillin - 250-1000 mg PO, 1M, N q4-6 hr Amoxicillin - 250-500 mg PO tid

Spectmm of Activity - streptococci, enterococci - gram negatives (E. coli, P. mirabilis, Shigella,

Salmonella)

3. Semi-synthetic (penicillinase resistant) Methicillin Oxacillin Dicloxacillin Nafcillin Cloxacillin

Spectrum of Activity - staphylococci (not MRSA) - streptococci

4. Expanded Spectrum (anti-pseudomonal penicillins) Carcenicillin Piperacillin Mezlocillin Ticarcillin Azlocillin

Spectrum of Activity - increased gram negative (pseudomonas, Enterobacter) - streptococci - not active against Staphylococci

5. PenicillinlB-Iactamase Inhlbitors ticarcillinlclavulanic acid (Timentin) - 3.1 gm N q4-6hr piperacillinltazobactam (Zosyn) - 3.375-4.5 gm N q8hr ampicillinlsulbactam (Unasyn) - 1.5-3.0 gm N q6hr amoxicillinlclavulanic acid (Augmentin) - 875 mg po bid

Spectrum of Activity - staphylococci (not MRSA) - streptococci - anaerobes (including Bacteroides) - gram negatives (Pseudomonas, Enterobacter)

Adverse Reactions - hypersensitivity -diarrhea - neutropenia - transient elevation of LIT's - thrombocytopenia - high sodium (especially with ticarcillin) - myoclonic seizures

114

n. Cephalosporins Mechanism of Action

-bactericidal - inhibition of cell wall synthesis

Agents Available:

I" Generation ~1l.1 Creneration 3,,1 Generatioll ~ til Gl'ner.nillll Cefazolin(Ancef) Cephalothin(Keflin) Cephaperin(Cefadyl) Cephalexin(Keflix) Cephadine(Ansper) Cefadroxil(Duricef)

Cefoxiten(Mefoxin) Cefuraxime(Zinacef) Cefotetan(Cefotan) Cefamandol(Mandel) Cefonicid(Monocid) Ceforamide(Precef) Cefaclor(Ceclor) Cefpodoxime(Vantin) Cefuroxime axetil(Ceftin)

Spectrum of Activity 1 st Generation

- Staphylococci. Streptococci

Cefotaxime(Clafoxin) Cizaxime(Cefuax) Ceftriaxone(Rocepbin) Ceftaxidime(Fortaz) MoxaIactam(Maxam) Cefoperazone(Cefobid) Cefixime(Suprax)

Cefipime(Maxjphne)

- gram negatives (E. coli. P. mirabilis, Shigella, Salmonella) - anaerobes (not Bacteroides)

2nd Generation - Staphylococci (less active than 1 st generation) - Streptococci (same as 1st generation) - more gram negative (II. influenza, Proteus. Klebsiella, E.coli) - anaerobes (cefotetan & cefoxitan active against Bacteroides)

3rd Generation - Staphylococci. Streptococci (less active than 1 st & 2nd)

- Pseudomonas (ceftazadime & cefoperazone only) -anaerobes

4th Generation - same as earlier agents - greater gram negative coverage (including Pseudomonas)

Adverse Reactions - hypersensitivity (cross reactivity with PCN allergy 5-15%) - neutropenia - diarrhea - bleeding - phlebitis with IV administration

mOther B-Lactams lmipenemlCilastatin (Primaxin) - 500 mg IV q6-8hr

Spectrum of Activity - vety broad - most gram positive aerobes & anaerobes - gram negatives (including Pseudomonas) - anaerobes (including Bacteroides)

Adverse Reactions - seizures in patients with hlo seizures - nausealvomiting

115

Aztreonam - 1-2 gm IV q8h Spectrum of Activity

- gram negative aerobes(Pseudomonas) - not active against gram positive or aerobic organisms

Adverse Reactions - no major side effects

IV. Quinolones Mechanism of Action

- bactericidal - inlnbits DNA gryase

Available Agents Ciprofloxacin Lomef1oxacin Ofloxacin Levofloxacin Enoxacin Sparfloxacin

Spectrum of Activity - Staphylococci (!!Qt MRSA) - gram negative bacilli (Pseudomonas) - Enterobacter

Adverse reactions - GI (nausea, vomiting, diarrhea) - insomnia -headache - seizures

Trovafloxacin Sparfloxacin

- contraindicated in children -- defects in cartilage - drug interaction with theophylline & antacids

v. Aminoglycosides Mechanism of Action

- bactericidal - binds 30S bacterial ribosome to inlnbit protein synthesis

Available Agents Gentamycin Tobramycin Amikacin

Daily Dose 3-5 mglkg q8h 3-5 mglkg q8h 15 mglkgq8h

*Check trough after third dose

Peak(uglmJ) 4-10 4-10 20-30

Trough(uglml) 2 2 10

*dosing is now being recommended for q 24 to decrease toxicity (able to do this due to postantibiotic effect of the medication)

Adverse Effects

1. ototoxicity - irreversible

2. nephrotoxicity - reversible

3. neuromuscular blockade

Synergy with PCN Dose Gentamycin 3mglkglday q8h or q12h Adjust dose to 2mglkg/day in ESRD

116

VI. Sulfonamides - Trimetboprim Sulfamethoxazole (Bactrim) Mechanism of Action

- bacteriostatic - sulfamethoxazole ~ inlubits folic acid production - trimethoprim ~ inhibits bacterial dihydrofolate reductase

Dosage => I DS tablet bid - trimethoprim 160 mg/sulfamethoxazole 800 mg - excellent oral absorption; parenteral form rarely used

Spectrum of Activity - Staphylococci (including MRSA & MRSE) - Streptococci - gram negatives (pseudomanas)

Adverse Reactions - hypersensitivity

- hemolytic anemia - contraindicated with oral hypoglycemics & G-6-PD deficiency

YD. Macrolids Mechanism of Action

- bacteriostatic - binds 50s bacterial ribosome inhibiting protein synthesis

Agents Available Erythromycin (E-mycin) - 250-500 mg po qid Azithromycin (Zithromycin) - 500 mg 1st day, 250 mg qd x 4 days Clarithromycin (Biaxin) -- 250 Dig po bid Dirythromycin (Dynabac) - 500 mg po qd

Spectrum of Activity - Staphylococci & Streptococci - some anaerobes (not Bacteroides)

Adverse Reactions - gastrointestinal (nausea & vomiting) - hepatotoxicity - thrombophlebitis with IV infusion - hypersensitivity

YD. Vancomycin Mechanism of Action

- bactericidal

Dosage

- inhibition of cell wall synthesis

- 1 gram IV qI2h[22.5(CrCI) + 150] = 24h requirement - 125 mg po qid for C. difficile colitis only - must monitor peaks and troughs

peak -- 15-30 mg/mL(ideal peak is betw. 30-40) trough - < 10 mglmL(ideal trough is betw. 10-12)

get peaks!troughs after fifth dose Spectrum of Activity

-MRSA&MRSE - Staphylococci, Streptococci, Enterococci - gram positive anaerobes (Clostridium, Comybacterium) - not active against gram negatives

117

Adverse Reactions - nephrotoxicity - ototoxicity - reversible - red man syndrome

- anaphylactoid reaction whereby histamine is released by mast cells - dne to rapid IV infusion - erythema & pruritis especially of upper torso, neck and :face - treatment: antihistamines

IX. Clindamycin Mechanism of Action

- bacteriostatic - inhibits translation by 50s bacterial ribosome Dosage

- 600-900 mg IV q8h - 300 mg po bid-tid

Spectrum of Activity - Staphylococci, Streptococci - anaerobes (Bacteroides)

Adverse Reactions - pseudomembranous colitis - diarrhea, nausea

X. Tetracyclines Available Agents

Minocycline - 100 mg po q12-24h Doxycycline - 100 mg po q12-24h Tetracycline - 250-500 mg po qid

Spectrum of Activity - Staphylococci, Streptococci - some gram negatives and anaerobes - rare organisms (B. burgdorferi, Actinomyces, M. Marinum)

Adverse Reactions - gastrointestinal irritation - rash & photosensitivity - staining of bones and teeth

XI. Rifampin Dosage - 300 mg po bid Spectrum of Activity

- Staphylococci, Streptococci -Mycobacteria - some gram negatives (Neisseria, Haemophilus)

Adverse Reactions - red discoloration ofbody fluids (urine, tears, contact lenses) - skin rash - flu-like symptoms

xn. Metronidazole (F1agy1) Dosage

- 500 mg po tid - intravenous -- 15 mglkg load; 7.5 mglkg q6-8h

Spectrum of Activity - gram negative anaerobes (Bacteroides)

118

Adverse Reactions - metallic taste/dry mouth - antabuse reaction - seizures in patients with bJo seizures

Surgical Propbylaxis =:;;. Goal is to provide adequate drug level prior to and during the surgical procedure

Indications: - prolonged surgery (>2 hours) - use of implants (screws, k-wires, prostheses, etc.) - trauma surgery - immunocompromised patients - SBE risks

Selection of Agents: - active against most conmlon causative organism (Staphylococcus aureus) - long half life - intravenous administration - antibiotic level should be maximal at incision

Specific Agents: Cefazolin I gran1 IV Clindamycin 600 mg IV Vancomycin I gram IV

Miscellaneous Information

Antibiotics for MRSA - vancomycin - minocycline - ciprofloxacinlrifampin - bactrimlrifampin

Disulfiram! Antabuse Reaction - nausea, vomiting, diarrhea - occurs "\Vith concurrent ingestion ofEtOH and certain antibiotics - related with the MMT sidechain present on some antibiotics - specific drugs:

moxalactam cefomandol cefoperazone metronidazole

Antibiotic Associated Diarrhea 2 Types:

cefotetan

1. overgrowth of C. difficile (pseudomembranous colitis)

2. alteration of intestinal microbial population Characteristics:

- can be caused by any antibiotics - clindamycin is most common cause - occurs with oral or parenteral administration - independent of dose or duration of treatment

119

Treatment: - discontinue antibiotic if possible - no antidiarrheal agents (allows toxin to accumulate) - fluid and electrolyte support - antibiotic therapy

metronidazole 500 mg q8h vancomycin 125 mg po q6h

ANTIFUNGAL AGENTS

Amphotericin B Nystatin

Imidazoles Miconazole Ketoconazole

Triazoles Itraconazole Fluconazole

Imidazoles Miconazole Clotrimazole Ketoconazole Econazole Oxiconazole Sulconazole

Mechanism of action: FUNGISTATIC.

Terbinafine

Naftifine Terbinafine

POLYENES

Flucytocine Griseofulvin

Specific Cicloprox Olamine Haloprogen Tolnaftate lodochlorhydroxyquin

Nonspecific Whitfield's Ointment Undecylenic acid Castellani's Paint

Binds irreversibly with ergosterol (principal sterol in the fungal cell membrane). This results in altered membrane permeability, leakage of intracellular constituents, and cell death. Other possible mechanisms include oxidative membrane damage and enhancement of cell mediated immunity.

NYSTATIN (Mycostatin, Nilstat,) ·cream, ointment, powder ·apply to affected area BID ·inhibits cell membrane sterol biosynthesis -essentially no absorption with oral form- used to treat oral esophageal and GI candidiasis -indicated specifically for Candida

AMPHOTERICIN B (fungizone) -lotion, ointment, and cream in 3% concentration -apply to affected areas BID-QID -derived from Streptomyces Nodosus -active against saprophytes and yeast -oral form poorly absorbed

120

·used intravenously for potentially life threatening deep mycotic infections/systemic fungemia Dose: 0.25mg/kg/day infused slowly over 6 hours (important to monitor BUN/CR)

With incr. of Cr to>3.0 switch to lipophilic Amphotericin B (Amphotec) Side Effects: GI distress, fever, chills, headaches, hypotension, hypokalemia, hypomagnesemia, anemia, thrombophlebitis, lifer failure, renal failure Drug Reactions:

AZOLES

Aminogylcosides & Cyclosporine: synergistic nephrotoxicity Corticosteroids & K+ depleting diuretics: may potentiate hypokalemia, hypomagnesemia

Imidazoles and Triazoles Mechanism of action: FUNGISTATIC

·inhibit growth of fungi by interfering with cell membrane ergosterol biosynthesis by preventing the

14·alpha·demethylation of lanosterol ·may inhibit cytochrome c peroxidative and oxidative enzymes resulting in

increased intracellular peroxide generation

·effective against dermatophytes, saprophytes, candida and some gram positive bacteria

·many have anti· inflammatory activity

SYSTEMIC AZOLES- IMIDAZOLES:

MICONAZOLE (Monistat IV) ·NO oral preparation available ·intravenous or intrathecal Dose: 200·3600mg/day in 3 divided doses Side Effects: GI distress, phlebitis, seizures, tremors, anemia, hyponatremia,

thrombocytopenia, cardiac dysrhythmias Drug Interactions: may inhibit metabolism of Sulfonolureas, Coumadin, Phenytoin

KETOCONAZOLE (Nizoral) -well absorbed ·99% bound to plasma protein ·reaches skin via bloodstream and eccrine sweat glands ·excreted predominantly through bile (feces 57%, urine 13%) Indications: blastomycosis, coccidiomycosis, paracoccidiomycosis, histoplasmosis, chronic mucocutaneous candidiasis, superficial dermatophyte infections Dose: 200-400mg/day for 2-8 weeks (superficial infections) 8-18 months

(onychomycosis) Side Effects: Many! more common SE's include GI disorders.

Less common SE's: hepatotoxicity, CNS disorders (HA, dizziness), adrenal insufficiency, gynecomastia, impotence, thrombocytopenia, anemia, leukopenia ·asymptomatic elevation in liver transaminases occur in 2-10% of patients

121

Drug Interactions: Antacids, H2 Blockers, Rifampin, Isoniazid, Phenytoin, terfenadine, Astemizole, Chlordiazepoxide, Coumadin, Cyclosporin, Insulin, Amphotericin B, Corticosteroids, Alcohol

SYSTEMIC AlOLES- TRIAZOLES: -triazole ring may be responsible for increased potency, decreased toxicity, and wider

spectrum of action of these agents

ITRACONAZOLE (Sporanox) -rapidly absorbed -lipophilic -only 0_2% free drug in the plasma -"reservoir" effect- therapeutic levels persist in skin/nails/hair follicles for weeks after discontinuation of

therapy; detected in toenails for 6 months after cessation of therapy -hepatic metabolism-liver function tests (LFT's) should be monitored regularly -excretion: urine (35.2%) and feces (54.1%) -not removed by hemodialYSis Indications: blastomycosis, histoplasmosis, asprigillosis, dermatophyte onychomycosis

Contra indications: -coadministration with Terfenadine, Astremizole, Triazolam, And

Midazolam -avoid in pregnancy and in nursing mothers- dose dependent maternal toxicity and embryotoxicity

ITRACONAZOLE (Sporanox)-continued

Dose: for onychomycosis 200mg po BID for 7 days, then first week of each month for 3-4 months (ie. Pulse dosing)

OR 200mg/day for 3 months

for tinea pedis 100mg/day for thirty days

-clinical cure rate approx. 60-70%; mycologic cure rate approx. 74%; approx. 15% relapse rate

Side Effects (incidence 7·12.5%): GI disorders, HA, dizziness, dizziness, malaise, myalgia, rash, pruritis, fever, idiosyncratic hepatitis, vasculitis, edema, HTN, orthostatic hypotension, hypokalemia, gynacomastia, impotence -elevation of LFT's in 0.3%-5% of patients- usually transient

Drug Interactions: -decrease Itraconazole levels: Rifampin, Isoniazid, Phenobarbitol,

Carbimazepine, Phenytoin, H2 Blockers

·increases drug concentrations of: Warfarin, Digoxin, Cyclosporin, Oral Hypoglycemics

FLUCONAZOLE (Diflucan) -intravenous form available ·hydrophilic -more than 90% of ingested dose is absorbed

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-only 11 % bound to plasma proteins, majority of circulating drug in free form -no significant first pass metabolism. unlike other azoles -primarily excreted through the kidney: unchanged (80%) metabolites (11 %) -high concentrations in the stratum corneum and sweat -detected in skin 10 days after cessation of therapy Indications: vaginal and oropharyngeal/esophageal candidiasis, cryptococcal meningitis Dose: for onychomycosis 150-300mg/week for 6-12 months

for tinea pedis 150 mg/week for 4 months if creatinine clearance >50mllmin then give full dose if creatinine clearance is 21 to 50 ml/min then give half dose if creatinine clearance is 11 to 20 mllmin then give 1/4 dose

-clinical cure rate approx_ 60%; mycologic cure rate 65% Side Effects: GI disorders, HA, rash, increased LFT's Drug Interactions:

-increases drug levels of: Warfarin, Cyclosporine, Theophyline, oral hypoglycemic agents

-increases Fluconazole levels: Rifampin -Phenytoin metabolism inhibited

TOPICAL AZOLES:

MICONAXOLE NITRATE (Micatin, Monistat) -2% cream, aerosol, powder, solution -apply to affected areas BID

CLOTRIMAZOLE (Lotrimin, Mycelex) -1 % cream, lotion, solution -apply to affected areas BID

KETOCONAZOLE (Nizoral) -2% cream -apply once daily -avoid in pts with sulfite sensitivity

ECONAZOLE NITRATE (Spectazole) -1% cream -apply once or twice daily -may be effective against some g+ bacteria

OXICONAZOLE NITRATE (Oxistat) -1 % cream, lotion -apply once or twice daily -may be effective against some g+ bacteria

SULCONAZOLE NITRATE (Exelderm) -1 % cream, solution -apply to affected areas BID

CLOTRIMAZOLE AND BETAMETHAZONE (Lotrizone cream) -apply to affected areas BID -for more inflammatory dermatophyte and yeast infections

**stinging, burning, itching, blistering, and contact dermatitis can occur with any topical antifungal**"

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ALLYLAMINES

Mechanism of action: FUNGICIDAL vs. dermatophytes -potent inhibition of ergosterol synthesis by selective inhibition of squalene

epoxidase -lack of ergosterol can interfere with the integrity and growth of the fungal

cell wall -squalene epoxidase inhibition causes squalene accumulation that may be

fungicidal -weakens cell membrane and causes cell death -effective against some gram positive and gram negative bacteria

NAFTIFINE (Naftine) -1 % cream and gel -apply to affected areas BID -lipophilic- binds well to the stratum corneum and penetrates into hair follicles -has anti·inflammatory properties

TERBINAFINE (Lamisil) Topical:

-1% cream -apply to affected areas BID

Systemic: -lipophilic- high concentrations found in stratum corneum, hair, and sebum -70-80% of oral dose is absorbed -significant first pass metabolism -80% oral dose (metabolites) excreted in urine -drug levels exceeding the MIC for dermatophytes persists for 2 to 3 weeks after

cessation of therapy Indications: onychomycosis due to dermatophytes Dose: for onychomycosis: 250 mg/day for 12 weeks

for tinea pedis: 250 mg/day for 2-6 weeks -decrease dose in liver dysfunction and when creatinine clearance is <50ml/min -mycologic cure rate 70%; mycologic and clinical cure-38%; 85% pts with no relapse

Side Effects: hepatic dysfunction (rare), GI disorders, HA, skin reactions/rash, fatigue, loss of taste, visual disturbances, neutropenia

-avoid in pregnancy and nursing mothers

Drug Interactions: less potential for drug interactions than Azoles -Terbinafine clearance increased by: Rifampin (100%), Phenobarbital -Terbinafine clearance decreased by: Cimetidine (33%), Terfenadine (16%)

MISCELLANEOUS AGENTS SYSTEMIC:

FLUCYTOSINE (Ancobon) MOA: inhibits RNA synthesis in susceptible fungi containing the enzyme cytosine

permease -typically used in combination with Amphotericin B Uses: systemic mycosis, candidiasis Dose: 50-150mg/Kg po in divided doses every 6 hours

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Side effects: GI distress, CNS disorders (HA, dizziness), skin rash, abnormal liver function, bone marrow suppression, renal failure, cardiac arrest, respiratory arrest

GRISEOFULVIN (Grifulvin, Fulvicin, Grisactin) MOA: FUNGISTATIC

-inhibits cell mitosis and nucleic acid synthesis -possibly inhibits chitin synthesis -has anti-inflammatory properties -effective against recalcitrant skin, hair, and nail infections caused by dermatophytes

-not effective against candida -reaches stratum corneum by sweating and diffusion -not recommended in pregnancy -contraindicated in hepatic disease and porphyria Dose: 500mg po QD; 330-375mg po QD (ultramicrosize) Side Effects: Many!

-more common include: GI distress, HA -less common include: CNS disorders, urinary disorders, cutaneous disorders, neutropenia, Arthralgias, liver dysfunction

Drug Interactions: barbiturates, coumadin, oral contraceptives, cyclosporine, alcohol

TOPICAL:

HALOPROGEN (Halotex) -FUNGICIDAL against dermatophytes, Candida -synthetic 1% cream and solution -apply to affected areas BID

CICLOPROX OLAMINE (Loprox) -FUNGICIDAL --blocks transport of amino acids into the fungal cell and weakens fungal cell membrane -effective against dermatophytes, candida and some bacteria -1% cream, lotion -apply to affected areas BID -has anti-inflammatory properties

MISCELLANEOUS TOPICAL AGENTS (continued)

TOLNAfTATE (Tinactin, Aftate) -FUNGICIDAL -inhibits sqealene epoxidase -inhibits growth of hyphae -limited to dermatophytes -synthetic 1 % gel, powder, cream, aerosol -apply to affected areas BID

UNDECYLENIC ACID (Desenex, Cruex) -FUNGISTATIC -cream, ointment, powder, spray powder -apply to affected areas BID

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WHITFIELDS OINTMENT -12% benzoic acid (FUNGISTATIC) and 6% salicylic acid (keratolytic) -causes desquamation of kertinized epidermis containing fungal organisms

CASTELLANI PAINT (fuchsin, phenol resorcinol, acetone, SP alcohol40B, purified water) -topical antifungal drying agent -apply 1-3 times daily

LOCAL ANESTHETICS

Mechanism of Action a. surface charge theory:

-local binds to receptor in the Na channel in nerve membrane -Na channel is blocked -decrease in rate and degree of depolarization -lack of development of action potential -conduction blockade

b. membrane expansion: -ability of un-ionized compounds to possess anesthetic activity -altered configuration of the membrane -decreased diameter of the Na channel -inhibition of Na influx / conduction blockade

c. diffusion: -diffusion of LA depends on degree of ionization -LA exist as uncharged molecule and charged cations -proportion depends on pKa of LA and pH of solution -governed by HendersolJ-Hasselbalch equation

pH = pKa + log base/cation -as pH decreases equilibrium shifts toward cation which binds to receptor -as pH increases equilibrium shifts toward base which causes membrane expansion

Pharmacology Esters and Amides

metabolism stability in sol'n allergic rx Ester plasma esterase unstable rare(para-aminobenzoic acid)

Amide hepatiC enzyme stable very rare

Characteristics: I.Lipid Solubility

-LA that are lipid soluble penetrate nerve membrane readily -they have a greater potency

2.Protein Binding -influences duration of action -agents of short duration bind poorly

126

3.pKa -defines the pH at which the base and cation forms are equal -agents with a pKa closer to tissue pH have a rapid onset

4.1 ntrinsic Vasodilator Activity -influences potency/duration of action -inc. in vasodilator activity = inc. in vascular absorption -less LA available for nerve blockade

Agents: ESTERS

l.Cocaine-addictive, only vasoconstrictor, used as topical anesthetic 2.Procaine-weak potency due rapid hydrolysis, used for infiltration anesthesia 3.Chlorprocaine-rapid onset, less toxic, used in obstetrical cases 4.Tetracaine-slow onset,inc. toxicity, used for spinal anesthesia

AMIDES I.lidocaine-rapid onset, used in regional, topical anesth., antiarrythmic 2.Mepivacaine-used for infiltration, peripheral block, epidural 3.Prilocaine-least toxic, used for intravenous regional anesth_, 4.Bupivicaine-long duration, used in chronic pain, epidural (labor) 5.Etidocaine-rapid onset, intense motor blockade 6.Ropivacaine-rapid clearance,shorter half-life than bupiv.

Toxicity CNS

Initial events Tinitus I ightheadedness confusion

Excitation phase tonic-clonic convulsions

Depression phase unconsciousness general CNS depression respiratory arrest

Maximum Recommended Doses

Drug mg/70kg

chlorprocaine lidocaine lidocaine lidocaine mepivacaine prilocaine bupivacaine etidocaine etidocaine

Conc.

(%) 3.00 1.00 1.50 2.00 2.00 3.00 0_75 1.00 1.50

mg/kg

PI/(Epi) 11(14) 4(7) 4(7) 4(7) 4(7)

7(8.5) 2.5(3.2)

6(8) -(8)*

CVS Initial events

hypertension/tachycardia I ntermediate phase

myocardial depression decreased cardiac output mild hypotension

'Terminal phase peripheral vasodilation profound hypotension sinus bradycardia conduction defects ventricular arrythmias circulatory collapse

mg/70kg

Pl(EPI) 770(980) 280(490) 280(490) 280(490) 280(490) 500(600) 175(225)

420(560) - (560)

Pl(EPI) 25(33) 28(50) 19(33) 14(25) 14(25) 17(20) 23(30)

42(56) - (37)

*etidocaine 1.5 not available without epinephrine -doses in parentheses apply when epinephrine 5ug/ml is added to solution

127

Alternative agents: BENZYL ALCOHOL 0.9%:

Indicated with patients with amide/ester allergies For use in short lacerations and superficial wounds

GLUCOCORTICOIDS

Glucocorticoids are the most powerful but also the most toxic class of drugs used for the treatment of inflammatory conditions. The investigation and use of glucocorticoids began almost fifty years ago, yet many controversies still remain regarding their clinical uses, risks and benefits.

Glucocorticoid Structure - cortisone is the main endogenous glucocorticoid - structure is a 21 carbon steroid hormone - synthesized from cholesterol - activity depends on structure

- structure determines potency and rate of absorption - cortisone and prednisone are inactive until converted to cortisol and

prednisolone

Hypothalamic Pituitary Adrenal Axis - regulates cortisol secretion - basal induced glucocorticoid release

- 20 mg/day - diurnal - increased in evening and morning

- stress induced glucocorticoid release - cold, exercise, infection, surgery

. HPA axis suppression => adrenal insufficiency - due to increased endogenous or exogenous glucocorticoid - symptoms of adrenal insufficiency

- nausea, U BP,.hyperkalemia, CV collapse - surgical stress dosing

. for pt's on > 7.5 mg/dayof prednisone for 1 month - hydrocortisone 100 mg IV for total 300 mg

Mechanism of Action - work through the synthesis of other compounds - regulates transcription and ultimately protein synthesis - mechanism of action important because:

1. takes hours for a clinical response 2. action is indirect => causes many unwanted side effects

Metabolic Effects => glucocorticoids protect the glucose dependant tissues(brain & heart)

Carbohydrate Metabolism - increase gluconeogenesis - decrease peripheral glucose uptake

Lipid Metabolism - increases lipolysis => insulin release and gluconeogenesis

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Protein Metabolism - decreases synthesis and increases breakdown in muscle - increases free plasma amino acids

Fluids and Electrolytes - sodium and water retention - hypokalemia

Bone & Calcium Metabolism - decreases intestinal calcium absorption - inhibits osteoblast function

Connective Tissue - decreases collagen formation - impairs granulation tissue formation

Systemic Glucocorticoids TherapeutiC Effects

l. Anti-inflammatory - modulators of inflammation

- inhibit prostaglandin synthesis - inhibits COX-2 - inhibits cytokine, adhesion molecule, chemotactic factor prod.

- decreases vascular permeability - cellular effects - increases # of neutrophils but decreases accumulation at sites of inflammation - decreases # of macrophages, lymphocytes, eosinophils, basophils

2. Immunosuppressive - cellular> humoral - circulating lymphocytes and monocytes decrease - inhibit natural killer and T-cell proliferation - effective against acute graft rejection

3. Anti-asthmatic - inhibits lipooxygenase by promoting production of a protein called

Iipocortin - inhibits production of leukotriene C4 &04 ~ SRS-A - decreases bronchiole inflammation

Pharmacokinetics - absorbed orally, intramuscularly, intrasynovially, topically - metabolized in the liver, excreted in the urine

Dosing Regimens 1. Daily High Dose

- >15 mg prednisone daily - life threatening autoimmune diseases

2. Pulse Methylprednisolone - 1 gram IV over 45 minutes - used as last resort therapy

3. Daily Low Dose - <15 mg prednisone daily - most common dosing schedule - used for inflammatory arthritic processes

4. Alternate Day Dosing - less side effects - usually less effective

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Drug Interactions Increase Steroid Clearance

- phenytoin, rifampin, barbituates, carbamzepine Decrease Steroid Metabolism

- ketoconazole, estrogen-containing oral contraceptives Other Effects

- decrease plasma salicylate levels increase requirement for insulin/oral hypoglycemics

Adverse Responses Adverse responses to therapeutic uses of glucocorticoids are mainly due to

prolonged exposure to high doses_ Most adverse effects are dose related and a short course(2 weeks) even at high doses gives a low risk_ Although threshhold doses are varied for individual patients, studies have shown that all patients receiving 30 mg of prednisone daily for a three month duration will experience adverse responses_

Very Common - osteoporosis - increased appetite - centripetal obesity - impaired wound healing - increase infection risk - HPA axis suppression

Uncommon - glaucoma - benign intracranial hypertension - peptic ulcer disease - hypokalemic alkalosis

Comparison of Various Steroids Glucocorticoid Potency Short Acting

Cortisone(Cortone) 0_8 Hydrocortisone(Hydrocortonne) 1

Intermediate Acting Prednisone(Orasone) 4 Prednisolone(Delta-Cortef) 4 Methyprednisolone(Medrol) 5 Triamcinalone 5

Long Acting Dexamethasone(Decadron) 30 Paramethasone(Haldrone) 10 Beta methasone(Celestone) 30

Frequent - myopathy - avascular necrosis - hypertension

- edema - thin, fragile skin - cataracts

Rare - pancreatitis

- hirsituism - panniculitis

- impotence

Daily Dose(mg)

50 - 100

10 - 20 10 - 20 10 - 20 5 - 20

50 - 100

0_75 - 3_0 4-6 0_6 - 3

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Local Corticosteroids =>Maximize local effects and minimize systemic adverse effectsc:

Indications Contraindications - rheumatoid arthritis - infectous arthritis - gout and pseudogout - bacteremia - seronegative arthridities - periarticular cellulitis - acute traumatic arthritis - osteochondral fracture - osteoarthritis - jOint prothesis - SLE and MCTD - allergy - tendonitis/bursitis - osteomyelitis - nerve entrapment syndromes - bacterial endocarditis - plantar fasciitis - several days before joint surgery - intralesional/dermal

Adverse Responses - postinjection flare - due to crystal deposition in the joint - corticosteroid arthropathy - similar to Charcot osteoarthropathy - iatrogenic infection - very rare - tendon rupture - only if injected directly into tendonous substance - facial flushing - more common with triamcinalone - skin atrophy/depigmentation - periarticular calcification - especially in DIPJ's and PIPJ's of fingers/toes - systemic absorption - masks signs of infection (.J... edema, erythema, calor, dolar)

Topical Steroids Pharmacologic Actions

1. Anti-inflammatory vasoconstriction in the skin stabilizes lysosomal membrane prevents conversion of membrane phospholipids to arachidonic acids

2_ Dermal Atrophy inhibits fibroblast proliferation inhibits deposition of connective tissue collagen

3_ Inhibits Mitoses in Epidermis

Disorders Responsive to Topical Steroids Responsive

atopic dermatitis erythematosis

seborrheic dermatitis soles

lichen simplex chronicus lipoidica diabeticorum

allergic contact dermatitis(late phases) irritant dermatitis(late phases) numular eczematous dermatitis stasis dermititis psoriasiS of face and genitalia

Disorders Less

discoid lupus

psoriasis of palms and

necrobiosis

sarcoidosis lichen striatus pemphigus vitiligo

granuloma annulare

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Potency Classes of Topical Steroids Groups I & II

- high potency - short term therapy - not recommended for generalized dermatoses, chronic therapy, face of

intertriginous therapy - Gr. I examples: betamethasone dipropionate 0.05%, clobetasol

dipropionate 0_05% - Gr. II examples: betamethasone dipropionate 0.01%, fluocinonide .05%,

desoximetasone .25% Groups III, IV, V

- medium potency - recommended for trunk, extremities, scalp - use with caution in generalized dermatoses - Gr. III examples: triamcinalone 0.5% ointment, betamethasone 0.01 % cream Gr. IV examples: triamcinalone 0.1% ointment, betamethasone 0.025%

ointment · Gr. V examples: triamcinalone 0.1 % cream, hydrocortisone valerate 0.2%

Groups VI & VII - low potency - recommended for face, axilla, neck, groin - Gr. VI examples: flumethasone 0.03% cream, desonide 0.05% cream · Gr. VII examples: hydrocortisone 1 % cream, dexamethasone 0.04% cream

Topical Vehicles 1. Ointment

· almost pure grease with very little water · most occlusive and hydrating · provides greater steroid effect - use on dry rash, palms and soles; not for use on wet rash

2. Cream · grease with more water · steroid effect weaker · use for dry rash

3. Lotion · little grease with more water - steroid effect weaker - use on scalp, toe interspaces, axilla, groin

4. Solution · oily liquid of alcohol (propylene glycol) · steroid effect strong - fairly drying - burns on dry, cracked skin - use on scalp, toe interspaces, axilla, groin

5. Gel · steroid effect is as strong as in an ointment · may use under occlusion · very drying · use on scalp, toe interspaces, axilla, groin

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SEDATIVE HYPNOTICS/SLEEP MEDICATIONS

L 1EMAZEPAM (RESTORIL ) a..ASS : benzodiazepull hypnotic DOSAGE: 15-30 mgpoHSpm insomnia METABOLISM: heprtic EXCRETION: renal WARNINGS: l. do not use during pregnancy

2. combined effects with ETOH and CNS depressants 3. potential for abuse

2. 1RIAZOLAM (HALCION ) a..ASS : triazolobenzodiazepine hypnotic DOSAGE: 0.125-0.25 mg po HS pm insomnia METABOLISM: heprtic EXCRETION: renal WARNINGS: l.donmu~during~

2. use lower doses in elderly patients 3. may cause behavioral cl1al1ges 4. combined effects with ETOH and CNS depressants 5. potential for abuse

3. FLURAZEPAM (DALMANE) CLASS: benzodiazepam hypnotic agent DOSAGE: 15-30 mg po HS pm insomnia METABOLISM: hepatic EXCRETION: renal WARNINGS: l. do not use during pregnancy

2. combined effects with ETOH and CNS depressants 3. potential for abuse 4. do not use in children under 15 years of age

4. ESTAZOLAM (PROSOM) a..ASS : triazolobenzodiazepine hypnotic DOSAGE: 1-2 mg po HS pm insomnia METABOLISM: heprtic ( I3pid in smokers ) EXCRETION: renal WARNINGS: 1. do not use during pregnancy

2. combined effects with ETOH and CNS depressants 3. potential for abuse

5. DOXYLAMINE SUCCINAlE (UNISOM) CLASS : ethanolamine antihistamine DOSAGE: 25 mgpo HS pm insomnia METABOIJSM: heprtic EXCRETION: renal WARNINGS: 1. should only be taken at bedtime

2. combined effects with ETOH and CNS depressants

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6. ZOIPIDEM TAR1RA1E (AMBIEN) CLASS : IlOn-benzodiazepine hypnotic OOSAGE : 5-10 mgpo Hs pm insomnia METABOLISM: hepatic EXCRETION: renal WARNINGS: 1. use reduced dosage with elderly

2. oombined effects with EI'OH and CNS depressants 3. potential for abuse

ANTI-PRURITUS AND POTENTIATION OF NARCOTICS

1. DIPHENHYDRAMINE (BENADRYL) CLASS : antihistamine ADULT DOSAGE: 25-50 po tid-qid pm pruritus PEDS DOSAGE: 12.5-25 mg po tKkPd pm pruritus METABOLISM: hepatic EXCRETION: renal WARNINGS: 1. use lower doses in children and elderly

2. additive effects with ETOH and CNS depressants 3. do not give to patients taking MAO inlnbitors

2. PROME'IHAZINE (PHENERGAN) CLASS : phenothiazine derivitive with antihistamine, sedative, antimotion sickness, antiemetic, and

anticholinergic effects ADULT DOSAGE: 12.5-25 mg by deep 1M injection q 6-8 Hr PEDS DOSAGE: 12.5 mg by deep 1M injection q 6-8 Hr METABOliSM: hepatic EXCRETION: renal WARNINGS: 1. contains sodium metabisuIfite ( ? allergy )

2. avoid intra-arterial injection 3. intensifies and prolongs effects of CNS depressants and sedative hypnotics 4. may inteIact with MAO inlnbitors

3. HYDROXYZINE HCL (ATARAXIVISTARIL) CLASS: piperazine <b:ived antihistamine DOSAGE: 25 mg po ti<k}id pm pruritus ( AT ARAX )

50-100 mg 1M q 4-6 hr pm pain ( VISTARIL ) METABOliSM: hepatic EXCRETION: biliaIy WARNINGS: 1. potentiation of narcotics and CNS depressants

2. do not give to nursing mothers 3. indmationlsterile abscesses at injection sites

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ANTIEMETICS

1. CYCLIZINEHCL (MAREZINE) CLASS : piperazine derived antihistamine DOSAGE: 50 mg po q 4-6 hr MET ABOUSM : hepatic EXCRETION: renal W ARNlNGS : 1. combined effects with ETOH and CNS depressants

2. may cause hypotension especially after surgery

2. DIMENHYDRINATE ( DRAMAMINE ) CLASS: ethanolamine antihistamine DOSAGE: 50-100 mg po q 4-6 hr

50 mg 1M q 4-6 hr MET ABOUSM: hepatic EXCRETION: renal W ARNlNGS : 1. combined effects with ETOH and CNS depressants

2. use 'with caution ifhistory of seizure disorders

3. PROCHLORPERAZINE ( COMPAZINE ) CLASS: phenothiazine derivative OOSAGE : 5-10 mg po tid-qid

25 mg suPP pI" bid 5-10 mg by deep llvt injection q 3-4 hr

METABOUSM : hepatic EXCRETION: renal W ARNlNGS : L do not use in children ( symptoms similiar to Reye's syndrome)

2. strong extrapyramidal side effects 3, may cause orthostatic hypotension

4. TRIMETHOBENZAMIDE HCL (TIGAN ) CLASS : centrally acting antiemetic DOSAGE: 250 mg po tid-qid

200 mg suPP pI" tid-qid 200 mg 1M tid-qid

MET ABOUSM: hepatic EXCRETION: renal and biliaIy WARNINGS: L do not use in children

2. do not use with ETOH 3. Parkinson-like sytDJXoms 4. suppositories contain benzocaine

5. PROME1HAZINE (PHENERGAN) CLASS : phenothiazine derivative with antihistamine, sedative, antimotion sickness, antiemetic, and

anticholinergic effects OOSAGE : 12.5-25 mg by deep 1M injection q 6-8 HI METABOLISM: hepatic EXCRETION: renal WARNINGS: SEE PREVIOUS DESCRIPTION

135

6. ODANSElRONHCL (ZOFRAN) CLASS: serotonin 5 HI -3 receptor antagonist DOSAGE : 4 mg N pm nausea/vomitting METABOUSM : hepJtic EXCRETION: renal WARNINGS : RELATIVELY NEW WITH FEW ADVERSE EFFEcrs INCLINICAL 1RIALS

? Hepatic Toxicity

LAXATIVES AND STOOL SOFTENERS

1. YElLOW PHENOLPHlHALEIN AND OC:X:USATE CALCIUM (DOXIDAN) CLASS : irritant Jaxativelstool softener DOSAGE : 1-2 capsule po q day up to one week WARNINGS: (same as for COLACFJDIALOSE )

2. CASAN'IlIRANOL AND DOCUSATE SODRJM (PERICOLACE ) CLASS : irritant Jaxativelstool softener DOSAGE: 1-2capsulespoHS

15-30 mL (~) po HS WARNINGS: same as for COLACFJDIALOSE

3. DOCUSATE SODRJM ( COLACE, DIAWSE ) CLASS : surl3ctmt stool softener DOSAGE: 50-200 mg po q day ( COLACE )

100 mg po q day - tid (DIALOSE ) WARNINGS: 1. do not use with mineIal oil

2. do not use with abdominal pain, nausea, or vomitting

4. CASCARA SAGRADA CLASS : irritant laxative DOSAGE : 325 mg po HS

5. CALCIUMPOLYCARBOPHIL (FIBERCON, FIBERALL, MITROLAN) CLASS : bulk forming fiber laxative DOSAGE: 2 tabs up to qid (FIBERCON )

1 tab q day - qid (FIBERAlL) 2 tabs qid or pm (Ml1ROLAN )

1. should be taken with full glass of water to prevent choking ( tablets can swell in throat if not taken with WARNINGS at least 8 ounzes ofwater )

2. should be taken 1 hour before or 2 hOUl'S after tetIacyc1ine-like anbbiotics

6. PSYLlJUMHYDROPHlllC MUCllLOID (METAMUcn.) CLASS; bulk forming natural thempeutic fiber DOSAGE: avaiable in powders, pICkets, granules, and wafers

( see PDR for prescribing information ) WARNINGS: 1. patients may have an allergy to psyllium

2. contraindicated with intestinal obstruction and fecal impaction

7. SENNA CONCEN1RATE (SENEKOT) CLASS : irritant Jaxative

136

DOSAGE: 2 tabs po q day, preferably HS 10-15 mL (syrup) po q day. preferably HS 1 tsp (granules) po q day, preferably HS 1 StJR)OSitOly pr q day, preferably HS

8. SENNA CONCENTRAlE AND DOCUSAlE SODIUM (SENEKOT-S) a..ASS : irritant laxative/stool softener DOSAGE: 2 tabs po q day

9. BISACODYL (DULCOLAX) CLASS : irritant laxative DOSAGE: 10-15mgpoqday

1 suppository pr q day

10. DON'T FORGET PRUNE JUICE !!!!

ANTIDIARRHEAL AGENTS

1. NATIJRAL BELLADONNA ALKALOIDS WITII PHENOBARBlTOL (BELLATAL ) CLASS : anticholinergi.c/antisplsmodic DOSAGE: 1-2 tabs po tid-qid WARNINGS: 1. additive effects with Efoo and CNS ~

2. potential for abuse

2. DICYCLOMINE HCL (BENTYL ) CLASS : anticholinergic/antispasmodic DOSAGE: 80 mglday po in 4 divided doses WARNINGS: 1. contrnindications :

- obstructive llIOf81hy - obstructive disease of the GI tract - severe ulcerative colitis - reflux esophagitis -glaucoma - myasthenia gravis - nursing mothers

2. use with caution in patients with autonomic neuropathy, hepatic or renal disease, HIN, CAD, and CHF.

3. HYOSCYAMINE ( CYSTOSPAZ) CLASS : parnsympatholytic agent DOSAGE: 1-2 tabs po qid (fewer ifneeded ) WARNINGS: 1. contraindications :

-glaucoma - obstructive llIOf81hy - paralytic ileus - myasthenia gravis

137

4. GLYCOPYRROLA1E (ROBINUL) CLASS : anticholinergic agent DOSAGE: I tab po tid WARNINGS: 1. contraindications :

- autonomic neuropathy - hepatic or renal disease - ulcerative colitis - hyperthyroidism - hiatal hernia with esophageal reflux

5. DIPHENOXYLA1E HCL AND ATROPINE SULFA1E (LOMOTIL) CLASS : antidiarrheaV anticholinergic agent DOSAGE: 2 tab po qid WARNINGS: 1. :fluid and electrolyte monitoring a must

2. do not use for antibiotic associamd diarrhea 3. may interact with baIbituIates, tIanquilizers, ETOH, and MAO inhibitors

6. KAOLIN AND PECTIN (KAOPECfATE) CLASS : antidianheal agent DOSAGE: capsules, chewable tabs, and liquid preps

7. LOPERAMIDE HCL (IMMODIUM) CLASS : antidiarrheal agent DOSAGE : 4 mg po followed by 2 mg after each unformed stool

8. PINKBISMUlH (pEPTO BISMOL)

ANALGESICS

I. Morphine sulfate - adult dosage - 5-20mg q 4 hr SC,IM (also slow IV)

- 1O-20mg q 4 hr rectally - pediatric dosage - 0.I-O.2mg q 4 hr SC,IM - metabolism - liver - excretion - kidney - antidote - naloxone - (Narcan) - 0.4-2mg q 2-3 min IV,IM,SC up to O.lmglkg IV

MS Contin - 15,30,60,IOO,200mg in controlled release tablets with 200mg tablets only being used in

patients with tolerance - should titrate dose on an every 12 hoor interval starting V\-1.th 15mg q 12 hr PO

MSIR (Immediate release) - 15,30mg tablets or a solution of 5mgllml - should titrate dose 5-30mg q 4 hr PO is a good starting point

Morphine Derivatives: 1. Oxymorphone HCL (Numorphan)

- adult dosage - 1.0-1.5mg q 4-6 hr SC,IM or 0.5mg 4-6 IV 2. Hydromorphone HCL (Dilaudid)

- adult dosage - 2-4mg q 4-6 hr PO - 2mgq 4-6 hr SC - 3mg q6-8 hr Rectally

138

2. Methylmorphine S04 or P04 (Codeine)

- adult dosage - 15-60mg q 4 hr PO,IM,SC - pediatric dosage> I year old: O.5mglkg q 4-6 PO,SC - metabolism - liver - excretion - kidney and some liver - antidote - narcan as above

- Compounds containing Codeine

NAME CODEINE (mg) ASA (mg) ACETAMINOPHEN (mg)

Tylenol #2 15 300 Tylenol #3 30 300 Tylenol #4 60 300 Tyl/Cod Elixir 12 120 Empracet#3 30 300 Empracet#4 60 300 Emprin#2 15 325 Emprin#3 30 325 Emprin#4 60 325

Codeine Derivatives: 1. Oxycodone HCL

- Preparations and Dosages a. Percocet (5mg oxycodone, 325mg acetaminophen)

- 1-2 q 4-6 hrPO b. Tylox (5mg oxycodone, 500mg acetaminophen)

-lq6hrPO c. Percodan (4.5mg oxycodone, 0.38mg oxycodone terephthalate, 325 mg aspirin)

-lq6PO d Percodan Demi (pediatric)

- 112 the strength of regular percodan - 112 tab q 6 for children> 12 years old -114 tab q 6 for children 6-12 years old

e. Oxycontin (controlled release) - analgesia onset within one hour - sustained release over 12 hours - titrate every 1-2 days, if necessary - increase dose by 25-50% as necessary, do not increase dose :frequency - may give oxycontin immediate release for breakthrough pain - supplied in 10,20,40,80 mg tablets taken every 12 hours

139

2. Hydrocodone

Preparations and Dosages

NAME HYDROCOOONE (mg) ACETAMINOPHEN (mg) ASA(mg)

Lortab2.5 2.5 500 Lortab 5 5.0 500 Lortab 7.5 7.5 500 Lortab liquid 2.S 120 LortadASA 5.0 500 Lorcet 10.0 650 Hydrocet S.O 500 Vicodin 5.0 500 VicodinES 7.5 750

-- Dosages generally should not exceed 40mg of Hydrocodone

3. Propoxyphene HCLInapsylate (Darvon I Darvon-N) - adult dosage - Darvon 65mg q 4 hr PO

- Darvon-N 100mg q 4 hr PO or 10mglml susp at 10ml q 4 hr PO

- metabolism - liver - excretion - kidney - antidote - narcan as above - Preparations:

1. Darvon compound (32mg darvon.. 389mg ASA, 324mg caffeine) 2 .. Darvon with ASA (65mg darvon, 325mg ASA) 3. Darvon-N 50 (50mg darvon-N, 325mg acetaminophen) 4. Darvon-N 100 (100 darvon-N, 650mg acetaminophen)

** May be given to codeine/morphine allergic patients 4. Pentazocine HCLllactate (Talwin I Talwin Inj)

- adult dosage - SOmg q 3-4 hr PO, 30mg q 3-4 hr IM,SC,IV - contraindicated in children under 12

- metabolism - liver - excretion - kidney - antidote - narcon as above - Preparations:

1. Talwin compound (12.5mg pentazocine, 325mg ASA) -2tabq6hrPO

2. Talacen (25mg pentazocine, 650ng acetaminophen) -lq4hrPO

3. Talwin Inj *(caution with SC route - may cause skin damage Isclerosis!)

- 30mg q 3-4 hr IV,SC,IM 4. Talwin Nx *(contains Naloxone - an antagonist which

has no affect at 0.5mg PO however, it does have an narcotic antagonist affect if given IV at this

dosage - thus preventing abuse)* - 50mg pentaxocine, 0.5mg naloxone - 1 q 3-4 po (may be increased to 2 tabs if needed)

140

** All Talwin products may cause withdraw due to an antagonistic affect toward morphine and demerol regardless of the presence of naloxone

** May be used in morphine and codeine allergic patients

5. Meperidine HCL (Demerol) - adult dosage - 50-150mg q 3-4 hr PO,IM,SC

- lS-35mg/hr IV in divided doses or slow drip - pediatric dosage - 1.5mglkg q 3-4 hr PO,IM (single dose not to exceed lOOmg) - metabolism - liver - excretion - kidney - antidote - narcan - miscellaneous - May be given with 25-S0mg ofPhenergan or Vistiril in order to decrease the dose and not lose effect.

** This drug should not be given to dialysis patients due to its metabolite not being dialiazable and, this metabolite may induce seizures.

- Preparations: 1. Mepergan (2Smglml meperidine, 25mglml promethazine)

- adult - 2S-S0mg q 3-S 1M - children - O.5mg/lb q 3-4 1M

2. Mepergan Fortis (50mg meperidine, 25mg promethazine) - adult - 1 q 4-6 PO

6. Butorphanol (Stadol) - adult dosage - Img q 3-4 hr IV

2mg q 3-4 hr 1M - 1 mg puff up 1 nostril q 3 -4 hr

- pediatric dosage - contraindicated in patients under 18 - metabolism - liver - excretion - kidney - antidote - narcan as above

7. Non-narcotic agents with Narcotic-like pain relief A. Ketoralac (Toradol)

- adult dosage - 60mg loading dose then 30mg q 6 hr 1M - IOmg q 4-6 hr PO

* only for up to 5 days may this be used * This drug is a NSAID and has all the same precautions.

** General PrecautionslContraindications for these Medications -check: PDR if you are going to use these drugs and the following apply

1. compromised respiratory function 2. biliary tract dysfunction 3. increased CSF pressure 4. hepatic or renal disease 5. recent use of CNS depressants 6. Thyroid disease 7. recent use of MAO inhibitors 8. nursing mothers 9. be aware of acetaminophen and aspirin containing compounds and their relative contraindications

141

NON NARCOTIC I NON NSAID

- TRAMAOOL HCL (Ultram) CLASS: analgesic centrally acting DOSE: 50 - 100 mgpo q 4 - ~ brs.

max dose : 400mg I day METABOLIZED: liver CLEARED: renal WARNINGS: creatinine clearance< 30ml/min : dose: 50 -100mg po q 12 Ms.

cirrhosis pt. dose : 50mg po q 12 brs. may potentiate seizure risk with other medications associated with many GJ. complaints

NONSTEROIDAL ANTllNFLAMMATORY DRUGS

Pharmacology • With the exception of nabumetone, all NSAIDs are weak acids.

• Acidic environment of stomach I proximal small iiltestine • NSAIDs - nonionized lipophilic state allowing for rapid and complete absorption. • Most NSAIDs reach peak plasma concentIations- three hours. • Steady state plasma concentrations are achieved in 3-5 half lives.

• Extensively bound to plasma proteins (98-9CJOAl) • small volume of distribution. (1-2% of the drug is "free")

• Patients with hepatic dysfunction may require dose alterations. . • Sulindac and Nabumetone - prodl1lgs (converted in the liver to active form) • Most NSAIDs undergo hepatic biotransformation either through the cytochrome p450 system

or glucuronide conjugation • Elimination is predominantly through the kidney although some NSAIDs can be eliminated either

partially or totally through the biliary tract (e.g .. Sulindac, Indomethacin). • patients with renal failure conjugated metabolites can accumulate and be reabsorbed and

reconverted to the active drug. • Differences in NSAID half-life generally reflect differences in renal clearance

• The acidity of inflamed synovial tissue allows for increased penetration into joints and a larger portion of unbound drug in synovial fluid

• Joint concentrations ofNSAIDs will remain constant even when serum concentrations fluctuate.

Mecbanism of Action • NSAIDs possess analgesic. antipyretic, and anti-inflammatory effects. • The exact mechanism of action is not known. • Therapeutic effect is thought to be due to the inhibition of prostaglandin (PG) synthesis (yet for

many NSAIDs the dose required to suppress prostaglandin synthesis is lower than the dose needed to produce anti-inflammatOly effects.)

Prostaglandins: • Sensitize nociceptors to the effects of bradykinin,. histamine and other substances. • Raise the set point in the hypothalamic thermoregulatory center thereby causing fever. • Effects on inflammation are not completely understood

• Some PGs cause a direct vasodilation and are thought to potentiate the effects of bradykinin and histamine on blood vessels resulting in increased vascular permeability, vasodilatation, and edema.

• PGs are the byproducts of arachidonic acid metabolism

142

Arachadonic acid: • Stored in phospholipids of cell membranes • Liberated by phospholipases in response to noxious stimuli • Metabolized through cyclooxygenase or Iipoxygenase. • Leukotrienes are the endproducts of the lipoxygenase pathway, • prostaglandins, prostacyclin, and thromboxanes are the endproducts of the cyclooxygenase

pathway.

Cyclooxygenase: two distinct forms of the cycIoox-ygenase (COX) enzyme. 1. COX-l

• expressed in most tissues including the GI tract. kidneys, and blood vessels. 2. COX-2

• usually undetectable • induced by cells during inflammation.

• Most NSAIDs inhibit the COX-l enzyme and have a similar side effect profile. • Those NSAIDs that more selectively inhibit the COX-2 enzyme (i.e.

Nabumetone, Celebrex, Viox.x) are associated with less side effects.

ARACHADONIC ACID CASCADE

PHOSPHOLIPIDS

Phospholipase A2

ARACHIDONIC ACID

Cyclooxygenase (COX1&2)

CYCLIC ENDOPEROXIDASES

Prostacyclin Thromboxanes

5-HPETE

Leukotrienes

143

PGta

• Vasodilator

• Bronchodilator

• Sensitizes pain receptors

• Raises set point in hypothalamic thennoregulatOIy center

• Stimulates GI mucus secretion

PGF'l

• Vasoconstrictor

• Stimulates GI Mucus Secretion

Prostacvclin

PGI'l

• Vasodilator

• Inhibits platelet aggregation

• Inhibits gastric acid secretion

Thromboxane

TXA'l

• Promotes platelet aggregation

Adverse Effects of NSAIDs

1. Gastrointestinal

• Most common side effect ofNSAIDs. (10-20,000 people each year die from NSAID induced GI complications).

• Most complications involve damage to the mucosal layer and include

• indigestion • diffuse gastritis

• erosions • ulcerations • severe GI hemorrhage.

• Risk factors for the development of NSAID induced GI complications • prior histOIY of ulcer disease • advanced age • cigarette smoking • alcoholabuse • high dose/multiple NSAIDs • concomitant corticosteroid use. • The relationship with Helicobacter Pylori is unknown.

(NSAID induced ulcerations can be histologically distinguished from H. Pylori ulcers. Additionally, the majority ofH. Pylori ulcers occur in the duodenum and are symptomatic, whereas most NSAID ulcers occur in the antrum of the stomach and are asymptomatic.)

• NSAIDs have a dual insult on the GI tract- topical and systemic.

144

Topical (direct and indirect effect.)

• direct effect due to the transport of the lipophilic drug into the gastric mucosal cell where they are converted back to the ionized form which becomes "trapped" in the cell (Ion Trapping). The membrane permeability of the mucosal cell is then altered leading to an influx of very acidic gastric juice back into the mucosal cell (Back Diffusion).

• indirect effect occurs from the reflux of bile containing active metabolites.

Systemic • result from the inhibition of prostaglandin synthesis.

GI prostaglandins (predominantly PGE2, PGI2) have a cytoprotective effect. They stimulate mucus production and secretion, stimulate HC03- secretion, inhibit acid secretion, inhibit Gastrin secretio!!, and enhance mucosal blood flow. Various methods have been employed in attempting to decrease the incidence of GI Side effects. Most are directed at reducing the topical effect on the mucosa and have no systemic effect (e.g .. buffering, enteric coating, prodrugs, nonacidic NSAIDs, administration with food). Therefore, these methods are met with limited success. The use of cytoprotective agents (e.g .. Misoprostol, H2 blockers) has proven to be more efficacious. Some NSAIDs are associated with less GI side effects because they are thought to be less potent inhibitors of GI prostaglandins.

Cl1oprotective Agents I. Misoprostol (Cytotec)-

• PGE analogue • protects Born the gastric and duodenal mucosa • Side effects: Diarrhea- most common • Increases uterine contractility- AVOID in pregnancy (spont. abortion)

2. H2 receptor antagonists (Cimetidine, Ranitidine, Famotidine) • Block histamine induced release of acid from parietal cells • effective in protecting the duodenal mucosa

3. Sucralfate (Carafate)

• Neutralized stomach acids • may stimulate PG synthesis

• ineffective

4. Prilosec

Least Gastrotoxic NSAIDs 1. Nabumetone (Relafen)

• only nonacidic NSAID

• Prodrug • Selective COX-2 inhibitor

2. Etodolac (Lodine) 3. Choline Magnesium Salicylate (TriIisate) 4. Salsalate (Disalcid)

• Both TriIisate and SaIsalate are nonacetylated salicylates • Less potent inhibitors ofPG's

5. Celebrex

• COX - 2 inlnbitor

145

2. Renal

• Prostaglandins have seveml important roles in the kidney.

• regulate vascular tone • maintain GFR • enhance sodium and water excretion • stimulate Renin secretion The effect of renal prostaglandins is negligible in normal circumstances.

Renal Side effects:

• Acute Renal Failure (ARF) • Risk factors for the development of ARF include conditions that result in decreased

blood volume (liver disease, diuretic therapy, nephrotic syndrome, congestive heart failure, sepsis. etc.). Systemic vasoconstriction occurs in these circumstances to maintain blood pressure. Renal PGs are synthesized on demand and playa counterregu1.atory role attenuating the decrease in renal blood flow and GFR that would otherwise occur if the vasoconstrictive forces were left unopposed. Other risk factors in patients with normal blood volume include contrast induced nephropathy, chronic renal failure, and advanced age.

• interstitial nephritis • proteinuria • nephrotic syndrome • abnormalities of sodium, potassium, and water homeostasis

Least Nephrotoxic NSAlDs 1. Nabum.etone (Relafen) 2. Etodolac (Lodine) 3. Sulindac (Clinoril) 4. Choline Magnesium Salicylate (Trilisate) 5. Salsalate (Disalcid) 6. Celebrex (Cox-2 inhibitor)

3. Bronchopulmonary . asthma exacerbation.

• The degree of prostaglandin inhibition correlates to the potential for inducing bronchospasm. • PGEz is a bronchodilator and stabilizes histamine stores in mast cells. • Greater leukotriene production

• Theoretically, the inhibition of cyclooxygenase also funnels greater amounts of arachadonic acid through the lipoxygenase pathway resulting in. Many of the leukotrienes are bronchoconstrictors (L TC~ and function as slow reacting substances of anaphylaxes.

• For this reason NSAIDs that inhibit both the cyclooxygenase and lipoxygenase (Diclofenac, Ketoprofen) pathways are considered safer agents.

• Patients with nasal polyps, asthma, and nonallergic rhinitis are at increased risk to develop NSAID induced bronchospasms.

146

4. Cardiovascular

• Angina • Myocardial ischemia

• Leukotriene D4 (LTD4} is a potent coronary artery vasoconstrictor. Its production may be enhanced by NSAIDs by shunting arachadonic acid through the lipoxygenase pathway.

• Can increase blood pressure through its actions on the kidney. blood vessels. and from the increased salt intake associated with some NSAIDs.

5. Hematologic • impair platelet aggregation

• inhibiting the production ofthromboxane A2 (TXA2). • Aspirin irreversibly acetylates cyclooxygenase and its effect lasts for the life of the platelet

(8-12 days). Platelets lack a nucleus and are unable to synthesize a new enzyme. All other NSAIDs reversIbly inhibit cyclooxygenase and their effect persists for the time that effective serum NSAID concentrations are present. Therefore. to ensure return of normal platelet function aspirin should be discontinued 8-12 days prior to surgery. Other NSAIDs should be discontinued 4-5 half lives prior to surgery (Piroxicam because of its long half life requires 8-10 days for complete reversal).

• Blood dvscrasias - rare effects ofNSAID use • leading cause of death attributed to NSAID therapy.

• Aplastic anemia • Agranulocytosis • Hemolytic anemia • Thrombocytopenia (Aplastic anemia and agranulocytosis is more frequently implicated with Phenylbutazone and Indomethacin use.)

6. Hepatic A transient asymptomatic elevation in serum transaminases can occur in up to 15% of NSAID

treated patients. Possible mechanisms for hepatocellular injury include drug hypersensitivity and the formation of reactive intermediate metabolites. Pyrazoles, proprionic acids and indole derivatives show the greatest propensity for severe liver damage such as hepatitis and cholestasis. Diclofenac has also been reported to be relatively hepatotoxic.

7. Central nenrous system

• Headaches • Indomethacin causes dose related headaches secondary to its cerebral vasoconstrictive

effects.

• Tinnitus

• Confusion

• Irritability

• Insomnia

• Dizziness • Idiosyncratic aseptic meningitis

(most likely a hypersensitivity reaction) has been associated with Ibuprofen. Tolmentin and Sulindac used in patients with SLE or other collagen vascular diseases.

The majority of these effects are reversible with discontinuation of the drug.

147

8. Articular Cartilage NSAIDs are very effective in treatingjoint inflammation because of their ability to gain access to

synovial fluid, however there is evidence that they may actually contribute to joint destruction. There is conflicting information regardirig the role ofNSAIDs in preventing or producing cartilage destruction. Through the inhibition of prostaglandins and certain inflammatory cells NSAIDs prevent cartilage destruction. However, NSAIDs may inhibit certain aspects of cartilage repair by reducing the synthesis of hyaluronic acid and glycosaminoglycans.

DRUG INTERACTIONS 1. WarfariD

Warfarin is highly bound to plasma proteins and is rapidly displaced by NSAIDs. The active "free" level of Warfarin is then increased. The combination ofNSAID induced platelet inhibition and the Warfarin induced inhibition of the coagulation system predisposes these individuals to serious bleeding episodes (particularly GJ bleeds due to the effect ofNSAIDs on the stomach!).

2. Antiepileptic agents Pyrazole NSAIDs interfere with the metabolism of Phenytoin producing increased plasma

concentrations and increase the likelihood of toxicity. Additionally Phenytoin and Valproic acid are highly protein bound which can be easily displaced by NSAIDs.

3. Corticosteroids Corticosteroids increase the rate of salicylate clear.mce and reduce its plasma concentration.

Combination CorticosteroidINSAID therapy considerably increases the risk of GI side effects.

4. Probenecid Probenecid increases the plasma concentration of NSAIDs by reducing their renal excretion,

competing for albumin binding sites, and competing for liver glucuronidation enzymes.

5. Hypoglycemic agents Sulfonylureas are highly bound to plasma proteins and can be displaced from their binding sites

by NSAIDs leading to a dangerous hypoglycemic event Salicylates have a hypoglycemic effect themselves. Pyrazole NSAIDs can also inhIbit the metabolism of sulfonylureas.

6. Antihypertensive agents NSAIDs can antagonize antihypertensive agents through several mechanisms; most cause

sodium and water retention, suppression of plasma renin, suppression of adrenal receptors, and impaired prostaglandin synthesis.

7. Lithium Lithium is almost entirely eliminated through the kidney and its clearance is significantly

reduced by the coadministration of an NSAID.

8. Methotrexate Methotrexate is predominantly eliminated through the kidneys and its clearance is reduced by the

coadministration ofNSAIDs.

9. Digoxin NSAIDs increase serum Digoxin levels by decreasing its renal clearance.

148

Dru!! Clas, A!!ent Trade Ilame H(", Dose -'LlX D'lil.\ Supplied D(l'l'

Salicylotes Enteric coated Ecotrin 81mg 4000mgfday 4000mg 325mg in divided doses 500mg

Salsalate Disalcid, 500mg 3000mgfday Salflex 750mg I div doses

Choline Mg* Trilisate 500mg 2000-3000mglday Salicylate 750mg in divdoses

IOOOmg Trilisate liquid 500mgf5ml peds-5Omglkglday

Diflunisal Dolobid 250mg 500-1500mglday 1500mg 500mg in divdoses

Pyrazoles Phenylbutazone l00mg 400mgfday 400mg

indivdoses Indoleacetic acids

Indomethacin Indocin 25mg 75-15Omglday 200mg 50mg in divided doses 50mgsuppos 25mg/5ml susp

IndocinSR 75mg

Sulindac Clinoril 150mg 300-40Omglday 400mg 200mg in divided doses

Pyrrolacetic Acids Tolmentin Tolectin 200mg 600-1800mgfday 1800mg

600mg· in div doses; pediatr-TolectinDS 400mg lS-3Omglkglday

Proprionic Acids Ibuprofen Motrin,ffiU 200mg 1200-3200mglday 3200mg

Rufen, Nuprin 300mg in div doses Advil 400mg

600mg 800mg

Childrens Motrin lOOm.glSml 20-4Omglkglday 40mglkglda y

Childrens Advil suspension

Naproxen Naprosyn 250mg 500-1S00mgfday lS00mg (*ec=avail in 375mg(ec) in div doses; enteric coated) 500mg(ec) pediatric-

12Sm.gISml lOmglkglday lSmg/kg suspension

137Smg

149

Supplied Dose Proprionic Acids

continued Ketoprofen Orudis 25mg l00-300mglday 300mg

50mg indiv doses 75mg

Oruvail l00mg in single or (ext release) lSOmg divided doses

200mg

Fenoprofen Nalfon 200mg 1200-3200mglday 3200mg

300mg indiv doses 600mg

Flmbiprofen Ansaid SOmg 200-300mglday 300mg

lOOmg in div doses

Oxaprozin Daypro 600mg 600-1200mglday 1800mg or

in one or div doses 26mglkg Phenylocetic Acids

Diclofenac Na + Voltaren 25mg 50mg lOO-200mglday 200mg 7Smg in div doses

Diclofenac ~ Cataflam 50mg Anthranilic Acids

Meclofenamate Meclomen SOmg 200-400mglday 400mg

sodium IOOmg in div doses Oxicams

Piroxicam Feldene lOmg IO-20mglday 20mg 20mg

Napthylalkllnones Nabumetone Relafen 500mg IOOO-2000mglday 2000mg

7S0mg in one or two doses Tetrahydroindoles

Etodolac Lodine 200mg 800-1200mglday 1200mg 300mg in div doses 400mg SOOmg

Pyrrolopyrrole Ketorolac Toradol lSmglrnJ single dose: Tromethamine 30mglml <65yo-6Omg IM; 30mg IV

>65yo, renal failure, or <50kg-30mg IM; lSmg IV multiple dose: <65yo-30mg q6h IMIIV 120mg >65yo, renal failure, or <SOkg- ISmg q6h IMIIV 60mg ** IV bolus >15 seconds

lOmg lOmgq6h 40mg

*Maxmun Durati on of use is 5 Days PO, IM, And IV

150

Tables and Formulas

Creatinine Clearance = (Lean kg) (140 - age) (0_85 if female)

[normal> 80] (72) (stable creatinine)

Wt=[(actual- ideal) x 40%]+ ideal body weight

Ideal Body Weight:

Start at height of 5'0" equiv_ to 1001bs_

for males add 7fbsJinch >5ft

for females add 51bsJinch >5ft

Body Surface Area CBSA) = square root of [height (cm) x weight (kg)]. [in m2] 3600.

Therapeutic Drug Levels

Digoxin 0_5 - 2.2 ng/ml

Gentamicin peak 4 - 6 mg/mf

Gentamicin trough 1 - 2 mg/ml

Lidocaine 1 - 5 mg/ml

Lithium 0_5 - L5 meq/mf

Phenoba rbita I 15 - 40 mg/ml

Phenytoin 10 - 20 mg/mf

Theophylline 10 - 20 mg/mf

Tobramycin peak 4 - 6 mg/mf

Tobramycin trough 1 - 2 mg/mf

Vancomycin peak 18 - 40 mg/ml

Vancomycin trough 5 - 10 mg/ml

Antidotes Toxin Antidote

Acetaminophen

Benzodiazepi ne

N_ Acetyleysteine (mucomyst)

Flumazenil

151

Toxin

Heparin

Warfarin

Narcotics

Narcotic - Type Analgesic Comparisons

Drug Equi-Analgesic

Route Dose (MG)

(agonists)

Morphine 1M PO R

10 30- 60 60

Hydromorphine (Dilaudid) 1M 1.5 PO 4 - 7.5 R 6

(agonists) Levorpha nol(Levo-Dromora n)

1M 2 PO 4

Oxycodone PO 30

Methodone 1M 10 PO 20

Meperidine (Demerol) 1M 100 PO 300

Codeine 1M 130 PO 200

Duration

(HR)

4-5 4-5 4-5

4-5 4-5 4-5

4-6 4-6

3-4

4-6 4-6

2-4 2-4

3-5 3-5

Antidote

Protamine

Vitamin K

Naloxone

Drug Equi-Analgesic

Route Dose (MG)

(mixed agonist - antagonists)

Butorphanol (Standol) 1M 2

Buprenophine (Buprenex) 1M 0.3 - 0.6

Nalbuphine (Nubain) 1M 10

mixed agonist - antagonists)

Pentazocaine (Talwin Nx) PO 180

Duration

(HR)

3-4

4-6

3-5

2-4

152

Relative potencies and Equivalent Doses of Corticosteroids

Approx. Equiv. Relative Relative Duration Dose* Anti·inflam. Sodium of Action

GI ucocorticoid Potency Potency Retaining T 112 (hrs)

Short·acting (s) Cortisone 25 0.8 0.8 8·12 Hydrocortisone 20 1 1 8·12

I ntermediate·acting(l) Prednisone 5 4 0.8 12·36 Prednisolone 5 4 0.8 12·36 Methyl prednisolone 4 5 0.5 12·36 Triamcinolone 4 5 0 12-36

Long·acting (L) Beta methasone 0.6 30 0 36-54 Dexa methasone 0.6 25 0 36·54

*These dose relationships apply only to oral or intravenous administration; relative potencies may differ greatly when injected intramuscularly into joint spaces.

Topical Corticosteroid Potency

Potency Drug Level

High Betanethasone (Oiprolene. Oiprasone)

Triancinolone acetonide (Kenalog-HP. Aristocort-HP)

Oesoximetasone (Tropicat)

Ffuocinonide (Lidex)

ntermediate

Betanethasone (Valisone)

Desoxinelasone (T ropicort·LP)

Desonide (T ridesilon)

Tricmcinolone acetonide (Kenalog, Aristocort)

Strength

0.05%

0.5%

0.25%

0.05%

0.1%

0.05%

0.05%

0.05%

Potency Level

low

Very low

Drug Strength

Ffuocinolone 0.01% (Synatar)

Betarnethasone valerate 0.01%

Triancioofone acetonide 0.025% (Kenafog-LP, Aristocort·LP)

Hyctocortisone 2.5%

Hyctocortisone 1.00%

Hyctocortisone 0.5%

153

Substances which may discolor urine

Black/Brown/Dark

Cascara Chloroquine

Ferrous salts Ferrous sulfate

Furazolidone Methocarbamol

Metronidazole Nitrofurantoin

Quinine Senna

Methylene blue Triamterene

Blue/Green

Amitriptyline Indigotindisulfonate

Methylene blue Resorcinol

Tolonium

Drugs which may discolor feces Black

Acetazolamide

Aminophylline

Amphotericin B

Chlorpropamide

Corticosteroids

Black

Cytarabine

Ethacrynic Acid

Fluorouracil

Hydrocortisone

Melphalan

Methytrexate

Potassium salts

Procarbazine

Tetracycline

Thiotepa

Warfarin

Aluminum Hydroxide

Amphetamine

Bismuth salts

Clindamysin

CycIcophosphamide

Digitalis

Ferrous salts

Hydralazine

Iodide containing drugs

Methyprednosolone

Phenylephrine

Prednisolone

Sulfonamides_

Theophylline

T riamcinlone

Red

AminoPyrine

Doxorubinicin

Idarubicin

Phenyl butazone

Phenoth iazi nes

Rifampin

Orange/Yellow

Daunorubicin

Ibuprofen

Oxyphen butazone

Phenytoin (pink)

Phensuximide

Senna

Acetanilid

Phenazopyridi ne

Sulfasalazine

Heparin

Rifampin

Warfarin

Green

Indomethacin Medroxyprogesterone

Yellow

Senna

Pink/Red

Anticoagulants

Barium

Oxyphenbutazone

T etracyC\ine syrup

Orange/Red

Phenazopyridine

Black/White speckling

Aluminum Hydroxide

Barium

Aspirin

Heparin

Phenylbutazone

Rifampin

Antibiotics (PO)

154

Chloramphenicol

Drug-Lab Test Interferences

Test Serum ALT lAST

Serum Bilirubin

Serum Calcium

Urine Catecholamines

Serum Cholesterol

Serum Creatinine

Urine Glucose

Urine Ketone

CSF Protein

Serum Protein

Methylene blue

May increase results Erythromycin Methydopa

Ascorbic acid Dextran Epinephrine Methyldopa Rifampin

Hydralazine

Acetaminophen Chloral Hydrate Epinephrine Erythromycin La beta 101 Levodopa Methenamine Methydopa Tetracyclines Triamterene

Aspirin Corticosteroids Phenothiazines Vitamin D

Cefoxitin (Jaffe method) Flucytosine

Ascorbic acid Cephalosporins Levadopa (Clinitest) Nalidixic Acid

Levadopa Mesna Phenazopyridine Salicylates

Methicillin Phenothiazines Sulfonamides

Phenazopyridine

May decrease results

Aspirin Heparin Sulfisoxazole

Iodine containing Radiocontrast Media

Nitrates

Ascorbic acid Cephalosporins Levadopa (Clinistix, Test-Tape)

Cytarabine

155

Urine Protein

Serum Thyroxin

Blood Urea Nitrogen

Serum Uric Acid

Dru~ that can cause fever

Most common

Amphotericin

Cephalosporins

Halothane

Interferon

Iodides

Isoniazid

Levothyroxi ne

Methyldopa

Muromonab - CD3(OKT3 )

Penicillins

Phenytoin

Procainamide

Quinidine

Streptoki nase

Urokinase

Vaccines

Vancomycin

Aminogglycosides Magnesium Sulfate (Large IV doses) Nafcillin Phenazopyridine Tolbutamide Tolmentin

Heparin Heparin

Chloral Hydrate Chloramphenicol Streptomycin

Ascorbic Acid Caffeine Theophylline Levadopa

Less common

Allopurinal

Antihistamines

Atropine

Azathioprine

Barbituraates

Benztropine

Bleomycin

Carbamazepine

Chlorambucil

Cimetidine

Cisplatinum

Clofibrate

Cytarabine

Daunorubicin

Diazoxide

Doxorubicin

Folic Acid

Haloperidol

Hydralazine

Hydroxyurea

Ibuprofen

L-Asparaginase

6-Mercaptopurine

Methoclopramide

Nifedipine

Nitrofurantoin

Paraldehyde

PGE2

Procarbazine

Quinine sulfate

Rifampin

Ritodrine

Salicylates

Streptomysin

Sulindac

Streptozoci n

Tetracycline

Triamterene

Trifluoperazine

156

Drugs Causing Adverse Hematological Effects

1. Drug Induced Aplastic Anemia

Acetazolamide Oral Antidiabetics

Antihistamines Oxyphenbutazone

Carbamazepine Penicillamine

Chloramphenicol Phenobarbital

Chloroquine Phenothiazines

Chlorothiazide Phenytoin

Gold Salts Propylthiouracil

Indomethacin Quinidine

Methimazole Sulfonaamides

2. Drug Induced Aganulocytosis

Acetaminophen Isoniazzid

Acetazolamide Levodopa

Allopurinal Lincomycin

Para-Aminosalicylic Meprobamate Acid

B-Lactam Antibiotics Methazolamide

Benzodiazepines Methimazole

Brompheniramine Methyldopa

Carbamazepine Metronidazole

Captopril Nitrofurantoin

Chloramphenicol Oxyphenbutazone

Chlorpropamide Penicillamine

Cimetidine Pentazocine

a. Immune Hemolytic Anemia (continued)

Hydralzine Quinidine

HCTZ Quinine

Ibuprofen Rifampin

Isoniazid Sulfonamides

Levodopa Streptomyci n

Mefenamic Acid Tetracycline

Melphalan Tolbutamide

Methadone Triamterene

Clindamycin Phenothiazines

Clomipramine Phenylbutazone

Dapsone Phenytoin

Desirpramine Primidone

Doxycycline Procainamide

Ethacrynic Acid Propanolol

Ethrosuximide Prohythiouracil

Fenoprofen Pyrimethamine

Flucytosisne Quinine

Gentamicin Rifampin

Gold salts

Griseofulvin

Hydralazine

Streptomycin

Sulfa Antibiotics

Thiazide Diuretics

Hydroychloroquine Tocainide

Ibuprofen Tolbutamide

Imipramine Vancomycin

Indomethacin

3. Drug Induced Hemolytic Anemia

a. Immune Hemolytic Anemia

Acetaminophen Methyldopa

Para-Aminosalicylic Methysergide Acid

Cephalosporins Penicillins

Chlorpromazine

Chlorpropamide

Cylophosphamide

Cytarabine

5-Fluorodeoxyuridine

5- FI uorouraci I

Hydroxyurea

6-Merca ptopu ri ne

Methotrexate

Probenecid

Procainamide

Phenytoin

Primadone

Pyrimethamine

Sulfasalzine

Triamterene

Trimethiprim

Vinblastine

157

b. Oxidative Hemolytic Anemia

Ascorbic Acid Menadiol

Aspirin Methylene Blue

Benzocaine Nitrofurantoin

Chloramphenicol Nitrofurazone

Chloroquine Phenazopyridine

Dapsone

Sala~osulfapyridine

Diazoxide

4. Drug Induced Megaloblastic Anemia Para-Aminosalisylic Neomysin

Acid

Azathioprine

Chloramphenicol

Colchicine

Nitrofurantoin

Oral Contraceptives

Phenobarbital

5. Drug Induced Thrombocytopenia

Acetazolamide Hydrochlorothiazide

Allopurinol Isoniazid

Aminoglutethimide Meclofenamate

Para-Aminosalicylic Morphine Acid

Amrinone Peniccilin

Cephalothin Phenyl butazone

Chlorothiazide Phenytoin

Cimetidine Procainamide

Desipramine Quinidine

Diazepam Quinine

Drug Induced Thrombocytopenia (cont) Digitoxin Rifampin

Furosemide

Heparin

Sulfisoxazole

Trimethoprim

158

PERIOPERA TIVE MANAGEMENT PERI OPERA TIVE MANAGEMENT PERIOPERA TIVE MANAGEMENT PERIOPERA TIVE MANAGEMENT PERIOPERA TIVE MANAGEMENT PERIOPERA TlVE MANAGEMENT PERIOPERA TlVE MANAGEMENT PERIOPERA TIVE MANAGEMENT PERIOPERA TIVE MANAGEMENT PERIOPERATIVE MANAGEMENT PERIOPERA TIVE MANAGEMENT PERIOPERA TIVE MANAGEMENT PERIOPERATIVE MANAGEMENT PERIOPERATIVE MANAGEMENT

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HOSPITAL CHARTING

Pre-operative note 32 yo BF presents for smgical correction of her plinful bunion left foot Condition has not resolved with

conservative therapy. PMH: IDDM, HIN (well-controlled) Meds: insulin, procardia Allergies: no kno·wn drug allergies (NKDA) Social History: Past Surgical History: Labs: Chemistry= Na CI BUN

K CO creat

CBC = WBC· hemoglobin Platelets

hematocrit

Urinalysis: Serum HCG: Foot x-rays: Chest x-ray: no active lung disease ECG: normal sinus rhythm

Glucose

PfIINR/PIT =

Impression: hallux abductovalgus defonnity left foot

Plan: 1. smgical correction left bunion defonnity as per attending 2. patient medically cleared for procedure as Dr. PMD 3. consent sigued (Procedure reviewed with patient including risks, benefits and complications; all questions answered.)

Post -operative note eponym: "SAPPPA HEMl PC"

S: surgeon A assistant(s) P: pre-operative diagnosis P: post-operative diagnosis P: procedure A anesthesia (ie-general; spinal; local; IV sedation with local) H: hemostasis (ie-ankle or thigh pneumatic tourniquet inflated to __ mmHg for __ minutes; local control) E: estimated blood loss M: ~ (ie-sutures; drains; fixation; bone grafts; etc) I: injectables (ie-intra- or post-ilp local anesthesia; steroids) P: pathology (ie-bone; soft tissue; foreign body)

C: complications C: Condition - Stable, Fair, Guarded, Critical

Patient tolerated both procedure and anesthesia without <lpIm'ent complications and with vital signs remaining stable throughout procedure. Patient transported from OR to RR with vascular status intact to (RIL) LE, escorted by member of anesthesia department and podiatric surgical resident.

159

Post -op and Admission Orders eponym: "ADC V ANDILMAX"

A: Admit to the service of Dr. Mlodzienski (podiatric Surgery) D: diagnosis C: condition (ie-stable) V: vitals (ie-monitor vital signs q shift as per floor protocol) A: activity (ie-bedrest) N: nursing (ie-elevate left leg and apply ice to dorsum foot) D: diet 1: insIouts L:labs M: meds A: ancillary personnel (ie-physical therapy; social service) X: x-rays

In-Patient Progress Note 2/28/95 Podiatric Surgery 6:30 am S: Patient visited at bedside; offers no complaints

Patient denies experiencing SOB, chest pain, cough, ca1fJthigh pain Good appetite, - nausea!vomitting, - abd pain + void, +BM

0: T max , T presently , BP, P, R Lungs - clear to auscultation (CT A) Left foot - NVS intact wound edges appear healthy, viable wound margins approximated with sutures - dehisence, - drainage, - purulence - erythema, mild localized edema Labs - wound culture left foot [collected 2127/95] MRSA sensitive to vancomycin X-rays - no erosive changes consistent with osteomyelitis noted

A: 1. SIP I & D diabetic foot infection, wound status improving 2. IDDM, blood sugars well-controlled

P: 1. dressing change perfonne, will continue daily local wound care 2. continue IV Abx; will check peakItrough levels

vancomycin (day #5) 3. will repeat wound cultures and CBC tomorrow

Basic Pre-op Labs Reasons for ordering labs a) indication of infection b) indication of anemia c) indication of hemorrhage

Signature

d) indication of hyper- or hypoglycemic state e) indication of renal disease f) indicatioon of coagulopathies g) indication of metabolic disease

160

Normal Lab Values a) CBC with differential

WBC: 5000-10000 cellsIul RBC: males 4.7-6.1 x 10 cellsIul

females 4.2-5.4 x 10 cellslul hemoglobin: males 14-18!ifdl

females 12-16!ifdl hematocrit: males 40-54%

females 37-4'1'10 mean cell hemoglobin (MCR): 27-31 picograms mean cell hemoglobin concentration (MCHC): 33-3'1'10 mean cell volume (MeV): males 80-94 urn

females 81-99 um platelets: 150000-450000 ul

segmented neutrophils: 41-71% basophils: 0-1% stabs neutrophils: 5-10% lymphocytes: 24-44% eosinophils: 1-3% monocytes: 3-7%

reticulocyte count (normal = 1.5%) indicator of erythropoietic activity reticulocytes are immature RBC's which still possess a nucleus normal bone marrow responds to decrease in erythrocytes- (indicated by hematocrit value) with an increase in production of reticu10cytes

Left shift may be indication of infection, toxemia, hemonhage present in the CBC when more ~ 20% segs are seen or when the total PMN count is greater than 80%

b) Chemistry sodium: l34-149 meqIl potassium: 3.2-5.2 meqll chloride: 94-110 mmol caIbon dioxide: 19-32 mmolll BUN: 6-26 m!ifdl creatinine: 0.4-1.5 m!ifdl glucose: 56-124 m!ifdl

c) Coagulation Studies PT (prothrombin time): 10 .1-l3.1 seconds PIT (activated partial thromboplastin time): 23.5-34.3 sec

d) Urinalysis color: yellow appearance: clear glucose (glu ua): negative ketones (ket ua): negative occult blood (oc bId u): negative protein (pro ua): negative nitrates (nit): negative bilirubin (bili ua): negative specific gravity: 1.010-1.025 pH: 5.0-7.5 leukocyte esterase (leu): negative urobilinogen: 0.2-1.0 eu/dl

161

Interpreting the CBC with differential key points to note include:

a) WBC count >conelate count with differential to detennine extent of infection, left shift, elevation of a specific cell

lineage (ie-elevation oflymphocytes may indicate a state of chronic infection) b)RBCcount

>correlate with indices (MCR, MCV, MCHC) to detennine anemic states and specific types of anemias c) Hemoglobin

>indicates oxygen carrying GaJXlcity ofRBC to tissues; major concern in post-op healing d) Hematocrit

>correlate with RBC count and indices to detennine anemic states

Alterations in Lab Parameters There are numerous fuctors that can alter every aspect of the pre-op lab values. A complete listing of factors that may alter the various lab values can be found in any reference manual (ie-Clinician's Pocket Reference by Gomella, Braen & OIding)

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Peri-operative Complications

Fever

Oral temperature • normal range is 36.5-37.4 C (97.7-99.5), with an average temperature of 37 or 98.6 • rectal temperatures are usually 1 F higher because this value is unaffected by external cooling factors

associated with evaporation that occurs when oral temperatures are measured • body temperature greater than 100.4 F during the postoperative period is a significant finding and the

etiology should be detennined • current theory states that the anterior hypothalamus is responsible for thermoregulation • most people exlubit diurnal fluctuation oftemperature with the lowest reading in the am and the

highest reading in the p.m.

Peri-operative fever

• Malignant byperthermia • incidence ... 1112000 pediatric anesthetics ... 1140000 adults anesthetics • susceptible patients ... elevated CPK preoperatively (occurs in -70010 of susceptible patients) ... family histOIY (dominant inheritance) of anesthesia problems ... EKG abnonnalities ... diagnosis: skeletal muscle biopsy and in vitro isometric contracture testing in the presence of caffeine.

halothane, or both

• triggering agents ... anesthetic agents (inbalational agents such as ether, halothane, enflurane) ... neuromuscular blocking agents (i.e. succinylcholine) ... stress

163

• symptoms/signs '+ rapidly progressive reaction '+ first sign usually arrythmias '+ masseter muscle spasm '+ rapidly rising temperature '+ tachypnealtachycardia '+ profuse hyperhidrosis '+ metabolic and respiratory acidosis '+ dark, mottled skin '+ hyperkalemia leading to cardiac dysrythmias '+ elevated CPK levels '+ excessive myoglobin release

• treatment '+ Stop the administration of anesthesia '+ change anesthetic tubing '+ hyperventilate with 1000/0 02 '+ correct the acidosis '+ cool the patient ~ pack the patient in ice ~ gastric lavage with cold saline ~ cardiopulmonary bypass (in severe situations)

'+ Dantrolene sodium (dantrium) ~ skeletal muscle relaxant that prevents the release of calcium ~ intraoperative crisis

»> begin at minimum dose of I mglkg by continuous rapid IV push and continue until symptoms subside or until maximum dose of 10 mglkg has been reached

»> if abnormalities reappear, then regimen may be repeated ~ postoperative crisis

»> 4-8 mglkglday po in four divided doses for 1-3 day period ~ preoperative prophylaxis

»> 4-8 mglkglday po in four divided doses for 1-2 days prior to surgery with last dose 3-4 hours before scheduled surgery

»> Dantrium 2.5 mglkg IV approximately 1 hour before the anticipated anesthesia ~ theory: Malignant hyperthermia is chemically induced by anesthetic agents or catecholamines

produced by stress. The sarcoplasmic reticulum within muscle contains - 3000 times the amount of Ca ++ normally present in the sarcoplasm. In order for muscle contraction to occur, sarcoplasmic reticulum must release Ca++ into the sarcoplasm. The sarcoplasmic reticulum then must resequester the Ca ++ in order for muscle relaxation to occur. When malignant hyperthermia occurs the Ca++ ions cannot be reabsorbed by the sarcoplasmic reticulum; the concentration of Ca ++ inside the cell rises activating a series of metabolic reactions leading to the symptoms of malignant hyperthermia Dantrolene works by preventing the release of Ca ++ from the sarcoplasmic reticulum.

Postoperative Fever

• mnemonic [Wind, Walk, Water, Wound, Wonder drugs] • The mnemonic only serves as a guide to determine the possIble cause of a post operative fever. It

represents the more common etiologies of fever at a given time during the post operative period. Keep in mind that most of the etiologies can potentially occur at any time during the perioperative period (depending on why the patient is hospitalized and what procedures are performed).

• intraoperative '+ malignant hyperthermia • (Wind] 12-24 hours post op '+ atelectasis '+ post op hyperthermia

164

• [Walk] 24 hours post op '+- thrombophlebitis '+- pulmoruuy embolism • [Water] 48 hours post op '+- UTI • [Wound] 72 hours post op .. post op wound infection • [Wonder dmgs] anytime post op '+- drugfever • Other causes] anytime post op '+- IV catheter phlebitis/infection '+- catheter infection '+- constipation (?etiology) '+- benign postoperative fever (temperature increase of less that 2 F 48-52 and 72-78 hours post op

without any signs of complication) • workup • The work up of postoperative fever begins with a careful and thorough H&P. The patient should be

questioned specifically about symptoms such as SOB. chest pain. dysuria. pain at the IV site etc .. Look to see if the patient is on any new medications (ie. low dose heparin. antIbiotics) to try and determine if the fever may be a result of a medication Be sure to inspect all catheter sites. Laboratory evaluation can begin with simple tests such as a CBC with differential. UA., and CXR. Blood cultures should also be obtained if it is believed that the fever is from a septic source. It is recommended that 2 sets of blood cultures be obtained to avoid the potential of treating a contaminating organism that is found in only one bottle

Severe intractable pain

'+- sutures too tighl '+- constrictive/tight dressings '+- hematoma '+- ischemia

White toe

• arterial in nature (usually caused by macremboli, arterial insufficiency, over stretching of neurovascular bundle with toe lengthening or repositioning)

• usually an acute incident, therefore the onset of ischemia is rapid and severe (no time for collateral circulation to develop)

• symptoms/signs '+-excruciating pain '+-pale coloration with blue mottling '+-parasthesia '+-pulselessness

• treatment '+-avoid nicotine/caffeine '+-D/C ice/elevation '+-place foot in dependent position '+-loosen outer/inner bandage '+-piston/rotate toe on K wire '+-warm compresses to proximal neurovascular bundle '+-local nerve block proximal to area to provide distal vasodilation '+-vascular surgery consult

165

Blue toe

• represents stasis from poor arterial inflow or sluggish venous outflow

• etiology '+microembolic shower '+post op complication ~ tight dressing/cast ~ "tourniquet effect" of large volume of local anesthetic ~ poor tissue handling technique ~ impingement of tissue between bone or fixation device ~ dissecting hematoma

'+paraneoplastic digital thrombosis '+transient vasospasm of digital vessels ~ collagen vascular diseases (rheumatoid arthritis, SLE, scleroderma) ~ Raynaud's disease or phenomena ~ acrocyanosis

• treatment '+blue toe secondary to venous insufficiency ~ toe is usually warm and may blanch with pressure (may not blanch if severe) ~ inspect dressing ~ D/C ice and elevation ~ avoid dependency ~ do not attempt to increase vascular perfusion

'+blue toe secondary to arterial insufficiency ~ toe is cold and does not blanch with pressure ~ inspect dressingIK wires ~ D/C ice and elevation ~ avoid nicotine and caffeine ~ heat to popliteal fossa or anterior groin ~ thermostat controlled heat lamp over foot with temperature not to exceed 90 F ~ vasodilators

» oral (niacin, nifedipine, cyclospasmol) » nitroglycerin paste

~ if condition persists 12-18 hours, consider more xadical measures

• blue toe syndrome m~ also be seen in non-surgical settings '+drug induced '+anticoagulant thexapy (coumadin) '+prednisone therapy '+secondary syphilis '+pheochromocytoma '+hypercoaguable states "polycythemia vera '+thrombocytosis '+coagulation disorders '+arterioslerosis obliterans '+thromboangiitis obliterans .. cyanotic congenital heart disease

166

ANEMIAS

Classification a) relative

1. pregnancy 2. nutritional deficiency 3. splenomegaly 4. macroglobulinemia

b) absolute 1. decreased red blood cell production

>disturbance of proliferation and differentiation of stem cells -aplastic anemia -myelodyspIastic anemia

>distw:bance of prolifeIation and differentiation of erythroid progenitor cells -pure red cell apIasia -anemia of chronic renal disease -anemia of endocrine disease -<:ongenital dyserythrocytic

>disturbance of hemoglobin synthesis (hypochromic) -iron deficiency -thalassemia -idiiopathic pulmonary hemosiderosis

>distwbance of DNA synthesis (megaloblastic anemia) -vitamin Bl2 deficiency -folic acid deficiency -purinelpyrimidine metabolic defects

>unknown or multiple mechanisms -anemia of chronic disease -sideroblastic anemia -anemia associated with marrow infiltration -anemia associated with nutritional deficiency

2. increased red blood cell destruction >intrinsic abnormality

-membrane defects (ie-hereditary spherocytosis) ~e deficiency (ie-G-6PD deficiency; porphyria) -globin abnormality (ie-sieIde cell disease) -paroxysmal nocturnal hemoglobinuria

>extrinsic abnormality -mechanical -chemical of physical -infectious -antibody mediated -hyperactive macrophage system

4>loodl05S

Pre-operative Evaluation a) hemoglobinlhematocrit (Hgb'Hct)

1. should be evaluated in all patients (especially in menstruating females) since most anemias (unless severe) are asymptomatic

2. Hct should be above 4()0.4J (Hgb ~ 10 gm) for males and 37% for females, or elective surgery should be delayed determine cause; repeat test to rule-out lab error

167

b) Aplastic Anemia May be congenital (ie-Fanconi, Espren-Dameshek), idiopathic, acquired or associated \\'ith drugs,

chemical agents, radiation, infection, metabolic changes (ie- pregnancy) or immunologic factors. Condition is characterized by the loss ofhematopoetic cells, fatty replacement of marrow and pancytopenia. The anemia is generally normocytic and the prognosis is largely determined by severity of associated thrombocytopenia and leukopenia Recognition and removal of cause may lead to remission. Transfusions are usually not necesssary unless hemoglobin falls below 6-7 gmldL. Response to glucocorticoids, androgens and immWlosuppressive agents are variable. Bone marrrow transplants are being perfonned in patients with severe aplastic anemia with marlred bone marrow hyperplasia.

c) Iron Deficiency Anemia The most advanced stage of iron deficiency, characterized by decreased or absent iron stores, low serum

iron concentration, low transferrin saturation and low hemoglobin concentration or hematocrit value. May occur as a result of inadequate dietary iron intake, malabsorption of iron, chronic blood loss, diversion of iron to fetal and infunt erythropoiesis during pregnancy and lactation, intravascular hemolysis or a combination of these causes. The most common causes are excessive blood loss due to heavy menstrual bleeding, multiple pregnancies or GI bleeding. In severe WlCOmplicated iron deficiency anemia, the erythrocytes are hypochromic and microcytic, plasma iron concentration is decreased, iron binding capacity is increased, serum ferritin concentration is low and the free erythrocyte protoporphyrin concentration is increased

Fatigue irritability, palpitations, weakness and headache are common complaints of patients with iron deficiency. Once it has been established that a person is iron deficient and the cause identified, replacement therapy should be instituted immediately. Oral or parenteral treatment is required, with oral administration being the preferred route. Unless the anemia is extremely severe, blood transfusion is not indicated

d) Megaloblastic Anemia A family of disorders showing characteristic abnormalities of blood and marrow caused by impaired

DNA synthesis. Deficiencies of vitamin B12 and folate accOWlt for over 95% of the megaloblastic anemias. Anemia may be mild or severe, but because it develops slowly, few symptoms appear until the hematocrit becomes extremely depressed When they appear, symptoms include weakness, palpitations, fatigue, light-headedness, and shortness ofbreath. Patients characteristically show slight jaundice and severe pallor, producing the telltale "lemon-yellow" tint

Differentiation of pernicious anemia (inability to absorb vitamin B 12 secondary to lack: of gastic intrinsic facator) from other megaloblastic anemias is essential since treatment with B12 (cobalamin) must be continued for the patient's life. Although correction of the hematologic abnormalities of pernicious anemia may occur following the administration oflarge doses of folate, nemologic damage progresses and may even be irreversible. The most helpful diagnostic tests are serum vitamin B12 and folate levels, the Schilling urinary B 12 excretion test, and gastic analysis.

Initial therapy for pernicious anemia consists of 100-1000 ug 1M daily of cobalamin for two weeks, followed by 100-1000 ug 1M each month for life. To correct a folic acid deficiency anemia, 1-5 mg folate PO for 4-5 weeks is administered and usually adequate to replenish body stores and correct the anemia.

e) Sickle Cell Anemia Sickle cell anemia was first described by Herrick in 1910 and represents the most common form of

congenital hemolytic anemia, affecting 11600 blacks (homozygotes). Approximately 8"/0 of American blacks have the sickle cell trait (heterozygotes) and the incidence increases in areas such as Western Africa due to its protective quality against falciparum malaria

The term "sickle cell" disorder refers to states in which the red blood cell assumes a sickle shape when exposed to low oxygen tension. Under low oxygen tension the red blood cell sickles, causing sludging that slows blood flow; this stasis creates greater hypoxia that perpetuates the cycle and produces pain as well as infarction.

168

Hemoglobin is comprised of two alpha and two beta chains. Hemoglobin S represents a substitution of valine for glutamic acid at position 6 of the beta chain Red blood cells containing this type of hemoglobin are characterized by shorter survival and tendency to adhere to vascular endothelium, resulting in anemia and vascular occlusion.

Nonnal: Sickle Cell Trait: Sickle Cell Anemia:

HgbAl=96% HgbAl=55-75% HgbAl=1-25%

Hgb A2=3% Hgb F=l% HgbS=2545% Hgb S=75-95%

Screening for hemoglobin S can be done via the "sickle cell prep", whereby the red blood cell sickling is observable under a microscope. Positive screening tests should be followed Vl'ith hemoglobin electrophoresis to determine the specific hemoglobinopathy. Many patients with sickle cell anemia are in good health much of the time, but this state may be interrupted by a sudden crisis (infarctive, aplastic, hemolytic or sequestrative) which can occasionally prove fatal.

Typica1lab findings in sickle cell anemia include: decreasedHgb decreased Het normalMCV normal to increased WBC normal to increased platelets increased reticulocyte count elevated serum bilirubin elevated serum LDH

Though all systems may be affected, the heart is frequently the site of the most prominent physical findings. It is often enlarged to both the left and right with systolic and diastolic flow murmurs heard. Painful ulceration ar01md the ankles characterized by "punched out" appearance with rolled edges, are not an uncommon swquelae. Treatment generally consists of a combination ofbed rest, local wound care and occasional antibiotics. Bony sickling can predispose to osteomyelitis, most commonly due to Salmonella although pneumococcal and staphylococcal infection have been described.

Management of sickle cell anemia is mainly symptomatic and supportive. During painful crises maintain adequate hydration, improve oxygenation (ie-oxygen via nasal cannula), provide analgesia (ie-morphine, meperidine) and consider folic acid supplementation. Therapy to enhance production of hemoglobin F in these patients is still investiWUional. There is no increased risk of using pneumatic tourniquets in patients with sickle cell trait However, both pneumatic tourniquets and local anesthesia with epinephrine should be avoided in patients with sickle cell anemia. If general anesthesia is necessary, an inhalational anesthetic is preferred and adequate maintenance of oxygenation, hYdratiQll,.ventilationis essential.

BLOOD TRANSFUSIONS

Red Cell Antigens and AntIbodies: Serologic Considerations a) tests for red cell antigens

L red cell typing is usually performed by exposing the cells to specific anti-sera, incuOOting at 37 C and observing for agglutination.

2. the ABO and Rh types are determined for all blood donors and recipients to avoid transmission of ABO incompatible blood and to prevent allo-imTDlmi73tion by the Rh antigen.

>tests for additional Rh antigens and antIbodies and those in other genetic systems (ie-Ken, Kidd, Duffy) are often required when a patient has been allo-immunized

169

The ABO System a) serum of virtually all individuals contains antibodies corresponding to the A or B antigens not present on

their red cells. b) ABO typing is performed regularly by testing red cells for agglutination by kno\\'n anti-A and anti-B and

then by testing the serum for its ability to agglutinate knovm A, B and 0 red cells.

Blood Type Substitutions for Trnnsfusion (ABO and Rh) a) acceptable: A or B red blood cells to AB patients, Rh-negative whole blood or rbc's to Rh-positive patients b) usually acceptable: A or B whole blood to AB patients; 0 red cells to A, B, or AB patients c) acceptable in emergency: Rh-positive whole blood or rbc's to-

1. Rh-negative unsensitized men 2. Rh-negative unsensitized posbnenopansal women

d) never acceptable (exception: bone marrow transplantation) 1. A whole blood or rbc's to 0 or B patients 2. B whole blood or rbc's to 0 or A patients 3. AB whole blood or rbc's to 0, A, or B patients

The Rh System a) an individual inherits a complex balotype from each parent b) red cells of both donors and recipients are typed by testing them with anti-D. If cell agglutination occurs,

the type is Rh-positive >if cells are not agglutinated, patient is considered Rh-negative and is tested further for more weakly

reacting antigens c) all Rh-negative patients should receive Rh-negative rbc's

>obviously, Rh-negative blood may be given to Rh-positive patients, but this rarely occurs since only 15% of the population is Rh-negative d) the other Rh antigens (C, c, E, e) are much less immunogenic than D and it is impractical to match them in

donor and patient blood

Compatibility Tests a) pre-transfusion compatibility tests include typing patient and donor red cells for ABO and Rh, screening

patient and donor serums for significant unexpected antIbodies, and reacting donor red cells with patient serum (major crossmatch)

1. major crossmatch determines the presence of any allo-antibodies in the recipient's plasma that may destroy donor red cells and serves as a:final verification of the compatibility of donor red cells and the recipient's serum

2. while all transfusions must be preceded by an acceptable compatibility test, the crossmatch portion need not be performed prior to operative procedures that almost certainly will not require transfusion

3. crossmatchlng blood 00sed on intIa-operative usage (known as MSBOS - Maximum Surgical Blood Order Schedule) allows conservation of blood resources and contains laboratory costs

Transfusion of Red Blood Cells and Whole Blood a) RBCs in the management of chronic anemia and acute blood loss

1. RBCs should be transfused whenever the deficiency of circulating red cell mass is too severe to be treated conservatively

2. for immediate correction of acute and chronic anemia, tIansfusion ofRBCs should be the rule and whole blood the exception

170

Treatment of Hypovolemic Shock a) since restoration of tissue perfusion is of more immediate ~ than restoration of oxygen-<:arrying

capacity, immediate esaablishment of1arge IV lines and administnltion of IV fluids are required initially.

Available prepuations include -1. aystalloid solutions: primarily saline solutions 2. colloid solutions: produced artificially (ie-dextnm) or derivatives of plasma (ie-p1asma protein :fraction;

albumin) 3. whole blood and its components

b) the following guidelines are an aa:epIable approach to the management of these patients -1. almost all shock. patients with hypovolemia should receive ba1anced saline solutions initially; some use

dextran in saline or pIagna protein solutions 2. shock: patients with anemia (symptomatic) should receive piCked RBCs 3. pIasma protein losses producing serum albumin levels of 2 WdL or less can be corrected via infusion of

albumin or plasma protein fractions

prior to tranfusions give patients BenadrylSO mg polTylenol650 mg po to prevent possible minor reactions

Side Affects of transfusions: 1. Fever 2. Rash (Urticaria, pruritis) 3. Hemolytic anemia 4. Respiratory distress 5. Volume overload 6. Noncardiogenic pulmomny edema

Screening Procedures to Deted Coagulation Disorders

LAB'IEST

platelet count bleeding time prothrombin time (PI)

partial t:brombopJastin time(PfI)

thrombin time

PURPOSE

I' detection of platelet deficiency

evaluation of platelet :function evaluation of deficiencies of

factors II, V, VII, X evaluation of deficiencies of

factors V, vm, X, XL XII

I detection of abnormalities of fibrinogen (factor I)

also prolonged with cim1lating heparin and increased fibrin degradation products

PRE- and POST-OP MANAGEMENT

The Cardiac Patient a) Patients with cardiac disease should be evaluated by a cardiologist b) Elective surgery should be delayed as long as necessary to bring the patient to the OR in optimal medical

condition c) The risk of surgery is weighed against the risk of cardiovascular complications. d) Recent MI- due to high mortality rates, surgery should be postponed at least six months if possible e) Old MI- if evidence of old MI is found on the ECG without chest pain. a previous ECG should be

obtained for compuison

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f) Unstable Angina 1. careful observation and postponement of non-emergency surgery 2. maximize medical therapy with nitrates, beta-blockers and calcium channel blockers 3. if medical management is unsuccessful, get an evaluation for coronary bypass surgery before the elective non-cardiac surgery

g) Mild Stable Angina 1. may undergo minor procedures safely 2. beta-blockers and nitrate therapy should continue pre-op and be resumed post-op

h) Arrytbthmias 1. in generaL conventional anti-arrhythmic therapy should continue up to and through surgery for pltients already under treatment 2. five or more PVC'siminute are associated with increased cardiac mortality. Their significance remains controversial (puticularly if the patient is asymptomatic) and evaluation in terms of frequency, complexity and overall patient clinical status should be taken into account. These patients need to be carefully monitored and given anti-arrhythmic medications if more complex arrhythmia's occur.

Hypertension a) Mild to moderate hypertension is not a significant risk to the surgical pltient if:

1. diastolic BP is stable and <110 mm Hg 2. intra-operative and recovery room pressures are closely monitored and treated

b) In general, antihypertensive medications should be continued up to the time of surgery and post-operatively c) Get potassium levels on all patients on diuretics; replace ifsennn potassium is::: 3.5 mEqIL before surgery

Congestive Heart Failure a) Treat appropriately pre-operatively and postpone non-emergent surgery b) Swan-Ganz monitoring is essential in patients with CHF who must undergo emergency surgery. Patients

with borderline cardiac status undergoing major elective surgery may also benefit from Swan-Ganz monitoring.

Diabetic Patient a) General Information

1. stress of anesthesia and operation exacerbates diabetic patient's glucose intolerance 2. to maintain nutrition and}XeVent ketoacidosis and hypoglycemia, the patient must receive a minimum

of 100 gm caIbohydratdday and adequate insulin must be continuously available. One liter of D5W contains 50 gm of caIbohydrate.

3. this patient should have optimal nutritional status, hydIation level and electrolyte balance before surgery 4. correct ketoacidosis even ifbefore an urgent operation because of associated high mortality rate 5. hypoglycsemia is a more hazardous condition than hyperglycemia When there is no hyperketonemia,

moderate hyperglycemia (200-250 mg/dl) is not hazardous and should be expected during the early post- operative period Marlred hyperglycemia can lead to osmotic diuresis, dehydration and hyperosmlarity and thus, should be avoided.

6. there is evidence that high glucose levels alter leukocyte and fibroblast function, predisposing to infection and poor wound healing. P1asma glucose should be maintained between 100-200

m~dl. 7. insulin requirements may fall abruptly after the infection has been adequately decompressed. Anticipate

this be decreasing the last insulin dose by one-third b) Insulin and Glucose Schedules

1. no insulin, no glucose >minor operations under local where there is low stress and the patient is expected to eat after the surgery >no insulin or glucose is given the morning of surgery and intra-operative fluids contain no dextrose >blood sugars are checked and regular insulin given as needed until the next morning when the usual regimen is resmned

2. subcutaneous insulin with N glucose (most common) >management is most convenient if procedure can be done in the early morning

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>NFO (nothing by mouth) after midnight >In the early moming-

-start IV fluids consisting ofD5 1/2NSS -give approximately one-third to one-half of the patient's usual am dose ofNPH or lente inulin -hold regular insulin dose

>Upon completion of the operation-<ontinue the IV fluids until the patient receives 2 liters (100 gm of glucose) in a 24 hour period -give regular insulin every ~ hours blsed upon (fingerstick) blood glucose levels. The first

determination should be done as soon as the patient anives in the recovery room The dose should be based on the patient's response to previous doses of insulin.

INSULIN SLIDING SCALE blood glucose level Regular Insu1in

<200 no covemge 200-250 2 units SQ 251-300 4 units SQ 301-350 6unitsSQ 351-400 8 units SQ

>give omI fluids and food as soon as the patient's condition permits >resume diet and pre-op daily insulin dose >if the patient cannot be fed, start IV DSW or D10W to total 200 gm carbohydrate daily and divide usual NPH or Lente dose into two equal doses given 12 hours apart. <bain serum glucose levels every 6 hours and cover with regular insulin as needed. >lower dose ofNPH or Lente ifhypoglycemia occurs

c) Diabetics on Oral Hypoglycemic Agents 1. Minor Surgery

>withhold the medication on day of surgeIy

>if surgery is early in the morning and the patient is eating post-op, the omI agent is resumed > if the surgery is delayed or the patient is expected to be NPO for many hours, start D5W N and monitor glucose. Regular insulin is given as needed

2. Mgor Surgery >discontinue omI hypoglycemic agent >when possible an insulin regimen should be started several days before surgery to determine insulin

levels and to stabilize glucose levels >NFO after midnight the day before surgery >one-half to one-thitd intermediate acting insulin is then given on call to the OR and the patient managed with regular insulin based on blood glucose levels determined every 6 hours >with shorter time ftames, the om! agent is discontinued 24 hours before surgery. The patient should be NPO after midnight and receive regular insulin as needed based on glucose levels every 6 hours. D5W N is started the morning of surgery.

>omI hypoglycemic agents can be started when normal diet is resumed

Thyroid Disease a) This condition is not a contra-indication to elective surgery b) It is important to get the patient euthyroid before surgery c) Hyperthyroid Patient

1. these patients are apt to develop hypertension, severe cardiac dySIbythmias, h}'J)erIhennia and thyroid storm There is no apparent correlation between nature or severity of surgery to thyroid storm

2. bring to euthyroid state by (takes 1-6 weeks): >propylthioruacil 800-1000 mg/day for 1 week then 200-400 mg/day maintenance dose or 30-40

mglday methirnazol PO >beta-blockers (dose= 160 mglday) control tachycardia, palpitations, anxiety, etc.

3. all patients, unless contra-indicated, should receive combination of the above drugs

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d) Hypotbyroid Patient 1. bring patient to euthyroid state (takes weeks to months). Once achieved, there is no increase in

morbidity associated with surgery. 2. L-thyroxine's long half-life allows it to be stopped during the perioperative period without problems. 3. myxedema coma should be suspected in patients who fail to awaken from anesthesia and who

manifest CO retention. . Anemia a) Evaluate the etiology of the anemia before proceding with any elective surgery. b) Treatment is individualized on the basis of the etiology (Hct, Hgb, reticulocyte count, blood smears,

Coomb's test, bone marrow exams and the H & P are useful to pinpoint the etiology). A hemoglobin of 10 gmldI and a hematocrit of 30% have customarily been required to assure adequate tissue oxygenation during surgery.

c) Each patient's requirement is based on several factors; the values listed above are just guidelines. d) Decision for transfusion must be made weighing the benefits versus the risks e) Factors requiring higher pre-op hemoglobin levels

1. old age 2. acute blood loss 3. coronaIY artery disease (CAD) 4. pulmonary disease 5. peripheral vascuIar (PVD) or cerebrovascular disease 6. significant blood loss expected

f) Factors making lower pre-op hemoglobin level more acceptable 1. youth 2. chronic anemia 3. normal exercise tolerance 4. no cardiac, pulmonary or cerebrovascular disease 5. little blood loss expected

g) Therapy should provide only those blood components required to correct the defect. Oral therapy (ie-iron, folate. vitamin B12) is appropriate if the surgery is elective and can wait. Packed RBC's can be used for all but severe hemorrhage.

Neutropenia a) Etiology

1. drugs 2. infectious agents (especially viral) 3. preleukemia, myeloproliferative disorders 4. congenital 5. chronic rl1eumatic disease (ie-SLE, Felty's syndrome)

b) Cancellation of surgery if <1 OOOImm . Risk: of infection is marlredIy increased when granulocyte count is <500/mm . c) Treatment depends upon the etiology. Postpone surgery in viral or drug induced cases untilleukopoenia is

reversed. d) Granulocyte transfusions have little indication for surgery and only used in an infected patient \\'ith a count

<500/mm Hemostatic Disorders a) Careful bistory is crucial because it may give the :first indication of potential hemostatic problem;

questioning (include prior surgery, dental procedures, mucous membrane bleeding, transfusions, bruisability. epistaxis,

history of hematomasIhemar delayed bleeding, family history)

b) Certain hemostatic problems are seen with normal routine Jabs.

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LAB lEST PURPOSE p1atelet count detection of deficiency }XOthrombin time fuctor VII. extrinsic pathway

(PI) (warfurin) partial tbrombop1astin factors vm. IX. XII time (PIT) (heparin)

*factors V and X. prothrombin and fibrinogen are required for both Pf and PIT bleeding time evaluation of platelet fimction

ABNORMAL NORMAL DISORDER (faaors) PIT Pf hentopbilia (VllI)

Christmas disease (IX) factor XI deficiency Hageman fuctor (XII) deficiency von Willebr.md's disease

PI' PIT factor VB deficiency PIT & PI factors n, V, or X deficiency

dysfibrinogenem DIC

vitamin K deficiency broad spectrom antIbiotics malabsorption liver disease

PIT & Pf faaor XIII deficiency von Willebr.md's disease dysfibrinogenemia Ehlers-Danlos syndrome vasculitis R.endu-Osler-Weber disease

replace factors as specific as possible and postpone SUIgeIy if possible

c) anticoagulants l.coumadin

>coumadin interferes With action of vitamin K in the synthesis of factors n, vn, IX. X >discontinue coumadin - normalization within 36-48 hIs >vitamin K can be given but it is preferable to discontinue coumadin (SQ or oral administration 18-24

hours for nonnalization); vitamin K will interfere with post op anti-coagulation for 1 week. >emergency swgery: discontinue comnadin and transfuse 2-4 units of fresh frozen plasma; this may

need to be repeated post-op 2. heparin

>PIT will be normal if discontinued 8 hIs before swgery >mpid reversal may be achieved with protamine sulfilte (1: 1(0); usual dose is 50 mg N over 5 minutes >heparin induced thrombocytopenia is fuirly common

Obesity a) Defined as body weight> 30010 above ideal b) Severe obesity is not rare c) Mortality tate is 2-3 times that of the normal patient d) Pre--operative evaluation is made more difficult because fat curtains the ~ system of interest e) Careful questioning of previous lung disease, heavy snoring, blood prsssure, thrombopblebiti pulmon3IY

embolism are essential f) Thorough cardiovascular and pulmonary exams are essential g) Standard pulmoDaIy function tests, 12 lead ECG and ~ x-ray should be accomplished on all moderate to

severely obese patients

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h) Prescribe regimen for optimum pulmonary function deep breathing and coughing exercises, incentive spirometers and bronchodilators followed by chest percussion if needed

i) Unless contraindicated prescnbe mini-dose heparing to help prevent DVf and pulmonary embolism j) Avoid Trendelenburg position because the weight will decrease lung volume k) Use volume pressure monitors (ie: Swan-Ganz) in severely obese patients with cardiovascular or

pulmonary disease . I) Use spinal or local anesthesia where appropriate m) Consider waiting two days post-op to extubate if problems arise intra-operatively n) Early ambulation

Steroids a) Identify patients who will need supplemental steroids during the stress of surgery b) Glucocorticoid deficiency may result from:

1. primaIy dysfunction of the adrenal gland 2. secondary adrenal insufficiency due to pituitary disease 3. adrenal suppression due to administration of exogenous steroid

c) Corticosteroid coverage has become a standard practice when treating patients with even suspected adrenal deficiency who \DldeIgo surgery

d) Cardiovascular collapse is the major concern e) An adrenal reserve test is available 1) The daily requirement of cortisone is approximately 300 rug g) Suspect adrenal deficiency if:

1. >7.5 mg prednisone in single daily dose taken for> 1 mo. 2. any steroid in divided doses for >5-7 days 3. long acting preparations (ie-dexamethasone, betamethasone) taken for >5-7 days 4. >20 mg prednisone taken for >5-7 days 5. patient with Cusbingoid appearance 6. prolonged shock or unexplained shock or fever

h) A wide variety of steroid schedules have been proposed; no one has a distinct advantage over the other i) example of glucocorticoid coverage

1. minor surgery/limited procedure >m:inima1 to additional steroid coverage needed >give regular dose with surgery and maintenance dose after surgery

2. major surgery >hydrocortisone sodium succinate 100 mg 1M or IV every 6 hours for 24 hours to start with pre-op medications. Use IV route if there is tissue hypoperfusion >reduce by 500/0 daily beginning POD #1 until maintenance dose or equivalent is reached (20 rug AM, lOmgPM) >in patients with primmy adrenal insufficiency fludrocortisone 0.1 rug daily must be added. to provide sufficient mineralocorticoid activity when the dose of hydrocortisone is 100 rug or less per day >with short procedures give a single IV or 1M dose of hydrocortisone 100 mg with pre­medications and an extra 20 mg oral dose that evening. Resume regular regimen the next day

Renal Disease a) The history and physical, glomerular filtration rate, serum creatinine, BUN, urinalysis, and blood chemistry

profiles \\'ill be indicators for renal disease b) Risk of surgery is not likely to be increased if creatinine clearance is >50% normal (normal creatinine is

<2.0) The point of significant risk has not been determined c) Regulation of volume status is critical

1. mild to moderate renal impairment: these patients are unable to concentrate their urine and are therefore, at risk for vo1mne depletion. Observe fluids carefully and replace as needed Monitor body weight, Jlas (ins and outs), electrolytes, and pH

2. severe renal insufficiency: these patients are at risk for volume overload and hypeIka1.emia. Monitor fluid baJance and dialyze if necessary. Consider Swan-Ganz monitoring

3. UTI's are treated pre-operatively based on C & S results

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4. obstructive lesions are removed or corrrected before major surgery 5. fluid and electrolyte imbalances should be corrected pre-op 6. metabolic acidosis, even though compensated should be corrected with sodium bicarbonate 7. anemia: Hgb 9 gm/dl and Hct 25% are satisfactory for tbe patient with chronic insufficiency 8. correct coagulation defects seen in chronic renal disease pnH)p

9. hemodialysis, when necessary, should be planned for the day before surgery d) If renal function deteriorates or transfusion reaction occurs consider using an osmotic diuretic (ie-mannitol).

This may have a protective effect on renal tubular function e) Nephrotoxic drugs must be administered carefully and in reduced doses f) Post-operative urine output of <25 m1Ihr requires irnrnOOiate evaluation g) Diabetic patients are particularly prone to acute renal failure after contrast dye studies

SW AN-GANZ CATHE'IER Description a) flexible quadruple lumen tube approximately 110 em long and scored in 10 em increments b) lumens

l. distal (PA) lumen: ~ -records PAP, PCWP IF ~ mixed venous blood for oxygen content analysis

2. proximal (RA) lumen: -records RAP or CVP

3. balloon lumen -tenninates 1 em from tip of catheter

-when balloon is inflated, it moves in direction of blood flow

-the inflated balloon guides catheter through the RA, RV and into the pulmonary artery where it lodges in smaller branch

-records the pulmonary capillary wedge pressure (PCWP) in this position [pcWP: normally equal to the Left Atrial pressure

thus, sensitive indicator of presence of pulmonary congestion and left sided CHF]

4. thermistor lumen -contains temperature sensitive 'Wires -calculates cardiac output by thermodilution technique

Insertion a) percutaneous insertion via internal jugular vein safest b) location of catheter tip determined by recognition of characteristic pressure waveform of each heart

chamber

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Complications of right heart catheterization a) cardiac dysrhythmias b) thrombosis c) sepsis d) pulmonary infarction e) pulmonary valve perforation f) knotting of catheter g) rupture of balloon

Indications for hemodynamic monitoring a) severely ill. hemodynamically unstable patients b) acute cardiac conditions

(ie-complicated MI; RV infarction; mitral regurgitation)

c) chronic cardiac insufficiency

~.--, . .

J

. -') ................. _. ~f

(ie-constrictive pericarditis; congestive cardiomyopathy) d) miscellaneous

(ie-acute non-myocardial infarction pulmonary edema)

Differential Diagnosis of common PA catheter readings low RAP, low R VP: volume depletion high RAP, high RVP: volume overload

CHF cardiogenic shock

high PAP: CHF cardiac tamponade increased pulmonary vascular resistance (ic-hYJXlxia, pulmonary disease, ventilator effect of PEEP)

low PCWP: volume depletion high PCWP: cardiogenic shock

LV failure severe hypertension mitral regurgitation and stenosis volume overload cardiac tamponade

Alcoholic Patient a ) Screening:

l)ask: all patients: Do you drink alcohol, including beer, wine, or distilled spirits? 2)for current drinkers:

-On average, how many days per week do you drink alcohol? -On a typical day when you drink, how many drinks do you have? -What is the maximum number of drinks you had on any given occasion during the last month?

3)for current drinkers: (CAGE questionnaire) -Have you ever felt that you should Cut down on your drinking? -Have people Annoyed you by criticizing your drinking? -Have you ever felt bad of Guilty about your drinking? -Have you ever had a drink first thing in the morning (Eye opener) to steady your nerves or get rid of a

hangover?

b) Assessment for all patients at risk: of withdrawal: (Clinical Institute Withdrawal Assessment for Alcohol) I )nausealvomiting 2)tactile distIbances (itching, pins and needles, burning, numbness) 3)tremors 4 )auditory disturbances 5)paroxysmal sweats 6)visual disturbances 7)anxiety

178

8)headache, fullness in head 9)agitation

lO)orienlation and clouding of sensorium.

c)Treatment for withdrawal 1)Lorazepam 2 mg q 6 x 4 doses, then 1 mg q 6 x 8 doses (additional doses as needed) 2)Propb.y1axis:

-15-30 mg SeIax tid x 3 days -15-30 mg SeIax bid x 2 days -15-30 mg SeIax qd x 2 days -multivitamins 1 tablet po qd -start NSS at determined rate with 100 mg thiamine/I mg folate x I bag (may give folate and thiamine po)

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PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY PRINCIPLES OF SURGERY

IPL

REGIONAL AND LOCAL NERVE BLOCKS

Goal: • Provide local anesthesia to area of insult • Maintain minimal patient movement • Maximum relief to the patient

Indications: • Surgical intervention

• Diagnostic • Aspirate or soft tissue or joint

Equipment:

• Needle • Diameter- small gauge (25 or 27) • Length- adequate to reach target (typically 1.5 inch)

• Syringe (3ec, 5ec, or 10 ec) • Local Anesthetic (LA) • Antiseptic solution (Alcohol, Betadine, etc.)

• Prep area distal to proximal

Technique: 1. Identify peripheral nerve(s) innervating region to be anesthetized 2. Dmw-up adequate amount of LA (insure pt is non-allergic) 3. Prep entry site with antiseptic solution

• Joint entry requires betadine paint prep (three times) 4. Optional topical anesthetic prior to breaching integument (i.e. ethylchloride spray, topical

lidocaine) 5. Swiftly enter needle perpendicular to integument 6. Infiltrate intradermal wheal 7. Advance needle to desired neural structure 8. Biplane aspimte

** ALWAYS, ALWAYS, ALWAYS aspirate prior to iof'dtrating LA 9. Infiltrate appropriate amount of anesthetic solution

* Use least number of skin entries necessary to acquire desired anesthesia * When redirecting needle always withdraw needle to subcutaneous layer, then follow steps 6 through 9 * Abide by OSHA regulations for handling, recapping and discarding of needle and syringe

Complications: • Direct injury to nerve trunk • LA toxicity- watch for CNS and CV symptoms

• Allergic reaction

Nerve Blocks: Popliteal

• Indicated for intra and/or post -op analgesia of rearfoot and leg procedures • Tibial nerve/Sciatic nerve at the level of the popliteal fossa • Optional use of nerve stimulator for proper site infiltration is recommended • Set nerve stim. at 2.0-3.0 rnA • Enter 7-8 em proximal to popliteal skin crease, medial to biceps femoris

muscle/tendon • Advance nerve stimulator slowly until triceps surae and/or toe flexors twitch • Infiltrate approx. 30-40 ec's oflong acting LA • Ancillary saphenous nerve block may be indicated

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Common Peroneal • Diagnostic for: assessing spastic peroneal muscles, stress inversion radiographs for

lateral ankle instability • Very superficial 1-2 cm deep to skin • Palpate fibular head and nerve • Enter laterally 2.5 cm distal to fibular head • Infiltrate approx. 3-6 cc's LA

Ankle Block • Indicated for multiple forefoot and midfoot procedures <2 hours, I&D • Total of 10-15 cc's LA

I. Posterior Tibial NenJe • Medially at the level of the malleolus bisect the tendo achilles and tibial

malleolus • Enter at the bisection infiltrate 1-2 cc's LA • Redirect needle distal anterior at 45 degrees to skin, bury needle to hub and

infiltrate 1-1.5 cc' s LA • Again, redirect distal posterior at 45 degrees to skin, bury needle to hub and

infiltrate 1-1.5 cc' s LA 2. Superficial Peroneal Nerve (lntennediate and A1edial Dorsal cutaneous)

• Plantarllex the foot at the ankle joint and identify the superficial peroneal or it's terminal branches in the distal1l3rd of the leg

• Enter directly over nerve(s) approx. 1 cm proximal to ankle joint • Infiltrate 1-1. 5 cc' s LA

3. Deep Peroneal Nerve • 1 cm proximal to ankle joint identify tendons of tibialis anterior and

extensor ballucis longus • Enter bisection T A and EHL, bury needle to hub (if tibia is encountered

retract needle 2-3mm • ASPIRATE, then infiltrate 1-2 cc's LA

4. Saphenous Nerve • Identify the Great Sphenous Vein at the anterolateral aspect of the medial

malleolus • Without exiting from DP block, redirect needle in subcutaneous plane

directly medially, just lateral to the GSV • ASPIRATE, then infiltrate 1 cc LA

5. Sural Nerve

MayoB/OCk

• Palpate for nerve trunk 0.5-1 em inferior to lateral malleolus • Enter directly lateral at this level • Infiltrate 1 cc LA wheal directly over nerve • Redirect anteromedial in subcutaneous plane infiltrating 1-1.5 cc's LA • Again, redirect inferior and distally in subcutaneous plane infiltrating 1-1.5

cc's LA

• Indicated for first metatarsal and hallux procedures (i.e. HA V Surg., closed reduction fracture, etc.)

1. Deep Peroneal Nerve • Palpate the dorsal aspect of 1 sl and 2nd metatarsal bases • Enter interspace dorsal, raise wheal, aim plantarly burying needle to hub,

aspirate, infiltrate 1.5-2cc's LA

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2. First Proper Digital Branch of the Medial Dorsal Cutaneous Nerve • Without exiting DP injection site redirect directly medially • Infiltrate 1-l.5 ce's LA along subcutaneous plane

3. First Proper Digital Nerve of the Medial Plantar Nerve • Enter medial to lit metatarsal through wheal, direct needle plantarly • Infiltrate 1-1.5 ce's LA along subcutaneous plane

4. Second Proper Digital Nerve of the Medial Plantar Nerve • Enter medial to 1st metatarsal through wheal, direct needle laterally just to

inferior 1st metatarsal base infiltrate 1-1.5 ce' s LA • Redirect plantar lateral in subcutaneous plane and infiltrate 1-1.5 ce's LA

Reverse Mayo BlDek

Hallux Block

1. Intermediate Dorsal Cutaneous Branch to Fourth Interspace and Lateral Plantar Branch • Palpate the dorsal aspect of 4th and 5th metatarsal bases

• Enter 4th interspace dorsally, raise wheal, aim pIantarly bury needle

• Infiltrate l.5 ce's LA 2. Lateral Dorsal Cutaneous Nerve (Sural Nerve)

• Without exiting interspace injection site redirect, directly laterally • Infiltrate 1-1.5 ce's LA along subcutaneous plane

3. Proper Digital Branch to Fifth Digit of the Lateral Plantar Nerve • Enter lateral to 5th metatarsal through wheal, direct net:dIe medially • Infiltrate 1-1.5 ce' s LA along subcutaneous

• Indicated for nail procedures, subungual exostectomy, etc. • Two-point stick

1. First Proper Digital Branch of the Medial Dorsal Cutaneous Nerve & First Proper Digital Nerve of the Medial Plantar Nerve

• Enter the dorsal medial aspect of the proximal phalanx base • Raise wheal, direct needle plantarly infiltrate 0.5-0.75 ce's in

subcutaneous plane 2. Deep Peroneal Proper Digital Branch to Hallux & Second Proper Digital

Nerve Branch of the Medial Plantar Nerve

DigitJ.Il Block

• Enter the dorsallatera1 aspect of the proximal phalanx base • Raise wheal, direct needle plantarly infiltrate 0.5-0.75 ce's in

subcutaneous plane

• Indicated for arthroplasty, amputation, nail procedures, etc. • Enter the dorsal central aspect of the proximal phalan..x base • Raise wheal, direct needle plantar medial, infiltrate 0.5 ce's in subcutaneous plane • Redirect plantar lateml, infiltmte 0.5 ce's in subcutaneous plane • Plantarly, look for cutaneous blanching and wheal formation

182

BONE HEALING

Definitions a) osteoblasts: bone fonnation whether embryonic or through a healing process requires the presence of

osteoblasts. The osteoblast is the only cell capable of bone production. Osteoblasts are derived from precursors located in the walls of blood vessels. These mesenchymal cells or pericytes differentiate into osteoblasts in areas of fracture, osteotomy or growth. An adequate blood supply must be present for the cells to reach these sites. TIle relationship between osteoblastic bone formation and a functional vascular network is a key component to understanding bone healing.

b) osteoclasts: large multinucleated cells located in the tip of the "cutting cones", which dissolve bone matrix fonning canals through existing bone. Responsible for bone reformation. c) osteoid: a noncalcified organic matrix formed by osteoblasts, which contains 95% collagen and 5%

proteoglycans d) mineralization: the process by which osteoid becomes deposited with calcium phosphate, mainly in the

fonn of crystalline hydoxyapatite. In mature bone, mineralization occurs 8-10 days after osteoid is formed. Normal mineralization in lamellar bone occurs at the rate of 1 um per day as determined by Frost in 1%3.

e) woven bone: type of bone which fonns healing bone callus. The intercellular substance contains a disordered three dimensional anay of collagen fibrils. Osteoid seanlS are narrow fu.d osteoblastic cell population is dense. Woven bone rapidly mineralizes following formation. It may proliferate ridges and trabeculae to form extensive networks.. Osteoblasts extrude matrix in all directions. Eventually remodels to lamellar bone. f) lamellar bone: highly o~ed bone laid do\\n in congruent layers with parallel collagen fibers which

change directions from one lamella to the next. Osteoblasts are highly polarized extruding matrix only in their basal cell surfuce. Requires a flat smooth substrate in order to be synthesized.

Stages of Bone Healing I. Inflammation: day 1 to day 3-4

initial hematoma formation around site followed by necrosis of bone margins macrophages invade area to remove dead bone and tissue

II. Induction: day 1 -(duration unknown) osteoblasts or chondroblasts induced

good oxygen supply, vascularity and stability -osteoblasts form poor oxygen supply, vascularity and stability -chondroblasts form

pro-ca11us develops from the maturing hematoma ill. Soft Callus: day 4 to 4 weeks

clinical union noted with elimination of motion across site formation of callus noted

IV. Hard Callus: 4 weeks to 4 months callus converted to mature lamellar bone radiographic union noted

V. Remodeling: 4 months to 2 years

Types of Bone Healing a) Primmy (direct)

1. occurs when bone fragments are rigidly immobilized 2. stages of bone healing undifferentiated and callus formation absent 3. with rigid immobilization, framework provided by callus not necessary 4. due to the rigid immobilization., the fixation device assumes partial load applied to the bone; the result is

bone resorption due to reduced biomechanical demand

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5. types ofprimaIy bone healing -gap healing: hematoma fills the microscopic gaps

• area is infiltrated by capillaries and osteoblastic cells. then filled with woven bone and remodeled osteoblasts initially form IamelIa oriented 90 to the long axis of the (fracture) site and are then rep1aced by axialIy oriented IamelIa

-contact healing: smfaces in direct contact "cutting cones" cross interfi1ce, producing concentric pattern of new lamellar bone "cutting cone" advances approximately 70-100 urn per day, as per research done by Schenk

b) Secondary (indirect) 1. occurs when bone is not rigidly immobilized 2. motionlinstability allow for additional hemonbage, wbich fuvors fibrocartilage formation and

ultimately callus 3. bone callus creates a framewOIk so that bone healing may occur. A layer of bigh tensile strength

connective tissue is laid down between fragments followed by granulation tissue, wbich resists compression. This framework is repJaced by fibrous cartilage. Eventually chondroclasts remove the cartilage and osteoblasts begin to produce woven bone

4. bone remodels in accordance to Wolffs Law, whereby bone deposition takes place on the concave side and resorption on the convex side. Adaptation may correct some angular deformity, but cannot correct misalignment of articular ends.

Complications of Bone Healing 1. malunion: a nonanatomic position of fracture fragments following the healing process. Malunion can

result in structural defonnity and reduced or total loss of fimction. Usually the result of poor reduction combined with inadequate fixation.

2. delayed union: union is considered delayed when healing has not advanced at the average rate for the location and ~'})e offracture. Prolonged casting or dynamic loading of bone may be needed to hasten healing.

3. nonunion: the difference between delayed union and nonunion is not clear cut. The time when a given fracture should be united cannot be arbitrarily set and depends on location, type, physical characteristics of the patients and mode of therapy. A nonunion may not be diagnosed until there is clinical or radiographic evidence that healing has ceased and union is unlikely. Generally a fracture of the shaft of a long bone should not be considered a nonunion until at least 6 months after surgery. The final status of a nonunion is the formation of a pseudo-arthrosis.

Diagnosis of nonunion a) standard radiograph: presence of sclerotic borders or osseous void at the fracture site b) stress fluoroscopy

manually manipulate fracture site under fluoroscope should be virtually no movement between ends ands osseous bridging should be present [not fully diagnostic of nonunion]

c) (fc-99m) bone scan normal fracture healing stages on bone scan week I-week: 4: diffuse uptake at fracture site and 3(ljoining areas of bone week 4-week 12: biphasic pattern with uptake more localized to fractured ends of bone week 12-2 years: coalescence stage with focal uptake at

fracture site alone hypertropbic nonunion will demonstrate persistence of biphasic stage atrophic nonunion "ill demonstrate low uptake activity at fracture site; may see focal uptake with

intervening void ("cold spot") d) tomograms: help visualize presence of ttabeculation or persistent fracture line e)Cfscan

184

f) osteomedullangiography radiopaque dye injected on one side of fracture if venous continuity is seen across fracture site, nonunion can be ruled out if venous continuity present (positive test), immobilize and initiate NWB status ifvenous continuity absent (negative test), open reduction with bone graft recommended

C~ailionofNonuniom Based upon vascular supply and osteogenic potential a) Hypertrophic or Hypervascular Nonuniom

This type of nonunion is capable of a biologic reaction. The ends of the fragments are viable and highly vascularized. There are three subgroups within this category -

1. Elepbant Foot nonunion: very hypertrophic with heavy callus fonnation. Results from unstable fixation or premature weightbearing. .

2. Horse's Hoof nonunion: mildly hypertrophic with poor callus formation. Results from moderately umtable fixation.

3. Oligotrophic nonunion: not hypertrophic and callus is absent Results from displacement of fracture, distraction of fragments or fixation without direct apposition of fragments.

Elephant Foot Horse's Hoof

b) Atrophic or Avascular Nonunions This type of nonunion is not capable of a biologic reaction. There are four subgroups within this category -

u n Oligotrophic

L Torsion Wedge nonunion: this type has an intermediate fragment in which the blood supply is decreased or absent The intennediate fragment is healed to one main:fragment but not to the other.

2. Comminuted nonunion: characterized by the presence of one or more intermediate :fragments which are necrotic. Typically results from plate breakage and callus formation is absent

3. Defect nonunion: characterized by a loss of a fragment, usually in the diaphysis. The ends of the fragments are viable, however, the gap is so large that bridging cannot occur. The ends eventually become atrophic.

4. Atrophic nonunion: results when the intermediate :fragments are missing and scar tissue (which lacks osteogenic properties) fills the void

Torsion Wedge Comminuted Defect Atrophic

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Electrical Properties of Bone a) Wolff: electric potentials are created under the application of stress to bone b) Fukada and Yasuda (1950's): bone piezoelectricity bone becomes electrically polarized

when it is defonned the compte&ii.on side is electronegative with callus production and the tensionside is electropositive

c) Freidenberg and Brighton (1960's): bioelectric potential nonstressed bone demonstrated electronegative potential in areas of active bone growth and electtopositivepotentials in areas ofless activity

d) Anderson and Erikson: electrical properties and bone growth result from ''streaming potentials" [the pH difference between collagen hydroxyapatite and the surrounding liquid medium causes an electrical gradient]

e) .AthenstaOOt: collagen fibers have asymmetrical chaIge distribution [parallel anangement of collagen sets up a net dipole moment with growth occmring towaId the negative end of the fiber]

Tmdment ofNonunions a) Hypertrophic nonunions - stabilization offiacture ends b) Atrophic nonunions

I. resection of nonunion and bone graft with fixation 2. llizarov technique

corticotomy followed by distraction (to induce local necrosis and neovascularization) compression-distraction ("accordion technique")

3. electrical stimulation does not correct for shortening of malposition

the exact mechanism by which electrical current stimulates bone growth is unknown. In the 1970's many investigators developed different electrical stimulating devices. All reportedly have the same

overall success rate of 80-850/0, however, the principles of good fracture management must be strictly followed. All forms cannot induce bone growth in large gap nonunions. In general a gap larger than one­half the diameter of involved bone is a contraindication to electrical stimulation All forms require approximately 3~ months for bone healing.

types of electrical stimulation systems ->invasive electrical stimulator Electrodes and power pack are directly implanted in the nonunion site. This does not require patient cooperntion to maintain, however, two opel3tions are required - one to place and one to retrieve the unit

>semi-invasive stimulator Percutaneous electrodes are placed at the nonunion site and are attached to an external power pack This requires one operative procedure and patient coopeI3tion is necessary to maintain the unit.

>non-invasive stimulator Involves the use of an externally applied pulsed electromagnetic field to induce an electrical potential in the nonunion site. Totally noninvasive, however, requires patient to apply and maintain

the unit.

compression-distIaction ("accordion technigge") , r

go St~ LJ.

1+ 186

corticotomy and distraction bone pegging technique

CE':::]

~ D

graft interposition technique compressed bridging graft technique

BONE STIMULATION Stimulation of bone to promote healing has indications for more thanjust nonunions. Currently osteogenesis is stimulated through either electrical or mechanical (ie-ultrasound) means. Three methods are available for electrical stimulation-

1. Faradic 2. Capacitive (ie-Osteogen by EBI) 3. Inductive - pulsed electromagnetic field; noninvasive

Although electrical stimulation has achieved promising results, research continues to define optimal treatment parameters. Keep in mind that electrical stimulation will not correct angular deformity, rotational deformity, shortening or articular surfuce defect. Also. its potential for oncogenesis is still uncertain as of yet.

Tissue Effects of Electrical Stimulation a) increased pH: promotes bone formation

1. inlnbit osteoclast resorption 2. stimulate mineral deposition in fracture rerair

b) decreased pO : enhances calcium deposition 1. stimulates optimal bone growth in vitro 2. growth plate cartilage and bone cells follow an anaerobic metabolic pathway 3. found in bone and cartilage cells in fracture callus

c) desensitize osteoclast to PfH

Indications nonunions; delayed unions congenital pseudo-arthrosis enhance survival rate of bone graft repair following resection of massive tumor Charcotreconsttuction AVN

187

Contraindications uncontrolled motion synovial pseu<krarthrosis fracture gap > 1 em (or 112 diameter of the bone) pregnancy active osteomyelitis (invasive techniques) pathologic fiacture secondary to malignant tumor

Exogen, Inc developed a different method to stimulate osteogenesis based upon low intensity, pulsed ultrasound called SAFHS (sonic accelerated fracture healing system) therapy. This method provides a mechanical stimulus and its low energy level differentiates it from conventional (high energy) ultrasound utilized in rehabilitation therapy. Possible mechanisms of action -a) direct mechanical effect b) increased perfusion through microvasculature c) increased blood flow d) indirect electro-kinetic effect

Studies involving mbbit tibial fractures have yielded 87-91% success rntes. Also, a femoral fracture study from the Mayo Clinic concluded that the effects of the ultrasound therapy were not inhibited by the presence of an intramedullary rod. Electrical or ultrasound stimulated osteogenesis are options to promote healing, but are not substitutes for sound surgical principles regarding fracture care.

Osteogen: EBl product implantable device OC power supply/capacitive method

generator placed in subcutaneous tissue, 8-10 em from cathode -generator removal not mandatory -tester available to make sure it was implanted COrrectlyflS still working

bone geposition OCQJTS in 5-8 mm radius around (cathode) wire anock or cathode should not touch metal "cuiable cathode wire configurations

• "li ()'"?J lJ

~

-helix

-zigzag

-<hill hole (fish --y-y-ry scale)

this configuration allows greatest control in preventing contact with fixation

188

WOUND HEALING

Surgical Layers a) skin: epidermis and dennis b) superficial fascia

1. outer layer ~culus adiposis) 2. inner layer - thin membranous layer

All vessels, nerves and lymphatics lie between these layers c) deep fascia

1. beneath this layer are muscles and tendons 2. the deep fascia may be continuous with the joint capsule and periosteum

d) bone

Classification of Wounds a) clean: a non-traumatic, non-infected wound which does not enter the respiratory, alimentary or

genitourinary tracts or the oropharyngeal cavity. Accounts for 75% of all operative wounds.

b) clean-contaminated: contains normal flora without unusual pathogenic contamination. A clean wound contaminated by a minor break in aseptic technique is considered clean-contaminated c) contaminated: includes soft tissue lacerations, open fractures, penetrating WOilllds and other fresh traumatic

injuries. A procedure with a major break in aseptic technique is considered contaminated. d) dirty and infected: heavily contaminated or clinically infected prior to surgery

Types of Wound Healing a) primary intention: initial closure of an incision "With accurately approximated wouknd edges; produces the

least amount of scarring. b) secondary intention: healing occurs by formation of granulation tissue containing fibroblasts which close

the wound by contraction and secondary growth of epithelium. c) tertiary intention: delayed primary closure

Phases of Wound Healing a) substrate phase (lag phase): day 1 to day 3-4

vascular response -increased vasodilation and permeability hemostasis via activation of clotting cascade and formation of platelet -fibrin plug leukocyte response (margination & emigration of WBCs) capillary redirection toward wound edges in order to contribute to granulation tissue

inflammatory response -PMNs predominate during the first few days macrophages predominate by day 5

b) proliferative phase ( repair phase): day 3-4 to day 21 controlled by macrophages fibroblasts lay down collagen; wound edges "heap up' due to collagen proliferation new fibers and vessels bridge defect myofibroblasts ("surgeon's cells") migrate from surrounding tissue to lay down collagen and

glycosaminoglycans these cells have a contractile characteristic

collagen fibers initially laid down in random pattern c) remodelling phase (maturation phase): day 21-

collagen fibers re-align along long axis of (linear) scar strongest scar has its fibers arranged in same direction as the collagen fibers in the native surrounding dermis [ideally, original scar will be parallel to RSTL]

189

Complications of Wound Healing a) local mctors delaying wound healing

l. incisions: incisions improperly placed within relaxed skin tension lines or made at an angle other than perpendicular to the skin surface

2. traumatized tissue: rough handling of the wound during surgery can lead to excessive tissue damage which will delay wound healing

3. improper irrigation: fililure to irrigate properly will allow foreign bodies to remain and delay healing 4. inadequate hemostasis: creates pooling, distention of tissues and dead spaces 5. desication of tissues: drying of tissue during surgical e.-xposure 6. infection: infection occurs if the innoculum and virulence of the organism overcame the resistance of

the host; purulence separates wound edges 7. prolonged dependency: leads to edema, which mvors sepatation of wound edges 8. local corticosteroids: large amounts delay granulation tissue, depress capillaJy proliferation and

suppress fibroblast proliferation Corticosteroids iIUected around the surgical site, and in proper dosage, limit excessive edema formation.

b) systemic mctors that delay wound healing 1. uncontrolled diabetes mellitus 2. alcoholism: alcoholics are nutritionally depleted, especially in protein. Alcohol also reduces protein

metabolism; hypoproteinemia prolongs the lag phase and slows the onset of proliferative phase. 3. gastroiontestinal malabsorption 4. ascoIbic acid deficiency: synthesis of collagen and epithelial regeneration are dependent on ascorbic

acid 5. steroids: high levels inhibit collagen synthesis and mucopolysaccharide production 6. platelet inhibiting drugs: drugs that impair platelet aggregation include aspirin, phenylbutazone,

sulfinpyrazone, antihistamines, indomethacin, chloropromazine, tranquilizers and heparin 7. 7. anemia: hemoglobin less than 10 gmldl with a hematocrit less than 33% is considered inadequate

tissue oxygen supply for proper healing 8. hepatic disease: decreases clotting mctors and albumin production 9. obesity: unsatisfactory oxygen tissue levels and hypercoa.guability 10. age: decreased healing caused by autoantIbodies., altered proteins and diminished connective tissue

production

Wound healing agents 1. ACCU.2YME® (papain-Urea Debriding Ointment)

-Papain, the proteolytic enzyme from the fruit carica papaya, is a potent digestant of nonviable protein matter but is harmless to viable tissue. It is relatively ineffective when used alone as a debriding agent and requires the presence of activators to stim~ate its digestive potency.

-In Accuzyrne®, papain is combined with urea (a denaturant of proteins) to bring about two actions: (1) to expose the activators of papain and (2) to denature nonviable protein matter in lesions and thereby render it more susceptible to enzymatic digestion

INDICATIONS AND USAGE

-indicated for debridement of necrotic tissue and liquefication of slough in acute and chronic lesions such as pressure/decubitus ulcers., varicose and diabetic ulcers.. burns, post-operative wounds and miscellaneous traumatic or infected wounds -it digests all non-viable substrates found in necrosis even in the presence of infection (and it does not harm healthy, viable tissue) -usually see results in a few days - 30g tubes (and store in a cool place) -adverse reactions include skin irritation and "burning" sensation

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ADMINISTRATION

1. clean wound with saline 2. apply Accuzyme® directly to the wound and cover with a dry, sterile dressing 3. qd or bid applications preferred -'1-. irrigate wound at each redressing to remove any accumulation of liquefied necrotic material

2. REGRANEX®GEL (becaplermin)

-Regranex gel contains a recombinant hwnan platelet-derived growth factor (becaplermin) for topical administration -Becaplermin is produced by recombinant DNA technology by insertion of the gene for the beta chain of platelet-derived growth factor (pDGF) into the yeast, Saccharomyces cerevisiae -acts to promote chemotactic recruitment and proliferation of cells involved in wound repair and enhancing the formation of granulation tissue

INDICATIONS AND USAGE -indicated for the treatment of lower extremity diabetic neuropathic ulcers that extend into the subcutaneous tissue or beyond and have an adequate blood supply -used as an adjunct to good ulcer care including initial sharp debridement, pressure relief and infection control -it has not been evaluated for the treatment of diabetic neuropathic ulcers that do not eAiend through the dennis into the subcutaneous tissue or ischemic diabetic ulcers -contraindications include hypersensitivity (contains parabens) and known neoplasms at the site of application - 2, 7.5 and 15 gram tube sizes -must store in refrigerator (do not freeze)

APPLICATION 1. wash hands thoroughly 2. rinse wound with saline solution or water 3. do not touch tip of tube to any surface 4. apply a carefully measured quantity ofRegranex® gel to the wound (enough to cover the

surface) 5. after gel is applied, dress the wound 6. after 12 hours, remove dressing and gently rinse with saline or water 7. apply new dressing for next 12 hours without Regranex®

Types of Scar Formation a) hypertrophic scar

1. results from abnormal collagen proliferation. Buudles of collagen are laid do"n parallel to the skin surface; ncapsuIated and stays within margins of original scar.

2. begins to neutralize and soften after approximately 18months 3. can be treated with topical steroid applications

b)keloids 1. fibrous tissue hyperplasia with fibroblasts arranged in randomly oriented parallel strands. Keloids are

devoid of seblceous glands and are non-encapsulated. The lesion extends beyond the margins of the original scar; frequently entraps nerves and produces extreme pain

2. differential diagnosis . • dermatofibrosarcoma protuberans • rare malignant variant of dermatofibroma

• continues to enlarge; no history of prior trauma • hypertrophic scar

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3. treatment surgical excision contra-indicated intIa-Iesional steroid injection may cause keloid to flatten pressure dressings helpful after surgery andIor injection silicone gel sheeting may be effective

Skin Tension

Tension is the force that causes wounds to widen and scars to hypertrophy. Incisions must be placed in areas of least tension to insure minimal scarring. a) Langer's Lines

Described in 1861, thought to be a reflection of underlying muscle pull. In 1941, Cox determined new skin cleavage lines utilizing LangeI's techniques

b) Relaxed Skin Tension Lines Determined by Burges and Alexander in 1962. Their lines are created by underlying structures such as muscle, tendon, bone or any st:rucWre tenting the overlying skin. An incision made perpendicular to the relaxed skin tension lines will gap widely, whereas an incision made parallel to these lines will remain well approximated

PRINCIPLES AND TECHNIQUES OF FIXATION

AOIASIF a) AO: AIbeitsgemeinschaft fur Osteosynthesisfragen or The Association of Osteosynthesis b) ASIF: Association for the Study oflntemal Fixation c) Goals of the AO - rapid recovery of the injured limb

L anatomic reduction 2. preservation ofblood supply 3. stable internal fixation 4. early active mobilization

Principles of Rigid Fixation PrimaIy vascular bone formation a) consists of simultaneous remodeling and formation of new bone at the fracture site b) bypasses fibrocartilage formation seen in secondary bone healing; new bone is intentionally formed at the

fracture margins aka-contact healing: direct reconstruction of fragment edges by haversian remodeling c) absence of micromotion is necessary for direct haversian remodeling and for the cutting cones to cross the

fracture site and unite the ftacture d) if motion ocaus, periosteal and endosteal callUs forms resulting in secondary bone healing

Principles of Internal Fixation a) Interfragmentary Compression

1. static (compression remains constant) >lagscrew >eccentric loaded plate >external fixation

2. dynamic compression >tension band

implant absorbs tension and bone absorbs compression k-wires provide rotational stability

b) splintage 1. internal

>nails; k-",lles, intIameduIlary nail >cerclage wire; stainless steel wire

192

>neut::rn1 plating neutralizes forces applied to the fracture site *stress shielding: In the absence of physiologic stress, bone resorption occurs in accordance to Wolff's Law. This causes disuse osteoporosis and possible refiacture. Recent research demonstrated a direct correlation between the disturbance of blood supply upon application of internal fixation and the resultant osteoporosis from revascularization of the area a few weeks later.

2. external >e>.:ternal fixation

CONCEPTS AND TERMS OF MECHANICS Stress and Strain a) "stress-press, strain-gain"

Stress is the pressure that you put on a material in IbsIsquare inch. Strain is the length or a measured deformation that results in a material after a certain stress has been applied to it.

b) Stress-Strain Curve 1. when stress is plotted versus strain, we get a load deformation curve; this curve represents a picture of

the mechanical behavior of a particular implant under a load 2. yield point

>Represents the point beyond which the material is no longer Hookian (ie-the strain of a material is no longer proportional to the stress applied to it)

> When you pass the yield point of a material, further Jl1ll or stress causes an disproportionally larger stretch or strain

>Beyond the yield point the material cannot return to its original shape and you have entered the range of plastic deformation

3. Ultimate Failure Point • continued stress through the rnnge of rnnge of plastic deformation eventually leads to fuilure of the

material • Hook's Law: the amount of strain in a material tmder a load is proportional to the amount of stress

applied to it • Once the applied load is removed the material will spring back to its original shape (range of elastic

deformation). The resulting slope represents the stiffuess of the material [aka-Young's Modulus of Elasticity or the "E" modulus]

• Since implanted materials that we use are much stiffer than bone, the material absorbs the stresses and strains instead of the bone. This is known as stress shielding and causes disuse osteopenia in the bone.

Materials 316LVM:

1. the ''L" stands for low caIbon content

193

the "VM" indicates that the base alloy was remelted in a vacuum, which reduces the number of impurities that affect the material's physical properties

2. composition iron and CaIbon: provide strength chromium: anti-corrosive, but weakens alloy nickel: restrengthen alloy; anti~rrosive 1ll01ytxJenum: anti~rrosive manganese silicon copper nitrogen sulfur phosphorous

Other Terms a) Fatigue fililure

Failure of a material from repetitive loading and unloading. Many materials can undergo a certain level of stress and if not exceeded, will not show any evidence of fatigue failure. Tensile stresses cause a material to fail at its surface.

b) Creep A pennanent deformation in a metal Bridges are built in a semi-arc to prevent creep. Creep is temperature

dependent (ie-tbe higher the temperature, the greater the creep). Creep rates at body temperature are low, and thus, an implant in the body takes several months to :fuil from creep. c) Viscoelasticity

The ability for a material to "flow" (ie-the material shows eIastic behavior, but also a "iscous flowing behavior). The best example of a viscoelastic material is cartilage - cartilage molecules rearrange themselves allowing for the acceptance of more stress. d) Neutral Axis of Bone

When a long bone is loaded, a tension side and a compression side develops. The axis that experiences neither tension nor compression is called the neutral axis of bone. Plates could withstand tension well, but not

bending. Therefore, plates are placed on the tension side of the bone.

BONE SCREWS Two types of screws: wood screws and machine screVr"S.

Wood screws have a threaded tip and predrilling is not necessary. As they are driven into bone, they crush and compact the material This is not well tolerated by cortical bone, and therefore, their application is limited. Machine screws have a blunt end and require both predrilling and tapping for insertion. Self tapping screws have a fluted tip and cut a leading thread as they are driven. Almost all scre\\'S in current use are machine screws.

194

.. \ \, }--E .-' \\

H I

Screw Anatomy

r ..... ~ ~ ... ;;o$ji,,,

. . ~~---

a) Head: with some exceptions, it is hexagonal. The hexagonal recess allows for most efficient translation of torque from the screwdriver to the screw and reduces cam-out (lifting out of the screwdriver from the screw head).

Torquing a screw too much on bone increases the pressure at the bone-screw interface, causing hyperemia and bone resorption around the screw with subsequent loosening.

b) Land: undersurface of the head which comes in contact with the bone c) Shank: unthreaded portion of the screw (cancellous) d) Run-out: junction between the shank and threaded portion of screw. It is the weakest point on the

screw. The threads should cross well into the fracture fragmen~ otherwise screw breakage at the run-out is inevitable as well as distraction of the fragments.

*Keep in mind that a screw could break anywhere depending upon the forces at the bone­screw interface. However, a screw is "veakest at the run-out.

e) Thread diameter: represents the diameter of the screw f) (ie-a 4.0 mm screw has a 4.0 mm thread diameter) g) 1) Pitch: represents the distance between the threads. A cortical screw has a tighter pitch than a

cancellous screw, which makes it more suitable for hard cortical bone. h) Core diameter: represents the diameter of the screw between the threads; determines the size of

the thread hole. i) Tip: either trochar, round or fluted (self-tapping screw) j) Axis: central line of a screw k) Tip angle: tip to the axis 1) Rake angle: thread to axis angle

Self tapping vs. Non-self tapping screws a) self tapping

1. pilot hole larger than with non-self tapping screws and screw threads do not penetrate as deeply into bone

2. once pilot hole is drilled into the bone, the screw can be inserted (screwed in) 3. may have advantage over non-self tapping screws in thin cancellous bone and in flat bones (ie-skull,

pelvis) b) must perform insertion carefully - if unintentially angled, the screw will cut a new path and destroy the

already cut threads b) non-self tawing

1. require pre-drilled pilot hole and then cutting of screw thread pattern with a tap 2. less heat generated with insertion due to decreased resistance

Cortical and Cancellous Screws Cortical a) For use in hard cortical bone and function as positional (ie-hold a plate in place) or as a lag screw (ie­

threads of screw do not engage proximal cortex of fracture) b) sequence of cortical screw insertion

glide hole, threaded hole, countersink, measure depth, tap and insert screw depth measured before tapping to prevent the gauge from disrupting the thread pattern

195

Cancellous a) The pitch of this screw is higher than that of the cortical screw. It is either fully or partially threaded.

Designed for soft metaphyseal and epiphyseal bone. When used in lag fashion, all the threads must cross the ftacture of the osteotomy site.

b) sequence of cancellous screw insertion tbreacbI hole, countersink, measure depth, tap and insert screw

Lag Screw Principles Three conditions must exist for a screw to function as a lag

1. the near cortex must be drilled with a clea.t"aJ:la: hole or a glide hole to allow the screw to glide freely 2. the filr sur:filce must be threaded 3. when tightened, the screw head must contact the near mrf3ce or cortex so it can compress the fracture

segments Lag screw is best positioned perpendiruJar to fracture sur13ce for maximum compression If screw thread engages both near and far cortices, compression across fracture site will not be achieved and

gapping will ocarr across site

Malleolar Screw Originally designed for fixation of medial malleolus ChaIacteristics -partially threaded have same thread profile and pitch as cortical screws trephine (self-cutting) tip

Cannulated Screws These scre'\\'"S are designed to minimize complications associated '\\'ith screw insertion (ie-redirecting screws

and repeated bone penetration,. which compromise bone fixation). A k-wire is used to achieve reduction and an intIa~e x-ray is taken to confirm placement. The k-wire then serves as a guide for the screw placement. Avai1able in 3.0 nun, 4.0 nun, 4.5 mm, 7.0 mm sizes, 7.3 mm.

Effects of Screw Holes in Bone a) decreases the bone's resistance to bending and to torsional forces b) stress concentration is increased up to 1.6 times around a screw hole c) fractures through old screw holes have been documented up to II months after screw removal; greater

incidence in diaphyseal bone since it is under greater torque moments than metaphyseal bone, which experiences greater compressive stresses. d) following screw removal, a 34 week period of casting is recommended

Plates a) Description

Plates function through interfragmentary compression, buttressing and neutralization 1.1nter:fragment: Compression

>plate may perform more than one :function at the same time (ie-neutralization plate can protect lag screw and also exert compression along long axis of bone) >eccentric loading of bone creates tension on one side and compression on the other if plate is applied to tension side, deformity will be prevented (with load, the plate is put under tension and cortex opposite plate under compression) likewise, if plate is applied to the compression side, cortex opposite plate will gM> under load

196

.1' ...

2. Buttress plates Plate is applied to fracture site so as to prevent shift of the fragments under load Special designs: "T", "L", "spoon". "cloverleaf'

3. Neutralization Plates

.-

Protect screw fixation. Interfragmentary screws are used to stabilize a fracture and the plate is applied to neutralize the bending, torsional and shear forces that would otherwise jeopardize the fixation obtained by lag screws alone.

b) Plate Sizes 1. tubular plate: tube with radius of 6 mm and thiclmess of 1 mm 2. semi-tubular (accommodates 4.5 mm screws) 3. one-third tubular (accommodates 3.5 mm screws) 4. one-quarter tubular (accommodates 2.7 mm screws) 5. posterior anti-glide plate

>used for Weber B fractures with posterior spike. The fracture has the tendency to displace superiorly and posteriorly, which is prevented by this plate position.

>the plate can reduce the fi:acture >no potential for the screw to go into the joint >also recommended for osteoporotic bone >the distal fragment does not require screws

c) LC-OCP: limited contact~c compression plate Further development of the DCP and DCU Based upon the concept ofhiological plating

1. minimal surgical disruption of blood supply 2. improved healing in the zone covered by the plate 3. reduced risk of re-fracture following plate removal because of minimal damage to bone beneath the

plate 4. titanimn as the implant material provides optimal tissue tolerance

197

5. grooves on the undersur.face of the LC-DCP >minimize damage at bone/plate interface, which preserves blood supply >allows for small bone bridge beneath plate, in an otherwise weak spot >allows for more even distribution of the stifihess of plate (more resistant to bending and torque)

6. description >equal distance between screw holes along the plate >screw holes symmetrical and have oblique undercuts at each end to allow for up to 40 tilting of

screw in each direction in long axis of the bone >1Uldercuts between holes >trapezoid cross-section

7. healing with the LC-DCP >1atera1 undercut areas allow for bone fonnation at plate side of periosteal surface >:fracture gap exhibits band of remodeling rather than resOIption of ftacture surface >small amount of plate-induced remodeling

Other Forms of Internal Fixation a) Kirschner Wires (1909) - "k-wire"

1. supply primary, supplemental and provisional fixation 2. supplementaIy: to augment screw or other wire fixation. Readily preformed with low morbidity.

When used with a screw, the k-wire affords rotational stability. 3. primary fixation: used for metatarsal osteotomies, fractures and fusions 4. provisional fixation: used intra-operatively in the reconstruction of a comminuted fracture. Also

fixation of choice in physea1 injuries. 5. the rigidity ofk-wire fixation can be increased by increasing the diameter of the k -wire and the

number of them used 6. threadedk-wires provide greater fixation per diameter versus the smooth k-wire. They tend to slip on

insertion and once insertion is started, they are harder to redirect and have lower failure threshold compared to a smooth k-wire of the same diameter

7. Sizes (diameter in inches): 0.028, 0.035, 0.045, 0.062 b) Steinman Pins

1. considered large k-wires and function the same as k-wires 2. sizes in inches or millimeters

>5/64 to 12164 inch diameter (in 1164 increments) > 1. 9 to 4.7 nun in diameter

3. tip design: applies to both K -wires and Steinman pins >trochar, diamond or cut tips cut tip has an eccentric point producing a large hole and sub-optimal fit trochar tip allows for the least slippage on insertion, and thus, highest accuracy of placement diamond tip has slightly less initial holding power than a trochar tip

>at acute approach angles, diamond and cut tips walle along cortical surface, while the trochar tip penetrates

c) Stainless Steel Malleable Wire 1. monofilament from 24-30 guage stainless steel 2. used when fracture fragments are too small, osteoporotic or comminuted to be

suitable for screw fixation 3. best used in awlsion fractures and in tension band technique 4. the right angle loop configuration is the most stable loop configuration

ill

198

d) Staple Fixation L suitable in bone with high cancellous/cortical ratio

(ie-calcaneus); the thicker the cortex, the greater the propensity of comminuting it on insertion 2. propensity to distract the fracture fragments if not properly compressed prior to application 3. manual insertion causes rocking of the staple legs and an enlarged elliptical channel for the legs as

well as, sub-optimal holding power 4. power driven staple fixation allows staple to penetrate the bone without rocking, thus improving

fixation; will need to pre-drill when used in cortical bone 5. staple size is determined by bridge width and leg length.

longer the leg length, the greater the pullout power 6. recommended application in circumferential fashion to prevent fracture gapping upon weightbearing 7. barbed staples increase staple purchase and holding power; they are hard to remove and produce a

significant defect in bone

e) Absorbable Fixation L two types

>Biofix: composed of polyglycolic acid >Orthosorb: composed of poly-p-dioxanone tapered pin attached to stainless steel pin for drilling completely eliminated within six months gradually loses tensile strength as the bone heals PDS histologically more inert; less rapidly degraded

2. undergo hydrolysis when placed in living tissue 3. possess much less stiffness and shear strength vs a

k-wire; 50010 decrease in holding power 4-6 weeks after insertion 4. indications: fixation of osteochondral fragments; digital fusions; metatarsal osteotomies 5. complications: late inflammatory reaction and sinus formation; adverse tissue reactions (ie-rejection,

irritation, encapsulation) f) Herbert Bone Screw

I. originally designed for fixation of caIJlIl scaphoid bone 2. rom screw diameter; 16-30 rom length in 2 rom increments 3. screw is "headless", compared to cortical and cancellous screws; this feature allows for insertion of the

screw through articular cartilage 4. can be inserted manually or by the use of a jig 5. screw removal not normally required 6. threaded portions distal and proximal with tighter pitch proximally; the difference in pitch provides 7. compression between the acljacent bony fragments 8. composed of Titanium alloy - titanium alloy with 9. 6% aluminum and 4% vanadium 10. indications: fixation of osteochondral fragments; metatarsal osteotomies; Akin osteotomy

g) Reese Arthrodesis Screw L designed to create greater compression across arthrodesis site 2. stainless steel screw with clockwise (right-handed) threads proximally and

counterclockwise (left-handed) threads distally; smooth portion between the threaded segments (2.0 rom core diameter)

3. indications: hallux IPJ fusion; digital arthrodesis

41 r..

~~

199

h) Tension Band Concept 1. the combination of static intediagmentaI compression with the .functional loading of the part to

create a dynamic degree of interfragmentaI compression 2. two basic components:

Load Beam (osseous segment) Tension Band Device

-+tension lmtd plate -+dynamic compression p1ate -+eerclage wire

3. examples in the ankle and foot +avulsion fractures of the medial and 1ateral malleoli and 5th metatarsal base (although there is some dispute with the 5& metatarsal base)

4. used for transverse and short oblique fractures but not amenable to long oblique, spiral fractures, or comminuted ftactures

Complications ofIntemal Fixation a) Intra~e complications

1. screw strips: longer screw; larger diameter screw; redirect the pilot hole and different form of fixation 2. screw, drill or tap breaks: hollow reamer/extraction bolt; trephine it out or leave it in

b) Post-operative complications 1. nonunion: results from poor fracture reduction. incorrect fixation or patient noncompIiance 2. infection: follow infection protocol-if internal fixation unstable, remove and replace with external

fixation device applied away from site to insure stability and maintain blood supply of osteotomy or fracture site

c) necrosis: secondary to stripping of periosteum and/or excessive compression at fracture ends d) breakage: usually due to inappropriate application of fixation device (ie-size; method; post-op course)

Complications of Specific Fixation Devices a) K-wires and Steinman pins

1. skin protrusion as a possible site of pin tract infection 2. loosening - causes necrosis ofbone at pin site and most common cause of pin tract infections 3. migration - smooth k-wires are most prone to migration

mechanical motion at or near fixation site is important bending, prompt removal. proper application and use of threaded pins reduces chances of migration

b) Monofilament wire 1. initation of tendon or overlying skin 2. shifting of fulgments on breakage of the wire 3. loss of fixation secondary to poor criteria and application

c) Staples 1. cortical shattering 2. distraction of the fracture ends 3. fracture displacement on insertion of the staple

d) Screws 1. poor reduction of fracturelosteotomy 2. screw thread across fracturelosteotomy site 3. one point of fixation 4. hitting the near cortex of adjacent bone 5. incorrect placement 6. incorrect choice or sequence of insertion 7. incorrect type, size or length of screw 8. overaggressive countersink with cortical disruption

e) Plates 1. increase in operative time secondary to extensive dissection of soft tissue and periosteum 2. initation and need for removal 3. disuse osteopenia secondary to stress shielding or revascu1arization after periosteal stripping and the

need for casting post removal

200

Bioenvironmental Properties and Reactions a) Galvanic Corrosion: caused by two dissimilar metals in body b) Crevice Corrosion: caused by one metal moving against another c) Fretting Corrosion: occurs when the protective oxide layer is broken down due to micromotion. When a

metallic implant is placed in the body, the nickel from the implant reacts with its surrounding tissue fluid fonning a protective oxide layer (passivation layer) that protects the metal from corrosion.

d) Stress Cracking: cracking of the metal due to cyclic stresses. Cracking results from corrosion. fatigue and stress corrosion cracking.

EXTERNAL FIXATION Classification ofEx1ernal Fixators

a) Sinlple Pin Fixators 1. utilize half pin or trnns-fixation pins with one or more longitudinal side arms 2. simple to use and versatile 3. disadvantage = the bone segments must be properly reduced prior to the application of the fixator 4. examples: AO tubular system; Wagner single half frame; the original Roger Anderson device

b) Modular Pin Fixators 1. the pins inserted into the bone are stabilized by one clanlp to which a universal joint is attached,

connecting the longitudinal rods 2. extremely versatile_ allowing movements and adjustments in variety of planes 3. disadvantage = the apparatus is complex, heavy and bulky 4. example: the Hoffman-Vidal frame

c) Ring Fixators 1. components include circular and selni-circular rings that attach to side longitudinal rods 2. pins connect the bony segments to the circular rings 3. disadvantage = bulky and difficult in gaining access to soft tissues 4. advantage: capable of adjusting in all planes and uses k-wires which can be inserted in a 360 orientation

without complicating the frame design 5. example: the classic llizarov frame

Functions a) lengthening b) neutralization c) compression

Uses of External Fixation a) open fractures b) comminuted fractures c) arthrodesis d) osteotomy fixation e) soft tissue stabilization/fixation

Configurntion a) unilateral (one or two planes)

1. excellent wound access 2. not as stable as biplane

b) bilateral (one or two planes) 1. increased stability 2. increased chance of damage to anatolnic structures

201

Unilateral

Biodegradable Fixation

Ideal osteosynthesis device should remain firm enough for the duration of bone healing and then lose its strength and transfer the nonnal stress to the healing bone. It should then disappear from the body after healing is complete.

Fixation types (Currently available in U.S.) * Screws *Rods/Pins

Historical: 1973-84: Basic research on animals 1985: Clinical trials on humans, absorbable rods 1987: First totally absorbable self-reinforced screw used

Basic Polymers: PGA - polyglycolide PLLA - poly-L-Iactide PDS - polydioxanione

* Fixation devices are produced by a self-reinforcing procedure that combines polymers to improve strength (SR-PGA, SR-PLLA)

Bilateral

202

* Degraded by hydrolysis - eventually entering into the Kreb' s cycle and excreted in urine, feces or expired CQ.

Loss of mechanical resistance: SR-PGA - 30-60 days SR-PLLA - 3-12 months

Complete absorption: SR-PGA - 5-10 months SR-PLLA - 15-60 months

• Actual time depends on the shape, size, molecular weight and variable tissue en"ironments of implantation.

Advantages: 1. Avoids stress shielding or stress protection osteopenia 2. Eliminates burden (Physiologic and financial) of secondary procedures for fixation

removal. 3. Does not lead to image artifacts when using MRI or CT post implantation. 4. May be left in sites of infection as implants are bacteriostatic.

Disadvantages: 1. Screws are Iadiolucent - unable to confirm fixation position with x-ray. 2. Less interfragmentary compression than with conventional screws. 3. Possible foreign body reaction.

Cortical Bone Pins 1. Allofix ® made by M1F TM (Musculoskeletal Transplant Foundation) 2. Studies underway using pin to augment fixation of Chevron (Austin) osteotomies

(and its modifications) and to fixate PIPJ toe fusions 3. made from cortical bone that has been turned on a lathe to varying sizes

a. 2.0 111Ill. 2.4 111Ill. 2.7 111Ill. 3.0 111Ill. 3.5 mm b. insertion kits available corresponding to size of pin

SUTURE MATERIALS

Purposes: a) approximate tissue until healing takes place b) ligate vessels c) tag fragile or important structures

Selection based on: a) biologic and mechanical performance b) structure to be sutured (tendon, fascia, skin, vessels, bone) c) bacterial presence

I) contaminated 7 monofilament (nylon, polypropylene) 2) clean

203

Suture characteristics: a) strength and thread dimension

1) varies with basic material composition and dimensions

b) most used standard. measurement 1) USP (United States Phannacopeia) 2) denotes dimension and knot pull strength

c) suture volume 1) nse of smaller sutures decreases foreign body volume but sacrifices knot pull strength

d) elongation 1) elasticity

~ return to original length with cessation of strain ~ stainless steel, braided polyester, catgut, silk:

2) plasticity ~ elongation persists with cessation of strain ~ polypropylene

3) intermediate

e) flexibility

~ posses both elastic and plastic properties ~ nylon, polyglactin 910

1) based on material and diameter of suture ~ small diameter is more flexible than large diameter ~ silk, dexon = flexible ~ nylon, catgut = stiff

f) monofilament vs. braided 1) monofilament has a low coefficient of friction and is better suited for contaminated wounds 2) braided has a high coefficient of friction, greater strength, and capillarity

g) capillarity 1) fluid and bacteria may penetrate into interstices of braided sutures 2) PMN's, macrophages too large to reach interstices(increases risk of infection)

h) coating 1) helps decrease capillarity 2) improves handling 3) reduces tissue drag

Suture needles: a) desirable characteristics

1) made of high quality stainless steel 2) slim as possible without compromising strength 3) sharp enough to penetrate tissue with minimum resistance 4) rigid enough to not bend but ductile enough to not break:

204

b) needle anatomy 1) suture attachment 2) body 3) point

c) measurements I Chord Length _~ I

Needle 1oEk''-----~--:ii'_i~ Point i . 1) chord length

2) needle radius 3) needle diameter 4) needle length

d) suture attachment

e)

f)

1) closed (eyed) 2) French (split or spring) 3) swaged (eyeless)

body 1) 2)

3) point

1)

2)

3)

~ most common ~ suture attachment

directly into needle ~ decreases tissue damage

Needle length

straight, Y2 curved, Y4 circle, Y2 circle (most common), 3/8 circle, 5/8 circle geometric shape

~ round, flat, oval, triangular length (4mm-60mm)

blunt ~ used for friable tissue

tapered ~ useful for tissue offering slight resistance ~ paratenon, tendon sheath, subcutaneous tissue

cutting ~ conventional

+ cutting edge on concave curvature + cuts through dense, difficult to penetrate areas (tendon, ligament) + care must be taken not to "rip" through tissue

~ reverse + cutting edge on convex curvature + prevents needle from "ripping" through tissue (skin) + greater strength

• ~ A Regular Cutting

Spatula ~ y

Reverse Cutting

Suture types: a) absorbable

I) generally lose tensile strength within 60 days 2) natural

~ degraded by lysosomal enzymes ~ catgut

+ name may originate from "kitgut" meaning violin string

205

b) c)

3) synthetic

+ made from submucosa of sheep intestine or serosa of bovine intestine + can be treated with chromic salts and formaldehyde for greater strength + stored in alcohol for preservation + highest tissue reactivity of all sutures

}> collagen + made from long flexor tendon of steer + primarily used in ophthalmic surgery

+less tissue reactive than catgut

}> degraded by hydrolysis }> polyglycolic acid (Dexon)

+ braided + good knot-pull and tensile strength + very inert + completely hydrolyzed in 100-200 days + may be coated with polycaprolate for improved tissue passage, handling, knotting + skin and subcutaneous tissue

}> polyglactin 910 (Vicryl) + braided + 65% tensile strength remains at 14 days + very inert + completely hydrolyzed in 80 days + may be coated "'ith polyglactin 370 and calcium stearate for better handling

}> polydiaxonone (PDS) + monofilament + high flexibility and tensile strength + completely hydrolyzed in 90 days + very inert + 70% tensile strength at 14 days

}> polyglyconate (Maxon) + monofilament + resists kinking and curling + becomes softer as it's exposed to tissue fluid + completely hydrolyzed at 180 days (longest of any "absorbable" suture)

}> poliglecaprone (Monocryl) + monofilament + very pliable and inert + completely hydrolyzed in 90-120 days + 20-30010 tensile strength remains at 14 days

d) nonabsorbable I) generally maintain tensile strength longer than 60 day 2) natural

}> silk + made from silk of the silk worm + known for superior handling properties especially when braided + impregnated and coated ",ith mixture of waxes and silicone + low tensile strength which is completely lost at 360 days (very slowly absorbable) + highly tissue reactive

}> cotton, linen + similar to silk + increased tissue reaction + very low tensile strength, weakest suture

206

3) synthetic ~ nylon (Etbilon, Surgilon)

+ possesses "memory" ( the tendency for a filament to want to straighten) + elastic in nature therefore well suited for retention and wound closure + high tensile strength and low tissue reactivity + monofilament and braided + may be used in contaminated wounds

~ polyester (Ethibond, Dacron) + braided + high tissue strength + low tissue reactivity + may be coated with silicone for smoothness, reduces tissue trauma + used when strong apposition of tissues is needed indefinitely

~ polypropylene (Prolene, Surgilene) + very inert + monofilament + better pliability and handling than nylon therefore holds knots better + excellent tensile strength + passes through tissue with minimal drag + often used in contaminated wounds and plastic surgery

~ stainless steel (Flexon = braided) + monofilament and braided + measured in the Brown and Sharpe (B&S) gauges and not in the USP method + may corrode especially at stress points + mild to moderate tissue reactivity + may fracture, fatigue, or kink + used for bone fixation, tendon repair. and retention sutures

Staples: a) common uses

1) gastrointestinal anastomoses 2) wound closure 3) ligature substitute

b) better resistance to infection than wounds contaminated by the least reactive suture c) often used to affix skin grafts d) implementation

I) evert skin edges \\'ith two atraumatic forceps 1) deliver the staple at 60 degree angle to the skin 2) when staple assumes an upright position the top span will not be in contact with the skin - this

helps

Flattened Topspan

~1 ! lJ Dimple Dimple Point

J ~

00

to prevent "cross-hatching"

STAPLE ~

~

STAPLER

207

~ a) made in a variety of forms that vary in backing and adhesive formulation b) porous structure of adhesive and backing allows for evaporation c) superior resistance to infection over any other wound closure technique d) may only be used as primary closure device on wounds with minimal static and dynamic tension e) may be supplemented with dermal sutures on the high tension skin of the extrenllties

Fibrin sealants: a) biologic tissue adhesive b) Derma Bond®

208

I I I I

FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SURGERY FOREFOOT SUR(if~r{ .. F'nR·r··FO()T· sLrR ---ir: 1-< . . \.J -"c.. ... j. lJ L_ ~ \'. r (' ....... ~i-' r)c T rlrF-~ ( .. '. r' IT) .'" . ~_i. i l) t" t-·, \ J "'" l 1< . Jr". t~ '\ J~ -....~~1"'-. J.A 'It...... __ ,_/1....--". '- .. l~....;.;:.'\;. ~~

ACCESSORY BONES OF THE FOOT AND ANKLE

Accessory Bones • Developmental Anomalies • May be multiple in the foot • Unilateral in ~ 500;0 of cases

Most Common • Os Trigonum • Os Tibiale Extemum • Os Intermetatarseum

Os Trigonum • Near posterolateral tubercle of talus • "Interns Fracture" • When fused. - called "Trigonal Process" • More often bilateral • Frequency R:! 2.7 -7.7%

Os Tibiale Extemum I Accessory Navicular • Incorporated by T. Posterior Tendon • Typically pyramidal in shape • Fibrous or fibrocartilaginous

connection • Frequency R:! 3 - 12%

Type! • Really a sesamoid bone in T.

posterior tendon

• Round • Account for 30% Type II • Accessory ossification center in

the navicular • Separated from navicular body

by fibrocartilage

• Triangular

Os Intennetatarseum • Between Medial cuneiform and base

of 1st and 2nd metatarsals • Projects between the 1st and 2nd

metatarsals • Spindle shaped - tapers distally • Usually fused to distal lateral comer

of the medial cuneiform • Frequency R:! 1.2 - 10%

Os Sustentaculi • Posterior aspect of sustentaculum tali • Rarely a distinct bone (0.47%)

uncinaI:us

• Fibrous or fibrocartilaginous connection to sustentaculum tali • More common in males • Frequency R:! 2 - 3%

Os P""Y:;;t-tI-l--.Llrtermetatarseum

Os cuboideum seconclarium

209

Os Calcaneus Secundarious • Interval between anteromedial calcaneus, cuboid navicular. and head of talus

• Located dorsal • Frequency"" 7 -11% (male); 6-7% (female)

Os Cuboides Secundarium • Interval between cuboid, navicular, talus, and calcaneus

• Locatedplantar • Process can connect to cuboid • Frequency "" 1 - 3%

Os Talonavicular Dorsale • AK.A Os Supranaviculare, Pirie's Bone) • Located Dorsally an T -N joint - near midpoint • Frequency "" 15% (male); 11% (Female)

Os Intercuneifonne • Located dorsally between proximal segments of intermediate and medial cuneiforms and navicular

• Wedge shaped • Frequency "'" 1%

Os Cuneo - Metatarsale - Plantare • Located plantarly between I st metatarsal and medial cwleifonn

• Frequency "'" rare

Os Vesalianum • Located just proximal to the tuberosity of the 5th metatarsal • Must be differentiated from ossifying apophysis

• Frequency z rare

Os Subtibiale • Plantar to medial malleolus • Round or angular appearance • Frequency z 4%

Os Subfibulare • Plantar to lateral malleolus • Round or c.omma shaped • Frequency z ?

Os trigonum .

tarsi" I Talus ~ accessorius /

i i

Os versalianum pedis

Anomalous os ,..talocalcaneum

Sustentaculum tali

Acessory navicular

.iioiIr,.,.......~-J\r-Os tibiale externum

Processus uncinatus

Os intercuneiforme ~~:a::~_ Os

210

OSSIFICATION OF THE BONES OF THE FOOT

Bone Primary Center Secondary Center

Tibia 7-8 wks intrauterine Prox., before birth; Dista13-12 mos Fibula 7-8 wks intrauterine Prox., 3-4yrs; Distal 9-12.5 mos Calcaneus 3rd mo intrauterine Post., 6-8 yrs Talus 6th mo intrauterine Navicular 3rdyr Cuboid Birth-6mos Medial Cuneiform 2ndyr Intennediate Cuneiform 3rdyr Lateml Cuneiform Istyr Metatarsal I 10th wk intrauterine Base,3rdyr Metatarsal II, ill, IV 9th wk intrauterine Head, 3-4 yr Metatarsal V 10th wk intrauterine Head, 3-4 yrs Proximal Phalanges II-IS wks intrauterine Base, 2-Syrs Middle Phalanges variable, after ISth wk intrauterine Base, 2-8yrs Distal Phalanges 9-12 wks intrauterine Sesamoids in FHB 10-12 yrs

DIGITAL SURGERY

Anatomy of the Extensor Apparatus of the Toes a) the EDL tendon:

1. divided at the level of proximal phalanx into three slips

2. a middle slip inserts into base of the middle phalanx

3. medial and 1aternl slips into base of distal phalanx

4. the combined EDB and EDL tendon has no insertion at the baSe of the proximal phalanx

Base, 2-8yrs

mterosseous muscle belly

Lumbrical

Fuse

14-17 yrs

17-20yrs 17-2Oyrs 17-20yrs lS-18yrs lS-18yrs 15-18yrs

b) EDL is held in central position on the dorsum of the toe by a fibro-aponeurotic structure extending from MIP joint to PIP]

1. the proximal segment is a sling-like structure 2. wrnps around the capsule of the MIP joint 3. inserts at the junction of the plantar plate, deep transverse metatarsa1ligament and flexor tendon sheath 4. thus, the EDL tendon is finnly held to the plantar aspect of the proximal phalanx, not the dorsum

c) extensor wing or hood is distal segment of extensor apparatus I. provides insertion for the lumbricales 2. 1umbrK:a1 muscle passes plantar to the deep transverse metatarsal ligament to insert into the extensor

hood

Extrinsic Musculature Extensor Digitorum Longus a) originates from anterior compartment of the leg b) passes beneath e:l\.iensor retinaculum and cfu.ides into four slips

211

c) at the MIP joint., gives off expmsions -proximal ex1ensions are vertically oriented -distal extensions are oblique fibers and provide insertion to the lumbricales

d) inserts at the mse of the distal phalan.x e) creates a dorsiflexory force at the metatarsophalangeal joints in s\\'ing phase of gait f) also dorsiflexion at the ankle joint

Flexor Digitorum Longus a) originates in the deep posterior compartment of the leg b) divides into four slips in the second layer of the foot c) each tendon passes plantar to the MIP joint and inserts into the distal phalan.x d) four lumbrical muscle originates from the four tendonous slips medially e) the quadratus plantae inserts into it's lateral portion, fonning a conjoined tendon

Intrinsic Musculature to the Lesser Digits Flexor Digitorum Brevis a) originates from plantar aspect of calcaneus in the first layer of the foot b) passes plantar to the MIP joint c) at the level of proximal phalan.x it splits to allow the long flexor to pass through d) inserts into the base of the middle phalanx e) functions to plantarflex the IPJ along with the long flexor; this causes a retrograde dorsiflexion at the

MfPjoint

Dorsal Interossei a) are bipennate muscles b) originate from adjacent sides of corresponding metatarsals c) the first dorsal interossei originates from adjacent first and second metatarsal shafts, and inserts medially

. into the second toe d) the remaining interossei originate from the adjacent sides of the corresponding lesser metatarsals and

insert laterally into the bases of proximal phalanges two. three and four

Plantar Interossei a) unipennate muscles b) originate from plantar medial aspect of metatarsal shafts c) insert medially into the third, fourth, and fifth digits at the base of the proximal phalanx d) the flexor digiti quinti brevis originates from the lateral plantar aspect of the fifth metatarsal and inserts

laterally into 00se of proximal phalan.x of the fifth digit

Quadratus Plantae Muscle a) originates from interior swfuce of the calcaneus b) inserts into the lateral aspect of the FDL tendon c) provides porximal stability to both the lumbricals and FDL d) straightened out the medial proximal pull of the FDL; if it loses it's mechanical advantage, adductovarus

fifth toe will result

Lumbricales a) four in number originating from the medial aspects of the FDL tendon slips b) travel plantar to the transvserse metatarsal ligament and insert medially into the extensor hood c) their function in gait is theoretical at present

212

NAIL SURGERY

Nail Anatomy Nail Plate

. overl.yiDg posterior skin

fold· suzface ofpostuiorskin fold

Divided into three areas derived from three different germinal sites: dorsal nail plate - from upper nail root matrix

intermediate nail plate - from lower nail matrix ventIa1 nail plate - from the nail bed

Nail Bed a) is located underneath the exposed and. concealed portions of the nail plate b) consists of a germinative layer and a dense dermis c) the deepest part of the dermis is fused to the periosteum of the distal phalanx d) the concealed portion where nail growth happens is called the matrix e) the outer limit of the matrix is a semicircular whitish area called the lunuJa f) the hyponychium is a thickemxi portion of epidermis under the distal free edge and is continuous '\lith the

germinative layer of the nail bed

Nail Wall a) folds of epidermis on either side of the nail and covers the nailproximally b) at the proximal nail fold, the horny layer spreads onto a free surface as the eponychium or cuticle

Nail Groove a) it is a furrow between the bed and the wall b) the epidermis loses all of its layers here except the germinative layer, as it continues onto the undersurface

of the nail plate

Afatrixec/Omies Indications: a) onychoayptosis (ingrown) b) onychomycosis (fungus) c) onychauxis (thickened) d) onychogryphosis (dystrophic) e) onychohlysis (separated) f) incurvated nail

Contraindications: a) infection b) vascular compromise

213

Partial Matrixectomy - Chemical Phenol and Alcohol technique

a) done under local anesthesia and a digital tourniquet b) ingro\\'n nail border is freed with a spatula or Freer elevator c) English Anvil splitter is used to split the offending edge d) the nail spicule is removed e) matrix area and nail bed are curretted to remove debris f) the posterior nail fold is curretted to remove any debris g) phenolization is performed (89"10 pure phenol)

1. protect adjacent tissue with ointment (ie-petroleum jelly; betadine ointment) 2. apply phenol on cotton swab for 30 sec intervals x 3 3. apply alcohol on a cotton swab to wash the phenol 4. dress toe with a dry sterile dressing

Sodium Hydroxide technique a) descnbed.first by Travers and Ammon in 1980 b) done in a similarfushion as the Phenol & Alcohol technique, but uses NaOH 10% and neutralized. with 5%

acetic acid c) supposedly is more predictable, high success rate, low recurrence rate and less drainage with fuster healing

time d) NaOH is applied. anywhere from 3 seconds to 3 minutes until there is visible coagulation of the nail bed

capillaries e) after care includes soaks with saline and dilute acetic acid for 20 minl3x day for 7-10 days depending on the

drainage

Complications of putial chemical matrixectomies a) recurrence resulting from:

1. improper application of the chemical 2. not enough currettage 3. dilution of the chemical secondary to bleeding 4. impropoer removal of the nail and matrix segment

b) cyst formation resulting from: 1. unaggressive matrix removal and cautery 2. sand allowed. beneath the posterior nail fold

Thermocautery a) descnbed by Kobak in 1980 b) done under local anesthesia and a distal tourniquet c) nail bolder is freed. and offending edge cut with nail splitter d) the nail spicule is removed. and the nail fold is curretted e) hand held disposasble cautery loop at temp. of2200 F is used for one or two seconds f) after care is the same as for Phenol & Alcohol technique g) advantage = no caustic chemical used with this technique

Electrodessication Partial Matrixectomy a) described. by Vernon in 1938 b) involved. using electrocautery hyfrecator writ c) needle ofhyfrecator inserted. under the posterior nail fold d) the unit is set at 50 and hyfrecation is performed. in intervals of 34 seconds, until all the matrix is destroyed e) Kerman and K1amus reported this technique to be safe and extremely effective

214

Total and Partial Matrixectomy Procedures

Winograd Partial Matrixectomy a) described in 1929 b) one-fourth inch of the edge of the

nail along with matrix and nail bed is removed and auretted

c) done via a linear incision down to bone

d) a strip of the nail fold is removed e) margins are undermined and the

incision is closed with suture

Frost Partial Matrixectomy

a)descnbedin 1950 b) a modification of the Winograd

procedure c) transverse incision for better

visibility of the underlying matrix d.) initially did not use sutures for

closure e) follow-up studies on both above

procedures are promising t) the flap created could cause avascular

necrosis of the tip g) the technique could be modified by

using a "J"-sbapedincision

Whitney Total Martixectomy (Acisional) a) first described in 1968 b) a spatula is used to open up the nail

distally. worlring proximally c) the nail is removed in toto d.) the posterior nail fold is bluntly

elevated e) the nail matrix is secured with fon:eps

and removed in toto t) technique does not provide full

exposure to the nail matrix

215

Whitney Total Matrixectomy a) descnbed in 1968 b) skin incisions similar in design

to the Frost technique c) two pamllel incisions are made

and flapped open d) the nail is removed first and

the matrix fonows e) the skin incisions are closed

with suture 1) this technique provides good

exposure to the matrix g) lower recurrence rate compared

to the Acisional technique

Terminal Syme Total Matrixectomy a) most radical procedure for

dystrophic nails b) removes the entire nail, nail weill,

and matrix c) close defect with plantar skin

flap after resecting the distal half of the distal phalanx

d) acquired the name S}me because of the plantar flap

e) disadvantages: shortens the toe potential slough creates bulbous terminal stub

Zadik Total Matrixectomy a) ,",-as first described by Quenu in 1887 b) the operation removes the nail matrix and the nail without shortening the distal phalanx c) the eponychium is excised and the skin flap is advanced and sutured d) the procedure should not be done in patients with PVD or uncontrolled diabetes mellitus because of

complications (ie-sloughing of the flap; increaesed risk of infection; de1ayed healing) e) Kaplan modified this procedure by removing the nail bed completely down to terminal pha1anx f) Owens modified the Kaplan technique removing the medial and lateral nail borders along with the

entire nail bed

216

HAMMERTOES

Hammertoe a) most common digital deformity b) the proximal phalan.~ is dorsiflexed and the middle pbalanx is plantaIflexed c) this may buckle the MfP joint and make it prominent pJantarly d) primarily caused by biomecbanical ma1function e) shoes play a role in formation f) long second toe has a tendency to develop hammertoe defonnity g) may present with heloma occurring at the PlPJ or DlPJ levels h) radiographically one sees a dorsiflexed proximal pbalanx with flexion of the middle or middle and distal

phalanges; . -may see a "gun banel" sign

Types of Hammertoes a) Flexor Stabilization Hammertoe

1. usually occurs in a pronated foot 2. usually in late stance phase of gait 3. pronation causes hypermobility of the forefoot 4. the flexors fire early in gait to stabilize a hypennobile forefoot 5. this causes overpowering of the interosseous muscles leading to hammering or cla\\-ing of digits 6. weak interosseous muscles secondary to a neuroplthy will allow overpowering of the long flexors 7. the most common etiology ofhammertoes

b) Flexor Substitution Hammertoe 1. occurs in the supinated foot 2. occurs in the late stance phase of gait 3. there is strnigbt contracture of all lesser toes 4. usually the triceps are weak 5. deep muscles of the leg try to substitute for the triceps 6. tibialis posterior,Flll., and FDL :fire earlier and longer causing contracture of all lesser digits 7. a high arched foot with contracted digits is the usual presentation 8. the least common etiology of hammertoes

c) Extensor Substitution Hammertoe 1. occurs in swing phase of gait 2. the EDL overpowers the lumbricales 3. see a strnigbt gorsal contracture of the MIP joint 4. occurs during propulsion, swing phase, and heel contact 5. deformity is demonstrated by having the patient dorsiflex the ankle in a non-weigbt bearing situation 6. in anterior pes caws foot type, passive pull on the EDL tendon is created; this causes dorsiflexion at

the MIP joint and passive contracture at the DlPJ by the flexor 7. also occurs in ankle equinus defonnity 8. in peripheral neuropathy and neuromuscular diseases, the lumbricales are affected and the EDL gains

advantage leading to an extensor substitution phenomenon.

CLA WTOE DEFORMITY

Clamoes a) flexion of the middle and distal phalanges on the proximal phalanx b) most often involve all the lesser toes including the hallux c) usually associated with cavus foot and neuromuscular conditions d) always associated with dorsal contracture of the MIP joint and plantar contracture of the lPJ's e) often see hyperkeratosis and painful metatarsalgia beneath the metatarsal heads f) early stages may be flexible and strnigbten out \\-ith the push-up test

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g) late stages, the interphalangeal joints will flex, when the metatarsals are loaded h) x-ray findings show dorsiflexed position of the proximal phalanx and plantarllexed position of the middle

and distal phalanges i) a "gun barrel" sign ",ill be seen on DP radiograph

Mallet Toe a) distal phalanx is flexed on the middle phalanx b) no involvement at the PIPJ c) associated with a long digit d) extension of the joint is limited e) difficult to manually reduce if long standing condition f) x-ray see DIPJ contracture with evident gun barrel sign g) surgical correction is via resection of the head of the middle phalanx h) may need to release the plantar contracture "ia tenotomy and capsulotomy i) splint in corrected alignment for three weeks in surgical shoe

FLOATING TOE a) a condition in which one or more toes fail to purchase the weight bearing surface in stance phase and

walking b) caused by a failure of the flexor mechanism to function effectively c) [normally, weight bearing tenses the flexors and plantar fascia, which stabilize the proximal phalanx on

the metatarsal head; failure of the ray to load results in failure to load that strand of plantar fascia and flexor cap. Result is unstable toe]

d) other causes include a short metatarsal; brachymetatarsia; iatrogenically short or excessivesly elevated metatarsals; severe hammertoe or clawtoe deformity, dislocation of the MTP joint

e) important is the loss of the internal cubic content from within the MIP joint; this occurs with plantar condylectomies.. metatarsal head resections, and with resection of proximal phalangeal base

f) e) correction is aimed at the cause of the floating toe (ie- brachymetatarsia, lengthen the metatarsal; base of proximal phalanx resection, syndactyly)

g) stabilizing arthrodesis of the PIPJ, K-wire fixation and extensor release h) surgical correction of floating toe

• based on the cause of the floating toe (ie-brachymetatarsia) -ifthe cause is related to chronic adhesive capsular release along with arthrodesis should be attempted

• if the etiology is an elevated lesser metatarsal, then a plantar displacement osteotomy should be performed

• other options for floating toe syndrome include syndactylization and V-Y advancement

1. syndactyIization

• salvage procedure secondary to prior surgery ie-resection of the base of the proximal phalanx with resultant floating toe or floppy toe resection of metatarsal head with resultant floating toe

• loss of toe purchase secondary to iatrogenic causes • contraindications to syndactyIization

infected inter5Jm:e macerated interspace

• third and fourth toe syndactylization is contraindicated since these digits lie in between the lateral and medial columns (thus, second toe is syndactylized to third toe and fourth toe to fifth toe)

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2. v-v advancement flap >a salvage procedure for the correction of iatrogenic floating toe >produces a digit with no active dorsiflexion or pJantarOexion >good reported cosmetic result

ARTHROPLASTY (ofPIPJ) a) indicated for flexIble to semi-rigid digital deformity b) the digit is 3J¥OOChed through a linear or semi~cal incision c) the incision is aciried through su1:H:utaneous tissue to the level of the EDL tendon d) a transvesrse tenotomy is made at the level of the PIPJ e) medial and 1ateral collateral ligaments are incised f) the extensor tendon is retracted proximally g) the head of the proximal pha1anx is resected h) Kelikian push-up test is performed if defonnity is not reduced

sequential release is performed in the following manner: 1. extensor hood resection 2. extensor tendon lengthening 3. dorsal capsulotomy 4. pIantarcapsule release 5. arthrodesis

ARTHRODESIS OF THE LESSER DIGITS a) converts the toe to a rigid lever b) indicated where intrinsic muscle stability is compromised:

1. lack: ofMIP joint stability 2. semi-reducible or non-reducible contracture of the IPJ 3. hyperlreratotic lesion overlying the 1P joint 4. transverse plane defonnity of distal aspect of the toe 5. claw toe defonnity 6. abnonnally long toe 7. to neutmlize the long flexors and extensors ~"--

c) procedures .. 1. end-fo.end fusion

>done via a standard arthroplasty incision >IP joint freed from soft tissue attachments >cartilage from head of proximal phalanx resected along with the base of the middle phalanx >K-wire driven through mic:klle and distal phalanges (exiting through tip of toe beneath the nail) >resected smfuces aligned >K -wire driven across site and stability is checked >0.045 K-wire can be usedifnot crossingMIP joint >0'<)62 K-wire can be used if crossing the MIP joint (anything smaller would break) >main1ain K-\\'1re fixation for ~ weeks

2. peg-in-hole fusion >most optimum procedure for fusion of a digit >poduces significant shortening of the digit >difficult to perform >dorsal cortex of phalangeal peg left intact to provide stability

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>good bone stock is needed to perform >although stable. needs a K-wire fixation

3. spike-in-hole fusion >same as peg-in-hole fusion, but the proximal phalan.x is fashioned into a spike >dorsal cortex of phalangeal spike left intact >no great advantage over the peg-in-hole fusion

CONGENITAL OVERLAPPING FIFTH TOE a) definition: deformity occurring at the fifth MTP joint

synonyms = overriding fifth toe hyperextension of the fifth toe elevated, contracted varus of the fifth toe digiti quinti vams

b) etiology 1. usually congenital and bilateral 2. less commonly unilateral, traumatic or iatrogenic in nature 3. incidence is equal between males and females 4. three main components of the deformity

>adduction contracture >dorsiflexion >external rotation

c) clinical appearance 1. the toe usually appears smaller,

smaller, shortened and flattened or "plddle shaped"

2. supra-adductus: the fifth toe over the fourth

3. infra-adductus: the fifth toe under the fourth

d) deforming forces 1. dorsal and medial skin is usually tight 2. in severe cases,. the skin of the web space can be contracted as well 3. medial coI1ateIallig:ament and

dorsomedial MPJ capsule are shortened and tight

4. the EDL tendon is contracted e) conservative treatment

1. usually reserved for children or for deformity that is not longganding 2. stretching and strapping into pIantarflexion and abduction

f) surgical treatment 1. consideration depends upon the age of the pltient and location and severity of the deformity:

>skin pIasty to lengthen dorsal-medial skin >tenotomy, tendon lengthening or tendon transfer >dorsal-medial capsulotomy >ostectomy >syndactylization of the fourth and fifth toes >amputation >a combination of procedures

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g) historical surgical procedures 1. Anderson: removal of a plantar skin wedge, dorsal V-Y skin pIasty, lengthening of the EDL tendon.

fifth metatarsal head resection. and svndactvlization of the fourth and fifth toes 2. Butler: dorsal raquet incision with a J,tanta; haodl~ extensor tenotomy and MPJ capsulotomy 3. Duvries: dorsal Z skin plasty, extensor andMPJ capsulotomy 4. Kaplan: plantar skin wedge plasty, extensor tenotomy, dorsal, medial and lateral MPJ capsulotomyand

partial }XOximal phalangectomy 5. Kelikian: syndactylization of the fourth and fifth toes and a proximal phalangectomy 6. Lantzounis: mainly a sagittal plane COIreCtion; it involves an MPJ capsulotomy and a tnmsfer of the

EDL tendon through a drill hole placed through the neck of the fifth metatarsal 7. Lapidus: division of the EDL tendon and transposition to the distal end of the abductor digiti minimi

tendon 8. Wilson: dorsal V-Y skin p1asty and extensor tenotomy and elongation

h) post-operative care L compresssive dressings 2. observe neurovascular status 3. toe splinted 4-6 weeks to maintain correction

i) complications 1. recurrence 2. dehiscence 3. shortened digit 4. instability of the fifthMPJ

POLYDACTYLY Definition: presence of an acessory, supernumerary or extra digit

a) very common congenital anomaly b) may present as a hypoplastic digit without osseous structure or as a fully developed digit c) can be either preaxial or medial to the second metatarsal (the axis of the foot) or postaxial d) can form part of a SJ'lldrome or can present as a nonsyndromatic or isolated deformity

Classification Postaxial polydactyly (fifth digit duplication) according to Temtamy & McKusick:

Type A:. characterized by a fully developed accessory digit that articulates with the fifth metatarsal or a duplicated :fifth metatarsal

Type B: characterized by an accessory digit without osseous substance this classification :fuils to address the range of forms between digit devoid of osseous substance and

completely duplicated digit ~

r~ E~: s>cM:C~:>tI¥-~~fII;.-L~ ;:! I L~c~cm-r~ ~

~lyPl' II ~M~~:otIl'

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Venn-Watson Classification of postaxial polydactyly based upon degree of duplication fonn least differentiated to the most differentiated: soft tissue duplication, wide metatarsal head T -metatarsal, Y -metatarsal and complete duplication

wide met head

T -metatarsal

Preaxial Polydactyly (first digit duplication) rarely involves the foot

Y -metatarsal

not well documented compared with preaxial polydactyly of the hand Temtamy & McKusick classified four types in the hand Type I - polydactyly of the first digit Type 2 - polydactyly of a triphalangeal first digit Type 3 - polydactyly of a second digit Type 4 - polysyndactyly

Blauth & Olsson Classification (1988) classification according to radiomorphologic alteIations based upon position of duplication on both the longitudinal and transverse planes

complete duplication

a) longitudinal: arrangement is blsaed on the duplication of a phalanx or ray from distal to proximal and is subdivided into five types:

distal phalanx middle phalanx proximal phalanx metatarsal tarsal

b) transverse: arrangement indicates the number of duplicated rays which are then numbered with Roman numerals medially to latern11y

permits classification of the hand and foot accounts for special malfonnations, such as triphaJangism and multiple duplications aids in accwate diagnosis and in developement of a surgical plan

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¢

PREDISLOCATION SYNDROME (Lesser MTPJ Instability)

Descriptive: • Patients usually middle age 30-50 • Acute/subacute pain plantar mtpj(2nd most common) • Pain disproportionate to physical findings • History of increased activity, trauma, steroid injection • Sharp pain, bruise, throbbing • Gmpe-size lump beneath mtpj (bursal sac)

Stages: (not used clinically) I. mild edema, tenderness plantar/distal joint, no change in alignment II. moderate edema ID. clinical deviation of digit, loss of toe purchase '''lith weight-bearing

Differential DX:

• stress fracture • synovitislcapsulitis

• hammertoe • neuroma • metatarsalgia

Imaging: X-ray findings

• long 2nd met • altered MfPJ congruity • + dIaw sign (vertical stress test)

1. stabilize met • hypertropbic

cortex of involved met 2. hold prox phal parallel to met

3. translocate digit in sagittal plane greater than 500/0=p0sitive test

Bone &an

MRl » inc. uptake in angiogram phase indicating inflammatory process

l.edema along distal slip of plantar fascia 2. thickening of plantar plate or rupture visible 3 .capsulosynovial joint effusion

Conservative Therapy:

Surgery

» 60-90% relief » reduce pain » stop progression

» Splint/strapping Metatarsal splint pad Cross-ever tape method

Stabilize prox phalanx in plantar direction Can be used as a diagnostic tool

» Medrol dose packlNSAID » ultrasound, whirlpool

» flexor tendon transfer » "z" lengthening ofEDL » extensor hood recession » total MTPJ capsulotomy » K-wire fixation in overcorrection » PrimaIy plantar plate repair from plantar incision

**Both the Weil and Helal osteotomy aJ

utilized to shorten the metatarsal and to aIlo' joint decompression

» Weil osteotomy (oblique at metatarsal neck from plantar-proximal to dorsal-distaI) » Helal osteotomy (oblique at metatarsal neck from dorsal-proximal to plantar distal) » Post -op splint to maintain correction

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BRACHYMETATARSIA

Def"mition: A short, hypoplastic metatarsal due to premature closure of the epiphyseal plate; when more than one metatarsal is involved the condition is called brach)'metopody

Etiology: • congenital • developmental • iatrogenic • traumatic

Associated congenital anomalies: - Down's Syndrome - Turner's Syndrome - sickle cell anemia - dystrophic dwarfism

Characteristics:

• unilateral or bilateral • 25: I female to male ratio • 4th metatarsal most common

- Albright's Congenital Osteodystrophy - pseudohypothyroidism I pseudo-pseudohypoth)TOidism - poliomyelitis - myositis ossificans

• usually becomes evident between ages 4-15

Clinical presentation: • short, contracted toe seen clinically • short metatarsal seen radiographically • cosmetic or psychological concern • metatarsalgia blc increased load to adjacent metatarsals • plantar callus formation • floating toe of associated affected metatarsal • overlapping toe causes:

extensor & flexor tendon contIactures skin contracture

Conservative Treatment: • orthotics or accomadative devices

• padding

Surgical Treatment ~ Soft Tissues • V -y skin plasty to relieve tension of contracted skin • Z-plasty lengthening of long extensor tendon • tenotomy of short extensor tendon • MIPJ capsulotomy (dorsal, medial, lateral release) • sectioning of deep transverse intermetatarsalligament

Surgical Treatment ~ Osseous

1. Osteotomy lengthening procedures (many options to restore metatarsal parabola): I. single metatarsal osteotomy with insertion of bone graft 2. combined lengthening and shortening metatarsal osteotomies 3. slide lengthening metatarsal osteotomies

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Complications of osteotomy lengthening: lengthening too aggressive -+ neurovascular compromise lesser MlPJ limitus delayed union I nonunoin resorption I collapse of bone graft

2. Callus Distraction (Callastosis)

Description • Technique in which bone lengthening can be achieved by slow distraction of the bone callus that forms

at the open ends of a surgically osteotomized bone. • First performed by llizarov on lower extremities using a circular external fixator device. • Based on the law oftension-sttess

Procedure

Advantages

living tissue when distracted slowly becomes metabolically active

anatomical dissection to the level ofbone incision and reflection of periosteum osteotomy or corticotomy -+ initiates callus formation

= osteotomy - through and through cut of bone = corticotomy - cut ortex only to maintain endosteum

-+ studies show equal success with either technique placement of external fixation device latency period - time between osteotomy/corticotomy and distraction

= varies with each bone and patient age = optimal latency 5 days to 2 weeks

rate of distraction (also varies with bone and patient age) = 1 mmlday in 4 equal increments = according to llizarov for tibial lengthening

distraction stopped when desired length is achieved period of ossification at distraction site fixation left in place until rndiographic evidence of osseous union

no need for bone graft no neurovascular compromise because all structures are gradually lengthened can gain more length than other bone lengthening procedures can gradually lengthen soft tissue structures (tendons, skin)

Disadvantages pin tract infections need compliant patient

IndicationsIUses brachymetatarsia callus distraction Evans procedure for pes piano valgus lengthening of medial cuneiform for metadductus tibial lengthening or correction of angular deformity

Callus Distraction Procedure for Brachymetatarsia longitudinal incision over affected metatarsal anatomic dissection to level of bone linear periosteal incision placement of external fixator pins

= 2 proximal to osteotomy (1 in cuboid or cuneiform; 1 in metatarsal) = 2 distal to osteotomy

osteotomy/corticotomy closure of periosteum and anatomic layers

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placement of external fixator device (EBITM M-IOO mini external fixator most common) begin distraction 5-14 days post-operatively tum device ~ tum 2-3 times per day (.5 - .75 mm total length gain per day) serial mdiogmphs - will see mdiolucent gap at distmction location nonweightbearing recommended

osseous consolidation - then remove external fixator

LESSER METATARSAL SURGERY

Historical Review 1916 - Meisenbach: osteotomy 3 em proximal to MIP joint 1917 - Davis: metatarsal head resection 1940 -Man: resectionoftmpezoidal wedge 1948 - Borggeve: same as Mau, except performed distal 1952 - McKeever. subcapital osteotomy; telescoped, spiked end of shaft into capital piece; shortening

osteotomy 1953 -DuVries: pJantarcondylectomy 1954 - Giannestras: step-down shortening osteotomy 1954 - Rutledge & Green: removal of metatarsal head and one-tbird of the shaft 1 %5 - DuVries: metatarsal head arthroplasty and plantar condylectomy 1 %9 - Addante: osteoclasis 90 degrees to the shaft 1%9 - Wolf: dorsifle..xory osteotomy on distal metatarsal shaft 1971 - Scarlato: dorsiflexoty base wedge osteotomy or elevational osteotomy procedure 1973 - Jacoby: classic "V" osteotomy

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Neck osteotomies (most commonly performed osteotomies for isolated tylomas) a) V-osteotomy

1. Jacoby described the procedure 2. allows :free motion in the sagittal plane, but stable in the transverse pIane due to "wings"

b) Osteoclasis 1. performed at the level of the metaphyseal neck 2. free motion in sagittal and tIansverse planes 3. bigh incidence of pseudoarthrosis and nonunion

c) PMO (percutaneous metaphyseal osteotomy) 1. transverse osteotomy through the head. of the metatarsal 2. instability and heaIing problems similar to osteoclasis

d) DFWO (dorsifiexory wedge osteotomy) popu1ar procedure that has spawned many similar procedures

e) V-wedge 1. also known as the Bartel wedge 2. more oblique wedge than DFWO, allowing for increased bone-to-bone contact

Shortening osteotomies (wilen tyloma may be secondary to an elongated, rather than a pJantarflexed metatarsal) a) cylindrical osteotomies: through and through osteotomy with removal of the wedge b) Chevron osteotomy: similar to Jacoby wxcept a second "V" cut is made proximal and the wedge is

removed

Basal osteotomies a) EO (extensor osteotomy)

1. similar to the DFWO but done 1-2 em distal to the meIatarsal<Uneiformjoint 2. usually perfOImed to relieve an isolated IPK

b) EOA (extensor osteoarthrotomy) same indications as the extensor osteotomy except that it is used when stabilization of the metatarsal-

cuneiform joint is desired c) Buckholz osteotomy

1. similar indications as the above basal osteotomies 2. more oblique and proximally located apex than the extensor osteotomies descnbed above 3. the greater obliquity allows pJacement of a 2.7 mm cortical screw for fixation 4. most stable

The California (left coast) approach Principles

a) perform surgery on only first, third and fifth metatarsals b) will peIform smgery on all subtne:latat"W lesions c) no surgery on second and fourth metatarsals

Philosophy a) first and fifth metatarsals have independent axis of motion (triplanar), and thus, have significant influence

on the second and fourth metatarsals

b) the third metatarsal is the most independent ofbiomechanical and other metatarsal influence c) arthrodesis or arthropJasty of the second and fourth digits to remove retrograde plantarfiexory forces

Surgical treatment a) submet 2 lesion

1. address first metatarsasl deformity (HA V, hypermobility, sagittal plane position) 2. arthrodesis or arthropJasty second digit (remove retrograde force at the second MP])

b) submet 4 lesion 1. address fifth metatarsal deformity (Tailor's bunion, hypermobility, adducted fifth digit) 2. arthrodesis or artbrop1asty fourth digit (remove retrogI3de force at the fourth MP])

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c) submet 3 lesion 1. usually due to long third metatarsal or iatrogenic transfer lesion 2. can perfonn appropriate metatarsal procedure

To Float or to Fix? Floating philosophy

a) metatarsal will find its own level b) weight bearing and soft. tissue binding (fibrosis) will pro"ide appropriate and stable level c) decrease chance of transfer lesion

FL'I:3tion philosophy a) why guess? can place metatarsal at desired location b) difficult c) prevent nonunion, pseudoarthrosis, etc

TAll.,ORtS BUNION

Introduction predilection of Tailor's bunion occurs in 2: I female to male ratio

Types six osseous pathoanatomical types of Tailor's bunion have been described: a) rotation of the lateral plantar tubercle into a lateral position b) increased intermetatarsal angle c) increased lateral deviation angle d) a large round dumbbell-shaped fifth metatarsal head e) arthritic changes rresulting in exostosis fonnation at the fifth metatarsophalangeal joint f) any combination of the above conkditions with the first three being the most common

Etiol0R.v (as described by Root) a) abnormal STJ pronation b) uncompensated forefoot or rearfoot varus with a pronating foot c) congenital plantarflexed fifth ray d) congenital dorsiflexed fifth ray e) idiopathic condition caused by absence of transverse head of the adductor hallucis into the fifth MIP joint

Radiographic Evaluation Intermetatarsa1 Angle: Buckholz & Fallat method, which takes into consideration the lateral bowing present within the fifth metatarsal a) represented by the angle between formed between two lines -

>line drawn aqjacaent and parallel to the medial proximal surface of the fifth metatarsal shaft >line bisecting the long axis of the fourth metatarsal shaft

b) normal value is 6.47 degrees c) pathological value is 8.71 degrees (bunion defonnity)

Lateral Deviation Angle: Buckholz & Fallat method, which takes into consideration the lateral bowing ·within the fifth metatarsal

a) represented by the angle formed between two Iines ->line bisecting the head and neck of the fifth metatarsal at the articular surface >line drawn adjacent and}malleI to the medial proximal surface of the :fifth metatarsal shaft

b) normal value is 2.64 degrees c) pathological value is 8.05 degrees

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c) submet 3 lesion 1. usually due to long third metatarsal or iatrogenic transfer lesion 2. can perfonn appropriate metatarsal procedure

To Float or to Fix? Floating philosophy

a) metatarsal will find its own level b) weight bearing and soft. tissue binding (fibrosis) will provide appropriate and stable level c) decrease chance of transfer lesion

Fixation philosophy a) why guess? can place metatarsal at desired location b) difficult c) prevent nonunion, pseudoarthrosis etc

TAU,OR'S BUNION

Introduction predilection of Tailor's bunion occurs in 2:1 female to male ratio

Types six osseous pathoanatomical types of Tailor's bunion have been described: a) rotation of the lateral plantar tubercle into a lateraI position b) increased intermetatarsal angle c) increased lateral deviation angle d) a large round dumbbell-shaped fifth metatarsal head e) arthritic changes rresulting in exostosis fonnation at the fifth metatarsophalangeal joint f) any combination of the above conkditions with the first three being the most common

Etiology (as described by Root) a) abnonnal STJ pronation b) uncompensated forefoot or rearfoot varus with a pronating foot c) congenital plantarflexed fifth ray d) congenital dorsiflexed fifth ray e) idiopathic condition caused by absence of transverse head of the adductor hallucis into the fifth MIP joint

Radiographic Evaluation Intennetatarsal Angle: Buckholz & Fallat method, which takes into consideration the lateral bowing present \Vithin the fifth metatarsal a) represented by the angle between fonned between two lines -

>line drawn adjacaent and parallel to the medial proximal surface of the fifth metatarsal shaft >line bisecting the long axis of the fourth metatarsal shaft

b) nonnal value is 6.47 degrees c) pathological value is 8.71 degrees (bunion defonnity)

Lateral Deviation Angle: Buckholz & Fallat method, which takes into consideration the lateral bowing ,,;thin the fifth metatarsal

a) represented by the angle fonned between two lines ->line bisecting the head and neck of the fifth metatarsal at the articular surface >line drawn a£ljacent and parallel to the medial proximal surface of the :fifth metatarsal shaft

b) nonnal value is 2.64 degrees c) pathological value is 8.05 degrees

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Intermetatarsal Angle Lateral Deviation Angle

Historical Review 1949 - Harris & Davis: first to descnbe "bunionette" deformity

proposed simple lateral condylectomy 1951 - Hohman: transverse osteotomy of metatarsasl neck without fixation 1953 - Dixon: prominent fifth metatarsasl head due to splaying

treatment consisted of wearing "ider shoe or excision lateral condyle and bursa 1956 - Leliever: felt Tailor's bunion was due to three mecbansims

1. supernumerary bone 2. increased intermetatarsal angle 3. cross-legged sitting position (tailor's)

1959 - Brown: fifth digit and metatarsal resection to narrow foot 1959 - Do Vries: bunion due to three reasons and recommended lateral condylectomy

1. hypertrophy of soft tissue overlying metatarsal head 2. congenitally wide fifth metataI5al head 3. lateral bo'wing of the fifth metatarsal

1961 - Ambrey: lateral condylectomy or metatarsal head resection if a submet lesion existed 1969 - Yaney: base osteotomky to decrease the 1M angle and head remodeling 1971 - Sgarlatto: talked about lateral bowing of fifth metatarsal 1971 - GeIbert: base wedge osteotomy using binge axis 1974 - Leach & Igou: reverse Mitchell 1974 - Rapapport: base wedge osteotomy and arthroplasties

Surgical Approach based upon radiographic rersults from 1M and lagteral deviation angles a) high 1M angle: procedure should be some type ofbasal osteotomy b) nonnal 1M and high lateral deviation angle: procedure should be an osteotomy at the metatarsal neck c) all nonnal angles: if tailor's bunion is present, then resection of the lateral surfuce of the fifth metatarsal

head is performed d) surgical procednres:

1. ostectomy 2. reverse Hohman 3. reverse Wilson 4. reverse Austin 5. reverse Offset-V 6. adductory rose wedge

osteotomy 7. fifth metatarsal head

resection 8. joint arthroplasty

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IMPLANTS

Indications:

a) eliminate pain

b) regain or retain motion (questionable!~ spacer)

c) correct deformity

Historv:

a) 1962 - Seeburger 1) used durallium for his hemi 1st MIPJ implant

2) functioned to cover a necrotic 1st metatarsal head

b) 1965 - Downey

1 ) total (ball and socket)

c) 1973 - Sutter 1) double barrel stem with an external dacron mesh jacket

d) 1974 - Feder and Feder 1) ulnar head prosthesis used at 1 s[ metatarsal head

2) madeofsilicone

3) repeated by Karp ('74) and Freed ('79)

e) 1978 - Calman-Nicolle

1) total implant made of polypropylene

2) hinged in the middle with an arm into metatarsal and phalanx

f) 1982 - Swanson

1) total finger implant design made of silicone

2) dacron mesh impregnated into prosthesis

3) redesigned an earlier version of a total finger implant by Neibauer and Cutter

h) 1983 - Sgarlatto 1) used at the PIPJ and DIP! for hammertoe deformity

BiomateriaIs:

a) stainless steel 1) may cause resorption of bone

2) steel may corrode

b) Silicone

1) low elastic modulus (returns to normal form after a physiologic load)

2) does not have potential for corrosion

3) soft tissue response (fixation by encapsulation)

4) may cause detritus synovitis (chard of silicone in synovium causes chronic inflammation)

5) bone response c) pol)'methylmethacrylate

1) bone cement used to hold implants in place

2) exothermic reaction while mixing may cause A VN

d) titanium, cobalt, polyethylene

Implant design I function:

a) hemi - Y2 of the joint 1) indication is arthritis on one side of joint 2) Swanson great toe - concave head with a long stem 3) Weil modification great toe - 15 degree DASA to compensate for abnormally high

PASA; shorter, tapered stem

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4) Sutter - with or without internal or external dacron mesh 5) Titanium - biocompatable; titanium oxide coating resists corrosion 6) Implant should be wider than stump of remaining bone

b) total - both sides of joint 1) one component total

+ Swanson - central "U" hinge with opening dorsally; no angulation

+ Sutter - proximal stem angled 15 degree dorsally to accommodate for metatarsal declination angle -7 LaPorta - neutral or 15 degree angle with plantar angle on distal side-? Lawrence

+ Sgarlatto similar to Swanson 2) two component totals

+ Koenig - ti1anium proximally (plantar lip replaces metatarsal condyles); polyethylene distally; NO transverse stability

+ Bioaction & Kinetic - metatarsal component = cobalt chrome; pba1angea1 component = ti1anium with polyethylene covering; NO transverse stability

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Host Response: a) materials must be biochemically inert, durable, non-irritating, non-toxic, hypoallergenic, non­

carginogenic, non-pyogenic, and handle physiologic stress

Indications: a) hallux valgus with subluxation, hallux rigidus (should not be used as sole procedure if IM angle is

greater than 14 degrees)

b) revisional surgery

c) rheumatoid, DID, gout d) osteochondral fracture. intra-articular fracture

e) hammertoe, cIa-wtoe, mallet toe

Surgical Technique:

a) maintain length of metatarsal and proximal phalan:x

b) all require some reaming of the medullary canal

c) maintain capsular integrity

Radiographic Analysis:

a) check: alignment and position in the medullary canal b) the initial x-ray may show some separation between implant and bone

1) normal until the 3rd month

Complications:

a) material failure 1) intrinsic (metatarsal head irregularities, stress fractures)

2) extrinsic (eccentric placement, inadequate bone resection, or soft tissue release)

b) microfragmentation I) initial abrasion of stem during implantation

2) head abrasion at bone/implant interface -7 grommet used as Cl D CQJ metal interface to protect implant from being eroded by 0 bone .. '

c) juxta-articular bone cysts

d) frozen toe 1) due to proliferation of bone secondary to DID

e) intramedullary fibrous hyperplasia 1) secondary to aseptic necrosis from enlarged metatarsal head or proximal phalanx base

f) infection 1) acute (40010 of infections) within 5-7 days to a month post op

+ contamination during surgery + hematogenons spread + contiguous spread from hematoma, sutures, etc.

2) delayed & late (60% of infections) within 1 month to 2 years post op + "time lapse" effect -7 bacteria enter at time of surgery and proliferate when

the environment is optimal

3) treatment + removal of implant + synovectomy + bone grafting of cysts + fusion of joint ( dramatically shortens toe) + prophylactic antibiotics -7 staph. epi.

+ vancomycin +clindamycin

232

LOWER EXTREMITY AMPUTATIONS

I. General Concepts A Disarticulations - done in children because it preserves the epiphyseal plate allowing full limb

growth B. Amputation length - in general the longer, the better both physically and mentally C. Gait velocities decrease with more proximal amputations D. Complications are the rule with difficulties in healing, prosthesis fitting, rehabilitation, and

possible additional amputations

II. Indications for Amputations A. Trauma (crushing, mutilating) B. Malignant neoplasia C. Uncontrollable infections D. Arterial vascular diseases leading to gangrene E. Severe deformities (non reconstructable)

III. Amputation Statistics A. 33% of patients having unilateral amputation \\-iIl have the contralateral limb amputated after

3 years B. 33% survival rate 5 years post-op Below Knee Amputation

IV. Lower Extremity Amputations A Hemipelvectomy (malignancies and failed Above Knee Amputations) B. Hip Disarticulation (malignancies and failed Above Knee Amputations) C. Above Knee Amputation (AKA) D. Knee Disarticulation E. Below Knee Amputation (BKA) F. Proximal Symes Amputation G. Pirogoff Amputation H. Chopart Disarticulation I. Lis Franc Disarticulation J. Tenninal Symes Amputation K. Ray Resection L. Transmetatarsal Amputation (IMA) M. Digital Amputation N. Guillotine (open amputation at any level which requires granulation or delayed surgical

closure)

IV. Principles of Amputation A. site must withstand friction from prosthesis I shoes which makes plantar skin more ideal for

weightbearing flaps B. scars should not adhere to bone C. avoid unnecessary procedures to improve cosmetic outcome D. tendon balancing E. amputation site should be free from cellulitis, lymphangitis, and edema F. flaps should be under no I minimal tension G. adequate hemostasis to avoid a pabulum

v. Proximal Symes Amputation A. total foot amputation that may be used in healthy patients \\-ith severe foot trauma B. medial and lateral malleoli are resected C. preservation of the calcaneal fat pad as a posterior I plantar flap to use for weight bearing

surface D. dog ears are revised at second stage of procedure to prevent ulceration E. high rate of complications with prosthetic fitting and distal ulceration

233

VI. Pirogoff Amputation A modification of proximal Symes that preserves the calcaneus for length of limb B. fusion between calcaneus and tibia C. high rate of complications with fusion and prosthetic fitting

VII. Chopart Disarticulation A preserves a long plantar flap if needed B. high complication rate, especially equinovarus deformity (TAL or achilles tenotomy

recommended) C. prosthesis recommended

VIII. Lis Franc Disarticulation A preserves a long plantar flap if needed B. medium complication mte, especially equinovarus deformity (TAL or achilles tenotomy

recommended) C. prosthesis recommended D. do not leave articular cartilage and plane remaining uneven joint surfaces because uneven

cartilage surface at incision site delays healing and can lead to pressure points

IX. Transmetatarsal Amputation A Most commonly used proximal foot amputation B. metatarsals transected at dista1113 in a smooth parabola with the second being the longest,.

and the cuts of the metatarsals should be angled distal-dorsal to proximal-plantar with metatarsall angled proximal-medial to distal-lateral, and metatarsal 5 angled proximal-lateral to distal-medial

C. must have long plantar flap D. ankle foot orthosis (AFO) and custom molded shoes with toe filler and rocker bottom are very

beneficial in rehabilitation E. low complication mte (TAL or achilles tenotomy and possible anterior tibial tendon transfer

to lateral stump for tendon balancing

X. Terminaf Symes Amputation A removal of all or part of a toe B. flaps used for closure

1. fish mouth (mostly done on hallux) 2. long plantar 3. side to side 4. racquet

C. remove cartilage (receives its' nourishment from synovium) if disarticulating

234

INTERMETATARSAL NEUROMA aka Morton's Neuroma " ... a peculiar and painful affection of the foot"

- Thomas G. Mortoo 1876

HISTORY 1845 1876

1883

Durlacher. L Morton, TG

HoadIey,AE

Original description of disease Etiology: Compression oflateral plantar nerve between '" & 5th Metatarsal heads; recommended surgical excision ~r '" me/head First to excise third interdigital nerve

1897 Jones & Tubby Etiology: A communicating branch blw medial and lateral plantar nerves was compressed hili' the '" metatarsal head and the ground Etiology: Secondary to stretching of r & '" interdigital nerves under deep transverse inJennetatarsalligament; also :r interdigitai nerve is larger because of additional fibers from lateral plantar nerve rommunicating branch Etiology: Ischemic origin to nen>e lesion

1940

1948 1951

Betts, W

Nissen,Kl Mulder,JD Etiology: Weakness of the transverse arch of the forefoot results in

hypennobility of the metatarsals alJowing the interdigital nerves to become im·tated and inflamed with jib1'QUS

1963 Kopel/& Etiology: Entrapment neuropathy of the interdigital nerve secondary to trauma Thompson

PATHOGENESIS ~ Truly unknown? ~ Most likely etiology is an entrapment neuropathy secondary to stretching and irritation of the

interdigital nerve as it passes under inferior to the deep transverse intermetatarsailigament with repetitive dorsiflexion at MTPJ during ambulation

HISTOPATHOLOGY The term "neuroma" is a misnomer, it is not a tumor or mass out growing from a nerve

~ Sclerosis and edema of epineurium ~ Thickening and hyalinization of endothelial vessels in and around the nerve ~ Thickening and fibrosiS of epi-.peri-, and endoneurium ~ Demyelinization of nen'e fibers

DIFFERENTIAL DIAGNOSIS

• Abnonnal Metatarsal Parabola • Metatarsus Proximus • Freiberg's Infarction

• Vascular Ischemia • Plantar Fat Pad Atrophy • Hypennobile Metatarsals

• Capsulitis

• Ganglion c.yst

• MFP Joint Synovitis • Occult Fracture

• Tarsal Tunnel Syndrome

CLINICAL EVALUATION

Presentation characteristics ~ Female»Male ~ Third to seventh decade

• Neuritis

• Epitheloid C.VSl

• Rheumatoid Nodule

• Radiculopthy

• Synovial Cyst

~ Most common interspace involved is the 3rd, closely followed by 2nd ~ First and fourth interspace are rare

• Traumatic Bursitis

• Foreign Body

• Metatarsal Stress Fracture

• Pre-Dislocation Syndrome (PDS)

~ Multiple interspace involvement rare <4% (Thompson & Deland, FAI, Jan 1993)

235

~ Gradual onset of symptoms present many months prior to office visit )- Symptoms y Forefoot burning pain );. Aggravated »7th ambulation, squatting, and tight shoe gear y Sharp stabbing pain ~ Pain radiating to involved digits y Reliefby rest and massage

Signs y Lngimlh}~~esia

,. Reproducible pain with lateral compression of forefoot y Sullivan's sign (Splaying of digits) y Pain between and just proximal to metatarsal heads ~ Palpable intermetatarsai mass y Alulder's Click

ADmCTIVE CLINICAL MEASURES

1. R.adiograpIry ~-ray) • To RIO osseous or arthritic pathology

2. Magnetic resonance imoging (MRl)

• Best seen on TJ -weighted images as focal area of decreased signal intensify • Good for determining extent of lesion

3. UlJrasonography (US)

• Rely on ability to interpreter • Up to 98% sensitive

4. Electromyograph (EMG)/ Nerve tXlnducIion velocity (NCV) • Not routine diagnostic procedures • Used for atypical presentation • RIO more proximal neural pathology

CONSERVATIVE TREATMENTS Y Provides good temporary relief of symptoms in 20-50010 cases Y Generally poor long-term effectiveness

1. Diagnostic local anesthetic block to interdigiml space 2. Wide-toe shoe box 3. Padding and/or strapping ("Cookie pad") 4. Orthotics 5. Physical therapy 6. Ionophoresis, phonophoresis 7. Metatarsal bar 8. Corticosteroid injection(s)

Y SURGICAL TREATMENT , Offers best def"mitive treatment Y Effective in 70-100% of cases in the literature

Incisional Approach 1. Dorsal

A Longitudinal (McKeever 1952) ~ Provides good exposure to interdi.gital nerve Y Avoids weight bearing scar ~ Approx. 3 em incision bIw metatarsal heads Y Transect deep transverse intermetatarsalligament (DTIL)

236

B. Web-space (McElvenny 1943) ~ Incision through the web-space extending 1-2cm dorsally ~ Proximal exposure can be difficult ~ Allows for early weight-bearing ~ Avoids weight bearing scar

2. Plantar Use large gauge suture

A Longitudinal (Hoadley 1893) ~ Approx. 3cm incision bisecting metatarsal beads ~ Nerve is very superficial from this approach therefore, excellent visualization of

nerve » Less dissection ~ Preserve DTIL ~

» Can transect nerve more proximal

No residual dead Space therefore, decreasing opportunity for hematoma fonnation

~ Best approach for "re-do neuroma" or "stump neuroma"

B. Transverse (Nissen 1948)

Procetb,,·es:

~ 2-3cm curvilinear incision over interspace(s) just proximal to plantar digital sulcus ~ Option for multiple interspace neuroma ~ Less potential for hypertrophic scar formation vs. longitudinal ~ More potential to disrupt plantar fat pad ~ Increased risk of compromising perpendicu1ar uaversing superficial neurovascular

1. Neurectomy ~ Excision of the interdigital nerve and its concomitant branches ~ Most commonly peIformed surgical procedure ~ Dorsal or plantar approach ~ Identify and expose all nerve branches prior to resection ~ 80-85% good results

2. Epineurolysis ~ InteIdigital nerve is freed form surrounding soft tissue structures, without excision of

. nerve » DTIL: (a) remains intact, (b)is 1Iansected or (c) is transected and repaired ~ Preserves sensation to the interdigital space ~ Addresses etiology of entrapment neuropathy ~ Results:

~ »

Dellon .• A- trQ1lsected DTIL; 80% complete relief Guthier, G- ttansected DTIL; 83% excellent, 14% improved

~

exceHent

POST -OPERATIVE COURSE ~ Compressive dressing

Diebold et aI.- follow-up Dl1L released; 92.5%

~ Use of a drain may be considered with excessive bleeding ~ Ice QI1.d elevation for 72 hours ~ Pain medication ~ Parliai weight bearing to heel with crutches in surgical shoe ~ Suture removal 2 weeks dorsal incision and 3 weeks plantar ~ Return to regular shoe gear at 2-3 weeks

237

POST-OP COMPLICATIONS

y Hematoma );> Stump neuroma (with neurectomy) y Recurrence (with epineurolysis) yEdema y Digi tal contracture ~ Wrong interspace addressed );> Hypesthesia

ALTERNATIVE TREATMENTS

~ Incisional scar y Wound dehiscence y Injection y Hyperkeratotic lesion y Paresthesia ~ Anesthesia y S7dn sloughing

1. C02 LASER 2. Endoscopic decompression for intermetatarsal neuroma (EDIN)

y Described by Barrett & Pignetti JFAS 1994 3. Cryogenic denervation 4. Percutaneous electrcoagulation

RECURRENCE y Rate is approximent(v 20% ~ Eti%gv

Wrong diagnosiS Wrong interspace Poor surgical technique Failure to divide the transverse metatarsal ligament Incomplete removal Transect common plantar digital nen'e too distal

., Treatment y Conservative- same as original, but more likely to fail >- Surgical- resection of nerve or stump

Mann and Reyno/ds- 81 I)/{)()j pis. had seventy-jive to one hundred percent relief

238

ANATOMY OF THE FIRST METATARSAL PHALANGEAL JOINT

Ligaments (9) 1. medial sagittal hood 2. Iateral sagittal hood 3. medial sesamoidal 4. Iateral sesamoidal 5. intersesamoidal 6. medial col1ateral 7. Iateral collateIal 8. plantar fuscia (slip inserts into Iateral sesamoid) 9. transverse metatarsal ligament

Sesamoids a) two in number b) artiaJ1ate in the grooved smface of the

first meIafaISal head c) crista of the first metatarsal head

separntes the two bones d) fibrous pJantar pad anchors each

11 sesamoid to base of proximal phalanx e) held securely in place by medial

sesamoidal, intersesamoidal, lateral sesamoidal ligaments and the plantar filscia

f) muscles and ligaments of the sesamoid complex:

Musdes(7) 1. extensor hallucis longus 2. extensor hallucis brevis 3. abductorhallucis 4. adductor hallucis (combined insertion) 5. (2) flexor hallucis brevis (medial and

1ateral heads) 6. fle.xor hallucis longus - as it travels

through the groove of sesamoids 7. Extensor Capsu1aris

• (the ligament splits into superior and inferior slips; this accommodates the adductor hallucis tendon to insertion at base of the proximal phalanx)

239

BLOOD SUPPLY TO THE FIRST RAY

1. dorsalis pedis artery 2. ttansverse plantar arterial arc 3. first plantar metatarsal artery 4. first dorsal metatarsal artery 5. branches of the first dorsal metatarsal artery 6. medial division branch of the first plantar metatarsal artery 7. 1ateral division branch of the first plantar metatarsal artery 8. hallucal branch - medial plantar artery fOIming cruciate anastomosis 9. cruciate anastomosis

1) medial branch of the first plantar metatarsal artery 2) lateral branch of the first plantar metatarsal artery 3) hallucal branch from medial plantar artery 4) first plantar metatarsal artery

10. descending portion of the first dorsal metatarsal artery 11. common plantar haIlucal artery 12. medial and 1ateIal hallucal arteries with transverse anastomotic branch 13. transverse anastomotic branch 14. collateral arteries of the second toe

Il:-~ofJ

.ll-T--............,;.

~--cp...".

t,---'r----H~~~

l'-----4---Hi---T.V E:-~-&-orjj II--~;..r.;-"" ~,--riiii~

240

-"- ... ~-.. ~ ... --

) BUNION SURGERY

RADIOWGY OF THE FIRST RAY

Metatarsus AMJdns Angle a) measumd on a DP view b) formed by a line perpendicular

to the bisection of the lesser tarsus and a line Jepresenring the lesser metataISus

c) the lesser metataISus is represen1ed by the bisection of the dorsal longitudinal axis of the shaft of the second meIatarsal

d) the normal metatarsus adductus angle is 15

e) as the foot becomes more adducted,

this angle increases and a greater chance exists for abductus deformi1;r at the first MIP joint

Metatarsal Prolusion Distance a) measured on a DP view b) Iepleseuts the distance between two art:S

and demonsttates the length between the first and second metatarsals

c) a positive millimeter distance is used to indicate that the first metatarsal is longer than the second metatarsal

d) a negative millimeter distance is used to indicate that the first metatarsal is shorter than the second metatarsal

e) normal range of the metatarsal protrusion dist;lJJre is +/- 2 mm

f) ideally, the length of the first metatarsal should be about the length of the tbiId metatarsal

Metatarsal Split Distance a) measures the split between the first

and second metatarsals b) measured from the most lateIal aspect of

the first metatarsal base to the medial cortex of the second metatarsal

c) measurement must be made parallel to the bisection of the second metatarsal

d) 2 mm or greater is significant e) important in evaluating soft tissue

deforming forces at the metatarsal­ameiformjoint

241

) Proximal Articular Set Angle a) fonned by a line drawn perpendicular

to effective articular cartilage of the head of the first metatarsal and line representing 10ngibJdjnaJ

bisection of the first metatarsaI b) if the angle measured is greater than

7.5 • adaptive changes have taken place at the first metatarsal head, which indicates a structural adaptation of the articular cartilage

c) this indicates a structural deformity and not a positional one

Distal Articular Set Angle a) on a DP view, it is formed by a line

drawn perpendicular to the effective articular cartilage of the base of the proximal phalanx

b) represents structUIal adaptation of the base of proximal phalanx on the shaft

c) abnormal Jateral epiphyseal closure at the base of the proximal phalanx, which causes more gIO\\th medially with a resulting bowing of the s.baft may alter this angle

First Metatarsophalang Joint Position a) the joint position on a DP view is a comparison of lines representing the effective articular cartilage of the first metatarsal head and a line Ieplesenting the effective articular cartilage at the base of the proximal phalanx

congruent joint: a joint is said to be congruent when the two articular swfaces are wholey articular and the joint space is equal

deviated joint: a joint is said to be deviated when the lines representing the articular surfaces intersect outside of the joint

subluxed joint: a joint is said to be subluxed when the lines Jeplesenting the articular surfaces intersect inside the joint

b) a congruent first M1P joint wither represents a nonnal first M1P joint or a structural adaptation of the first metatarsal latemlly, creating hallux abductus deformity c) a deviated or a subluxedjoint occmring at the first MIP joint indicates a positional deformity

243

Determination of Procedure I. angular deformities - post-op goal to get 1M angie to 0

A 1M angles up to 16 usually respond to head procaiures B. 1M angles above 16-18 require base proa::dures

ll. increased PASA A Reverdin B. Peabody C. bipJanar Austin D. offset V with swivel

m. HA V with metatarsus adductus A HA V deformity is accentuated in presence of metatarsusaddnchlS: however, the 1M angle may appear

IV.

Y.

VI.

B.

A B.

A B. C.

A B. e. D.

Normal or slightly incresed consider distance between first and second metataIsal heads when choosing procedure

condition of the joint Iadiographic changes clinical exam (ie-I3llge of motion, pain, crepitus)

condition of the bone presence of cystic degeneration excessive sclerosis mar.ked osteoporosis

individual patient oornmeters age ambulatory status medical status

Vil. compliance

foot type

hypermobility elevatus

A B.

*REMEMBER: do not treat the x-rays*

Soft Tissue Correction (capsule tendon balance procedures)

I. Silver (1923) A resection dorsomedial eminence of first metatarsal bead B. lateral capsulotomy and medial capsulorraphy

ll. McBride (1928) A resection dorsomedial eminence of first metatarsal head B. lateral capsulotomy with removal of fibular sesamoid C. transfer the conjoined tendon of adductor hallucis and lateral bead of FHB to dorsolateral aspect of the first

metatarsal head

ill. Hiss A resection dorsomedial eminence of first metatarsal head B. lateral capsulotomy C. transfer abductor hallucis from plantar to medial to the first MPJ (abductor tendon sutured into hole in base

of proximal phalanx; acts as ligament to strengthen capsule medially)

245

BUNION SURGERY

RADIOLOGY OF THE FIRST RAY

Metatarsus Addndus Angle a) measured on a DPview b) formed by a line perpendicular

to the bisection of the lesser tarsus and a line lepIesenting the lesser metatatsus

c) the lesser metataISUs is represented by the bisection of the dorsal longitudinal axis of the shaft of the second metatatsal

d) the normal metatatsus adductus angle is 15

e) as the foot becomes more adducted, this angle increases and a greater chance exists for abduclus deformity at the first MIP joint

Metatarsal Protusion Distance a) measured on a DP view b) lepresents the distance between two arcs

and demonstrates the length between the first and second metatarsals

c) a positive mi11imeter distance is used to indicate that the first metatarsal is longer than the second metatarsal

d) a negative mi11imeter distance is used to indicate that the fust metataIsal is shorter than the second metatarsal

e) normal mnge of the metatarsal protrusion distance is +/- 2 mm

f) ideally, the length of the first metatarsal should be about the length of the thitd metatarsal

Metatarsal Split Distance a) measures the split between the first

and second metatarsals b) measured from the most lateral aspect of

the first metatarsal base to the medial cortex of the second metatarsal

c) measurement must be made pmillel to the bisection of the second metatarsal

d) 2 mm or greater is significant e) important in evaluating soft tissue

deforming forces at the metatarsal­cuneiform joint

241

Metatarsal Deformation Angle a) angle fonned by the bisection of the

proximal metatarsal base and the shaft of the first metatarsa1

b) measures any osseous defonuity of the metatarsal shaft relative to the base

c) nonnal is 8 or less d) greater than 8 indicates a

structural defonuity within the metatarsal shaft

Metatarsa1-Cuneifonu Angle a) tills angle is fonned by the proximal

first metatarsal base facet and the medial cuneifonn distal articular facet

b) nonnal is 25 or less c) greater than 25 implies a structural

defonuity

Hallux Abdnctus Interphalangeal Angle a) measured on a DP view b) represents the angle made by the

bisections of the distal phalanx and the bisection of the proximal phalanx

c) nonnal is 0-10 d) an increase in tllls angle represents

eitIler a congeIlltal bowing of the distal phalanx or a transverse deviation of the distal phalanx on tile proximal phalanx

e) may also increase when the motion at tile first MIP joint is limited (ie-hallux limitus or rigidns)

Hallux Abdnctus Angle a) on a DPview, it is the angle resulting

from the bisection of tile dorsal longitudinal axis of the proximal phalanx and the first metatarsal

b) nonnal is 10-15 c) an abnonnally high angle indicates a

positional defonnity at the first MIPjoint

d) this angle increases in all cases of HA V defonuities

242

Proximal ArtiaJ1ar Set Angle

a) formed by a line drawn perpendicular to effective articular cartilage of the head of the first metatarsal and line representing longitudinaJ bisection of the first metatarsal

b) if the angle measured ~ greater than 7.5 , adaptive changes have taken place at the first metatarsal head, which indicates a structural adaptation of the articu1ar cartilage

c) this indicates a structUIal deformity and not a positional one

Distal Artiwlar Set Angle

a) on a DP view, it is formed by a line drawn petpendicular to the effective articular cartiJage of the 00se of the proximal phalanx

b) represents structural adaptation of the 00se ofproximal phalanx on the shaft

c) abnonnal Jateral epiphyseal closure at the 00se of the proximal pba1anx, which causes more growth medially with a resulting bowing of the shaft, may alter this angle

First MetltarsQphaJangeal Joint Position a) the joint position on a DP view is a comparison of lines representing the effective articular cartilage of the first metatarsal head and a line representing the effective artiwlar cartilage at the 00se of the proximal pbalanx

congruent joint: . a joint is said to be congruent when the two artiwlar surfuces are wholey articular and the joint space is equal

deviated joint: a joint is said to be deviated when the lines representing the articular surfaces intersect outside of the joint

subluxed joint: a joint is said to be subluxed when the lines representing the articular surfaces intersect inside the joint

b) a congruent first MIP joint wither represents a normal first M1P joint or a structnral adaptation of the first metatarsal laterally, creating hallux abductus defonnity c) a deviated or a subluxed joint occmring at the first M1P joint indicates a positional deformity

243

Shape of the First Metatarsal Head (seen on DP vie,,\') a) Round

1. round first metatarsal head creates a high degree of instability at the first MTP joint

2. the hallux is prone to drift laterally on a convex surface

b) Square first metatarsal head 1. provides more stable joint

configuration versus a round first metatarsal head

c) Square with a ridge 1. represents square metatarsal head

with an oblique or central ridge 2. stable configuration; helps

prevent lateral de",iation of the hallux

3. a compensatory hallux interphalangeus may be seen with this

Tibial Sesamoid Position a) measured from 1-7 relative to the

longitudinal bisection of the first metatarsal

b) measured from medial to lateral; the normal tibial sesamoid position is 3

c) when the tIbial sesamoid position is 4, the sesamoid is overriding the crista of the first metatarsal, causing DID

d) the tIbial sesamoid could dislocate past

the crista without eroding it: this is best evaluated on a sesamoid axial view

Metatarsus Primus Adductus Angle a) formed by the bisections of the first

and second metatarsals longitudinally b) represents a deviation of the first

metatarsal in a transverse plane medially c) rectus foot type, 1M angle = 8-12 d) adducted foot type, IM angle = 8-10 e) the 1M angle could be increased in a

congenitally bowed metatarsal or a premature closure of the medial epiphysis secondary to trauma

f) in post-operative films. if the foot is held supinated secondary to guarding, false positive decrease in IM angle will be noted

g) this angle should be assessed on weigllt -bearing views h) os intermetatarseunl found between the 00ses of the first and second

metatarsals could contribute to an increase in the IM angle and to a hallux valgus deformity

244

IV. component procedures A. adductor transfer B. various capsulorraphies

1. frontal plane versus transverse plane correction 2. Washington monument 3. elliptical 4. "T" shaped 5. "U" shaped 6. inverted "L"

C. EHL tendon lengthening D. EHB tenotomy

Phalangeal Osteotomy

1. A B. C. D.

II. A. B. c.

proximal Akin corrects for DASA osteotomy perfomled 5-10 nml distal to MPJ proximal osteotomy parallel to surface of the base of the proximal phal3.IL'\: distal osteotomy perpendicular to long axis of the shaft

distal Akin corrects for hallux abductus interphalangeus osteotomy perfomled at distal end of proximal phalanx fixation of either osteotomy varies (ie-absorbable pin; k-wire; screw; suture; monofilament wire)

Capital Osteotomies

1. A. B.

C. II.

A B. C.

Austin (1974) resection medial eminence; lateral release osteotomy perfonned in the center of metatarsal head with 60 degree angle between the anIlS

I. unicorrectional: nonnaIizes 1M angle 2. bicorrectional: nonnaIizes 1M angle and P ASA

axis guide - utilized to lengthen .. shorten, plantarflex or dorsiflex Reverdin (1881)

primarily used in conjunction with other procedures by itself - only corrects hallux abductus (P ASA) osteotomy

1. performed in metaphyseal bone 2. first cut is 1 em proximal and parallel to the articular surface 3. second cut is perpendicular to long axis of metatarsal shaft (wedge shaped with base medial) 4. lateral cortex intact

ill. Reverdin-Green (1977) A modification: initial cut is made parnllel to the weightbearing surface being sure to exit just proximal to the

articular swfuce of the first metatarsal head B. avoids plantar sesamoidal grooves of the metatarsal head C. avoids scoring the sesamoid apparatus D. sanle indications as for the Reverdin

IV. Reverdin-Laird (1977) A modification ofReverdin-Green: lateral cortex is cut allowing lateral translation of the capital fragment B. corrects for P ASA and 1M angle

246

V. Reverdin-Todd (1978)

A modification: proximal osteotomy is either angled dorsal~ to plantar-proximal (pIantarflexes capital fragment) or dorsal-proximal to plantar~ (dorsiflexes capital fragment)

B. distal osteotomy is still parallel to the articular surface and proximal osteotomy parallel to the weightbearing surface

Neck/Metatarsal Osteotomies

I. Peabody

n.

m.

N.

v.

A same procedure as Reverdin except that the osteotomy is performed at the anatomical neck B. disadvantages over Reverdin -

A B. e.

D.

A B. e. D. E.

A

B. e.

A

B. e.

1. poorer healing area ofbone 2. requires secure fixation or non-weightbearing status

DRATO(Smith, 1971)

distal osteotomy - perpendicular to the long axis of the first metatarsal; through and through proximal osteotomy - angled proximal-medial to distal-lateral (to produce PASA correction) dorsiflexes capital fragment to place the articular cartilage in a more fimctional postiion, and thus,

attenpts to increase dorsiflexion at the first MPJ

1. 2. 3. 4.

l. 2. 3. 4.

disadvantages poor healing bone highly unstable requires secure fixation or non-weightbearing status technically difficult

()ffi;et V (Vogler)

apex of osteotomy at metaphyseal~yseal junction (versus center of metatarsal head with Austin) angle of winge; is less than 60 degrees longer osteotomy allows for greater bone-to-bone contact length of dorsal wing determines amount of swivel posSIble advantages

can correct for 1M angle and hallux abductus good bone-to-bone contact ease offixation (ie-pin; screw) patient can be weightbearing

Kalish apex of osteotomy in center of circle around metatarsal head; as with Austin procedure (metaphyseal

osteotomy)

1. 2. .., .J.

long dorsal wing allows for screw fixation unable to swivel capital fragment to correct P ASA

Scarf or Z osteotomy (diaphvseal osteotomy) two ways to perform osteotomy

distal cut dorsal and proximal cut plantar (avoids posSIbility of scoring sesamoid apparatus; easier to fixate) distal cut plantar and proximal cut dorsal

similar advantages and uses to Offset V trough effect: dorsal segment of the "Z" (cortical bone) wants to sink down into the plantar segment when

screws are tightened down

247

VI. Ludloff(1918) A oblique osteotomy oriented dorsal-proximal to plantar-distal exitingjust proximal to metatarsal head B. unstable osteotomy configuration e. can swivel for PASA correction

VII. Mall (1926) A oblique osteotomy oriented dorsal-distal to plantar-proximal, exiting just proximal to metatarsal-ameiform

joint (osteotomy exactly opposite to Ludlom B. unstable osteotomy configuration e. advantages:

D.

1. both Ludloff and Mau are higbly versatile osteotomies 2. the capital fragment can be elevated, depressed, lengthened, shortened, adducted or abducted 3. good degree ofbone contact is maintained re~ess of capital fragment displacement 4. the Mau osteotomy would appear easier to fixate (especially if using screws) and bave somewhat

better stability aginst the forces of weightbearing versus the Ludloff

1. 2. ... J.

disadvantages diaphyseal osteotomies - poor healing bone proximal location of osteotomy demands fixation and/or non-weightbearing status requires significant dissection about the first ray

VIII. Hohmann (1924)

IX.

A

B.

e.

D.

A B. e. D.

1. 2. 3.

1. 2.

trapezoidal osteotomy (with base oriented medially) made at the level of the metatarsal neck; through and through osteotomy advantages

capital fragment rotated medially to correct for hallux abductus capital fragment could also be translated laterally (1M angle correction) and/or dorsally or plantarly shortening of the first metatarsal could decompress the MPJ and slightly increase motion

disadvantages significant shortening of first metatarsal unstable osteotomy; requires fixation and non-weightbearing status

original procedure performed outside capsule and medial eminence was not resected

Mitchell (1945) oblique osteotomy similar to Hohmann, except with lateral cortical shut intact originaly fixed with 1-0 chromic catgut similar indications and disadvantages as Hohmann indications: long first metatarsal

X. Wilson A oblique osteotomy oriented distal-medial to proximal-lateral (through and through) B. capital fragment is shifted proximally and laterally along the osteotomy e. capital fragment can also be translated dorsally or pIantarly D. disadvantages

1. poor healing bone 2. unstable; requires secure fixation and/or non-weightbearing status 3. produces significant shortening

248

Basal Osteotomies

PRINCIPLES OF THE BASE OS1EOTOMY

hinge axis concept • binge has an axis and anus • motion about the hinge occurs perpendicular to the axis of the hinge; keep hinge perpendicular to the

weightbearing surface so the distal segment remains parallel to the ground when osteotomy is closed

• binge axis must be perpendicular to the ground in the sagittal plane, to avoid iatrogenically induced metatarsal elevation

• dorsomedial cortical hinge plantarflexes the distal segment upon closure • plantar medial cortical hinge (runs dorsomedial to plantar lateral) dorsiflexes the distal segment upon

closure / ..

"

complications • first ray elevatus • lesser metatarsalgia

• hallux varus

PROCEDURES

1. A B. c.

l. 2. 3.

D. 1. 2. 3.

Transverse closing base wedge (Loison, 190 1) osteotomy originally descnbed as being at a point just distal to the insertion of the long peroneal tendon base lateral with medial cortical apex intact advantages

longer lever arm allows for correction of significant IM angle deviations good vascular bone relatively little dissection required

disadvantages proximal location of osteotomy (longer lever arm) demands fixation and non-weightbearing status greater potential for disturbing blood supply about the first metatarsal requires pttient compliance

249

ll. A

B. 1. 2. 3.

e. 1.

D. 1. 2.

Ill. A

B. e. D. E.

Oblique closing base wedge (Juvarra, 1919) originally descnbed as a "double oblique section of the metatarsal" perfonlled at the junction of the middle and proximal thirds modification:

oblique osteotomy from proximal-medial to distal-lateral proximal cortical apex is maintained fixation with one or two screws

disadvantages requires more dissection than Loison osteotomy

advantages easier to fixate more bone-to-bone contact

Opening base wedge (Trethowan. 1921) linear osteotomy from medial to lateral across the base of the first metatrsal keeping the lateral cortical binge intact fashioned the resected medial eminence into a wedge and forced it into the osteotomy site good for maintaining or increasing length of first ray must be cognizant of jamming at the MP]

the high level of load at the proximal aspect of the first metatarsal often causes the autograft to resorb

IV. Osteotomy (Kotzenberg) A osteotomy oriented in transverse plane with apex proximal

V. Crescentic (Weinstock) A osteotomy created approximately 1.5 em distal to the first metatarsal-cuneifonn joint B. e.

when looking at the metatarsal from dorsal to plantar, the concave portion of the osteotomy faces distally the distal segment of the first metatarsal is rotated until the desired correction is attained

D. the dorsal segment can also be dorsiflexed or plantarflexed as necessary E. results in less shortening than with CBWO F. fixation and immobilization is required G. cmplications

1. elevatus 2. difficult to fixate 3. inaccurate reduction of the IM angle

VI. Epiphysiodesis A fuse lateral side of epiphysis during growth years B. (allows gro\\1b on the medial side to reduce the IM angle)

Combination procedures

I. Logrescino (1948) A double osteotomy of first metatarsal

1. for short first metatarsal: Reverdin + Trethowan 2. for long first metatarsal: Reverdin + Loison

B. advantages 1. corrects for high IM angle and deviated PASA 2. both osteotomies are placed in good metaphyseal bone

ll. 3:1 A capsule tendon balance procedure (Silver or McBride) B. closing abductOIy base wedge osteotomy C. proximal Akin osteotomy

250

Arthrodeses I. ~(1952)

II.

A head of the first metatarsal is &shioned into a peg B. hole is fusliioned into the base of the proximal phalanx C. the bones are implCted and a compression screw is driven from the plantar aspect of the base of the proximal

pha1anx into the shaft of the first metatarsal D. McKeever advised 15-20 ofMPJ extension with 15 of hallux abductus in men and 15-25 ofMPJ extension

with 25 ofbal1ux abductus in women E. Indications

1. grossly arthritic joint in a person whom you deem. too young to have a Keller artbroplasty 2. salvage procedure after unsuccessful Keller 3. severe RA with Iateml deviation of the toes

F. Advantages

A B.

C.

D.

1. weight-bearing function of the great toe is maintained 2. lessen the tendency to develop lesser metatarsalgia

1.

1. 2. 3. 4. 5. 6.

1. 2. 3. 4.

Lapidus (1934)

denuded cartilage offfirst metatarsal~ormjoint decorticated JateIal aspect of the base of the first metatarsal and the CKljacent surface of the second metatarsal base

packed bone chips obtained from the resected medial eminence in the space between the first and second metatarsal bases

Indications pain on motion offirst metatarsal-cuneiformjoint h}]JerD1Obility of the first metatarsal-omeiform joint DID of the :first metatarsal-cuneiform. joint velY long first ray excessive first metatarsal elevation or plantarllexion excessive angulation or gapping at the first metatarsal-cuneiform. joint

Disadvantages produces marlred shortening of the first ray comparatively long post-q> period increased potential for distUIbing the blood supply about the first metatarsal technically difficult

ArthropIasty oftbe First MPJ I. Keller

A technique 1. resection of one-fourth to one-tbird ofbase of the proximal phalanx, with cut perpendicu1ar to long axis

of the shaft 2. resection of medial eminence of first metatarsal head 3. medial capsulonaphy

B. eliminates reverse buckling forces across the first MPJ C. mainly reserved for elderly sedentaty population D. modifications

1. EHL lengthening to help prevent retraction of toe >sesamoid removal 2. pin fixation to maintain length 3. capsule interposition at MPJ 4. reauachment of short flexor tendon to stump of phalanx to increase stability of joint function

E. complications 1. cock-up hallux 2. Jack ofpurchase power 3. shortening of hallux 4. lesser metatarsalgia

251

II. A B.

Stone ---;;blique ostectomy oriented dorsal to plantar leaving plantar condyle and sesamoid apparatus intact

resection of medial eminence of first metatarsal head

ill. Mavo A excision of 5 mm of metatarsal head including the articular surfuce B. interpose capsule and bursal tissue between the metatarsal and base of proximal phalanx

Miscellaneous I. Opening wedge osteotomy of medial cuneifoIDl

A described for metatarsus adductus by Fowler B. bone graft may be allogenic or autogenic e. complications

1. overcorrection 2. nonunion 3. fracture of intermediate cuneifoIDl

Implants • simply intended to maintain space between bony surfaces • cannot correct for osseous deformity • any osseous deformity must first be corrected prior to implant use • osteotomies must be precise to prevent eccentric loading. of the implant • good bone stock is required to receive stem of implant • foreign body reaction etiher due to primary rejection or to inlplant breakdown with detritic synovitis is

possIble • patients must be made aware of short lifespan (tempotaIy nature of the implant)

I. Hemi (Swanson, 1971) [Dow Coming Wright]

II.

ill.

IV.

A originally designed to supplement the Keller bunionectomy B. medical grade, high performance silicone elastomer C. flat base - provides no correction for PASA D. available in titanium as well

A B.

A B.

e. l. 2. .., J.

A B. e.

HeIDi-Angled (Well modification) [Dow Corning Wright] base is angled - having increased depth on lateral side designed to articulate with an adapted metatarsal head (deviated P ASA)

Total Implant - Swanson Design (Dow Coming Wright) double stemmed implant resected surfaces ofbase of proximal phalanx and head of first metatarsal must be cut to lie flush with implant surfuce - eccentric load distribution will lead to early inlplant failure note:

again - the various osseous angular deformities ust be corrected prior to implant placement total inlplants cannot be used in the presence of cystic deformation of the first metatarsal head total joint implants available with titanium grommets which provide protective interface between bone

and implant

Total Implant - LaPorta Design [Sutter) proximal stem is angled 15 in sagittal plane to account for first metatarsal declination distal stem is angled 10 laterally to provide for physiological hallux abductus binge allows for 60 of motion

252

V. Total Implant - Lawrence Design [Sutterl A proximal stem also angled 15 in the sagittal plane B. distal stem is not angled (neutral) C. binge allows for 85 of motion D. allows for bevelled phalangeal base resection in attempt to preserve plantar insertions

Two Component Total Joint Systems

1. Koenig Total Toe lBiometl A noncemented system; the metatarsal component has a plantar ledge to help translate loading forces to

the metatarsal B. the metatarsal component is a titanium alloy hardened with ionized nitrogen to improve wear

characteristics C. the phalangeal component is ultrahigh molecular weiglu polyethylene (UHMW) and is available with a

titanium backing

II. BioAction Great Toe Implant IMicroAirel A cemented system B. the metatarsal component is cobalt chrome and angled for right and left geometry (no plantar ledge) c. the phalangeal component is ultra high molecular weight polyethylene with titanium backing is

available angled

AUSTIN

1 Aust.in

253

MITCHELL WILSON

/ ( .... , .. TRETHOWAN JUVARA JUV.AJiA (MODIFIED)

~~~ OPENING BASE WEDGE CRESCENTIC McKEEVER

LAPIDUS LOGRESCINO 3:1

254

Sf; STONE OPENING WEDGE MEDIAL CUNEIFORM

HEMI IMPlANT

~ ~

HEMIANGLED TOTAL IMPLANT IMPLANT (Swanson)

MAYO

PEABODY

255

REVERDIN-GREEN-LAIRD

HOHMAN

~ ~f:

o REVERDIN-TODD

256

Juvenile Hallux Abductovalgus

Def'mition: aberration in the function or alignment of the first metatarsophalangeal joint in persons below the age of twenty.

Incidence -Females> males -Significant positive family inheritance (maternal transmission)

Etiology -Autosomal dominance with incomplete penetrance -Biomechanical: pes planus/limb length discrepancy/STJ pronation/equinus -Metatarsal primus varusladductus -Neuromuscular deformitieslligamentous laxity -High rate of recurrence

Adult vs. juvenile HA V -Juvenile: less valgus rotation of hallux, general absence of chronic tissue reaction and degenerative joint disease, few adaptive changes of the first MIPJ (these are general guidelines, but not always the case)

Symptoms -Pain is not common -Deformation of shoe gear, difficulty fitting shoes -Concern with self image and appearance (common presentation age 11-14 y.o.) -Reluctance to engage in physical activity -Children <6 y.o. rarely have symptoms (usually present with concerned parent)

Staging of First MIPJ ROM Stage I: slight alxluction of the hallux with full ROM and presence of dorsomedial irritation of prominence Stage II: more advanced, greater transverse plane deviation, may be reduced passively with pain free and full

ROM Stage ill: greater deviation in the alignment of the first MIPJ, ROM in defornled position is full, but defonnity is

not passively reduCIble and all attempts to DF hallux on first metatarsal when the great toe is rectus results in "tracking" back into deformed position. This is indicative of fixed adaptive contraction

within the first intermetatarsal space. Usually with moderate to severe lateral displacement of sesamiods

Stage IV: rare, lack of ROM, crepitus, pain in first MIPJ

Radiographs -Metatarsus adductus/true 1M angle -PASAlDASNdistal metatarsal articular angle (DMAA) -Metatarsallengthlparabola -Hallux length -SesanlOid position

Treatment -Conservative:

-splints, toe wedges, bunion shields, 'wider shoes -orthoses

Surgical intervention: -Indications:

-pain, rapid progression of deformity, severe deformity, failure of conservative treatment, cosmetic concerns, secondary deformity of the lesser digits

257

-Goals: -restoration, improvement, and preservation of joint function -relief of pain -restoration of proper forefoot dynamics -improved cosmetic appearance offoot

-When? -< 6 y.o. : 40-50% of total metatarsal growth remains; surgery only in severe defonnities -6-10 y.o. : 60-80% of metatarsal length attained, physeal plate clearly defined radiographically,

surgery for severe defonnity and in cases in which significant adaptive changes have occurred in the articular surfaces of the MTPJ on radiographs

-10-15 y.o.: ideal period; 90% of normal metatarsal length attained in most boys by age 12 and 95% in girls the same age; osseous, cartilaginous, and collagenous tissues have relative plastic qualities that achieve excellent repair and adaptation

-Procedures: -soft tissue: ineffective -opening wedge osteotomy of medial cuneifonn -Lapidus -epiphysiodesis/epiphyseal stapling -digital procedures: Akin -distal first metatarsal osteotomy: Mitchell, Austin, Reverdin -crescentic osteotomy

-*closing base wedge osteotomy*

HALLUX LIMITUS

Definition a) hallux limitus: decrease in the range of motion at the first MTP joint b) halllLX rigidus: absence of motion at first MTP joint c) nonnal first MTP joint ROM: dorsiflexion = 65-75

plantarflexion = 40

Etiology a) hypennobile first ray b) immobile first ray c) excessively long first ray d) first metatarsal elevatus e) degenerative joint disease f) neoplasms g) trauma h) septic arthritis i) iatrogenic

(ie<orrecting functionally adapted joint with soft tissue release; failure to correct pre~xisting dorsiflexed first metatarsal or abnoramlly long first ray, over aggressive medial capsulorraphy; displacement of osteotomy; etc)

j) neuromuscular disorders k) systemic arthritides (ie-RA; psoriatic; gouty arthritis) 1) osteonecrosis secondary to avascularity of metatarsal head m) foreign bodies (ie-implants)

258

Classification of Hallux Limitus a) primary vs seamdary

1. primaIy hallux limitus >occurs in adolescent patients and is associated with a long first metatarsal >congenitally long first metatarsal

2. secondaIy hallux limitus >occurs in older patients >usually caused by DID, trauma, septic arthritis and systemic arthritides

b) structural vs functional 1. structural hallux limitus

>dorsiflexion of first MIP joint is decreased when the forefoot is both loaded and unloaded 2. functional hallux limitus

>dorsiflexion of first MIP joint is decrreased only when the forefoot is loaded

Clinical Findings a) symptoms

1. gradual onset of pain and limitation offirst MPJ ROM 2. pain localized to dorsal aspect of first MIP joint 3. pain experienced with ambu1ation and prolonged weigbtbearing

b) physical examination 1. dorsal or dorsomedial prominence of first MPJ

(aka-dorsal bunion) 2. hallux position is most commonly rectus 3. tenderness with passive dorsiflexion of hallux 4. test the first MP] dorsiflexion with the forefoot loaded and unloaded 5. excessive hallux IPJ dorsiflexion associated with:

-EHLspasm -ganglion cyst or adventious bursa associated with EHL tendon secondruy to irritation from shoe gear -plantarmedialIPJ hyperkeratotic lesion

(aka-pinch callus) 6. check sesamoid mobility:

>load the first ray and palpate the sesamoid apparatus while dorsiflexing the MPJ >arthrodesed or fibrosed sesamoids prevent normal and any MPJ dorsiflexion

7. antalgic, apropulsive gait with an early heel-off

Radiographic Findings a) nonuniform joint space narrowing b) flattening of the first metatarsal head c) osteophytes on first metatarsal head and base of proximal phalanx (aka4rsal flag sign) d) subchondral sclerosis e) loose bodies (joint mice) within the first ray f) first metatarsal elevatus (lateral view)

1. proximal phalanx articulates with the plantar aspect of the first metatarsal head 2. bisection of the first metatarsal is superior to the talar bisection {lateral view)

g) positive metatarsal protrusion distance

Surgical Management of Hallux Limitus a) ol:!iectives

1. removal of osteophytic spurring 2. creration of slack in the fle.xor apparatus 3. shortening of an excessively long first metatarsal

259

4. plantarflexion of an ele\ 'ated first metatarsal 5. reorientation of first metatarsal head articular surface

b) joint presen'ing procedures 1. cheilectomy (aka-:ioint remodeling)

>removal of osteophytic proliferation on the first metatarsal head or base of the proximal phalanx 2. Kessel & Bonney

>dorsiflexory osteotomy ofbase of the proximal phalaILX 3. Regnauld (aka-Mexican hat procedure; enclavement;

auto-implant; joint decompression) >base of proximal phalanx is resected and fashioned into a peg then reinserted into the proximal phalanx >LaPorta modification utilizes the resected proximal phalangeal base as the hole and the distal component

of the phalanx as the peg 4. Hoillruum type procedure

>indicated for long first metatarsal etiology 5. Waterman

>dorsiflexory osteotomy of the first metatarsal head >through-and-through osteotomy 0.5 em proxiam1 to the articular cartilage which converts plantarflexory

ROM to dorsiflexoI)' ROM >increases joint ROM by reducing the internal cubic content of first MfP joint

6. modified Waterman >dorsiflexory wedge osteotomy of the first metatarsal head leaving plantar articular cartilage intact

7. Waterman-Green >shortens and plantarflexes the first metatarsal >involves two osteotornies -

-trapezoidal wedge wider medially perfOIDled in dorsal to plantar direction, 0.5 cm proximal to articular cartilage -oblique, transverse osteotomy (through and through) 45 to the trapezoid which avoids the plantar articular cartilage

8. Youngswick modification of the Austin procedure 9. dorsal "V" osteotomy 10. plantarflexory wedge osteotomy

>Van Ness [transverse osteotomy] >plantar closing wedge osteotomy

II. Cotton >opening wedge osteotomy of the medial cuneifurm

(dorsal based wedge plantarflexes first ray) 12. reverse Cotton

>plantar based wedge osteotomy of the medial cuneiform to dorsiflex first ray

13. Lambrinudi >plantarflexory wedge osteotomy of the base of the first metatarsal to correct metataraI elevatus

14. sagittal Logriscino >Waterman + Lambrinudi

c) Joint destructive procedures I. Keller arthroplasty

>resection of one-third of the base of proximal phalanx 2. Implant arthroplasty

>totaI or herni-implant (with or "Without grommets) >must surgically address IDlY first metatarsal deformities for implant to succeed

3. Stone >dorsal to plantar wedge resection of one-fourth of first metatarsal head

260

4. Mayo >excision of 5 mm of first metat:ar5al head including the articular surface

5. McKeever arthrodesis >fusion of metatarsa1-phaJangeal joint

6. Lapidus arthrodesis >fusion of metatarsa1-cuneiform joint

Post-Operative Management a) biotm::banicaJ

1. orthotics 2. ptdding; aa:ommodative devices

b) continuous passive motion 1. excellent form of therapy which should be started immediately after surgery 2. hallux CPM machines available

c) intermittent active motion 1. most oommon type of therapy 2. usually instituted after one week of immobilization post-operntively 3. patient is instructed to stabilize proximally (first metatarsal) and to gently dorsiflexJp1antarllex to tolerance for a

few minutes daily d) there is no substitution for recognizing the etiology of the deformity and correcting the problem; not just performing

surgety to "soothe" symptoms

~c;::=3 Cl'

CHEILECTOMY KESSEL & BONNEY ~v REGNAULD

~ eo WATERMAN MODIFIED WATERMAN

WATERMAN-GREEN

R YOUNGSWlCK

DORSAL V OSTEOTOMY ~J .... conON

261

~~~ '-lAN NESS PLANTAR CLOSING WEDGE

(LAMBRINUDI) JUVARA (MODIFIED)

~ A-::::\ ~~q~~

HOHMANN TYPE OSTEOTOMY

HALLUX VARUS Definition a) deviation ofthe hallux at the first metatarsophalangeal joint

COMBINATION (HOHMANN + WATERMAN)

b) may exist as a transverse plane deformity of hallux adductus or present as an adductus, varus and malleus deformity

Classification a) congenital hallux varus

1. primaIy: an isolated deformity 2. secondary: associated with equinovarus deformity

b) acquired hallux varus 1. static: muscle balance undistUIbed

(ie-metatarsal osteotomy) 2. dynamic: muscular imbalance (ie-adductor transfer)

Etiology a) excessive resection of the medial eminence with disruption of the sagittal groove b) medially sublu..xed tibial sesamoid c) excision of the :fibular sesamoid d) overzealous medial capsulorraphy e) medial malposition of the sesamoid apparatus after adductor tendon transfer f) muscular imbalance through disruption of both the adductor hallucis and lateral head ofFHB g) overcorrection of the intermetatarsal angle by osteotomy h) overcorrection of the proximal articular set angle (PASA) i) aggressive post-operative bandaging and splinting

Symptoms of Hallux Varus a) histOIY ofHA V surgery b) unable to wear conventional shoe gear comfortably c) prin present along medial aspect of hallu..x secondary to shoe pressure d) prin along the medial aspect of the arch secondary to muscle contracture e) pain at the first MPJ with or without shoe gear

262

Clinical Signs of Hallux Varus a) adducted position or varus rotation of the hallux b) contracture at the IPJ or involving the EHL or abductor hallucis tendons (cocked-up hallux) c) pain on palpation of abductor hallucis d) pain and crepitus at the first ray e) hallux limitus or rigidus

Radiographic Signs of Hallux Varus a) hallux adducted at the first MPJ b) staked head offirst metatarsal with a peeking tIbial sesamoid c) absent fibular sesamoid d) previous osteotomy of the first metatarsal e) reduced or negative 1M angle f) negative proximal articu1ar set angle g) arthritic changes at the first MPJ and/or IPJ of the hallux

Correction of Hallux Varus a) conservative

1. abductovalgus strapping and splinting b) surgical

I. soft tissue release >medial capsulotomy >JateI3l capsulorrnphy

2. dynamic soft tissue procXldures >abductor hallucis tendon transfer >retransfer adductor haIlucis tendon laterally

3. osseous procedures >correct abnormal 1M angle or PASA (ie-reverse Austin)

4. joint destructive procedures >arthroplasty (ie-Keller,. KeUer with implant) >arthrodesis (ie-McKeever)

c) step-wise surgical approach 1. total soft tissue release at the first MPJ 2. medial capsulotomy 3. tibial sesamoidectomy (if30-500Al of the tIbial sesamoid is peeking medially) 4. address abductor hallucis as a deforming force (t:mnsfer of abductor ballucis to the pIantar-JateI3l flexor

apparatus and Iateral base of the proximal phalanx) 5. osseous correction

>determine the level of the osseous deformity >revise the previous first metatarsal osteotomy >if the 1M angle is negative, must reverse the overcorrection with apploptiate osteotomy

(ie-reverse Austin, reverse Offset Y, reverse CBWO) 6. arthroplasty of the first MPJ for severe deformity and for non-functional joint SlII'fuces

>Keller >Keller with berni-implant or total implant >Keller with fusion of hallux IPJ

7. arthrodesis of the first MPJ >McKeever >Lapidus

263

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BONE GRAFflNG

Bone Graft Indications 1. Induction of new bone formation: the process of osteogenesis, the stimulation of new bone formation, is

an important characteristic of certain bone grafts. The property is useful in the treatment of delayed unions, nonunions and arthrodesis by bone grafting techniques. .

2. Immobilization: bone grafting in combination with rigid internal fixation will aid in stabilization of arthrodesis sites and unstable fmcture sites.

3. Defect replacement: a major use ofbone grafts are to replace Jarge segments of tr.wmatically lost or surgically resected bone in order to maintain function and length of the affected segment.

Bone Graft Healing In order for bone grafts to heal properly they must be placed in a vascuJar recipient bed in close contact with surrounding bone fiagments and rigidly stabilized The graft site must be protected against external shearing forces to insure proper healing. The means by which bone grafts are inoorporated into host tissue differs for autogenous vet'SUS allogenic bone and for cortical versus cancellous bone, but generally involves five processes: I. vascular ingrowth: this process usually occurs within the first or second week following grafting.

Initially hemostasis and in:t1ammatory cell infiltration occur. In allogenic grafts the bone antigenicity may prolong the inflammatory process until host blocking antibodies can neutralize the graft antigens. Vascular budding quickly follows the inflammatory response.

2. osteoblast proliferation: once vascular ingrowth is eslab1ished, the osteoprogenitor cells or mesenchymal pericytes differentiate into osetoblasts and begin new bone formation.

3. osteoinduction: the process by which nonosseous tissue is induced to produce bone. The exact mecbanism is unknown., however, Urist descnbes a bone morphogenic protein present in bone matrix that acts as an inductor substance.

4. osteoconduction: the process in which the bone graft functions as a scaffold or conduit for migration of new bone as it rep1aces necrotic "old" bone. Axhausen used the term creeping substitution to describe this process.

5. graft remodeling: a process that may last for several months and results in reformation of the graft in response to biomechanical forces in accordance with Wolffs law.

Types of Bone Grafts 1. autogenous bone grafts: autogenous grafts are considered to be superior, primarily because of cell

viability and iImmlllologic compatibility. Autogenous bone grafts are considered to be a true transplant because the tissue is viable and will continue to survive and grow in the recipient site. Autogenous grafts area primarily indicated for use in areas where vasculari1y is most important A disadvantage to autogenous bone grafting is the creation of a second surgi.cal site and the formation of a bone defect in that area. Specific types of autogenous bone grafts include:

a) cancellous autogenous bone grafts: a fragile lattice netwOIK which provides the largest amount of viable cells and inductive morphogenic protein. The lattice provides an ideal structure for ingrowth of new vessels filcilitating osteogenesis. Cancellous grafts are fur too fragile to lend any stability to the graft site, however, they heal quickly and become progressively stronger and therefore more radiodense as they heal. This type of graft is preferred for llOmmions especially avascular nonunions. b) cortical autogenous bone grafts: a dense, compact strudure which provides strength and stability to the graft site. Cortical grafts transfer very viable cells and incorporate slowly. Vascular penetration takes twice as long as cancellous bone because osteoclastic resorption must precede osteogenesis. In contrast to cancellous grafts, cortical grafts lose strength as they heal and becomes more radiolucent. Approximately 400/0 of their strength is lost within a six week to six month period Cortical grafts are ideal for areas where strength and stabilization are required. Cortical grafts also allow secure attachment of fixation devices. c) corticocancellous autogenous bone grafts: these types of grafts combine the strength of cortical bone with the rapid osteogenic capabilities of cancellous bone. The iliac crest is a common donor site for this type of graft. d) free vascularized autogenous grafts: this form of graft is a segment of bone with its nutrient artery and veins intact. Utilizing microsurgical techniques, the graft is harvested and reanastomosed

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usually in areas of large bony defects. The most common donor sites include the nbs and the shaft of the fibula. Incorporation of this fonn of graft, when rigidly stabilized, follows primary bone healing.

2. allogenic bone grafts: allografts are considered implants because the tissue is, for the most part, nonviable. Living allografts are rarely utilized primarily because of immunologic incompatibility leading to host tissue rejection and possible transfer of infectious disease. All donors must meet strict guidelines developed by the American Association of Tissue Banks. The donor must be free from malignancy, infection or transmiSSIble disease. The donor must also have no history of viral hepatitis, syphilis, malaria, tuberculosis, leprosy, severe trauma, drug overdose or poisoning. Most allograft bone is processed to reduce the risk: of disease transmission. There are several different types of allogenic bone grafts reflecting the modification process utilized:

a) frozen allograft: this type of allograft is removed via sterile technique or sterilized following harvesting by ethylene oxide gas, irradiation, autoclaving or prolonged antibiotic washes. Freezing is perfonned to prevent enzymatic degradation. The temperature utilized, must be -70 C or below. Freezing does not affect the biomechanical properties of the graft, however, little reduction of antigenicity is accomplished b) freeze-dried allografts: the process of freeze-drying removes 95% of the moisture in the graft. Through a process called lyophilization, the bone is stored in a vacuum with infinite shelf life. The process also reduces allograft antigenicity, however, torsional and bending strength is significantly decreased The tensile and compressive strength are affected very little. c) demineralized or decalcified allografts: this fonn of allograft was primarily designed to promote osteoinduction while decreasing antigenicity. Urist developed the Autolyzed Antigen - Extracted Bone Graft which strips the minerals from the bone exposing the bone morphogenic protein to induce new bone production. This type of graft is very malleable and incorporates quickly into host tissue. d) artificial allografts: many materials have been proposed, however, the most noteworthy is the hydroxyaratite implant. This material is osteoconductive, but does not stimulate osteogenesis or osteoinduction. Strength is excellent and little immunologic incompatibility is demonstrated

3. xenogenic bone grafts: not recommended for use currently, primarily because of immunologic incompatibility leading to foreign body reaction which inhibits osteogenesis. Two commercially available fonns of bovine bone graft are marlreted under the names Boplant and Kiel Bone.

4. 4. composite bone grafts: the combination of allogenic and autogenous bone grafts can be useful to take advantage each graft's special properties. Autogenous bone is highly osteogenic while allogenic bone is highly osteoinductive.

Tecbniques of Bone Grafting 1. onlay bone graft technique: described by Cambell, the technique utilizes a large autogenous cortical

bone graft to bridge a nonunion. The graft was then fixated in place with screws or wire. Prior to grafting, the nonunion fragments were decorticated via a bone chisel. Phemister descnbed an onlay bone graft which was not fixated and placed the graft ubperiosteally.

2. a) dual onlay bone graft technique: a modification of the onlay technique in which the nonunion is centered between two cortical grafts. The technique was indicated for use in difficult or unusual nonunioDS.

3. inlay bone graft technique: simply involves the formation of a slot or window in which the bone graft is placed

4. sliding bone graft technique: originally described by Gill, the technique involved creating a graft from the shaft of

5. a long bone approximately one-half the diameter in width. This graft was then moved forward across the nonunion/arthrodesis site onto the recipient fragment

6. 4. Papineau bone graft technique: originally descnbed for treatment of chronic osteomyelitis and infected nonunioDS. The necrotic bone was excised, then the wound was cleansed and allowed to granulate. Small pieces of cancellous bone are then packed into the bone cavity and the wound is closed. The technique was designed for rapid revascularization.

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Deminera1ized Bone Matrix <DBM)

An autologous bone alternative

Bone matrix

• Or~c • Collagen • Noncollagenous proteins

• Bone Morphogenetic Protein (BMP) • Inorganic (mineralized)

• Hydroxyappatite (calcium, phosphorus)

DBM-• Allograft bone containing only the organic matrix • Exposes non-collagenous proteins (BMP) to the osteogenic precursor cells • BMP has been shown to be osteoinductive

DBM function:

• Osteoinduction Process by which osteogenic precursor (mesenchymal) cells are stimuJated to differentiate into chondroblasts and ultimately into osteob1asts

DBM Prodncts: l. Grafton

• Gel

• Flex

• Putty

• Crunch 2. Dynagraft

• Gel

• Putty 3. Osteofil

• Gel 4. AIloMatrix

• Putty

Inferior Calcaneal Heel Spur and Plantar Fasciitis

Diagnosis a) pain on palpation of the medial aspect of the inferior aspect of the calcaneal tuberosity. b) post static dyskinesia: pain of the insertion of the plantar fuscia when first weight bearing after a period

of rest The pain is usually partly relieved by further activity. c) x-ray: spur may or may not be present

Pathogenesis Any or many of the following structures may be involved in pulling on the periosteum of the calcaneus. This leads to periostitis which produces pain. a) plantar fascia pull (most common) b) abductor hallucis c) flexor digitorum brevis d) long and short plantar ligaments

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Differential Diagnosis a) calcaneal apophysitis b) calcaneal fracture c) nerve enttapment: usually the medial plantar calcaneal nerve d) plantar fascial tear or herniation e) avulsion injury f) tumor g) acromegalic fat pad alteration h) connective tissue disorders with associated fat pad alterations or autoimmune arthritides (ie-rheumatoid

arthritis, Reiter's syndrome, psoriatic arthritis, ankylosing spondylitis) i) infection: soft tissue or osteomyelitis j) contusion k) tendinitis (ie-first layer plantar musculature)

Treatment Inferior heel spur syndrome and a plantar fasciitis are considered self-limiting entities and will resolve without treatment However, the course of spontaneous resolution is long and the pain can be very debilitating thus treatment is very often indicated

a) conservative 1. steroid injections 2. NSAIDs 3. padding and strapping (ie-low dye) 4. physical therapy 5. inunobilization: casting Oow priority since this treatment is also debilitating) 6. orthoses: can be used as treatment for the chronic variety as well for prevention of recurrence. b)~

1. Griffith: plantar U-shaped incision around the heel

2. Steindler: rotates the posterior aspect of the calcaneus forward into a notch in tmderside of the calcaneus need to do a tendo Achilles lengthening

3. Michele and Kruger: COtmtersinking, L-shaped osteotomy of the inferior calcaneus decreases the "high point"

4. Hassab and El Sherif: several drill holes into the calcaneus theory is that it reduces venous congestion of the calcaneus

5. Duvries: resect inferior calcaneal spur through a medial incision ...... '" .... :fasciotomy

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6. ENDOSCOPIC PLANTAR F ASCIOTOMY Indications -surgical alternative in patients with recalcitrant heel pain/pIantar fasciitis -patients should have a minimum 6 month attempt of conservative care

Advantages -faster recovery time -less post-op pain

Technique -PT and sural nerve block -incision placement

-anterior & inferior to medial calcaneal tubercle based on NWB lateral x-ray -5mm vertical stab incision -blunt dissection to plantar fascia

-instrumentslEndotrac system -fascial elevator -hook probe -slotted obturator/cannula -handles for hook & triangle blades

-resection of medial 113 to Yz of plantar fascia

Complications -Lateral column destabilization(most common)

-calcaneocuboid/midtarsal joint pain -peroneal tenosynovitis -sinus tarsi syndrome

-Medial column destabilization -central arch pain -intrinsic myositis -hammertoe

-Other -continued heel pain -infection -incision pain -nerve entrapment-rare -plantar fibroma

-MANAGEMENT OF CALCANEOCUBOID JOINT SYNDROME -several weeks of restricted /partial weight bearing -short leg weight bearing cast -stretching -night splint -NSAID/steroid injections -orthosis/cuboid pad -physical therapy -removable cast boot -NWB short leg cast 4-6 weeks

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METATARSAlrCUNEIFORM EXOSTOSIS

(aka-tarsal bossing; peak of Lampi ere)

Etiology a) hypennobility of the first ray creates jamming of the first metatarsocumeifonn joint b) jannning of the first metatarsocuneifonn joint causes dorsal osseous lipping at the joint and an arthritic

process within the joint. c) bump pain, tendonitis of the extensor hallucis longus tendon and neuritis of the dorsal intennediate

cutaneous nerve can result from shoe pressure on the bump

Differential diagnosis a) ganglion b) neuroma

Treatment a) conservative

1. padding (to take pressure off the bump) 2. change of shoe lacing (skipping islets so the shoe laces doesn't pass over the bump) 3. orthoses (prevents hypennobility of the first ray)

b) surgical 1. exostectomy: must actually make a divet in the bone to prevent recurrence 2. arthrodesis of the first MfP joint: indicated when there is significant DID, recurrence of the exostosis

or an unstable first ray -HAGLUND'S DEFORMITY (Haglund's disease: osetochondrosis of the accessory navicular)

Diagnosis a) history and physical: posterior lateral osseous bump on the calcaneus. T)'pically, females arc

symptomatic due to irritation from shoe gear. b) differential diagnosis

1. calcaneal bursitis 2. achilles tendonitis 3. tendo Achilles calcification 4. tendo Achilles rupture 5. gout 6. tumor 7. fracture 8. connective tissue disease (ie-rheumatoid arthritis, Reiter's syndrome, psoriatic arthritis, ankylosing

spondylitis)

Pathogenesis the osseous bump and soft tissue overlying are irritated by shoe gear causing pain.

Radiology a) Fowler and Philip angle: measured on lateral radiograph.

1. intersection of a line tangent to the posterosuperior prominence at the insertion of the tendo Achilles and a line tangent to the anterior tubercle and medial process of the plantar tuberosity.

2. nonnal = 44-69 3. when greater than 75 = Haglund's deformity

b) Total Angle (Vega): measured on lateral radiograph 1. the calcaneal incljnation angle can also contribute to the fonnation of a retrocalcaneal bump (Rueh) 2. the total angle is calculated by adding the calcaneal inclination angle to the Fowler and Philip angle. 3. a total angle above 90 is considered pathological

269

Calcaneal Inclination Angle

c) Parallel Pitch Lines: measured on lateral radiograph

Fowler" Phi lip .Angle ~

1. the first pitch line (pPL 1) is the line tangent to the anterior tubercle and medial process of the plantar tuberosity. A perpendicular line is then drawn between the posterior lip of the talar articular facet and

the first pitch line (PPLl). 2. the second pitch line (PPL2)is dra"n parallel to the first pitch line and perpendicular to that

perpendicular line. 3. pathology is demonstrated if the bursal projection (the most superior posterior portion) of the calcaneus

projects superior to the second line. Bursal projection touching or below PPL2 is considered nonnaL

J-li1II:!,~::--.v' Burnl Projec1ion

PPL2

PPLI

d) Valgus Curve of the Calcaneal Tuberosity: demonstrated on the Harris and Beath view.

Treatment a) conservative: heel pads and shoe modification b) surgical

l. Keck and Kelly: remove wedge from the posterior superior aspect of the calcaneus 2. Duvries: transverse resection of the bump through a lateral incision 3. Fowler and Philip:

transverse skin incision through posterior heel with a Mercedes incision through the tendo Achilles resect bump through this incision

4. Dickenson: curvilinear medial incision from superior-medial to inferior-lateral

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Complications Avoid chasing the bump. With bone resection a new prominence is created The bump created should be

carefully rounded or additional bumps will be created with each resection.

Retrocalcaneal Exostosis

Retrocalcaneal Exostosis • Ensethopathy at Achilles insertion • Not Haglunds disease

Haglunds disease • Enlarged bursal peojection of the posrterior and superior calcaneus

Retrocalcaneal Exostosis- etiolog)' • Repetitive trauma / overuse • Equinus • Faulty biomechanics

Pathophysiology Dystrophic calcification -

• Haglund's deformity • Retrocalcaneal bursitis

• calcification of soft tissues with normal calcium metabolism • Usually initiated by trauma which causes tendon fiber disruption. scar fomlation" hypovascularity

and ultilllately calcification

Symptoms and findings

• Pain • Palpable painful bony prominence • Pain with passive ankle dorsiflexion

• Swelling • Thickening of tendon • Possible Equinus

Treatment - conservative • Rest • Physical therapy - stretching

• NSAID"s • Cast Immobilization • Heel lifts / padding I orthotics • Corticosteroid injection with cast immobilization

Treatment - surgical

1. Incisional approaches:

• Transverse • Central midline longitudinal • Medial or lateral longitudinal • Medial or lateral L • Lazy S

2. Procedures: • Tendon splitting - partial detachment • Complete detachment • "V' tendon flap • Tendon advancement • Calcaneal osteotomies

271

3. Post-op course: • Immobilization - NWB 4-8 weeks • Physical therapy • Orthotics I change shoegear • Change exercise

Eauinus

Definitions a) functional equinus: the foot cannot dorsiflex at least 10 degrees past the right angle relationship between

the foot and the leg. This degree of dorsiflexion is required for nonnal foot function. b) classical equinus: the foot cannot dorsiflex 90 degrees in its relationship to the leg.

Types a) gastrocnemius equinus: identified using the silverskiold test. The silverskiold test is performed by

measuring the re1ationship of the foot to the leg with the knee flexed at 90. If the equinus relationship is demonstrated with the knee straight and not demonstrated with the knee bent at 90 , then a gastrocnemius equinus is present.

b) gastrosoleal equinus: this form of equinus is not resolved by performing the silverskiold test. Osseous and pseudoequinus must be ruled out before a gastrosoleal equinus can definitively be identified.

c) osseous equinus: identified by bony abutment between the talus and the tibia anteriorly on a lateral stress dorsiflexion radiogmph.

d) pseudoequinus: the apparent equinus is due to an abnormal forefoot to rearfoot relationship. This is a cavus foot type.

e) combination equinus: any combination of the above.

Treatment a) gastrocnemius recession

1. indications: gastrocnemius equinus 2. advantages: quick rehabilitation period 3. disadvantage: limited indication and limited deformity can be corrected. 4. procedures

Vulpius: "V" shaped cut through the aponeuronsis of the gastrocnemius muscle Strnyer: tr.msverse cut through the aponeurosis of the gastrocnemius muscle Baker: tongue and groove procedure in the gastrocnemius aponeurosis with the tongue portion proximal McGlanuy and Fulp: tongue and groove procedure with the tongue portion distal Silferskiold: resect heads of gastrocnemius muscle releasing them from their origin

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c) tendo Achilles lengthening: all performed on the conjoined tendon of the gastrocnemius and soleus muscles (tendo Achilles)

I. indications: gastrosoleal. severe gastrocnemius and combination types of equinus

2. procedures open "Z"/closed "Z": transverse plane Hauser: section posterior 2/3 proximally and medial 2/3 distally White: section anterior 2/3 distally and medial 2/3 proximally (based upon anatomical torque of tendo Achilles) Hibbs: section the medial 2/3 proximally and then a longitudinal split in a distal direction at the lateral end of the incision: section the lateral 213 distally and then a longitudinal split in the proximal direction at the medial end of the incision Stewart: for when tendo Achilles insertion is more medial than normal and contracted, extending anteriorly on the surface of the calcaneus. An open transverse "z" was performed. with sectioning of the medial I12 at the insertion and laterall/2 more proximally. Sgarlato: "Z-plasty" in frontal plane, sectioned anterior 2/3 distally and posterior 2/3 proximally Hoke: triple hemi-section \Vith first and last sections medially and second cut laterally

c) tendo Achilles advancement: for spastic equinus (i.e. cerebral palsy) see Murphy's triceps advancement under section covering tendon transfers

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FLATFOOT

Flexible vs Rigid Flatfoot is evaluated by the following: 1. Active and passive range of motion of ankle, STJ. MfJ

• Flexible feet have full r.mge of motion at the STJ and MfJ 2. Hubscher maneuver. passive dorsiflexion of the hallux with the patient standing creates the windlass

effect of Hicks in the flexible flatfoot

• Arch elevation • Plantarflexion of first ray • Supination· of rearfoot in medial arch height • External rotation ofleg

Flexible Flatfoot

Etiology: 1. Equinus 2. Congenital: talipes calcaneovalgus 3. Structmal forefoot-to-remfoot relationship

• Compensated forefoot varus • Compensated forefoot valgus • Rearfoot equinus

4. Torsional abnonnalities • Adduction: metatarsus adductus, internal tibial torsion • Abduction: external tibial or femoral torsion. etc.

5. Frontal Plane abnormalities

• Genu varum I valgum 6. Neural-nmscu1ar-ligamemous

• Neurotrophic • Muscle imbalance • Flaccid paralysis • Ruptured tibialis posterior tendon. accessory navicular • Li~tous laxity I hypermobility: Ehlers-Danlos syndrome. Marfim's syndrome

**Note: The flexible flatfoot can eventually become rigid with the development of tarsal arthritis**

Radiology

*** Radiographic changes will reflect the primary plane of compensation (pIanal dominance)

1. Transverse plane (AP radiograph) • Talocalcaneal angle increases • Talonavicular congruency decreases (Talar head uncovering)

• Normally- approx. 75% of the talar head is in contact with the navicular • Forefoot adductus angle decreases • Cuboid abduction increases • Wedge shaped navicular

2. Sagittal plane (lateral radiograph) • Talar declination angle increases • Calcaneal inclination angle decreases • Talocalcaneal angle increases • Midfoot sagging; naviculo-cuneiform breach • Talo-lst metJtarsal angle increases (negative Meary's angle)

274

3. Frontal plane (calcaneal axial, lateral radiographs) • Flearfootever.rion • Increased superimposition oflesser tarsus • Decreased first metatarsal declination angle • Decreased height of sustentaculum tali

***Note: In severe flatfoot ankle views should always be obtained to rule out ankle valgus***

Surgical Procedures Categorized by: • Planal dominance • Osseous vs soft tissue procedures • Medial colwnn vs calcaneal procedure

Plana! Dominance: • Flefers to the primary plane of the flatfoot deformity (i.e., the plane in which is most

effected. • Although procedures are divided into the primary plane of correction, the other planes

are effected to a lesser extent, therefore all procedures provide triplaner correction

Transverse Plane 1. Evans calcaneal osteotomy

• Osteotomy of calcaneus 1.5 em proximal to calcaneocuboid joint and insertion of a bone graft lengthens the lateral colwnn and realigns the midtarsal joint

• May unmask metatarsus adductus 2. Calcaneal-cuboid joint distraction arthrodesis

• Also lengthens lateral colwnn • Thought to eliminate symptomatology at calcaneal-cuboidjoint created by the Evans

3. Kidner Procedure • Theoretically for transverse plane • Flemoval of prominent naviaJ1ar tuberosity or accessory navicular and transposition of

posterior tibial tendon plantarly into the naviaUar

Sagittal Plane 1. Lowman

• Talonavicular fusion • Tendo Achilles lengthening • Tibialis anterior under the navicular into the spring ligament • Medial achilles tendon as accessory ligament for tenodesis of the medial arch

2. Hoke • NaviaJ1o-cuneiform fusion • Indicated with obvious fault or hypermobility at the naviaJ1o-cuneiformjoint • Can modify and fuse with plantarflexory bone graft

3. Miller • NaviaJ1o-cuneiform-first metatarsal fusion • Posterior tibial and spring ligament advancement using an osteoperiosteal flap

4. Cotton • Opening p1antarflexory wedge osteotomy of the medial cuneiform

5. Lapidus • 1 st met - cuneiform arthrodesis

6. Young • Tendosuspension of the tibialis anterior through a keyhole in the naviaUar • T. anterior rerouted through the navicular (not detached from insertion) • Posterior tibial advanced under the navicular

275

7. Cobb • Hemisection ofT. anterior left intact at its insertion then reflected inferior and medial to

the tarsus and used to augment T. posterior 8. Tendo Achilles lengthening / gastroc recession

K1DNER LOWMAN

HOKE MILLER YOUNG

Frontal Plane 1. Orthotics 2. Chambers

• Artbroereisis concept • Raises the posterior mcet of the subtalar joint using a bone graft under the sinus tarsi

3. Baker-hill • Osteotomy inferior to the subtalar joint posterior facet with bone graft

4. Selakovich • Opening wedge osteotomy of the sustentaculum tali with bone graft which restricts

abnormal subtalar joint motion 5. Calcaneal Osteotomies

• Gleich: oblique osteotomy displaced anteriorly • Lord: displaces the calcaneus anteriorly, inferiorly and medially • Silver: lateral opening wedge with graft • Dwyer: medial closing wedge

• Koutsogiannis: transpositional osteotomy • Straight cut performed parallel to and behind the peroneal tendons • Fragment shifted medially / can also be shifted anteriorly • Increases the supinatory moment arm of the tendoachilles

6. STJ Blocking Procedures a) Arthroeresis

• Really limits triplane motion at the subtalar joint • Plantarflexion of the talus • Transverse plane adduction of the talus • Frontal plane eversion of the calcaneus

276

Examples: • Addante: Villadot umbrella • Stapeg • Sgarlato mushroom • ValIente • MBA (Maxwell-Brnncheau)

b) Extra-articular STJ arthrodesis (EASTA) Green-Grice arthrodesis

• Extra-articular Fusion of the STJ in the sinus tarsi using bone graft • Appositional bone growth is not disturbed • Indicated in ages up to 12-14 years

FroJttal Plane FlaifDo1 Procedures

Arthroeresis Procecblres

CHAMBERS BAKER-HILL SD.AKOVICH GREEN-GRICE

Arthroeresis hnplaJl'ls

o (spllere)

ADDANIE

~s t3 ~ VlLADOT STA peg SGARLATO

GLEICH LORD sn.vm DWYER KOUTSOGIANNIS

Rigid Flatfoot

Etiology

• Congenital • Oven:orrected flatfoot • Tarsal coalition -• Peroneal splSDl • Trauma (e.g. Lis Frnnc'sFracture I Dislocation) • Tarsal arthrosis I Charcot

Tarsal Coalition 1. Types

• Syndesmosis: fibrous • Synchondrosis: cartilaginous • Synostosis: osseous

277

2. Incidence: approximately 500,4 are bilateral • Talocalcaneal (middle facet) - most common • Calcanea-navicular bar - second most common; "comma sign" • Talonavicu1ar - third most common

Clinical findings • Sudden onset of pain after increased activity • Symptoms usually occur at times re1ated to ossification of the coalition • T -N 3-5 yrs; C-N 8-12 yrs; T -C 12-16 yrs • With complete synostosis there is no acute pain because no motion occurs at that joint • Decreased STJ ROM • Progressive valgus deformity associated with bow-strung peroneal tendons behind the lateral

malleolus - peroneal spastic flatfoot Usually secondary to synovial irritation of the 81'J and traumatic tenos}novitis; not due to a spasm of the tendon.

Radiographic findings 1. STJ coalition

• I...ateralview • Irregular narrowing or absent middle :facet • Halo-effect: sclerosis surrounding the STJ caused by increased density • Late findin&,,~

• Talarbeak • Broadening and flattening of laternl taIar process • Ball and socket ankle joint

• Harris and Beath calcaneal axial views • Evaluates middle and posterior facets • Standard:;:: 35,40,45 axial views • Three views determined by the angle of posterior facet declination reIative to

the weigh1bearing SUIface, 10 above and 10 below

• Isherwood views • Oblique DP: anterior facet • Medial oblique: middle and posterior facets • I...ateral oblique: posterior facet

2. Calcaneon3vicu1ar coalition • Medial oblique: Anteater sign

Treatment 1. Conservative (ie-orthoses, PT, NSAIDs, BK cast) 2. Surgical

• Excise the coalition • C-N bar: excise and interpose EDB muscle (Badgely) • Arthrodesis: selected joint or triple arthrodesis

Congenital Vertical Talus

Radiographic findings • Navicular dorsally dislocated on the taIar neck • Dorsiflexed, plantarflexed stress view:

• Df stress - rearfoot remains in equinus • Pf stress - t-njoint remains dislocated

278

Treatment 1. Serial casting in younger patients 2. Surgical

• Release soft tissue contractures • Tendon lengthening • Relocation of the T-N joint with pinning • lfnecessary, triple arthrodesis

CAVUSFOOT

Etiology a) neuromuscular: most common cause

1. myopathy: muscular dystrophy 2. peripheral nelVe or lumbosacral spinal nelVe root pathology

>Charcot-Marie-Tooth disease >Dejerine-Sottas's interstitial hypertrophic neuritis >polyneuritis >traumatic lesions of the sciatic nerve

3. anterior hom cell >poliomyelitis >myelomeningocele >spinal cord tumor

4. spinocerebellar tracts >Friedrich's ataxia >Roussy-Levy syndrome

5. pyramidal or extrapyramidal tracts >cerebral palsy >extrapyramidal and spastic hemiplegia

6. cerebral cortex >hysteria

b) other causes of cavus foot 1. infection: syphillis 2. idiopathic 3. trauma

>peripheral Den'€: damage >tendon ruptures with subsequent fibrosis and contracture

4. congenital disorders >myelomeningocele >spina bifida >myelodysplasia >clubfoot

ClassifJCation a) anterior cavus

1. metatarsus cavus: Lisfranc's joint 2. lesser tarsus cavus: lesser tarsal bones 3. forefoot cavus: Chopart's joint 4.locaJJgloballcombined

b) posteriorcavus 1. muscle weakness or spasticity of gastrocnemius or soleus 2. pseudoequinus: inadequate ankle joint dorsiflexion secondary to rigid anterior cavus deformity

279

Oinical Evaluation of the Caws Foot a) subjective

1. age of patient/age of onset of caws deformity 2. symptoms and progression of caws foot type

-frequent inversion ankle sprains -early futigue with arnhdation or stmding ~aint of muscle weakness of the lower extremity

3. medical and fiunily history -history of congenital spinal disorders -fiunily histol)' of caws foot type and/or neuromusadar disorders

b) objective 1. neurological examination

-muscle and sensory testing -assessmesnt of reflexes <OOIdination tests -electromyography and nerve conduction studies

2. physical examination -test for flexible or rigid medial arch with the Kelikian push-up test -assess ankle equinus -evaluate calcaneal position - fixed varus? -first ray: plantarflexed, fleXIble or rigid? -digital deformities: flexible or rigid?

extensor substitution? p1antar submetatarsallesions?

3. radiographic evaluation -1ateral13diograph

decreased talocalcaneal angle increased calcaneal incljnation angle decreased talar declination angle posterior break in the cyma line ''bullet hole" sinus tarsi

-AP radiograph decreased talocalcaneal angle increased metatarsus adductus

Principles of Cavus Foot Surgery a) determine the underlying etiology b) address the plane of deformity and the level at which the defonnity occurs. Examples:

>m!Ifoot varus - Dwyer >ankle equinus - gastrocnemius rescession or TAL >pJantarflexed first my - Jones suspension; DFWO >rigid anterior caws - Cole; Japas >digital clawtoes or hammertoes - DIPJ and PIPJ arthrodesis; Hibbs

c) cavus foot requires multilevel surgei)' (ie- digitslLisfranclmidfootlrearfoot)

Soft TISSUe Procedures (indicated for flexible defonnity) a) p1antar fascial release b) Steindler stripping: includes fascia, abductor hallucis, FDB, abductor digiti quinti and the long plantar

ligament c) Bost and Larsen

-release of medial column joints -release of plantar intrinsics

d) Garceau and Brahms -resect the motor branches of the medial and lateral plantar nerves

280

Tendon Procedures a) Jones suspension

-EHL is transferred to the neck of the first metatarsal -hallux IPJ fusion

b) Hibbs suspension -Steindler stripping -long extensor tendons transferred to lateral cuneiform

c) modified Hibbs -long extensor tendons transferred to the intermediate or lateral cuneiforms -Jones suspension (EHL to first metatarsal with hallux IPJ fusion) -anastomosis of the distal long extensor tendon stumps to the EDB tendons

d) Split Tibialis Anterior Tendon Transfer (ST A TT) -transfer of lateral half of the tendon to insertion site of peroneus tertius tendon at base of fifth metatarsal

e) Tibialis Posterior Tendon Transfer -tibialis posterior tendon is released from its insertion on the navicular and transferred through the

interosseous membrane i] passed dOm} EDL sheath to insert in the lesser tarsus or ii] half of tibialis posterior tendon is passed do\'\'n the peroneus tertius sheath and the other half is

passed dOm} the tibialis anterior sheath f) Peroneus Longus Tendon Transfer

peroneus longus is released at the level of the cuboid and transferred through the intermuscular septum, dO\,\,TI the EDL sheath and inserted into the lesser tarsus

peroneus longus may also be split in half; half anastomosed to tibialis anterior at its insertion and the other half anastomosed to peroneus tertius

Osseous Procedures Indicated for unreducible rigid deformity and in neuromuscular cases for stabilization of the foot: may also

require soft tissue release a) Cole: dorsifle.xory wedge osteotomy

through the navicular-cuneiform joints and cuboid

b) DuVries: dorsiflexory fusion through the MTJ

c) Japas: displacement V-shaped osteotomy through the cuboid, navicular and medial cuneiform

d) IMyer: lateral closing wedge osteotomy of the calcaneus

e) McElvenny-Caldwell: first metatarsal -cuneiform fusion

f) DFWO of first metatarsal g) triple arthrodesis

Caws Osteotomies

&a~ Cok DuVr.res

~. Japas Dwyer

M.cElv.umy & ~ll DFWO

281

TARSAL TUNNEL SYNDROME:

• classically, entrapment of the posterior tibial nerve. This discussion will be limited to the classical type, however, an anterior tarsal tunnel syndrome involving the deep peroneal nerve does exist.

Etiology: Type A (direct)

7. local disease: usually either processes which produce edema or space occupying processes occurring within the closed compartments under the Jaciniate ligament.

1. trauma: to the nerve itself or structures surrounding the nerve. 2. varicosities: causes venous congestion within the tarsal tunnel. Most common cause ofbilateIal cases. 3. congenital anomalies: accessory nmscles 4. os trigonum syndrome: inflammation with edema of the FHL tendon 5. abductor hallucis nmscle hypertrophy: space occupying 6. space occupying lesions within the tarsal tunnel: neurilemotl13, neurofibroma, lipoma,. ganglion.

aneurysm. 7. tenosynovitis: produces edema 8. iatrogenic: intra-operative, steroid nyections, tourniquet trauma, casting.

b) systemic disease 1. diabetes mellitus with associated neuropathy 2. inflammatory arthritides (ie-rheumatoid arthritis, ankylosing spondylitis) 3. crystal deposition diseases (ie-gout, pseudogout): producing crystals and edema within the tunnel. 4. mixed connective tissue disease (ie-SLE) 5. myxedema: synovial thickening

Type B (functional) a) pronation: internal rotation of the leg with tightening of flexor retinaculum.

Diagnosis a) History and Physical: neurological signs and symptoms on the plantar aspect of the foot

1. pain: shooting, burning or electric type sensation 2. burning sensation 3. symptoms worsen with prolonged weight-bearing and at night. 4. palpation of COId-Iike swelling 5. venous tourniquet test (causes symptonis to worsen due to congestion) 6. Tinel's sign 7. Valleix's points 8. sensory changes: two point tactile, pin prick and proprioception 9. diagnostic tibial nerve block: should resolve the pain temproarily 10. atrophy of the plantar intrinsic nmscles and plantar changes in sweat production (severe cases)

b) Electromyographic studies: prolonged latency as well as decreased nerve conduction Velocity support the diagnosis of tarsal tunnel syndrome.

1. electromyography 2. nerve conduction velocity

Treatment Conservative a) corticosteroid injections b) posterior ubial nerve blocks c) immobilization (ie-casting) d) orthosis: to prevent pronation

Smgical a) external neurolysis: consists of releasing the laciniate ligament swgically. The ligament is not

reapproximated during closure. Recurrence rates of 5-20010 have been reported.

282

TRIPLE ARTHRODESIS

Definition: fusion of the following three joints a) talocalcaneal (subtaIar) b) calcaneal-cuboid c) talonavicular

Indications a) correct deformities

1. valgus deformity 2. varus deformity 3. flatfoot 4. caws foot 5. talipes equino varus 6. fixed equinus 7. fixed dorsiflexion

b) relief of pain 1. tarsal coalition 2. arthritis 3. ruptured tIbialis posterior tendon 4. salvage for severe calcaneal fractures

c) stability/improve motor power 1. lateral ankle instability 2. neuromuscular disorders

Fixation of Triple Arthrodesis a) screws b) pins c) staples d) external fixation

Triple Arthrodesis procedures a) Ryerson:"classic triple arthrodesis" simple

joint resection b) Hoke: remove head of talus, resect articular

surface and replace head c) Haughton Dunn: remove l1a\>;cular d) Elmslie: indicated for fixed calcaneus foot

type e) Lambrinudi: indicated for fixed equinus foot type f) Brewster: countersink talus g) Grice: extra articular fusion of subtalar joint h) dowel graft: uses dowel plugs of bone to fuse the joints

Complications a) intra-operative neurovascular injury b) ankle arthrosis c) malalignment (can cause callosities) d) malunion e) nonunion (talonavicular joint most common)

TripJe Arthrodesis Procecl'ures

\ Naughton Dunn Hoke

Lamltrinwli Ebnslie

B:rews-rer Ryerson

G:rh:e

283

TENDON TRANSFERS

Objectives a) provide active motor power; in generaI, one grade of muscle strength is lost through tendon transfers b) elimination of deforming force c) produce stability d) cosmesis e) elimination ofbI3Cing

General indications a) muscle imbalance

1. flexible hammertoes 2. hallux valgus 3. dorsal bunions

b) paralytic foot I. poliomyelitis 2. Duchenne's muscular dystrophy 3. Charrot-Marie-Tooth disease 4. cerebral palsy 5. spinal cord impingement 6. sciatic nerve palsy 7. common peroneal nerve palsy ("Saturday night palsy") 8. drop foot

c) congenital deformities I. recurrent clubfoot 2. forefoot equinus 3. flexible flatfoot

d) iatrogenic deformities 1. hallux varus

Procedures:

Jones tendosuspension procedure a) procedure: the extensor hallucis longus tendon is transected at its insertion and transferred through a

transverse hole in the first metatarsal. The tendon is anchored by suturing it to itself dorsally. b) indications: hallux extensus (cock-up hallux deformity) due to flexible cavus foot deformity or flexible

plantarflexed first ray. c) 3(ljunctive procedures: fusion of the hallux interphalangeal joint to prevent an interphalangeal flexion

deformity. .

Panmetatarsal tendosuspension procedure a) procedure: any or all the metatarsal heads can be suspended as in the Jones suspension b) indications: flexible hammertoes c) adjunctive procedures: digital fusions and/or transfer of the distal attached portion of the tendon to the

extensor digitorum brevis.

Kidner procedure (refer to flatfoot procedure section) a) procedure:

resection of the accessory navicular and/or hypertrophied navicular tuberosity transposition of the tibialis posterior tendon insertion from a more lateral navicular attachment to a more plantar navicular attachment

b) indications: adjunctive procedure for a medial column flatfoot c) 3(ljunctive procedures: usually performed with an osseous flatfoot corrective procedure

284

Hibbs tendosuspension a) procedure

transection of the extensor digitorum longus tendons b) transfer the tendons to the midfoot (usually into a trephine hole in the intermediate or lateral

cuneiform)the distal portions of the tendons are usually transferred (sutured) to the EDB tendon c) indications: functional equinus (this gives the EDL tendon greater mechanical advantage in

dorsiflexing the foot and prevents the formation of hammertoes) d) aq;unctive procedures: may be performed with a Jones suspension of the hallux and/or digital fusions

Tibialis Anterior Tendon transfer a) procedure: transection of the tibialis anterior tendon at its insertion and transferring it to the

intermediate supination deformity from muscle paralysis (ie-CM1) or congenital muscle imbalance (ier. ecurrent clubfoot). Also used to correct drop foot.

b) ru:ljunctive procedures: tendo Achilles lengthening or gastrocnemius recession to weaken the posterior muscle group and/or fusion procedures of midfoot or rearfoot.

Split Tibialis Anterior Tendon transfer a) procedure:

incisions are made over the tibialis anterior tendon at its insertion and between the middle and distal thirds of the leg. the tendon is split from its insertion to the level of the proximal incision. the lateral half of the tendon is transected at its insertion and passed through the proximal incision a third incision is made at the cuboid/peroneus tertius insertion area the lateral half of the tibialis anterior tendon is passed either through the tendon sheath of the peroneus tertius then sutured to the peroneus tertius near its insertion or, when the peroneus tertius is absent, attached to the cuboid via tenodesis.

b) indications: flexIble varus and/or equinus deformities at the rearfoot or midfoot levels (increases dorsiflexion and eversion)

c) aqjunctive procedures: dorsiflexory osteotomy of the first metatarsal, digital deformity correction, calcaneal osteotomy and tendo Achilles lengthening.

Young tendosuspension (actually a transposition) a) procedure: the tibialis anterior tendon is passed through a slot in the navicular without distwbing the

insertion. The ubialis posterior tendon must be detached from its insertion to perform the procedure. It is reattached to the plantar surface of the navicular.

b) indications: flexible pes p1anus c) aqjunctive procedures: other flatfoot procedures

Tibialis Posterior Tendon transfer (a non-pbase transfer; can also cause flatfoot)

1. procedure: incisions are made dorsally over the midfoot and over the posterior tibial muscle between the middle and distal thin:Is of the leg. The tendon is transected at its insertion and passed through proximal incision.

two piths for passing the tendon -1. Ober technique: the ubialis posterior tendon is passed from the proximal incision and brought

around the medial malleolus and transferred into the lateral cuneifonn. 2. Putti technique: the tibialis posterior tendon is passed from the proximal incision and brought

t:brougb the interosseous membIane and transferred into the lateral cuneiform. b) indications: flexIble or spastic equinus deformities

285

Peroneus Longus Tendon transfer a) procedure:

an incision is made at the level of the cuboid where the peroneus longus tendon is identified the distal portion of the peroneus longus tendon is pulled tight and sutured to the peroneus brevis the peroneus longus tendon is transected just proximal to where it is sutured to the brevis the tendon is then transferred through the intermuscular membIane to the IateIal ameiform

(alternatively the tendon can be split and attached to the peroneus tertius and the anterior tibial tendons)

b) indications: flexible equinus (drop foot) deformity

Murphy triceps advancement theoretically reduces the lever arm of ankle pIantarflexion by 50% 'while reducing the lever arm of

propulsion by 15% a) procedure

transection of the tendo Achilles at its insertion advancement of the tendon anteriorly, just posterior to the posterior facet of the subtalar joint

b) indications: spastic triceps in cerebral palsy

Tendon Function Around The Suhtalar Joint Axis

286

ANKLE SURGERY

Medial Ankle Instability Surgen-

Deltoid ligament injuries 0CC\lI' when the foot is forcibly everted on the leg. Chronic isolated deltoid injury is rare. usually an old fibular :fracture is involved or undiagnosed tibiofibular diastasis.

a) Anatomy of the deltoid ligament The deltoid ligament is divided into two portions, the deep and superficial deltoid ligaments. The superficial portion is composed of the tibiocalcanealligament. The deep portion is composed of. from anterior to posterior, the anterior tibiotalar, tibionavicular, intennediate tibiotalar and posterior tibiotalar ligaments. Frontal plane instability is demonstrated by stress eversion mortise radiographs. Generally 10 or greater degrees of talar tilt is considered positive and indicates rupture of the tIbiocalcaneal and intennediate tibiotalar ligaments.

b) Surgical procedures 1. Schoolfield's procedure: the damaged deltoid ligament is detached at the origin in the tibia. The

foot is then forcibly inverted and the deltoid is sutured into the periosteum superior to the detachment site. This effectively advances the deltoid ligament

2. Du Vries' procedure: the deltoid ligament is cfu,ided vertically and horizontally creating a cruciate defect, which is then resutured Du Vries' suggested the resultant scar formation is strong enough to stabilize the medial ankle.

3. Wittberger and Mallory's procedure: the procedure utilizes a split portion of the tibialis posterior as a tendon graft to reinforce the medial ankle ligaments. Approximately 5 em proximal to the ankle mortise one half of the tibialis posterior is harvested and split to its insertion in the navicular. The portion of tendon is then passed inferiorly to superiorly through a drill hole in the distal tIbia and sutured blck onto itself with the foot forcibly inverted

Lateral Ankle Instability Surgery

Lateral collateral ligament pUhology is extremely common and is caused by repetitive inversion injury to the ankle. Chronic instability of the lateral ankle is a disabling condition which can predispose the patient to ankle fractures, osteochondral talar dome fractures and degenerative joint disease.

a) Anatomy of the lateral collateral ankle ligament: the lateral collateral ankle ligament is composed of three separate ligamentous structures.. The anterior talofibular ligament is an intracapsular structure which resists anterior displacement of the talus within the ankle joint mortise. The calcaneofibular ligament is extracapsular and oriented approximately 105 from the anterior CF talofibular ligamentIt resists inversion of the talus within the ankle mortise. The posterior talofibular ligament is a strong intracapsular ligament which is situated in a nearly horizontal plane. This ligament resists posterior displacement of the talus in the ankle mortise.

b) Diagnosis of lateral collateral pathology: rupture or weakness of the ATF can be confirmed with an anterior dJ:a\\'-er or push-pull lateral stress radiograph. An anterior displacement of2 em or greater as compared to the contralateral limb is considered abnormal. Rupture or weakness of the CF ligament can be confirmed utilizing stress inversion mortise radiographs. A talar tilt of 10 greater than the unaffected contra1aterallimb is considered abnormal. Ankle arthrograms or peroneal tenography are only indicated in acute ligamentous rupture with patients who have no prior history of ankle trauma. A peroneal tenogram is greater than 95% accurate for detennination of acute calcaneofibular ligament ruptures.

287

c) Surgical procedures: Procedures may be grouped into which ligament or ligaments they are designed to replace.

I. delayed primary ligamentous repair • Usually indicated in acute ligJImentous injury. In cases of chronic instability the

ligaments may be stretched and not tom Imbrication of the ligaments utilizing nonabsorhlble suture is then peIformed.(Brostrom)

• Gould modification: reinforcement of repair with extensor retinaculum

IT. anterior talofibular ligament replacement ::::> As a group these procedures reconstrud the A1F utilizing various structures usually passed

through the fibula, talus and occasionally the calcaneus following the anatomic orientation of the A1Fligament.

• >Watson-Jones procedure: utilizes peroneus brevis • >mini Watson-Jones procedure: utilizes peroneus brevis • >McLaughlin procedure: utilizes a split peroneus brevis • >Lee procedure: utilizes peroneus brevis • >Pouzet procedure: utilizes peroneus longus • >Storen I: utilizes a portion of the Achilles tendon • > Weber procedure: utilizes plantaris tendon • >Sefton procedure: utilizes p1antaris or long extensors • >Haig procedure: reinserts the A1F ligament • >Dockery, Toothaker and Suppan: utilizes split peroneus brevis and tertius

ill. anterior talofibular and calcaneofibular repIacement ::::> These procedures reconstruct the A1F and CF ligaments utilizing various structures passed

through and between the fibula, talus and calcaneus following the anatomic orientation of the A1F and CF ligJIments.

• >Elmslie procedure: utilizes fascia lata • >Christman-8nook: utilizes split peroneus brevis • > Winfield procedure: utilizes peroneus brevis • >Storen II: utilizes a free tendon graft of Achilles tendon • > Ahlgren-Larsson: a subperiosteal advancement of both A1F an CF ligaments • >Split Peroneus Brevis LateIal Ankle Stabilization:

• utilizes split peroneus brevis tendon

IV. A1F, CF and PIF ligament repIacement ::::> Designed to replace all three ligaments in anatomic or near anatomic position.

• >Spotoff. utilizes fuscia lata • >Rosendahl-Jensen: utilizes fascia lata

V. Extra-anatomic Lateral Ankle Stabilization ::::> These procedures reinforce the lateral ankle without following specific anatomically correct

ligamentous orientation. • >Nilsonne procedure: utilizes peroneus brevis • >Evans procedure: utilizes peroneus brevis • >Larsen procedure: utilizes peroneus brevis • >Viernstein procedure: utilizes peroneus brevis

288

Subluxated or Dislocated Peroneal Tendon Repair Procedures:

Dislocation and subluxation of the peroneal tendons is usually seen with sports injuries in which forced ankle motion takes places while the peroneal tendons are under maximum tension.

a) Surgical procedures 1. Kelly and Watson-Jones procedure: an osteoperiosteal

flap is created in the posterior aspect of the lateral malleolus. The procedure effectively deepens the sulcus preventing recurrent dislocation.

2. DuVries procedure: a wedge-shaped osteotomy is created in the posterior aspect of the lateral malleolus which forms a bone graft. The bone graft is displaced posteriorly and fixated forming a bony block to prevent dislocation.

3. Daimant -Berger: plicated and reinforced the peroneal tendon sheath. 4. Folschveiller: utilized a periosteal flap to reinforce the sheath and redirect the peroneal tendons

posteriorly. 5. Jones procedure: stabilized the peroneal tendons by reconstructing the retinacular ligament 'with a flap of

Achilles tendon.

:..--­Kelly & Wauon-Jones DUVRIES

AnierlorTalo6lndar lipmeni Repwemeni

Wabon-Jo:net

Se&.n,eial DodsIery, Suppan,

Too1LaJser

289

-Vieru1ein

ANKLE ARTHROSCOPY

In 1920 Takagi of the University of Tokyo was the first to view the inside ofajoint with an arthroscope. Since that time great strides have taken p1ace in equipment and techniques which continue to develop today. The surgical morbidity associated with arthroscopy is extremely low and the potential benefits to the patient are high.

Arthroscopic Equipment a) arthroscope: a lens containing, light-tnmsmitting tube which allows the transmission of a picture

to a television monitor or to the surgeon's eye. The arthroscopes of today contain GRIN (Gradient Refractive Index) lenses. This lens is a solid relay lens rod coated with black paint which allows the least amount oflight loss currently available. The tip of the arthroscope is angled from 0 to 90 . The oblique angle on the tip of the scope allows for a greater field of view, which allows the surgeon to peer around bends in joints. Arthroscopes are available in outer diameters of!.7 mm. 2.2 mm. 2.7 mm. 3.5 mm and 4.0 mm..

b) light somt:eS: there are three types oflight sources all of which transmit light into the joint via fiberoptic cables.

• ~ lamps: color tempeIatures of2900 K. least powerful • metal halide]amps: color temperature of 5800 K. intermediate power • xenon lamps: color temperature of 6000 K. which corresponds to daylight, most

powerful

290

c) cameras: two types are used. The Saticon tube camera functions very well in low light but is not submersible for sterility. The ceo integrated-circuit cameras are submersible and have much less bulk, but require more light.

d) hand instruments: include - trocars, obtwators and cannulas for entering joint spaces. Probes, knives, rasps, scissors, curettes and grasping forceps or basket forceps are also used. A very useful hand instrument is the suction punch which enables the surgeon to grasp tissue and aspirate it from the joint without removing the instrument.

e) power instruments: motorized cutters, shavers and abrasion burrs which allow arthroscopic debridement to procede at a much faster rate.

1) miscellaneous equipment: leg holders are padded U-shaped devices which secure the leg during surgery. Joint distraction devices are also available.

Arthroscopic Portals of the Ankle The ankle is divided into posterior and anterior joint cavities each with a medial, centrnl and lateral compartment. There are five classic portals of the ankle joint. Three are located anteriorly and two posteriorly.

I. anterior portals: anterocentral portal is placed between the extensor tendons and care is exercised not to injure the anterior tibial artery or deep peroneal nerve. Most arthroscopic surgery may be conducted through this portal. The anteromedial and anterolateral portals are designed for vie\\'ing medial or lateral gutter structures and for placement of hand or power instrumentation.

ll. posterior portals: posterolateral and posteromedial portals are placed just lateral or medial to the Achilles tendon. These are ancillary portals for examining the posterior ankle joint structures and for reaching deep posterior lesions.

ill. accessory portals: an accessory portal is placed anywhere it is needed. TI3DS-malleolar portals have been described.

Arthroscopic Technique Three basic principles are involved in arthroscopic maneuvering.

1. scanning: a sweeping motion from side-to-side and up-and-down. Scanning allows a large area to be viewed.

II. pistoning: moving the scope in and out, which allows the field of view to be enlarged or reduced.

ill. rotation: turning the arthroscope on its axis. Allows a larger field of view due to the obliquity of the arthroscope tip.

N. Arthroscopic Joint Pathology

Initially the arthroscope was simply a diagnostic instrument, however with the advent of hand and power instrumentation, the utility of the arthroscope is becoming evident.

I. synovitis: finger-like villi of hypertrophic synovium. Usually indicative of underlying joint disorders.

ll. chondromalacia: this condition is an arthritic change in the articular cartilage causing changes in consistency, texture,color and resilience. The affected cartilage must be debrided and the subchondral bone exposed, which will allow fibrocarti1age formation.

ill. osteochondrallesionlfracture: classi:fied by Berndt-Hardy, these lesions are ~ and sometimes difficult to visualize. The lesion must be resected by probing the extent of the fracture and abrading or grasping the fiacture itself

IV. jmpingement lesions: hyalinized meniscoid bodies or bands which restrict motion and cause pain. Easily resected with knives, graspers and/or suction pmches.

V. erosions: discrete focal areas of articular cartilage loss which may be abraded to subchondral bone and replaced with fibrocartilage.

VI. emprgjng arthroscopic techniques: arthroscopic stapling or suturing for chronic lateral ankle inslability and arthroscopic ankle fusion techniques are being developed.

291

ANKLE FUSIONS

Indications a) arthrosis b) severe angu1ar defonnity c) irreparable acute trauma d) bone tumor e) chronic osteomyelitis f) failed ankle prosthesis g) paralytic deformities h) salvage of avascular necrosis oftalar body

Anlde Fusion Fixation a) screws b) plates c) pins d) staples e) external :fixation

Intra-articular Grafts a) Hallock: bone chips b) ChuinaId and Peterson: iliac wedge c) Campbell: cortico-cancellous iliac graft in vertical fashion d) Wescott: graft:from proximal tibia e) Stauffer: salvage for failed total ankle prosthesis

cancellous bone packed around a cortical block f) Van Gorder and Chen: tIbial bone graft into ankle joint without resection of joint surfaces

Anterior Grafts a) GalIie: inlay grafts b) Kennedy: allogenic grafts with staple fixation c) Hatt: :fibu1ar spike d) BriUain: tibial graft through hole in pJafond

Posterior Grafts a) Carnrbill: :fish scale b) White: iliac wedge c) Gill: calcaneal wedge

Sliding Grafts a) Qamer: sliding tibia b) Soren: sliding tibia c) Blair: sliding tibia into superior aspect of neck of talus used for avascular necrosis of talar body

Malleolar Osteotomy a) Man:us. Balourdas and Heiple: chevron osteotomy of medial malleolus b) Wdson: used only anterior halves of both malleoli c) Bingold: :fibular spike through calcaneus d) Anderson: bimalleolar resection, crushing and used for cancellous graft e) Mead: bimalleolar f) Goldthwait :fibula g) Horwitz: split:fibu1a, and place half anteriorly and halflateraIIy h) Adams: spIit:fibu1a, fix lateral half on to fusion site and medial half used for cancellous chips i) Glissan: medial malleolus j) Stewart and Harley: bimalleolar osteotomy preserving the outer cortices k) Royal Air Force: :fibula

292

Dowel Fusion a) Baciu and Filibiu: medial approach, using image intensification b) Hone: dowel from anterior to posterior c) Pridie: medial approach d) Graham: cylindrical fibular graft

Internal Fixation a) Doctor's Hospital: uses two 6.5 mm cancellous screws from tIbia into talus

External Fixation a) Charnley b) Muller c) Calandruccio

bt.tra-articubr Grafls

Position of Arthrodesis a) sagittal plane is neutral b) valgus (0-5 degrees) c) externally rotated (5-10 degrees) d) posterior displacement of talus Hallock Ckuiltard & PeiersoJl

1. counteract JK1ll of tendo Achilles 2. preserve prominence of heel Anierior Tibial Grafis

Complications a) intra-operative neurovascular injury b) malunion c) nonunion

Cramer Hatt

Malleolar Osteo1Dmy Posterior ArtItrodesis

If) II ~~

Gill

293

PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLASTIC SURGERY PLi-\STIC SURGfiR'l' P'L}\STIC SURGER \~ PLi\STIC'~ SlJR,(} E~ f{ '\ ~ IJLl\STIC'< SURGEJ{ \ ·P·L. AS" '1T' 'lr'~ S'lTRC--- FI~'-~ _ .. _.'-- '- ) . J~J .. s

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1

Plastic Surgery

WOUND HEALING Healing by first intent: is the least complicated example of wound repair, and is the healing of a clean, uninfected surgical incision, approximated by surgical sutures.

a. narrow incision space immediately fills with clotted blood containing fibrin and blood cells. b. Dehydration of the surface clot forms the scab. c. Within 24 hoors, neutrophils appear on the margin of the wound d. Within 24-48 hoors, the cut edges thicken from mitotic activity of basal cells, epithelial cells from

the edges migrate along the cut margins of the dermis depositing basement membrane as they move. These cells fuse to form a thin but continuous epithelial layer.

e. By day 3, neutrophils are replaced by macrophages. Increased granulation tissue at the incision site. Collagen fibers are beginning to be manufactured along the margins, but do not bridge the gap. The thin epithelial cell layer thickens.

f. By day 5, Neovascularization is maximal. Collagen fibers begin to bridge the gap. Epidermis is back to its original thickens, and full differentiation.

g. During the second week, increased collagen and fibroblasts. Decreased to absent leukocytic infiltration, edema, and increased vascularity. Beginnings of blanching due to increased collagen and decreased vascularity.

h. End of first month, scar develops, increased tensile strength, maximal tensile strength achieved in several months.

STAGES OF SKIN GRAFT HEALING 1. plasmatic stage: occurs 2448 hours following graft application. A fibrin layer is formed between the graft and host

bed which serves to anchor and allow diffi.Jsion of nutrients to the graft. 2. inoscultation stage: this stage begins at 48 hours and involves revascularization of the grafted tissue. The graft will

demonstrate a pink hue during this stage. Lymphatic drainage will be established by the fourth to fifth day. 3. reorganization stage: the process of reorganization continues for months following grafting. Connective tissue will

reorganize and regulate vascular and lymphatic flow. 4. reinnervation stage: occurs simultaneously with the reorganization stage. The process may require one to two years

to complete.

FACTORS INVOLVED IN SCAR PROGNOSIS [Comprehensive Textbook of Foot Surgery]

Factors Effects Age* Race*

Body region *

Wound course and pattern** Wound Length**

Tension** Skin tension lines**

*Factors that are uncontrolled by surgeon **Factors that are controlled by the surgeon

Young patients may hypertrophy Blacks more likely to hypertrophy Among whites: blondes have a finer

scaring than brunettes Foot and leg heal well; related to

wound tension (See "Tension") Multiple small incisions heal better

than one long uninterrupted incision

Tension hypertrophies a scar Parallel lines give fine scars,

anti tension lines hypertrophy

294

FACTORS IN WOUND HEALING Pre-existing disease states. Nutritional status

Infection pH

Oxygenation Venous return

RESTING SKIN TENSION LINES -History of skin lines is very extensive, and very boring. -Basically, RSTL is recognized when a regularly shaped furrow is created upon pinching the skin area with index

finger and thumb. -These lines are often perpendicular to the long axis of muscles and their tendons, and often parallel to the axis of

joints at the level of the joint. -Ideal scar results can be acquired by placing incisions parallel to these RSTLs. -You will quickly notice that placing incisions parallel to RSTLs will not provide adequate exposure to the

surgical field. This is overcome by "zig-zaging" or creating an S-shaped incision. These incisions have become to be known as Anti tension lines.

WOUND COVERAGE TECHNIQUES -{}pen wounds must be provided with coverage. These coverage techniques are some of the most cleverly devised

and technically challenging to do in all of surgery. -Wound coverage should follow a step-wise approach. The simplest technique should be considered first. It

should follow this way: Direct closure -> Grafts -> local flaps -> distant flaps. - These include direct closure, skin grafting, flaps (including musculocutaneous and free flaps), artificial skin,

cultured cells, amnikon, and xenografts.

1. Skin Grafts This form of wound coverage involves removing varying thicknesses of epidermis and dermis from a donor site, and delivering it to the wound or graft site. Classified as:

a Autografts, Allografts, isografts, and xenografts. 1) autografts: a tissue harvested and applied within the same individual 2) isografts: a tissue harvested and applied within a set ofidentical twins 3) allografts: also called homografts, tissue is transferred between individuals of the same

species 4) xenografts: also called heterografts, tissue is transferred between different species.

Xenografts function only as biologic dressings and never area incorporated into the host's tissues

b. Full or spIit(0.OO8-0.012-0.016-0.020) thickness 1) split tbiekness skin graft (STSG): also called partial thickness skin grafts. Only a portion of the dermis is harvested. Split thickness grafts are the most commonly used free grafted tissue. There are four types:

a) thin grafts: grafts with a thickness of 0.008-0.0 12 inches. Excellent host tissue incorporation, however, this form of graft contracts the most. b) intermediate grafts: grafts with a thickness of 0.012-0.016 inches. This form is more durable and contracts less, however, host incorporation is slightly diminished. c) thick grafts: grafts with a thickness of 0.0 16-0.020 inches. The thicker the grafted tissue the less chance ofhost incorporation, due to greater tissue demands. Dmability and contraction are much improved. d) meshed grafts: this type of graft can be any thickness, but is placed through a meshing device which fenestrates the graft with unifmnly placed incisions. This process allows the graft to expand permitting greater surfuce coverage and prevents seroma and hematoma from collecting beneath the graft. Interposed spaces heal by epithelial migration from the surrounding graft tissue.

295

2) FaD thickness skin grafts: involves all of the dermis and portions of the superficial fuscia Any superficial fuscia or subcutaneous tat harvested must be removed prior to graft application. The primary indication for this type of graft is coverage in weightbearing areas or flexion points. The probability of host incorporatim is much lower than that of split thickness grafts. Donor sites usually include the inguinal or popliteal fossa areas. Small full thickness grafts may be harvested :from the foot in the areas of the medial arch and sinus tarsi. Donor site must be primarily closed or have a split thickness skin graft applied.

3) Apligraf (SEE BELOW) -Advantages: permanent coverage, technically simple, low risks, can be applied to almost any area of the body. -Disadvantages: increased failure rate over tendons and bone, graft contracture with split SO, increased failure rate with full thickness due to vascularization difficulties, infection or non healing donor site. Instrumentation for harvesting: Hand(Blair & Humby knives)or power( electric, gas or batteried powered dermatomes) instrumentation. Another useful device is the graft mesher. The graft mesher serves two purposes, first it allows the graft to remarkably increase its size, and second it prevents the biggest complication :from forming, seroma and hematomas. Another technique for preventing seroma and hematoma build up is via pie-crusting. Application of the graft:

a. graft must be in intimate contact with recipient tissue. b. all excess fluid must be removed :from recipient site. c. graft must slightly overlap the wound edges. d. suture graft into place. e. prevent shearing of revascularized graft by bulk dressings( cotton balls, fluffed gauze) secured by stent tie-over dressing. Moistening dressings may facilitate dressing removal later on. Excessive pressure must be avoided, because vascular channels can be occluded. f. limb must be immobilized in cast or posterior splint. g. post-operative dressings remain intact for 3-4 days. h. Storage of skin grafts: a skin graft should be harvested and applied immediately, however, excess skin graft may be stored in saline or anttbiotic solution soaked gauze and placed into a 0-5 refrigerator for up to 21 days.

Postoperative Course a. Removal of dressings 3-4 days post-op is done with great care. b. hematomas and seromas are recognized and punctured with a No. 11 blade. c. graft should be revascularizing and "pinking-up". d. necrotic tissue is to be removed. e.compression is maintained over graft for several months.

Complications of skin grafts: Any process which contacts between graft and host bed is interrupted will cause skin graft death.

seroma: the most common cause of skin graft failure. A transudative fluid accwnulation beneath the graft which tents it away :from the host bed. Seroma is prevented by proper application of a pressure dressing usually in the form of a stent dressing. The technique of "pie austing" or placement of multiple, small incisions in the graft will allow the seroma to escape the the dressing. Fluid may also be aspirated :from areas of concavity.

hematoma: similar to seroma, blood collection beneath the graft will also cause graft failure. Hemostasis of large bleeding vessels is necessary, however, capillary bleeding is normal and required for healing. Normal capillary bleeding may be controlled with proper fenestra tim of the graft and pressure dressing application. infection: greater than 9()01o of all skin grafts will take when the level ofbacteria is less than 10 bacteria per gram of tissue, however, certain organisms can destroy grafts quickly. Streptococcus pyogenes and pseudomonas pyocyanes produce fibrinolysins which disrupt the fibrin bond and devastate the graft. Systemic antibiosis has variable results in preparing recipient sites. Local wOWld care is far more important in reducing or eliminating infection.

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APLIGRAF

Description: a viable, bi-Iayered, skin construct: the epidermal layer (dull, matte finish) is formed by human keratinocytes and has a well-differentiated stratum cornewn; the dermal layer (glossy finish) is composed of human fibroblasts in a bovine Type I collagen lattice. While the graft contains matrix proteins and cytokines found in hwnan, Apligraf does not contain Langerhans cells, melanocytes, macrophages, lymphocytes, blood vessels or hair follicles. Apligraf is manufactured under aseptic conditions from human neonatal male foreskin tissue.

Indications: for use with standard therapeutic compression for the treatment of non-infected partial and full­thickness skin ulcers due to venous insufficiency of greater than I month duration and which have not adequately responded to conventional ulcer therapy.

Contraindications: • clinically infected wounds • patients with known allergies to bovine collagen • patients with a known hypersensitivity to the components of the Apligraf agarose shipping medium

How Supplied: • sealed in a heavy gauge polyethylene bag with a 1 0% C~/air atmosphere and agarose nutrient medium • should be kept in the sealed bag at 20°C-31°C until use (for single use) • supplied as a circular disk approximately 75 mm in diameter and 0.75 mm thick • should be used within 5 minutes of opening • To maintain cell viability, the product is aseptically manufactured, but not terminally sterilized

Preparation ofthe Venous Ulcer Wound Bed Prior to Apligraf Application: • Wound Infection: graft should not be applied over infected or deteriorating wounds until the underlying

condition has been resolved • Bacterial Containment: Antimicrobial agents may be used during the week prior to Apligraf application to

reduce the risk of infection. Dakin's solution, Mafenide Acetate, Scarlet Red Dressing, Tincoban, Zinc Sulfate, Povidone-iodine solution, and Chlorhexidine have been determined to be cytotoxic to Apligraf

• Wound Bed Preparation: graft should be applied to a clean, debrided wound after thoroughly irrigating the wound with a non-cytotoxic solution. Oozing or bleeding resulting from debridement should be stopped through the use of gentle pressure. Previous ulcer treatments other than standard therapeutic compression should be discontinued

• Control of Heavy Exudation: Heavy exudation may displace Apligraf and reduce adherence. Exudation should be minimized by appropriate clinical treatment. If exudation persists, Apligraf should be made permeable to exudate by perforating the graft to allow for drainage.

Suggested Technique for Application of Apligraf: • Prepare a sterile field and atraumatic instrwnents: forceps • Lift off the tray lid and note epidermal and dermal layer orientation: ApJigraf is packaged with the epidermal

(dull, matte finish) layer facing up and the dermal (glossy) layer facing down • When lifting Apligrafwith atraumatic forceps, be careful not to perforate or lift the polycarbonate membrane

beneath Apligraf • Apligraf should be placed such that the dermal layer (the glossy layer closest to the medium) is in direct

contact with the wound surface. Trim Apligraf so as to cover the wound bed with 1/8-1/4 inch margins • Secure Apligrafwith a three-layer dressing so as to assure contact to wound bed

FoUow-up: The wound should be inspected and the dressing changed at least once a week during the immediate post application period. More frequent changes may be required on highly exudative wounds. Additional applications of Apligraf may be necessary. The safety and the effectiveness of Apligrafhave not been established for patients receiving greater than 5 device applications.

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2. Skin Flaps

Skin flaps differ from skin grafts in that skin flaps retain their vascular supply. Indications: coverage of areas with poor vascularity (ie, bone and tendon), reconstruction of full

thickness, padding over boney prominences, coverage of areas requiring an operation at a later date, and restoration of sensation to an area. .

TermiJlology: Flap - refers to the tongue of tissue pedicle - refers to the base or stem of the tissue.

Classification: A. Vascular Anatomy Classification

1. random pattern (cutaneous flaps) derive their blood supply from the cutaneous dermal-subdermal plexus. They have no axial arteries. These are limited based on their dimensions (lengthlbreadth ratio). The pedicle must be wide enough to support the flap. The base should be at least as wide as the flap is long. If this is not possible, a delay procedure can be used to increase rate of survival. 2. Dial pattern (arterial flaps) - derive their blood directly from a cutaneous artery. The survival in these flaps are dependent on the dimensions of the artery and the length of the territory of the artery, not on the width of the pedicle. Examples are the dorsalis pedis flap and lateral calcaneal arterial flap.

a. Island flaps - no skin bridge b. Free flaps - transferred from distant site. More common in Podiatry. An example is the latissimus dorsi transfer.

B. Transposition Site classification 1. Local Oaps - adjacent to the defect.

a. Rotational flaps (rotation, transposition, interpolation)-pivot about the pedicle. Rotational flap - Ideally the flap should be a half circle. Movement is in a lateral orientation. Tension is relieved by Burow's triangle(excision of the triangle adjacent to the pivot point). Transpositional flap - usually rectangular or square. Movement is in an arc. Example: bi-Iobed flap, Limberg f1ap(rhomboid defect).

b. Advancement flaps - moved directly forward to cover defect, without lateral or rotational movement. Takes advantage of skin elasticity. Examples: V-V flap, V-V flap

2. Distant Oaps -indirect distant flaps seldom used in podiatry. -direct flaps - primarily taken from adjacent areas

3. Muscle & Myocutaneous Flaps The advantage of the muscle flap is its' bulk and vascularity.

* Preoperative considerations for muscle flaps should include: 1. viable length of the muscle on the dominant vascular pedicle 2. point and arc of rotation of the flap 3. the effect of the loss of function of the muscle

4. possible size of the cutaneous segment to be transferred with the muscle. muscles can, generally, support a cutaneous region 50% larger than the size of the muscle belly.

Lower Extremity Coverage with muscle Oaps: Upper 113 of leg. . . . . . . . . . . gastrocnemius/soleus

muscle bellies Middle 113 ofleg. . . . . . . . . . gastroc/soleusIFDU

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2. Distant flaps -indirect distant flaps seldom used in podiatry. -direct flaps - primarily taken from adjacent areas

3. Muscle & Myocutaneous Flaps TIle advantage of the muscle flap is its' bulk and vascularity.

Preoperative considerations for muscle flaps should include: 1. viable length of the muscle on the dominant vascular pedicle 2. point and arc of rotation of the flap 3. the effect of the loss of function of the muscle

4. possible size of the cutaneous segment to be transferred with the muscle. muscles can. generally, support a cutaneous region 50% larger than the size of the muscle belly.

Lower Extremity Coverage with muscle flaps: Upper 113 of leg. . . . . . . . . . . gastrocnemiUS/soleus

muscle bellies Middle 1/3 of leg. . . . . . . . . . gastroclsoleus/FDU

Tibialis Anterior mbs Distal 1/3 of leg. . . . . . . . . . soleus/peroneus

brevismbs Heel. . . . . . . . . . . . . . . . . FDBIEDB mbs Below medial malleolus. . . . . . .. abductor hallucis mb Below lateral malleolus. . . . . . . abductor digiti

minimimb Complications of muscle flaps -surgical errors of anatomy -traction, twisting. and transection of the vascular pedicle -larger defect than previous defect if flap fails

SKIN PLASTIES I. Derotational Skin Plasty

Indications: congenital clinodactyly, arthroplasty of the fifth toe. General Principle: skin wedge must be placed perpendicular to the axis of rotation of the toe. Also, wedge removal should only be deepened to derma1lsubQjunction, in order to preserve neurovascua1r components - unless exposure is critical.

2. Z-Plasty -essentially a transposition of two triangular flaps. General Principles:

-consider the gain in length at the expense of transverse shortening. Circumvented using multiple smaller Z-plasties. -should be planned so that the scar is in the RSTL. -arms of the Z should be equal.

-the angle of flap tips are ideally angulated 60 degrees(to ensure a sufficient vascular base). -the tip is secured using the Lambody suture(intraderma1 at tip and mattress at slot).

Complications: -tip necrosis due to tension, scar tissue across base, tissue undermining.

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3. v-v & y-VPlasties -a popular technique for skin lengthening General Principles:

*Maintain a wide angle V, for optimal blood supply * Apex should be proximal * A V-V will lengthen in one plane, and the Y -V will lengthen in the other(perpendicular) plane.

4. Redundant Skin Plasties --certain bone removal procedures will create skin redundancy, which can cause unacceptable cosmesis. Many of the times two semi-elliptical incisions will correct this surgical problem.

5. Double S Incision --use when incision is very large

6. Syndactylization --Goal is stability. Used when one digit is flail, and the adjacent is stable. --usually a salvage procedure.

DOG EAR REPAIR -Dog-ear is a term to descnbe the bunched-up tissue that may develop during wound closure. -can often be avoided by using cross hatch lines across planned incision site. -Smaller dog-ears will flatten with time, but larger dog-ears may be cosmetically displeasing. -These are easily rectified by extending the incision along the dog ear and allo\\'ing the flap to rotate. -other techniques describe cutting wedges out in line with RS1Ls -Another measure used is the Burow's triangle.

WOUND APPROXIMATION 1. Sutures 2. Steristrips 3. Staples

advantages:

disadvantages:

ereduce incidence of infection

ereduces overall cost of surgical procedure ereduces pt's exposure to anesthesia and tourniquet time ®cosmesis ®anatomicallimitations

WOUND EDGES - GENERAL PRINCIPLES -To ensure decreased scar formation, certain general principles must be followed:

.handle tissue gently heapproximate the tissue anatomically .close the deep tissues to decrease tension on skin tuse least reactive wound approximation devices tuse the proper gauge of suture to reapproximate to remove the tension tsubcuticular closure provides for excellent cosmetic results .Plantar incisions will require sutures to be left in for 3 weeks, nonweightbearing

MANAGEMENT OF KELOIDS AND HYPERTROPIDC SCARS -keloids and hypertrophic scars are benign gro\\'1hs characterized by an overabundance of collagen deposition. -both tend to be pruritic, raised, erythematous, and nodular. -they differ in that the keloid extends beyond the original incision site. Also, hypertrophic scars will improve in appearance, while keloids may worsen.

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-Keloids occur most frequently in adolescent blacks -Very important to do a thorough history and physical preoperatively Treatment: there are many modalities, none of which are consistently successful.

1. treatment should not begin less than 6-12 months postoperatively. 2. Surgical excision is more applicable to hypertrophic scars than to keloids. combined with one or more

Z-plasties to decrease the tension. 3. Use of nonabsorbable skin sutures with the least reactivity, ie polypropylene, surgical steel, or nylon.

Remove sutures in 7 days to minimize inflammatory reaction. 4. Strict adherence to atraumatic technique 5. Maintenance of good hemostasis 6. Postoperative irradiation and corticosteriods along scar will improve potential results. Corticosteriods

will decrease the level of collagenase inhibitors and thereby increase collagen degradation. Triamcinolone acetonide 40 mgflOOml is the preferred drug. Care should be taken to keep the drug within the scar, and away from the surrounding healthy tissue. Injections are preformed 3-5 weeks apart. When used with surgery, should inject 1 month prior to surgery, and for 3-4 weeks post-op.

7. Pressure over the scar exceeding 25 mm Hg for 4-12 months. This decreases vascularity, which thereby reduces cellular response and collagen deposition.

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PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS PEDIATRICS

1 t\ II"\.

METATARSUS ADDUCTUS

Definition: structural or positiooal medial deviation of the metatarsals in the transverse plane occurring at the tarsometatarsal articulation. • Erroneously tenned one-third of a clubfoot deformity as coined by Kite (1950)

talipes equinovarus: • forefoot adductim at midtarsal joint • rearfuot varus • rearfoot equinus

Incidence:

• 111000 live births • Risk to second in fiunily 1120 • 4.5% 151 degree relatives similarly affected • No sex predilection • 500"" bilateral • When willateral then left more commm than right

History:

Henke (1963)

• Germ.an literature • First to mention adductim of the fore part of the foot with valgus position of the heel

Bankart (1921) • First to report in English literature • Thought deformity was due to absence of the ''internal'' (medial) ameiform bone

McCormick and BIOWlt (1949) • Coined the tenn ''Skewfoot''

Kite (1950) • Erroneously tenned "Third of a Clubfoot"

Etiology - Unknown!

Theories: 1. Genetic 2. Atavistic medial ameiform 3. Intrauterine position

• Left sided cany

• Prima gravida 4. Environmental

• sleeping positions - belly sleeping 5. Arrest in fetal development 6. Muscle imbalance

• hyperactive abductor hallucis

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• shortened muscles (Abd hall / T. Post) gain mechanical advantage over lengthened muscles (peroneals)

7. Abnormal muscular insertions • Medial instead of plantarmedial insertion of abductor hallucis onto proximal phalanx • Tibialis anterior entirely onto 1 sI metatarsal instead of combined insertion with medial CWleifonn • Tibialis posterior primarily onto medial CWleiform instead of navicular

8. Absent medial CWleifonn

Associated Conditioos • IntemaI tIbial torsion (1 M-SOIo) • Congenital hip dysplasia (1.5-10%)

• Clubfoot • Windswept deformity (Met adductus on one foot and calcaneal valgus on the other)

Subjective Concerns

• In toeing • Tripping • Difficulty wearing shoes • Lateral shoe wear pattern • Bunion and hammertoes

Clinical Features:

1. Uncompensated

• C - shaped foot • Convex lateral border • Concave medial border • Prominent Sth met base • Separation of great toe from lesser toes

• Higharch

2. Compensated SkewfOOt (flatfoot)

• Adducted forefoot • Midfoot Iate:rally translated • Hindfoot valgus

• HAV • Digital cont:ractw-es

Clinical Exam Must determine: 1. Presence of tendon contractures / hyperactivity

• LicbtbIau test: the heel is stabilized, Sth met head is braced, and lateral pressure is applied to the medial aspect of the 151 metatarsal head ( abductory stress)

• A tight abductor halIucis will appear bowstrung 2. Concomitant presence of internal tIbial Union 3. Equinus?

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• Component of clubfoot 4. Flexible vs Rigid?

• If rigid then conservative therapy and soft tissue procedures are likely to full

Radiograpbic Evaluation

1. Metatarsus Adductus Angle - traditional • Normal = less than 21 degrees is a rectus foot • Pathologic = greater than 21 degrees • Consists of the longitudinal axis of the midfoot and the longitudinal axis of the metatarsals (which the

second metatarsal serves as a reference) • Line bisecting the talar head and extending distally win full medial to first metatarsal in metatarsus

adductus rather than laterally as seen in talipes equinovarus

2. Metatarsus Adductus Angle - Simplified (Engle's angle) • Utilizes the bisection of the second metatarsal and bisection of the middle ClIDeiform instead of the lesser

tarsus axis

3. Talo-1st metatarsal Angle-(Simons' Angle) • N=Oto-20 • Line bisecting the talar head will full medial to the first metatarsal in metatarsus adductus (negative) rather

than laterally as seen in talipes equinovarus (positive)

4. Talocalcaneal angle (Kite's Angle) • N = 20 - 35 (AP) • N = 25 - 45 (Lateral) • This angle is nonnal or increased in metatarsus adductus and decreased in TEV

Bisection Points of Lesser Tarsus

Lesser Tarsus Axis

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Metatarsus Adductus Angle Metatarsus Adductus Angle utilizing Engle.' s Angle

Metatarsus Adductus vs Uubfoot (lEV)

Clinical Comparison Metatarsus Adductus Clubfoot • Adducted forefoot • Adducted Forefoot • lateral navicular subluxation (or normal) • Medial navicular subluxation • Hindfoot neutral or valgus • Hindfoot varus • Noequinus • Equinus

Radiographic Comparison Metatarsus Adductus Simons' angle

• Positive Kite's angle • Normal or increased Talonavicular relationship • Normal or lateral navicular

Cooservative Tberapy

Clubfoot Simons' angle

• Positive Kite's angle

• Decreased TalonavicuIar relationship • Medial

1. Passive stretching and manipulation (up to 3 weeks old) 2. Serial plaster casting (up to age of ambulation ) 3. Modified Furlong cast 4. Modification of sitting or sleeping positions 5. Orthotics devices 6. Shoes I Splints

Biomechanically SOlDld Biomechanically lDlSOWld • Ganley Splint • Reverse last shoes

• Bebax • Denis-Browne Bar • Wheaton brace • Fillauer Bar

• Unibar

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• Ipos AntiaddndUs shoe

TIIREE POINTS OF PRESSURE: 1. Abduction at medial side of:first metatarsal head 2. Adduction at lateral side of cuboid 3. Inversion at heel

***Must be maintained to avoid valgus torque 00 hindfoot • The foot should be maintained in the corrected positioo for a time at least as loog as it took to gain the

desired oorrectioo

Surgical Coasiderations

1. Age • yotmger patients more amenable to soft tissue procedures

2. Has conservative therapy been attempted? • gm attempt conservative therapy up to the age of 5

3. Conamitant deformiti~ • '. Int tibial torsion • residual clubfoot • severe ~ valgus with HA V and hammertoe deformiti~

4. Severity of deformity • the more severe the deformity the greater the resistance to treatment and the more aggressive one needs to

be in surgery 5. Osseous maturity 6. FiexJ."le or rigid?

• the two above are related- with osseous maturity the metatarsal ~ square off and the deformity becom~ more rigid As the deformity becom~ more rigid soft tissue procedures are less likely to achieve the desired correction.

• Forceful manipulation of the rigid foot may force the hindfoot into valgus

SurgieaI Treatment

Guidelin~: I. Ag~ 2 to 6-8 years

• Soft tissue procedw-es 2. Ag~ 4 to 8 years

• Gray zone • Too old and too advanced osseous maturity to perform soft tissue procedur~ and yet not quite

mature enough to perform osseous procedw-es 3. Ages greater than 6-8 years

• Osseous procedw-es

Soft tissue procedures:

1. Heyman, Herndon and Strong procedure (1958) • procedure initially described using a transverse incision aa:oss Lisfranc's joint • three dorsal. linear longitudinal incisioos now used more commonly to avoid neuorvascu1ar embarrassment • release <bsal, interosseous and plantar ligaments along with the joint capsule • Modified HHS now more common (Kendrick et al., 1970)

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• preserve plantar lateral ligaments to prevent dorsal dislocation) • Complications:

• Dorsal dislocation • Degenerative arthritis (Stark et aI., 1987)

2. Thomson procedure (1960) • Resection of abductor hallucis muscle belly and medial capsulotomy

3. Lichtblau procedure (1975) • Modified Thomson procedure • Tenotomy or partial resection of abductor hallucis plUscle

4. LaPorta and Sokoloff • Tibialis posterior tendon lengthening with talonavicular capsulotomy, usually used in conjunction with

lUJ&S or Berman-Gartland procedures

Gray Zone (Cartilaginous procedures):

1. Johnson wedge chondrotomy (1978) • Resection of laterally based chrondrotomies from the bases of metatarsals 2- 5 laterally based closing wedge

osteotomy on the first metatarsal, just distal to the epiphyseal growth plate

Osseous procedures:

1. Bankart (1921 ) • Advocated excision of cuboid

2. Peabody & Muro (1933) • Excision of the bases of the three central metatarsals • Osteotomy of the fifth metatarsal • Mobilization and luxation of the first metatars<K:uneiformjoint • Correction of any abnormal insertion of the tIbialis anterior tendon

3. McCormick & Blount (1949) • Arthrodesis of the first metatarso-cuneiform joint • Osteotomies of metatarsals 2-4 • Wedge resection of the cuboid

4. Fowler (1959) • Opening wedge osteotomy of the medial cuneiform with bone graft

5. Steytler & Van Dec Walt (1966) • Base wedge "V - shaped" oblique osteotomies of all the metatarsals (lateral oriented base; apex - proximal)

6. Berman & Gartland (1971) • Proximally oriented crescentric dome-shaped osteotomies of each of the metatarsals • Osteotomy made at least 6 rom distal to growth plate of 1st metatarsal • First and fifth metatarsal osteotomies fixed with Steinman pins; second, third and fourth not fixed • Popular procedure today

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7. Modified Bennan-Gartland (actually the Steytler & Van Dec Walt procedure) • Transverse closing abductory base wedge osteotomies of all the metatarsals • Multiple fixatim techniques for all the metatarsal osteotomies • Popular procedme today

8. Lepird procedure (1982) • Oblique closing abdnctay wedge osteotomies m 1st sometimes (due to epiphysis) and sometimes the 5th

metatarsals • Rotatimal oblique base osteotomies of metatarsals 2-5

• Rotatimal osteotomies should parallel the ground supporting surfilce (thus, transverse plane motim)

• Technique: medial cortical binge initially preserved for stability, the screw is placed perpendicular to the supporting surfilce but not tightened, the medial cortex is then transected and the metatarsal is rotated to its corrected positim and the screw is tightened

• Popular procedure today

9. Brink and Levitsky (1995) • Cuneiform and wboid wedge osteotomies • performed through two incisions • Staple and K - wire fixatim

***Note: the above procedures can be performed alme or in combination ( ego Fowler and modifications of the Bankart procedure)

Johnson osteochondrotomies

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Berman & Gartland Steytler & Van Der Walt McCormick & Blount

Peabody & Mum Lepird

Brink & Levinsky

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CLUBFOOT

I. Congenital: A. Postural (Extrinsic):

1. Definition: Forefoot Adductus Rearfoot Varus Ankle Equinus

2. Mild, flexible defonnity with normal anatomy 3. Etiology: Intrauterine malposition 4. Prognosis: Good 5. Treatment: Conservative

B. Talipes Eguinovarus (Intrinsic): 1. Definition: Forefoot Adductus

Rearfoot Varus Ankle Equinus Talonavicular Subluxation Lateral Rotation o/Talus inAnJde Mortise

2. Severe, rigid defonnity with pathologic anatomy 3. Prognosis: Poor 4. Treatment: Surgical

II. Acquired: A. Neuromuscular Disorders:

1. Poliomyelitis 2. Meningitis 3. Cerebral Palsy 4. Spina Bifida 5. Myelomeningocele 6. Post-CVA

B. Post-Traumatic: 1. Spinal Cord Trauma 2. Peripheral Nerve Trauma 3. Tendon Laceration 4. MalINon-Union 5. Volkman's Contracture 6. Burn Contracture

Ill. Historical Review: A. 1210 BC: wall etchings of pharaoh Siptah with clubfoot deformity B. 1000 BC: 1st description of clubfoot in Indian literature C. Greek Mythology: Greek God Hephaestus with bilateral clubfoot deformities D. Aztecs: made splints from cactus leaves E. 300-400 BC: Hippocrates thought etiology was intrauterine position and recommended manipulation

and bandaging F. 6th - 15111 Centuries "Dark and Middle Ages": marked those with a clubfoot deformity as the devil G. 15th - 16!h Century 'The Renaissance': renewed interest in clubfoot deformity H. 1782: Lorenz advocated achillis tenotomy for treatment I. 1803: Scarpa believed osseous changes occurred secondary to soft tissue contractures J. 1831: Stromeyer performed achillis tenotomy on a recurrent clubfoot K. 1839: Little (Stromeyer's student) had a clubfoot defonnity secondary to an infantile febrile disease.

He wrote the "Treatise on the Nature o/Club/oot & Analogous Distortions" L. Late 1800's: Aggressive, radical treatment with forcible manipulation (Thomas Wrench) and resection

of large bone wedges M. 1933: Kite had an 88% success rate with conservative therapy consisting of gentle manipulation with

plaster of paris splinting. Kite's angle (talocalcaneal angle).

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N. 1884 - 1969: Staged, piecemeal soft tissue release o. 1971: Turco recommended a comprehensive, posteromedial release with temporary fixation of the

talonavicular joint P. 1982: McCay advocated circumferential release Q. 1985: Simons also advocated circumferential release R 1982: Crawford developed the Cincinnati incision

IV. Incidence: A. 2: 1 Male:Female B. 50% Bilateral (when unilateral Right> Left) C. Polynesian: 6.81/1000

Middle East & South African Blacks: 3.5/1000 White: 1.1211000 Asian: 0.57 f] 000

D. Most common pathologic, congenitalfoot deformity: 2.29/1000 live births

V. Etiology: IDIOPATHIC, possible factors include: A. Extrinsic & Environmental factors:

1. Intrauterine malposition: Hippocrates 400BC 2. Common peroneal nerve palsy secondary to intrauterine position (anterior muscle weakness):

White 1929 3. Amniotic strictures 4. Diseases: Diabetes, maternal hypothermia 5. Drugs: Aminopterin, d-tubocurarine, Methotrexate 6. Radiation 7. Malnutrition 8. Viruses 9. Multiple Pregnancies

B. Intrinsic & Anatomic factors: 1. Germ Plasm Defect: malposition of head and neck of talus: Irani & Sherman 1963, & Shapiro &

Glimcher 1979. The most widely accepted etiology. 2. Arrest of fetal development at 5th week of gestation: Bohm 1929 3. Arterial dysgenesis: absent or underdeveloped anterior tibial & medial plantar arteries 4. Anomalous tendon insertions: plantar insertion of TP or medial insertion of achillis & PL 5. Muscle maldevelopment 6. Congenital constriction bands: Keith 1940 7. Uneven rate of bone and muscle growth: Bechtol & Mossman 1950 8. Contracted deltoid ligament: Hirsch 1960

C. Hereditary factors: 1. Autosomal Dominant

Autosomal Recessive Sex-linked Recessive

2. Race Predilection 3. Unaffected By: Birth Weight

Birth Number Maternal Age

4. Incidence in Twins (Idelberger, 1939): Identical: 32.5% Fraternal: 2.')0/0

5. Incidence in Relatives (Wynne-Davies, 1973): 1st degree: 20-30 fold ina-ease zDCi degree: 6 fold inaease 3td degree: no ina-ease

6. Polygenic, multifactorial inheritance with sex-linked threshold: The number of abnormal genes must exceed the threshold Females have a higher tolerance; therefore, it takes more genes to a-eate the deformity. Since so many genes are required, the deformity is usually more severe in females. Males have a lower threshold; therefore, less genes are needed to create the deformity and when it is present it is usually less severe.

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VI. Pathologic Anatomy: A. Talus:

1. Reduced size 2. Head & neck anguJated medial and plantar 3. Anterior & lateral deviation in ankle mortise 4. Ta1ar Declination Angle = 115 - 135° (Normal = 150°) 5. Ta1ar Neck Obliquity = 50 - 65° (Nmnal = 15°)

B. Calcaneus: 1. Normal shape 2. Possible undecdeveloped sustentaculmn tali 3. Anterior & middle tilcets may be one 4. Plantarmedial angulation beneath talus (equinus & varus)

C. Navicular: 1. Normal shape 2. Hypertrophic tuberosity 3. Plantarmedial subluxatioo 4. May articulate with medial malleolus

D. Soft Tissues involved in deformities: 1. Skin, filscia, retinaculmn, vinculi (Master Knot of Henry), joint capsule, ligaments, tendons,

muscles, veins & arteries, and nerves 2. Tendons & Muscles:

a. Posterior: Contracted b. Medial: Cootracted c. Plantar: Contracted d Peroneals: Elongated e. Anterior Tibial: Dorsomedial displacement

3. Ligaments: a. Calcaneofibu1ar: Cootracted b. Posterior Talofibular: Contracted c. Bifurcate: Cootracted d. Interosseous: Contracted e. Spring Ligament: Contracted

VII. Pathomechanics: A. Lateral rotation of talus with head and neck angulated medial & plantar B. Posterior displacement of fibula (reason for contracture of CF lig)

1. Horizontal Breach (Angle between the bisection of the rearfoot and the malleolar plane) a. Normal = 75 - 90" b. TEV= < 75°

C. Calcaneus in varus & equinus D. Navicular medial and plantar (may abut medial malleolus) E. Forefoot adductioo

VIII. Clinical Evaluation: A. History:

1. Pregnancy: Gestation, illness, drugs, tramna 2. Delivery: Duration, anesthesia, complications 3. Growth & Development: Milestones

B. General Examination: 1. Neurological: Motor tooe & fimction, reflexes, sensation 2. Back & knees 3. Skin

312

C. Lower Extremity Examination: 1. Appearance

a. "Club-like"( equinoadductovarus) b. Small drawn-up heel c. Adducted forefoot d. Calf atrophy e. Decreased foot size

2. Medial: a. Skin: creases/furrow b. Navicular prominent c. Forefoot adducted

3. Lateral: a. Skin: thin/stretched b. Talus prominent c. Fibula posterior

IX. Radiographic Evaluation: A. Talocalcaneal Angle (Kite's Angle):

I. AP: Normal = 20 - 40° TEV = 15° or less

2. Lat: Normal = 35 - 50° TEV = 25° or less

B. Talo-I 5I Metatarsal Angle: I. AP: Normal: 0 - (-20) °

TEV = 15° or more C. Talocalcaneal Index:

1. Add talocalcaneal angles together on AP & lateral 2. Normal is> 40°

D. Simons Rule 0(15: I. Predicts presence of talonavicular subluxation using measurements on AP radiograph

a. Navicular does not ossify until about age 3 2. Talonavicular subluxation is present if:

a. Talocalcaneal Angle < 15° AND b. Talo-l51 Metatarsal Angle> 15°

E. Positioning for Radiograph: I. Position of maximwn correction: dorsiflexion & abduction with foot plantigrade 2. Sitting with hips & knees flexed 90°

F. Sources of Erroc: 1. Poor position 2. Identification: Navicular does not ossify until about 3 years

Ossific nuclei in talus & calcaneus are eccentrically placed G. Indications for Radiographs:

1. Determine severity of deformity 2. Monitor response to therapy 3. Iatrogenic changes 4. Intra-operative realignment

X. Conservative Treatment: A. Performed on ALL congenital clubfeet B. Begin immediately C. Manipulatioo:

I. Gentle but firm 10 - 15 minutes 2. Reduce all components: Abduct forefoot

Evert Heel Distract heel

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D. Serial Casting: 1. Used to maintain reduction 2. Above-knee cast changed every 1 - 2 weeks 3. Continue until satisfactory correction obtained or until further correction is unobtainable 4. Bivalve last cast and use for night splints 5. Monitor therapy with radiographs every 1 - 2 months

E. Post-Reduction: 1. Night Splints 2. Prewalker Shoes 3. Orthotics 4. Stretching

F. Complications with Manipulation: 1. Rocker-bottom foot 2. Flat top talus 3. Wedge-shaped navicular 4. Dorsal displacement of navicular 5. A VN: talus, navicular, distal tibia

XI. Surgical Treatment: A. Soft Tissue Release:

1. Comprehensive, circumferentiol release: Posterior, medial, lateral, plantar 2. Summary: General anesthesia, thigh towniquet, soft tissue release, reduction, K-wire fixation of

talonavicular joint, intra-operative radiographs, compression cast 3. Ideal Age: 3 -12 months

a. No surgery before 3 months old because you need conservative therapy to stretch the tissues and it is also technically difficult due to the small size of the structures

b. Decrease success when age is> 3 years old 4. Incision Placement:

a. Posteromedial ([urco): decreased visualization laterally b. Cincinnati (Crawford): Cosmetically superior however great incidence of wound dehiscence c. Posteromedial + Lateral

5. Sequential Release: a. Retract tarsal tunnel contents b. TP tendon lengthening (Z-plasty): follow distal to navicular tuberosity c. Talonavicular joint capsulotomy d. Spring ligament e. FDL tendon lengthening (Z-plasty): follow distal to Master Knot of Henry f. FHL tendon lengthening (Z-plasty) g. Superficial deltoids h. Interosseous ligament i. Calcaneofibular ligament j. Achillis tendon lengthening (Z-plasty) k. Posterior ankle joint capsulotomy (including posterior talofibular ligament) 1. Plantar fascia

B. Osseous Procedures: 1. Indications:

a. Recurrence b. Severe, rigid deformities c. Performed only in the child & adult NEVER on infants

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2. Osteotomies (Ages 2 - 6 years old): a. Lateral Column Shortening:

1. 1902 Ogston: Cuboid closing wedge 2. 1961 Evans: Calcaneocuboid joint closing wedge and arthrodesis 3. 1973 Lichtblau: Anterior calcaneus closing wedge

b. Medial Column Lengthening: 1. 1959 Fowler: Medial cuneiform opening wedge

3. Salvage Procedures: a. Triple Arthrodesis (> 12 years old): Increases stability in severe, rigid deformities b. Talectomy (4 - 8 years old): Used for severe, rigid deformities such as arthrogryposis &

myelomeningocele C. Complications:

1. Wound dehiscence 2. Residual deformity 3. Navicular wedging & subluxation 4. Flat top talus 5. Rocker-bottom foot 6. Overcorrection: calcaneus, pes planovalgus

D. Residual Deformities: 1. Metatarsus Adductus:

a. Soft tissue release b. TA tendon transfer c. Osseous procedures

2. Rearfoot Varus: a. Calcaneal osteotomy: Dwyer

3. Equinus: a. Achillis tendon lengthening or tenotomy

CALCANEOVALGUS

Definition:

Clinical:

Incidence:

Etiology:

Radiograph:

Deformity identified at birth with the foot markedly dosiflexed at the ankle and valgus position of the foot with respect to the leg.

dorsum of foot in contact with anterolateral leg ("up and out") Severe limitation of plantarflexion and inversion Lateral-loose skin folds below lat mall. Medial-skin stretched and taught

most common congenital malformation 1 : 1 000 live births more common in females usually bilateral with one limb more severe than the other

first born of young mothers Compression of the prima gravada with small tight uterus

External rotation & contracture of hips Sleeping position with ext. rotated & abducted hips

(primary deforming structures = tendons of anterolateral ankle)

AP- inc. TC angle Dec. 1N congruity with FF abduction Medial angulation of head & neck of talus

315

CVvs. VT:

DiifDX:

Treatment:

Lat- plantarflexed talus(relative due to df foot) with respect to tarsal bones Bisection ofh&n of talus inferior to cuboid(normal=superior halt) Dorsifelexion of calcaneus

radiograph

CV VT(vertical talus) Nav medial to talus Relative PF of talus Inc. DF of calcan

dora! to h&n of talus (if ossified) verticaJ/PF position of talus calc parallel with low or neg CIA

Clinical

Reducible with manipulation Foot against antec. Leg

nonreducible foot 9Odeg. To leg or equinus

vertical talus Congenital medial posterior bowing of the tibia Neuromuscular disease

conservative

surgical

Manipulation in early dx with flexible deformity Daily passive manip.

PF & 1NV to stretcbllengthen dorsolat soft tissues 20-30x in 4 daily sessions

Serial casting toes to tib tuberosity correct component parts of deformity

foot held pf if adduction rf neutral to inv

(avoid using if as lever to cast rf in varus) cast weekly or biweekly 3-6 months gentle gradual persistent correction is the rule

post cast - maintain with splints(Ganley) 12-16hr/day up to 6 months

considerations

options

rigid deformity failed conservative tx age of patient development of secondary arthritis

division of soft tissue structw"es anterior ankle

peroneus tertius EDB EDL AITFL

Correct valgus Z lengthen peconeals Divide preoneal sheath Div lat lig of STJ

316

Correct FF abduction Div ligg of CCJ Section TNJ capsule Single K-wire across MTL

AK cast 10-12 weeks Other procedures

VERTICAL TALUS

Introduction • most rigid form of flatfoot

Calcaneal osteotomies-Evans STJ arthroeresis Arthrodesis

• other terms: congenital rocker bottom foot, congenital convex pes valgus, congenital flatfoot with talonavicular dislocation, ''Persian slipper foot"

• severe cases involve cc joint, less favorable outcome

• 50% occur BIL, right> left • males = females • 50% occur as isolated congenital

defonnity

DitJerential Diagnosis • Idiopathic Flat foot • Paralytic Flatfoot • Flat foot in cerebral palsy • Oblique talus

• Talonavicular joint subluxation with weightbearing only • plantarflexed view, total reduction of Talooavicu1ar joint • benign flexible flatfoot • requires orthotics, possible Tendo-achilles lengthening, serial casting, surgical interventioo rare

Etiology • 500/0 secondary to either spina bifida, arthrogrypbosis, or a chromosomal abnormality (trisomy) • Neural tube defects - usually rigid form

• Diastematomyelia, lipoma of cauda equina, sacral agenesis, myelomeningocele • Arthrogrypbosis multiplex congenita • Neurofibromatosis • Ischio-calcaneal band, rare contracture of triceps

• Acquired • Cerebral palsy • Poliomyelitis • Spinal muscular atrophy

• Part of clinical spectrum • Freeman-Sheldon • Smith-Lemli-Opitz

• Marfan • • • Hurler's DeBarsy Nail-patellae

317

• • • Inheritance

•

Pnme-belly (Eagle-Barrett Syndrome) Multiple Pterygium Syndromes

Autosomal dominant, incomplete penetrance

Pathologic Anatomy • Wedge-shaped navicular with hypoplastic plantar segment • Severe pIantarfIexion of ankle joint • Tibia articulates with talus in posterior I13 only • Calcaneus closely approximates with distal tip of fibula and is everted and plantarfIexed • SustantacuIum tali is hypoplastic,no support for talar head • Absent anterior talar facet • Dorsal Talonavicular ligaments thickened and blend with deltoid • Superior peroneal retinaculum - attenuated, allowing peroneal subluxation • TP tendon attenuated under talar head, subluxed anteriorly onto medial malleolus • Peroneus Longus muscle is major deforming force, with increased pronatory potential • Contractures seen in:

• Tibialis Anterior • Extensor Hallucis Longus • Extensor Digitorum Longus • Peroneus Brevis • Triceps Surae • Peroneus Tertius

• Dislocated tendons: • Tibialis Posterior

• • Peroneus Brevis Peroneus Longus

ClUUcalilppearance • Forefoot abducted and pronated, lateral clawtoes • Convex plantar surface, rocker-bottom foot • Palpable talar head medially and plantarly • Hindfoot equinovalgus • Tight heel cord • Crease over narrowed sinus tarsi • Hollow anterior to lateral malleolus is helpful sign to differentiate VI from calcaneovalgus

• Gait:

• • • Delay in ambulation is uncommon Older children with shortened stride Decreased balance

• Pain may not appear lDltil adolescence

Radiographic Findings • Include ankle in evaluation offoot • Forced plantarflexion lateral view paramount in diagnosis • Talus, calcaneus and metatarsals all visualized in newborns • Cuboid ossifies within first month of birth • Navicular ossifies in 3 to 5 years • Resting lateral view:

• Use lateral cuneiform as marker to locate navicular • Dislocation of navicular dorsal to talus, forfoot follows the navicular • Increased talar metatarsal angle • Calcaneus in equinus

318

• Vertical position of talus • Resting dorso-plantar view:

• Increased Kite's angle (talo-calcaneal angle) • Increased talar metatarsal angle

• Severe VT will present with dislocated calcaneal-cuboid joint • Osteochondritis of the navicular (Kohler' s disease) may sometimes occur

Classifications Dupont Institute - Aksu & Kumar • Group I - Supple foot that resemble calcaneovalgus • Group II - Rigid foot, part of a syndrome • Group III - VT associated with Trisomy 13 - 15 or 18 • Group IV - VT associated with neuromuscular disease such as spina bifida

Wenger & Rang • Teratogenic - bilateral stiff as seen in arthrogryphosis • Neurogenic - muscle imbalance, more supple - as seen in spina bifida • Acquired - malposition in utero - as seen in children with no other major problems

Coleman • Type I - absence of associated calcaneal-cuboid joint dislocation • Type II - presence of calcaneal-cuboid dislocation

Treatment • Goals:

• Plantargrade foot with balanced distribution of weight between hindfoot and forefoot • Re-establish normal anatomical relationship between hindfoot and forefoot • Restoration of medial column competency

• Conservative tberapy(Casting) is aimed at stretching soft tissue structures in preparation for surgical intervention

• Casting (forefoot in plantarflexion) - start at birth and continue for 3 to 4 months • Surgical approach:

• Cincinnati incision • mid-dorsal incision • medial arch incision

• Surgical treatment may be performed in two stages(forefoot correction followed by hindfoot correction) • Lengthen contracted and dislocated tendons • Capsulotomy of talo-navicular and ankle joints • Capsulotomy of calcaneo-cuboid joint in severe cases • Tendo-achilles lengthening • Maintain alignment of talo-navicular and ankle joint with Kirshner wires • Release of calcaneo-fibular ligament to allow dorsiflexion of the talus • Release of taIo-calcanealligament to allow reduction

• Tendon transfer (PB, TA) to talar head or neck has been described • Subtalar or Triple arthrodesis in severe cases, older patients or if above mils

319

TORSIONAL DEVELOPMENT I DEFORMlTIES OF THE LOWER EXTREMITIES

TRANSVERSE PLANE DEFORMITIES Femur • Antetorsion I retrotorsion • lllp malposition / contractures

Tibia • Internal / external tibial torsion • Knee malposition / contractures

Foot • Metatarsus Adductus

SUBJECfIVE CONCERNS • In Toe I Out Toe • Tripping I Falling • Clumsy Gait • KneePain • Knock Knees • Bowlegs

IN TOEING 1-3 Years • Internal Tibial Torsion • Metatarsus Adductus

>3Years • Internal Femoral Torsion

PATHOPHYSIOLOGY Heredity Intrauterine Position • Persistent Fetal Alignment Persistent MaIposture in Postnatal Life • Sleeping I Sitting Positions Iatrogenic

TERMS Torsion: • The act or process of twisting; turning or rotating about an axis Version: • The act or process of turning or changing direction Ante • Prior to I Before • In front of Retro • Backward • Located behind

PODIATRIC TERMS Version • Rotation at the joint level Torsion • Rotation about the long axis of a bone

IN • Antetorsion • Retroversion our • Retrotorsion • Anteversion

320

ORTHOPEDIC TERMS

Version • Angular difference between the transverse axis

of each end of a long bone Torsion • Present when the version is abnormal or

excessive

PODIATRIC Femoral Retroversion

1

.' ,..,

....... .. , ..• .

. ,.,. ....... . .......

ORTHOPEDIC

PODIATRIC Femoral Anteversion

Antetorsion (16)

Normal (~12)

Retrotorsion (6)

INTERNAL FEMORAL TORSION (Femoral Antetorsion)

Internal Deviation

•••••• .... ... •••••

FEMORAL .ANTEVEBSION - transverse plane angle between head/neck and femoral condyles Birth • Normal: ~ 40 degrees • Range: 31-52 degrees

Adult • Normal: ~ 8-16 degrees

321

• Range: 7-28 degrees

45

40

35 - Anteversion

30

25

20

15

lD

5

0 Birth 1 3 5 V-. 7 9 15 Adult

TIBIAL VERSION - transverse plane angle between tibial plateau and plafond (ankle axis) Fetus

.:. Internal/Medial Infant

.:. +/- Neutral

.:. Normal: 0 - 7 Degrees Child

.:. Slightly External/Lateral Adult

.:. Lateral/External

.:. Normal: 20 - 30 degrees

30

25

20

15

10

5

0

-5 Birth 1 3

TORSIONAL PROFILE .:. Foot - Progression Angle

5

.:. Medial Hip Rotation in Extension

.:. Lateral Hip Rotation in Extension

.:. Thigh - Foot Angle

.:. Transmalleolar Axis Angle

- Tibial Version

7 9 11 15 30 50 70

Years

322

.:. Foot Configuration

90 80 70 ..... ..... .....

60 " ..... "- .....

50 "---

40 30 20 10 0 Birth 1 3 5 7 9

Years

FEMORAL ANTEVERSION - Measurement Clinical

.:. Netter method • Patient is placed Prone • Palpate Gr. Trochanter - Femur • Internally rotate the leg - Knee bent

until Gr. Trochanter is the most prominent laterally

• Measure angle between tibia (leg) and vertical

Radiography .:. Magilligan technique .:. Dunn technique

• Both are not often used Computed tomography / MRI

.:. Best Methods

TIBIAL TORSION - Measurement Clinical

.:. Thigh - foot angle

.:. Second metatarsal

.:. Transmalleolar axis Radiography

.:. Hutter and Scott Method Computed Tomography Ultrasound

--Internal

---- External·

11 20 30 50 70

...... t .... 11°.." DO

INTERNAL FEMORAL TORSION .:. In-toeing> 2-3 years .:. Medial rotatation of thighs .:. Patellae turned inward .:. Int rotation> Ext rotation

INTERNAL FEMORAL POSmON .:. Shortened or Spastic Medial Hamstrings /

Adductors .:. Contracture of Hip Capule

• Pubocapsular • Illiofemoral

.:. Gait Analysis • Increased Adduction - Late Midstance

TIBIAL TORSION Internal

.:. Failure of normal external rotation to occur

External .:. Concomitant Internal Femoral Torsion

• Miserable MaJalignment Syndrome .:. Iatrogenic post treatment for ITT or 1FT

ADULT

323

TIBIAL'IORSION - Treatment Considerations .:. Usually resolves by age 3 .:. 4% of adults have unresolved lIT

• 1 % Incapacitating .:. Greater and Faster Correction?

FUNCTIONAL EFFECTS OF TORSIONAL ABNORMALITIES Internal Deviations

Prior to Age of Self Awareness: .:. Decreased Angle of Gait .:. Supination

Beyond Age of Self Awareness: .:. Conscious Pronation .:- Pronation

External Deviations .:. Heel Contact Pronation

TREATMENT - TORSIONAL ABNORMALITIES

CONSERVATIVE TREATMENT .:. Passive Stretching and Manipulation .:. Change Sitting / Sleeping Habits .:. Serial Long Leg Casting .:. Bars

• Denis-Browne • Ganly Splint • Counter Rotation System (CRS)

.:. Braces

.:. Wheaton Telescoping Brace

.:. Orthotics

SURGICAL MANAGEMENT Indications

.:. Child> 8 years old

CONSERVATIVE TREATMENT - Seguale .:. Recurrence .:. External Tibial Torsion .:. Chondromalacia of the Patella

• Miserable malalignment syndrome ·:·Long Term Effects Unknown

SURGICAL MANAGEMENT Femur

.:. Rotatinal Osteotomies • Multiple Locations

.:. Illizaorv Tibia .:. Significant Functional Disability

·:·Severe Cosmetic Deformity .:. Proximal or Distal Rotational Osteotomy

324

EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE EMERGENCY MEDICINE 'E"M"E','RGP"N' "C',\lf\Ar::, 0' ')' C~ 'I',<}, ," ' , ", '" ,.L.d. ]. , lL ,,_. ' , ,

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EMERGENCY MEDICINE

ANAPHYLAXIS

Introduction Anaphylaxis according to Dorlands is a manifestation of immediate hypersensitivity (type I) in which e:~posure of a sensitized individual to a specific antigen or hapten results in life-tbrea1ening respiIatory distress. usually followed by vascular collapse and shock and accompmied by urticuria. pruritus and angioedema. Anaphylactoid is a reaction similar to anaphylaxis but it is not immullologically precipitated and thus occurs after the initial e.xposure. Anaphylaxis means lack of protection due to immunization. Your body creates an antibody that will not defend you from certain antigen. but "in cause a reaction.

Pathophysiologic Mechanism The susceptible person has an initial exposure to an antigen or a hapten which produces a specific sensitizing antibody or reagin. This reagin is kept within circulatory IgE immunoglobulins. These antigen specific 19E comple.xes bind \\'ith mast cells and Imophils; Upon re-exposure to the antigen, bridging occurs between the antigen alld the sensitized 19E complexes that have developed on the surfaces of the mast ceslls and basophils. This bridging causes a change in the cells causing a decrease in cyciic AMP. leading to degrnnulation and a release of pbarmocoJogically active mediators such as histamine. SRS-A serotonin. bradykinin and also chemotactic factor for cosinophiIs • neutrophils and p1atelcts. The above mentioned mediators except for histamine and SRS-A are thought to have added effect on anaphylaxis, but it is histamine and SRS-A that are the true causes of the anaphylactic reactions. Histamine is thought to be a truYor mediator of anaphylaxis of man. Histamine causes bronchial oonstriction. increased capillary penneability and vasodilation. Slow-reacting substance of anaphylaxis causes constriction of bronchial smooth muscle. Histamine and SRS-A aJong "\\ith the other above mentioned mediators arc responsible for the manifestations of anaphylaxis. These manifestations are what we see clinically and what must be recongized so that treratment can be instituted immediately.

There is no universal pattern or step-by-step process of anaphylaxis. The manifestations of anaphylaxis are listed below: with any reaction. not aJI the manifestations may occur and those that do may not appear in any order.

1. Cutaneous: erythema pruritus. urticaria and angioedema (usually of the eyes. lips or tongue) II. Respiratory failure: two types

A) Upper airway obstructions 0\\1ng to edema of the larynx and/or epiglottis which can cause acute distress and death by suffocation.

B) Lower airway bronchoconstriction which leads to limited airflow that is not relieved by endotracheal intubation, leading to a problem of gas e.xchange and hypoxemia and hypercarbia.

III. Cardiovascular: probably the most severe reaction which leads to hypotension. arrhythmias and cardiac arrest

Signs and symptoms The typical manifestations of anaphylaxis aIC that the patient complains of a sense or aura of uneasiness.. and becomes agitated and flushed Reaction can occur "\\ithin 1 to 15 minutes or several hours after exposure to antigen. Symptoms progress to palpitations. paresthesias. pruritus, coughing. sneezing. urticaria and difficulty breathing. Cardiovascular collapse can occur concomitantly "With respiratory distress or in its absence. Unrecognized, anaphylaxis can lead to shock and ultimately death

Causes The causes of anaphylaxis and anaphylactoid reactions are infinite. The most obvious and important precipitants are: narootic anaJgesics. local anesthetics (more prevaJent with esters than arnides), antibiotics (ie­penicillin and sulfonamides). antifungaIs (ie-amphotericin) and radiopaque dye. Cross reactivity between drug<; is equally important (ie-ccphaJosporins should not be prescribed to a penicillin aJIergic pltiellt).

325

Treatment Because of the dire consequence of anaphylaxis/anaphylactoid reaction, quick recognition and immediate intervention is tantamount. Inullediate treatment consists of 0.3 ml epinephrine (1:1000 dilution) given intramuscularly, whether the clinical picture is generalized pruritus, laryngeal edema, bronchospasm or hypotension. Further treatment includes the use of a tourniquet, placing the patient in a recumbent position, monitoring vital signs, establishinglmaintainingan airway. ox-ygen. etc.

Key Points -difference between anaphylaxis and anaphylactoid reactions -anaphylaxis is type I hypersensiti"ity (inunediate) -drug of choice is 0.3 ml 1M epinephrine (1: 1000 dilution) -patient history of allergic responses to drugs. foods. etc.

APPROACH TO CHEST PAIN

There are many causes of chest pain. All complaints of chest pain should be taken seriously. Empiric treatment should be started immediately. if there is any suspicion of a cardiovascular or respiratory event.

I. History of trauma and/or reproducible prin with palpation -most likely musculoskeletal in origin

II. CardiovascuIar and/or Respiratory etiology a) begin ox-ygen - 5 Umin b) monitor vital signs c) appropriate STAT consuItation with internist or cardiologist when possible (if event occurs in hospital) d) transfer patient to Intensive Care or Cardiac Care Unit e) examine for shock. increase in venous pressure. pulmoruuy edema

Ill. Shock. Hypotension. Increased venous pressure and/or Pulmonary edema A) treatment

1.) insert Iarge bore IV 2.) obtain arterial blood gas STAT 3.) obtain ECG and chest x-ray 4.) examine patient 5.) insert urinaIy catheter and monitor fluid status

B) differential diagnosis 1.) myocardial infarction 2.) pulmonary embolism 3.) acute heart fuilure 4.) pericaIdial effusion 5.) others: cardiac tamponade, tension pneumothorax.. aortic dissection, leaking aortic aneurysm

IV. Acute distress from pain or dyspnea "ithout shock. hypotension. increased venous pressure and/or pulmonary edema

A) treatment 1.) history and physical 2.) insert IVandinfuseD5W 3.) obtain arterial blood gas 4.) obtain ECG - correct severe arrhytlunia 5.) N morphine 2-5 mg every 10-20 minutes

B) differential diagnosis 1.) all those listed in the above section 2.) cardiac. respiraIOJ),. abdominal and musculoskeletal causes

326

ELECfROCARDIOGRAM

L Basics A) EKG paper

1.) usually run at 25 mm/sec 2.) thin 1 mm box = 0.04 sec 3.) thick 5 rom box = 0.2 sec

B) Components L) P wave: represents atrial contraction 2.) QRS complex: represents ventricular contraction 3.) T wave: represents ventricular relaxation 4.) P-R interval: not to e.xceed 0.2 sec 5.) QRS complex: should be less than or equal to 0.12 sec

ll. Rate A determined by pacemaker

1.) sinus atriwnnode (SA node) a) normally the pacemaker b) normal rate = 60-100 beats/minute c) sinus bradycardia = less than 60 beatslminute d) sinus tachycardia = greater than 100 beatslminute

2.) ectopic pacemaker a) either atrium b)AVnode c) either ventricle

B. how to determine the rate by quick estimation count the number of thick (5 mm) lines between two R waves each thick line is given a value in succession -300. ISO, 100.75.60.50

III. Identifying arrhmthymias A) determine the rate B) identify tbe pattern or regularity of tbe arrhythmia

I.) premature beats (ie-a beat earlier than e.xpected) 2.) speeding up or slowing down of the rh~thm 3.) presence of any pauses 4.) total irregularity or chaos

C) recognize and define atrial activity 1.) identify the P wave 2.) P wave may change iftbere is an ectopic pacemaker in either atrium. bowever a P wave will be present

and the QRS complex will be nonnal 3.) ectopic A V node pacemaker may have an inverted P wave or no P wave

D) recognizing ventricular activity if ectopic pacemaker is in the ventricle then QRS comple.x will be greater than 0.12 sec and P wave will be

absent E) determine relationship of atrial to ventricular activity

1.) normal l:l, fixed 2.) prolonged 1:1, fixed 3.) multiple P waves to QRS complexes 4.) P waves and QRS complexes unrelated

327

T'or::RQl!$ des Pointes (gqjnidinQ ~oxic~~)

......... ~ ........ ~ ~ k A A­

V..... .-.;. ,~ '"15'""rr #II~

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• rate-

I ...... ,..--.­~_ .... -a.. . :ti -~ . .. -_. ", ---'./4

• ..., .. -... ---- ~!t-' _.-r .-'l- ... r:~:-;:l;j:~---~-;; -"-r'~

328

COMATOSE PATIENT

Initial management to ensure maximal recovery and avoid further damage.

I. Asses ABC's

II. Obtain blood for STAT analysis A) toxic substance screen B) electrolytes, glucose. calcium. BUN & creatinine C) liver function tests

Ill. ~ which may improve patient's status and will not bann A) glucose (ampule ofD50) - consider h:ypoglyoemia until proven otherwise B) thiamine - give it with glucose to avoid precipitating acute Wemicke-Korsakotr syndrome

(encephalopathy) in thiamine ~cient patient C) corticosteroids - decrease cerebral edema D) mannitol - osmotic agent to reduce an elevated intracIanial pressure E) naloxone 0.4-2.0 mg IV - reverse DaIOOtic overdose F) valium 5-10 mg IV - stop seizure activity G) flumazenilIV - reverse benzodiazepi.ne overdose

IV. Normalize metabolic abnonnalities and body temperature

SHOCK

General management of shock 1. Recognize the presence of the shock state 2. Identify the probable cause of the shock state. 3. Early intervention - treatment of shock is directcd toward restoring cellular and organ perfusion with

adequately oxygenated blood, rather than merely restoring pulse and blood pressure: therefore, vasopressors are contra-indicated in hypovolemic shock.

The goal of treatment i~ to re.Uore organ perfusion

Signs of Shock 1. Tachycardia: earliest sign of shock.

infant 160: preschool 140: school age 120: adult 100 2. Respiratory rate: when tissue perfusion decreases, ox-ygen tension decreases and cells switch to anaerobic

metabolism. Lactic acid is then produced which induces a metabolic acidosis. Respiratory rate will increase causing a transient respiratory alkalosis. Tachypnea represents another early sign of shock.

3. Capillary filling: capillary f"dling \\-ill decrease cansing cold extremities. Normal capillary filling is 1-2 seconds. This sign is not considered a criteria in the h}'J1Olhennic (Iltient.

4. Pulse Pressure: the difference between systolic and diastolic pressure. This value \vill reduce as the patient enters the shock state. A narrowed pulse pressure is considered less than 20 mmHg. The phenomenon is primarily related to a rise in diastolic pressure because catecholarnines released during the shock state increase peripheral resistance.

5. Change in memaI status: often subtle in the early stages of shock. htitiallyanxiety may be expressed as fright or hostility. In the late stages the mental status may degrade to unresponsiveness and eventually lack of consciousness.

6. Fall is systolic pressure: this does not occur until a significant amount of blood is lost. usuall:r between 1500-2000 ml. Requires immediate interventiOlL

329

7. Drop in uriruuy output: usual urinary output in the adult is 20-30 mJ/hOUT. Urinal)' output is only affected in severe shock states. Once fluid replacement has been initiated urinary output may be used as a gauge of effectiveness. Urinary output should be 50 mllhoUT for adults.. 2 mlJkg/hoUT for infants and I rnlIkglhour for pediatric JDtients.

8. Hematocrit (hemoglobin concentrntion): a massive blood loss may produce a minimal acute decrease in hematocrit. A low hematocrit suggests significant blood loss or anemia, however a normal or near normal hematocrit does not rule out a significant blood loss. Therefore. hematocrit is an unreliable measure of blood loss

Types of Shock * All patients in shock are treated initially as though they were in hypovolemic shock*

I. Cardiogenic shock: a shock state induced by myocardial dysfunction. In the trauma patient this fonn of shock is common, second only to hypovolemic shock. Characterized by increased CVP pressure and a history of chest trauma. Causes include cardiac tamponade (muffled heart sounds. engorged neck veins). tension pneumothorax. cardiac contusion. air embolism and myocardial infarction (rarely).

2. Neurogenic shock: in general, isolated head trauma does not cause shock. Head and spinal cord injuries may produce hypotension secondary to loss of S}mpathetic tone, however this only compounds the effects of hypovolenria. Characterized by hypotension without the classic signs of shock and \\1de pulse pressure.

3. Septic shock: shock due to infection is uncommon in trauma. however should be considered with penetrating wounds of the abdomen where bowel contents are spilled. Characterized by mild tachycardia \"ann skin fand a "ide pulse pressure.

4. Hypovolemic shock: defined as an acute loss of ciIt:ulating blood. The normal adult circulating blood volunte is ']010 ofbody weight or in a 70 kg man. approximately 5 liters. In children the blood volume is 8-9% of body weight or 80-90 mlJkg. Once hypovolemic shock is suspected immediate aggressive fluid resuscitation must begin.

5. Factors that alter vascular dynamics: a) JDtient age - the older the JDtient the more difficult)· they have in tolerating and compensating for

hemorrhage. b) severity of injury - special attention to anatomic location. c) time Iap;e - the tinte between occurrences of injury and treatment is significant d) prehospital therapy - fluid replacement or use of MAST (military antishock trousers) or PASG

(pneumatic antishock garments).

Classes of Hemorrhagic Shock

1. Class I ltemorrhage: a loss of 15% of blood volwne or 750rnl. No measurable signs of shock. are demonstrated with the exception of minimal tachycardia. Without therapy the body will compensate for the volume loss within 24 hours, however crystalloid fluid replacement is suggested.

2. Class IT hemorrhage: a 15-30% volume loss or 750-1500 mIs. Characterized by tachycardia, tachypnea, decreased pulse pressure. Systolic pressure and urinary output usually remain stable. Patient may ex-perience ~e CNS changes. The majority of patients in this stage of ltemorrhage may require blood transfusion eventually, however, are easily stabilized with crystalloid fluid

3. Class ill hemorrhage: a 30-40% blood loss or 1500-2000 mIs. This class of hemonbage presents the classical signs of shock (ie-marked tachycardia tachypnea. change in mental status and fall of systolic pressure). At least 30% of blood volwne must be lost before the systolic pressure drops. Treannent requires immediate crystalloid fluid replacement and eventual transfusion. The decision to immediately transfuse is based on the patient's response.

330

4. Class IV hemorrhage: more than 40",4. volume loss OT 2000 mls. This degree of exsanguination is immediately life- threatening. Characterized by the classic signs of shock, negligible urinary output and unobtainable diastolic pressure. Immediate fluid and blood replacement and surgical intervention to stop the hemorrhage is warranted

• Loss of 50% of blood volume results in loss of consciousness, pulse and blood pressure.

Soft tissue fluid loss Ma:ior soft tissue injuries and fractures affect the circulation in m"O ways-

L blood loss: a fractured tibialhumerus can lose up to 750 ml of blood. Femurs can lose 3 units (1500 mI) and the pelvis can lose 6 units (3000 mI) of blood

2. inflammatory edema: consists of plasma and e.macellular fluid

Roughly 25% of fluid fowtd at the ifYured area is circulating volume. Therefore the 3: 1 rule of fluid replacement is indicated For example, most patients in hemorrhagic shock will require 300 ml of electrolyte solution fOT each 100 ml of blood volume loss.

Initial management of hemorrhagic shock 1. Airwaylbreathing: restoring blood volume does nothing unless the blood being circulated is ox·ygenated

Maintenance of arterial oxygen tension at least 95% PI02 or better is necessary. 2. Hemorrhage control: bleeding from arterial wowtds is controlled with direct pressure. Internal bleeding

requires surgical evaluation immediately. 3. Gastric decompression: the GI tIact stops functioning in the tramnatized prtienL The danger of aspiration

with fatal sequela exists. 4. Vascular access: must be obtained promptly using large bore 16 gauge or larger catheters. If peripheral

access annot be obtained a saphenous vein cutdown is performed before a CVP is considered The cutdown is quicker and with less complications.

5. Initial fluid therapy: crystalloid isotonic electrolyte solutions are used for resuscitation only. Ringers Iactate is first choice followed by normal saline. Normal saline is not preferred due to the potential to cause hypochloremic acidosis especially in renally impaired patients. The initial bolus in adults is 1-2 liters and 20 ml/kg in children.

6. Blood replacement: once the decision to begin tIansfusion has been made, three types of blood are available depending on the urgenCy of the patient's condition.

• fully crossmatched blood : preferred, however, usually takes one hour to prepare. • type specific (saline crossmatched): compatible \\-ith ABO and Rh blood types but minor

antlbodies e.xist. Available within 10 minutes. • type 0 negative blood: reserved for use in patients with exsanguinating hemorrhage. Rh

negative mctor is suggested to avoid future sensitization.. especially women of childbearing years.

• Blood wanners should be used with blood and crystalloid fluids to prevent hypothennia. A 160 micron filter should be used to filter microscopic clots. All other filtering devices should be avoided because they do not allow rapid fluid administration.

7. Pewnatic Antishock Garment (pASG): this de\ice raises systolic pressure by increasing peripheml resistance and myocardial afterload. The device is a prehospital therapy designed to buy time.

Only two in-hospital indications exist • severe pelvic fracture with continous hemorrhage and hypotension • patients in-route to the OR with intra-abdominal trawna and severe hypovolemia Contra-indications • uncontrolled hemorrhage outside the confines of the garment

• pulmonary edema • suspected OT kno\,\TI rupture of the diaphragm • left ventricular dysfunction • respiratory distress: necessitates the deflation of the abdominal compartment

331

The device cannot be removed until the patient has been adequately managed and is stable or when there is adequate preparation for immediate surgical intervention. The deflation process is graduaL begirllling with the waist compartment and proceeding to each leg cOlllfwtment. Air is released until a 5 mmHg drop in blood pressure is noted.

Complications in treatment of hypovolemic shock A) Age the older patient has difficulty compensating and tolerating hypotension from hcmorrhage. B) Athletes: this group of patients have pulse rates of 50 and increases in blood volunle by 15-20%. Cardiac

output increases 6 fold and stroke volume by 50%. Assessment of this patient is difficult. C) Medications: beta-adrenergic receptor blockers and calcium channel blockers significantly alter the

paticnt's hemodynamic response to hemorrhage. D) Hypothemua: temperature is extremely important to record in tile suspected shock patient. E) Pacemakers: heart rate remains constant in these patients until blood loss causes myocardial failure. This

group should be monitored by CVP pressure. F) Continued hemorrhage: if hemorrhage cannot be controlled by initial treatment immediate surgical

intervention is requi.red G) Fluid overload: once the patient management is completed the risk of fluid overload is minimized by CV'P

monitoring or pulmonary wedge pressure. A pulmonary wedge pressure is technically difficult to perfonn in the emergency room setting, therefore CVP pressure can be employed much more simply

=> Central venous pressure monitors only the right hearl'S ability to accept fluid The precise measure of cardiac function is tlle relationship between end diastolic ventricular volume and stroke volume. Therefore right heart pressure to cardiac output as determined by CVP pressure is indirect and insensitive estimate of cardiac function. however. it is useful for gross evaluation of tlle clinical situation

• -a minimal rise in tlle initial low CVP values indicate need for further fluid replacement.

• -a declining CVP value indicates continued hemorrhage. • -an abrupt elevation in CVP value suggests replacement is too much or too rapid and

cardiac function is comprontised H) Acid-Base balance: the initial respiratory alkalosis gives way to metabolic acidosis of a mild fonn in tlle

early stages of shock and does not require treatment. In prolonged late stage shock a severe metabolic acidosis can occur. This is treated only witll increased fluid not bicmb Bicarbondate therapy is indicated whcn tlle pH drops below 7.2

n Recognition of other problems: when the patient fails to respond properly to tllerapy. consider other causes. 1) Constantly re-evaluate the patient.

332

TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMA TOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TRAUMATOLOGY TR. A 'CliVi A T'O' ,"" "\ ,.

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FRACTURE MANAGEMENT

Initial Assessment Extremity trauma is rarely Jife-threatening, but associated injuries can be potentially serious. Certain injuries and combinations of injuries to the skeleton may be pennanently disabling if not properly recognized

L Primary Survey: life-threatening conditions are identified with this exam AirwaY maintenance with cervical spine control ~reathing and ventilation ~ircu1ation with hemorrhage control Qisability: quick neurologic check using the A VPU method

A alert V: responds to visual stimuli P: responds to ~ stimuli U: unresponsive

~xposure of patient, remove all clothing

2. Secondary Survey: The secondary survey is a head to toe evaluation of the tIauma patient, which does not begin until the primaIy survey is

complete and the patient is stabilized Each region of the bocJy, beginning with the head and ending with the feet. must be thoroughly examined. Special procedures such as laboratory studies and radiographic examinations are conducted in this survey.

3 History: Information concerning the cause of the injury will help determine the direction and strength of the defonning forces. A

history can be obtained at any time during the evaluation of the patient, but cannot interfere with the primary and secondary survey.

4 Definitive Care Phase: In this phase, all the patient's injuries are managed This phase includes comprehensive management, fracture

stabilization and any necessary operative intervention, as well as stabilization of the patient in preparation for appropriate transfer to a fucility that can provide a higher level of medical care.

Fracture Assessment Fractures are generally classified into two major groups, open or closed fractures. Any obvious or suspected fracture near a wound should be assumed to be an open fracture, even if the fracture cannot be seen in the wound

1. Life-threatening fractures crush injuries of the pelvis and abdomen traumatic amputations of the arm, foreann, thigh or leg massive open long bone fractures

2. Limb threatening injuries vascular injuries with or without fracture crush injuries compartment syndromes dislocation of major joints open fractures

3. Associated or occult fractures

333

In the podiatric assessment of a trauma patient occult fractures are easily overlooked. Certain types of accidents and/or fractures have associated injury pattenlS.

=> Compression fractures - this t)-pe of fracture is most commonly seen in a patient who has fallen from a height and landed on their feet Calcaneal fractures are associated with tibial plateau fractures and vertebral body fractures. Spinal radiographs are required on all 'jumpers".

4. Neurovasuclar injuries Assessment of neurovascular status is the first step in evaluation of extremity injury. a) vascular injuries: vascular injuries disrupt the integrity of the vessel wall, with bleeding or thrombosis resulting

in impairment of distal circulation and ischemia. Bone is an extremely vascular organ. Fractures involving long bone and pelvis can result in hypovolemic shock. The pelvis can lose six units of blood, the femur three units and the tibia one and one-half units. Dopplers and angiograms provide the most accurate means of vascular evaluation.

b) comautment syndromes: a compartment syndrome occurs when the interstitial pressure rises above that of the capillary bed., local ischemia of nerve and muscle occurs. Compartment syndromes take several hours to fonn. The patient may have excellent pulses, however, the pain the patient is experiencing is out of proportion to the injury sustained Cannulation and measurement of compartment pressure is diagnostic. Pressures greater than 30 mmHg are indicative of compartment syndrome. Prompt fasciotomy is necessary.

c) nerve injury: injury to nerves may represent actual division of the nerve or a physiological disruption. In general, stretch injuries have a poor prognosis compared with compression injuries.

d) amputations: patients with amputations require rapid assessment and consultation with a specialized center. The amputated part should be cleansed of any gross debris and wrapped in a sterile towel moistened with saline and placed in a crushed ice cooler and the patient shonld then be transferred to a center capable of microvascular re­anastomosis. Amputated parts remain viable from 4-6 hours at room temperature or up to 18 hours if cooled properly.

Oassifications of Closed .Fractures Rockwood and Green devised a classification system based on fracture mechanism which help determine subsequent treatment.

1. Direct Trauma: closed fractures caused by direct blows of varying velocity a) Tapping :fractures: low velocity blow which results in no comminution and little soft tissue damage b) Crush:fractures: high velocity blow which creates extensive soft tissue injmy and comminution

2. Indirect Trauma: closed fractures resulting from forces acting at a distance to the fracture site a) traction:fractures: transverse avulsion fracture at the site oftenckm or ligament attachment b) angulation fractures: transverse fracture caused by bending forces on a long bone. The convex side

transversely fractures while the concave side splinters c) spiral :fractures: an oblique:fracture 45 to the long axis ofbone, caused by rotational forces d) compression fractures: result from impaction of the shaft into the soft cancellous bone e) angulation and axial compression fractures: cause transverse fractures with butterlly fragment f) angulation and rotation fractures: cause oblique fracture lines

334

Treatment of Closed Fractures Prior to definitive treatment, the primary and secondary survey must be completed. The neurovascular and tendon function are first priority.

1. Contra-indications to closed reduction => no disp1acement => no reduction is possible due to comminution => reduction cannot be held by external immobilization => traction forces produced the fracture => open fracture

2. Indications for open reduction => closed reduction technique have failed to approximate fragments => articular surfiIce involvement, anatomic reduction is necessaty

=> traction force fractures resulting in large avulsion fi:actures 3. Technique of closed reduction

=> anesthesia is necessaIy to prevent patient muscular guarding; guarding causes excessive reductive force to be used resulting in greater tissue damage

=> review of fracture mechanism is necessary to understand proper reductive movements => slow, steady traction applied along the axis of the bone with counter-traction applied by an assistant => restorntion oflength => correction of rotatory deformity => apposition of bone fragments => correction of angulational deformity => application of Jones compressive dressing

* tissue swelling usually peaks approximately 6-8 hours following injury => timely application of a compressive dressing will reduce soft tissue edema => evaluate neurovascular status => following a 3-4 day course of elevation with compressive dressing application, a "hard" cast may be applied

Fractures in Children and Adolescents Children's bones react much more quickly to fi:actures than those in the adult Within a few days, the fragments are joined by callus. Reduction of the fractme is easiest within the first 24 hours.

1. Indications for operative or nonoperative treatment: In general. closed reduction is preferred for children's fractmes. The healing capacity of growing bone is

considerable and pseudarthrosis seldom occurs. Malunion may be corrected by subsequent growth. Operative treatment should be considered when closed reduction fails or surgery will prevent a poor result

2. Aims of fracture treatment in children a) prevention of malunion: the ability of bone to spontaneously correct post-traumatic deformity

decreases with age. Anatomic reduction is indicated in the adolescent. b) prevention of growth disturbances: setmation of the epiphysis heals perfectly following precise

reduction. If closed techniques cannot precisely reduce the epiphysis, operative reduction is recommended Excessive longitudinal growth is regularly seen following fracture of the diaphysis. It is compensated for by allowing the fractme to unite with slight initial shortening.

335

DIGITAL AND SESAMOIDAL FRACTURES

Pedal digital and sesamoidal fractures are not incidental. trivial injuries. The sequela from mistreatment of these fractures can result in long tenn J:Xlinful disability.

Hallux fractures: Considered to be the most common fracture in the forefoot. Most hallux fractures occur at the distal phalanx and result from a stutbing injuIy or a crushing injury from a heavy oqject falling on the toe. Crushing injuries cause comminution of the distal phaiaIL'{ and are often associated with subungual hematoma due to a lacerated nail bed. Pressure caused by the hematoma can damage the nail matrix if not relieved within 6-12 hOUTS. If the hematoma involves more than 25% of the nail plate, avulsion of the entire nail plate should be considered. If a nail bed laceration is noted upon removal of the nail plate, the injury should be treated as an open fracture.

Sesamoid fractures: Usually caused by repetitive, high-impact activities or by crushing injury to the foot. Sesamoid fracture must first be differentiated from a bipartite or multipartite sesamoid

Findings supporting a diagnosis of sesamoid fracture­>fracture line usually jagged, irregular or uneven >large space between fragments is consistent with fracture >anatomical1y abnormal fragment positions indicate fracture >bone callus formation is suggestive of fracture >multipartite sesamoids are usually larger than nonna! >contralateral views demonstrate no evidence of similar findings on the uninjured foot >iffurther diagnostic studies necessary, Consider technetium 99-mdp bone scan, dorsiflexion stress radiographs of

the first MIP joint CT scans or MRI

=> Fracture of the tIbial sesamoid may be more common due to greater load during gait.

Lesser digital fractures: Fracture to the fifth digit due to night walking is the most common lesser digital fracture. The proximal phalanx is usually affected, demonstrating an oblique or spiral oblique pattem

Treatment

Hallux fractures: Comminuted tuft fractures usually respond to immobilization in a weightbearing cast or surgical shoe. Intra-articular condylar fractures may respond to conservative management (NWB cast immobilization), but may require ORIFdepending on the size of the fracture fragment. If conservative therapy fails, surgical excision may be necessary.

Sesamoid fractures: Conservative management consists of cast immobilization (with extension to end ofhalllL'<) NWB for 4-6 weeks. Surgical shoe pad::Jed to alleviate pressure under the first metatarsal head and "W-alking cast are other options, but may be more appropriate for sesamoiditis than for fracture management. In some cases of severe injury surgical excision of the affected sesamoid and long tenn management with functional orthoses may be required

Lesser digital fractures: If nondisplaced, support via buddy splint and avoiding narrow toed shoes is usually adequate. If displaced, reduction is required This reduction may be maintained with a simple buddy splint, percutaneous K -wire, or modified cast. Severe injuIy may necessitate ORIF or excision of fracture fragments.

336

Jabss' Classification of First MTP Joint Dislocation Injury

~ dorsal dislocation of the proximal phalanx and sesamoids with the intersesamoidalligarnent intact. The JDC'clwnism of injwy is hyperextension of the hallux.

=> Treatment: open reduction

Type ITA: dorsal dislocation of the proximal phalanx and the sesamoids with rupture of the intersesamoidalligament. => Treatment: closed reduction

Type lIB: dorsal dislocation of the proximal phalanx and the sesamoids with transverse fracture of one of the sesamoids.

=> Treatment closed reduction

Type IIC: dorsal dislocation of proximal phalanx and sesamoids with complete disruption of the intersesamoidal ligament and transverse fracture of either sesamoid

=> Treatment: open reduction

Type II variant: dorsal dislocation of proximal phalanx with complete disruption of sesamoid-plantar pIate complex and separation of previous bipartite tIbial sesamoid

=> Treatment: closed reduction

J ahss' Classification of First MTPJ Dislocation Injury

Type I Type lIA Type lIB

METATARSAL FRACfURES

Classification of Metatarsal Fractures: these injmies share the same classification as long bones, which have been descnbed by Salter.

=> site: diaphyseal, metaphyseal, epiphyseal or intra-articular => extent: complete or incomplete => configuration: transverse, oblique, spiral or comminuted => relationship of fracture fragments to each other: shifted sideways, angu1ated, rotated, distracted, overriding or

impacted => complicated or uncomplicated

*Gudas further classified metatarsal fractures into intemal metatarsal (2,3,4) and external metatarsal (1,5) fractures. He suggested that further consideration be given to the external metatarsals due to the effects of extrinsic muscles

and independent ranges of motion.

337

Treatment of metatarsal fractures: treatment varies according to the metatarsal involved anatomic location of the fracture as well as degree of displacement. Sagittal plane defonnity must be minimized in order to prevent subsequent metatarsalgia and/or frncture of the adjacent metatarsals.

Diaphyseal frnctures: treatment varies by the amount of displacement. Nondisplaced fractures are generally placed in a nonweightbearing cast. Displaced frnctures require attempted closed reduction followed by cast inmlobilizatio11. Should the reduction 110t be maintained in a cast, open reduction with internal fixation is required.

MetaphYseal fractures: usually transverse in nature, these f:rnctures can be managed conservatively \vith a cast.

Unstable fragments, however, may require intemal fixation.

F'IF"IH METATARSAL BASE FRACTURES

Radiologic Classification (after I.M Stewart) as translated from Courrier des Pedicures Romands bv Miss M Soufflet, MChs ~: supra-articular f:rncture occurring at the metaphyseal-diaphyseal junction

>this injury corresponds to a true Jones frncture mechanism - vertical and transverse forces act upon a fixed foot that cannot invert nonunions common due to the dynamic forces of soft tissue attachments, the fifth metatarsal's independent range of motion and vascular supply to fifth metatarsal => Treatment=if nondisplaced, 6-8 weeks NWB immobilization

surgical repair in competitive athletes and in cases when conservative therapy fails consist of ORIF with pins, screws, plate with screws, wire or bone graft with plate fixation

~: intra-articular avulsion fracture with one or two fracture lines Type III: extra-articular avulsion fracture in which the peroneus brevis tears a small fragment from the

styloid process => Treatment for avulsion fractures involves conservative therapy as outlined above and tension band wiring if

surgical intervention is required Type IV: intra-articular, comminuted fracture Type V: e>..1ra-articular avulsion fracture of the epiphysis in children

338

Fifth Metatarsal Base Fracture Classification

I II ill IV v

Stewart Classification from: Jones's Fl3Cture:· Fl3Cture of Base of Fifth Metatarsal by IMStewart, MB, FRCSE Clinical Orthopedics, 1960. This is the preferred classification.

Type I A TypeIB

339

TypeilA

n

Type lIB

Classification of Fifth Metatarsal Base Fractures from 51 cases Cases

Fracture at the· ction of shaft and base (JONES) - T I A 8 Comminuted - T I B 6 Fracture of the IIA 11 With Joint involvrnent - T 21

Stewart Classification from: Jones's Fracture: Fracture of Base of Fifth Metatarsal by I.M.Stewart, ME. FRCSE, Clinical Orthopedics, 1960.

TARSOMETATARSAL JOINT FRACTURE I DISLOCATION

FractUre/dislocation to this joint is rare and difficult to diagnose. The configuration of the joint is extremely stable due to a recessed second metatarsal base and strong plantar/dorsalligaments.

Two classification systems based upon radiographic appearance are most commonly employed-

A) Quenu and .Kuss :::::> Homolateral: fractureldislocation with all the metatarsals displaced in one direction corresponds to Type A Hardcastle

classification Isolated: involvement of a single metatarsal, usually dislocation of the first metatarsal => Divergent: fractureldislocation which forces the first metatarsal medially and the lesser metatarsals laterally

340

B) Hardcastle Type A total incongruitylhomolateral

=> total incongruity of the entire tarsometatarsal joint => with displacement in the sagittal or transverse p1anes Treatment =

• closed reduction if non-disp1aced • ORIF if severe

• stabilization with 2 K-wires is common, but depends on the stability of the tarsometatarsal joint (ie-one wire medially ~ :first metatarsocuneifonn joint and one wire JateraI1y across fifth mecatarsocuboid joint)

Type B: partial incongruity partial displacement involving partial incongruity of the joint complex in either sagittal or transverse planes or both

B 1 - medial dislocation => displacement of the first metatarsal in iso1ation or in combination with displacement of the lesser

metatarsals B2 -lateral dislocation

=> first metatarsal unaffected Treatment =

• surgical stabilization of joint complex • closed reduction, depending upon severity

Type C: divergent divergent displacements involving partial or total incongruity of the joint the first metatarsal is displaced medially and any combination of the lateral four metatarsals are disp1aced laternlly in the sagittal or transverse p1anes or both lateral plantar artery is compromised

Cl - partial displacement C2 - total displacement

Treatment =

=> surgical repair due to instabili1y of joint complex (ie-three or more K-wires)

Type A

TypeBl

341

TypeB2

TypeC

MIDFOOT FRACfURES (CUNEIFORM, CUBOID AND NAVICULAR)

Cuneiform and Cuboid Fractures Isolated fractures of the cuneiforms or cuboid are rare and usually caused by direct impact trauma. Fractures to these bones can also occur as associated injuries with tarsometatarsal frnctures, fifth metatarsal base fractures and navicular fractures.

Oassification of cuneiform and cuboid fractures 1) avulsion fracture 2) body fracture (simple, comminuted or crush) 3) fracture with dislocation

Treatment: these injuries usually respond to cast immobilization since the bones are strongly bound by intertarsal ligaments and surrounding bony structures. If avulsion fracture does not respond to conservative therapy, surgical excision offiagment should be considered.

342

NAVICULAR FRACTURES Watson..Jones classification

I1mJ: tuberosity fracture Type II: dorsal chip fracture

Type m: fracture of the body with or without displacement

Treatment: treatment varies acoording to location The tuberosity fractures are usually satisfactorily managed with cast immobilization. Pull of the tibialis posterior can

delay or prevent healing, necessitating the surgical excision of the fragment Chip fractures respond well to casting. Body fractures, depending upon the degree of displacement, will require closed reduction and frequently open reduction with internal fixation.

TALAR FRACfURES

The talus is almost wholly artiadar and has a unique blood supply which predisposes it to severe post-traumatic COmplications including crippling arthritis, delayed OT nonunion and avascular necrosis. Fractmes of the ta1ar head are frequently seen in sudden dorsiflexmy force injuries, however, usually have a good prognosis with cast immobilization.

Due to the large amount of artiadar surface, bloocJ. can only supply the talus through three main sources: through the neck, through the sinus tarsi, through the tarsal canal and through the medial side of the body. The three main arteries which supply the talus, in order of significance, are - the posterior ti.biaI, anterior tIbial and peIforating peroneal. Hawkins sign is frequently used to ~ the viability of the talus following fractureldislocation; it appears as a subchondral radiolucency on the AP view of the ankle approximately 6-8 weeks after injury and occurs when no avascular necrosis is present. It has been postuJated that Hawkins sign is caused by disuse osteopenia or vascular congestion, which suggests maintenance of blood supply to talar body.

343

Hawkins Classification of Talar FractureJDisJocations ~: nondisplaced vertical fracture oftalar neck

body of the talus retains its nonnal position in the STJ and ankle joint Type II: vertical fracture of the talar neck with STJ subluxation or dislocation Type ill: vertical fracture of the talar neck with STJ and ankle joint dislocation

all three sources of blood supply are disrupted Type IV: vertical fracture of the talar neck with STJ, ankle and talonavicular joint dislocation

all three sources of blood supply are disrupted

Ha\>vkins Classification ofTalar Neck Fractures

II

INCIDENCE OF AVASCULAR INCIDENCE OF

TYPE NECROSIS STJ AR1HRlTIS I II ill IV

20% 40010

100% 100%

rare 60-75% 100% 100%

Berndt-Hardv Classification of Talar Dome Fractures

~: small area of subchondral bone compression Stage II: partially detached osteochondrnl fragment Stage ill: completely detached, non~laced osteochondral fragment Stage IV: displaced osteochondral fragment

Treatment:

ill

stage I stagell medial stage ill

observe, immobilize. NWB cast immobilization, NWB 8-12 weeks cast immobilization

lateral stage ill stage IV

::::> small lesion - excise fragment dril1/curette subchondral bone early ROM exercises

surgical intervention surgical intervention

cast immobilization NWB 2 weeks, then PWB4weeks

:::::> large lesion - ORIF :::::> arthroscopy - recommended to remove loose bodies

pneumonic = ''DIAL-A-PIMP'

N

344

dorsiflexion-inversion causes an anteroIaternllesion shallow, wafer shaped lesion

pIantarflexion-inversion causes a medial posterior lesion deep, cup shaped lesion

Anterolateral Lesions

44%

KEY

Fractures

""'­Posteromedial Lesions

56€?/o

Miscellaneous TaJar Fractures: fractures of the talar head are frequently seen in sudden dorsiflexory force injuries, however, usually have a good prognosis with cast immobilization. Areas of ligamentous attachment such as the dorsal taJar neck and medial talus are sites of avulsion chip fractures. These, too, respond well to conservative therapy. The lateral taJar process is a common fracture site, referred to as a Shephard's fracture and must be properly immobilized to prevent prolonged pain due to delayed or nonunion.

Snepoen classification of talar body fractures Group I: transchondraI or compression fracture of taJar dome

(including osteochondritis dessicans of talus)

Group II: coronal, sagittal or horizontal shearing fractures involving the entire taJar body ~ coronal or sagittal fracture

IA: nondisplaced ill: displacement of trochlear articular surface Ie: displacement of trochlear articular surface with associated subtalar joint dislocation ID: total dislocation oftaJar body

Group II: Type I

IA IB Ie

Tvpe II: horizontal fracture

ID

345

IIA: nondisplaced lIB: displaced

Group II: Type II

ITA

Group ill: fracture of the posterior tubercle of talus

Group N: fracture ofIateral process of talus

Group V: crush fracture oftalar body

ITB

Group ill

Group IV

Group V

346

CALCANEAL FRACTURES

~ Calcaneal :fractures account for approximately (i()O/o of all major tarsal injuries and 1-2% of all diagnosed fractures.

~ Calcaneal fractures are arguably the most disabling of pedal fiactures.The most oommon mechanism of injury is a fall from a height of as little as two feet The talus is driven through the calcaneus. cteating fracture lines of three types - avulsion, oompression and shear. Asc;ocjated ftactures of the tibial plateau. femur, hip and lumbar spine must

also be considered

Diagnosis: patients oompJain of severe pain upon weightbearing and will usually give a history of a fall from a height Characteristic ecchymosis may occur below the medial and lateral malleoli as well as extending to the plantar aspect of the heel. referred to as "Mondur's sign".

Radiographic examination should include the following views: -dorsop1antar view: assessment of calcaneocuboid joint -laternl view: assessment of anterior beak. tuberosity and posterior filcet -axial view: demonstrates lateral cortical bllge and the presence of a superomedial fmgment -Broden I view: assessment of posterior filcet

~ central beam is cephaJad; 90 footlleg angle with foot and leg internally rotated 45; radiographs taken at 10, 20, 30, 40 angles. (central beam is caudal with Broden II views)

Radiographic measurements: interpretation of subtalar joint depression is oommonly derived from the measurement of two angles formed on the laternl view

1) Bobler's Angle (Crucial Angle: Angle of incidence): formed by a line joining the highest point on the posterior articular SUIfiJce to the most superior point of the calcaneal tuberosity and a line joining the high point of the posterior articular SUIfiJce to the high point on the anterior beak

Normal=20-40 Injury causing depression of the subtalar joint will cause this angle to decrease.

2) Gissane's Angle (Critical Angle): angle formed between the anterior laternl cortical shelf and the posterior margin of the posterior fucet

Normal= 120-140 Injury causing depression of the subtalar joint will cause this angle to increase.

Gissane's Angle

347

Oassification of Calcaneal Fractures

Many classification systems have been suggested, however, no one system completely integrates mechanism with treatment. Two commonly used systems will be descnbed which group calcaneal fractures into extra- and intra-articular fractures.

Rowe Classification Type IA: fracture of medial tubercle Tvpe IB: fracture of sustentaculum tali Type IC: fracture of anterior process

IA IB Ie

Type ITA: avulsion fracture of posterior superior calcaneal process Type DB: avulsion fracture of posterior beak. with involvement of tendo Achilles

d II A - Beak Fracture

~I1 B - Avulsion Fracture

Type ill: extra-articular fracture through body of calcaneus

Type IV: intra-articular fracture through body of calcaneus without joint depression

348

~: commjrnrted, intra-articu1ar fiacture through body of calcaneus with joint depression

I t5?J<QJ1 Essex-1opresti cJas;e:ification of intra-articuJar gdgmeaJ fractures This c1as<;ification system is commonly utilized to describe Rowe IV or V fractures. Both the tougue andjoint depression types contain a primary and secondaIy fiacture line. The primaIy fracture line runs from superior to inferior, extending from the apex of Gissane's crucial angle to the plantar aspect of the calcaneal body. The seoondaIy ftacture line is determined by the direction of foICe - vertical directed foICe creates tongue type and anterior directed foICe creates joint depression fractures. Further evaluation of articu1ar disruption through cr scan may be necessary

Type A:. Tongue type

=> talus carries the foICe into the subtalar joint

=> sharp spur of talus is driven inferiorly into the crucial angle, splitting it along the lateral cortex

=> secondaIy fiacture line extends to posterior border of the tuberosity

Type B: Joint Depression Type => primary (sagittal plane) fracture

divides calcaneus into medial and lateral fragments

=> the medial :fragment includes the sustentaculum tali and medial portion of posterior facet of STJ

=> the lateral :fragment includes the lateral portion of posterior facet and remaining body of calcaneus

=> the lateral talar process acts like a wedge causing sepmIlion and depression of (lateral portion) posterior facet into body of calcaneus

=> lateral wall fiacture occurs with lateral cortical extension or with distal extension into calcaneo-cuboid joint

349

Treatment: => calcaneal fracture treatment varies according to the location of the fracture and articular surface involvement.

tuberosity fractures: usually this type of calcaneal :fracture is minimally displaced and responds to cast immobilization. Occasionally, closed and possibly open reduction is necessary.

sustentaculum fractures: these fractures involve portions of the anterior and/or middle :fucets. If nondisplaced cast immobilization and non-weightbearing status is required Displaced fractures require closed or open reduction techniques.

anterior process fractures: these fractures are usually caused by an inversion mechanism about the ankle. This injury responds well to cast immobilization. If chronic pain results, the fragment may be excised

posterior beak fractures: should the Achilles tendon insertion run through or above the :fracture line, plantarflexory power will be compromised Open reduction with cancellous lag screw or tension band fixation followed by casting is indicated

eAm-articular body :fractures: usually little or no joint depression \\ill occur and the injury will respond "ill to non­weightbearing cast immobilization.

intra-articular body :fractures: always involve joint depression to some degree. Several methods of reduction have been suggested in the literature-1. immobilization with early weightbearing 2. skeletal traction or Bohler clamp reduction 3. primary subtalar joint or triple arthrodesis 4. open reduction with internal fixation via the medial approach as described by McReynolds 5. open reduction with internal fixation via the lateral approach with bone grafting as descnbed by Palmer 6. extemal fixation (ie-llizarov technique)

350

Syndesmosis Sprains -can range from minor strains to complete rupture ( diastasis) of the syndesmotic ligaments

Anatomy: -anterior inferior tibiofibular ligament (AITF) -posterior inferior tibiofibular ligament (PITF) -posterior inferior transverse ligament -interosseous ligament -interosseous membrane

Mechanism of injury: -forced external rotation of the foot with simultaneous internal rotation of the leg -hyperdorsiflexion with forceful external rotation

Classification of Syndesmotic Diastasis -latent diastasis: ankles that appear normal on routine radiographs but experience ankle mortise widening with stress external rotation radiographs -frank diastasis: syndesmotic separation visible on plain radiographs *deltoid ligament most likely concominantly ruptured with ankle diastasis

Symptoms: -marked, generalized edema -pain out of proportion for isolated lateral ankle sprain -ecchymosis -tenderness over the AITFIPITF that may extend proximally over the interosseous membrane -limited ankle ROM -inability to perform toe raise -toe to heel ambulation

Special Tests: -anterior drawerltalar tilt to rio ATF/CFL involvement -palpation of the syndesmotic ligaments -passive dorsiflexion of the foot (this wedges the wider anterior talus in the ankle mortise causing separation of the tibia and fibula) -external rotation of the foot on a neutral ankle with the knee held at 90 degrees -"squeeze test" (manual compression of the tibia and fibula above the level of the calf) *these test are considered positive if they result in pain within the syndesmosis*

Adjunctive Imaging: -plain radiographs (need to rio fracture) -stress external rotation radiographs (look for ankle mortise widening/increase in medial clear space) -arthrography -MRI

351

Treatment: Conservative: these patients take a longer time to rehabilitate then medial/lateral ankle sprams

-immobilization with gradual progression to protected weightbearing -physical therapy to include ROM, proprioreceptive training, strengthening -return to normal activities with protective bracing for the first 3-4 months

Surgical: -consider in complete tibiofibular diastasis or with continued ankle instability -transsydesmotic screw fixation

Possible Sequelae: -continued pain/instability -heterotopic calcification (usually causes no long term functional disability)

352

ANKLE FRACTURES

The mechanism by which an ankle fracture occurs must be fully understood in order to restore anatomic alignment of the joint. Ramsey found that experimentally 1 mm lateral ta1ar displacement within the ankle mortise decreased tIbiotaJar contact by as much as 42%. Yablon found that division of the lateralli~ents and/or lateral malleolus leads to greater ankle instability than sectioning of medial structures. He, therefore, concluded that anatomic reduction of the lateral malleolus is the key to restoration of ankle stability in bimaI1eolar fractures. The work: of these investi~rs as well as that of the A-O form the basis of our current understanding of ankle fractures.

Eponyms descrIbing ankle fractures Pott's (Dupuytren's) fracture: bimalleolar fractnre Cotton's fracture: trimalleolar fracture Bosworth's fracture: lateral malleolar fracture with ankle displacement Maisonneuve fracture: proximal fibular fracture Volkmann's fracture: posterior malleolar (tIbia) fracture Tillaux fracture (tubercle of~: avulsion fracture of the anterior lateral tIbia Wag$ffe fracture: avulsion fractnre of the anterior medial fibula

Classification of Ankle Fractures

Laug~Hansen Classification This classification system descrIbes 95% of all ankle fractures and allows one to predict the degree and severity of ligamentous injury based upon the type of osseous injury. Each type of fracture is descnbed by two terms. The first describes the position of the foot at the time of injury and the second descrIbes the direction the talus was driven by the injuring force.

Sutrination-Adduction Stage I: transverse avulsion fracture of the lateral malleolus or lateral ligament rupture Stage II: vertical fracture of the medial malleolus

Pronation-Abduction Stage 1: transverse avulsion fracture of medial malleolus or deltoid ligament rupture Stage II: rupture of Al1F and/or PITF ligaments Stage ill: short, oblique fracture of the lateral malleolus

Sutrination-Eversion Stage I: rupture of Al1F ligament Stage II: spiral fracture of the fibular malleolus Stage ill: rupture ofPITF ligament or Volkmann's fracture Stage N: rupture of deltoid li~ent or avulsion fracture of medial malleolus

Pronation-Eversion Stage 1: rupture of deltoid ligament or avulsion fracture of tIbial malleolus Stage II: rupture of the Al1F ligament or avulsion fracture (Tillaux or Wagstaffe) Stage ill: high fibular fracture (Maisonneuve) Stage N: rupture of the PITF ligament or Volkmann's fracture

Pronation-Dorsiflexion Stage I: vertical fracture of tIbial malleolus Stage II: fracture of the anterior tibial lip Stage ill: supramalleolar fibular fracture Stage N: transverse fracture of posterior tIbia, level with

proximal aspect of the anterior tIbial fracture

353

Supination-Adduction

! . ~ '\ Stage I Stage II

Supination-Eversion

Stage I Stage II Stage III Stage IV

Pronation-Abductio~

Stage I Stage II Stage III

354

Pronation-Eversion

Stage II Stage III Stage IV

Pronation-Dorsiflexion

Stage I Stage II Stage III Stage IV

Danis-weber classification This system represents a surgical classification based UJXln the level of the fibular fracture and its relationship to the syndesmosis

~ fibular fracture begins at or below the syndesmosis corresponds to supination-adduction classification

~: fibular fracture begins at the syndesmosis corresponds to supination~ersion and pronation-abduction injuries

~: fibular fracture begins above the syndesmosis corresponds to pronation~ersion injwy

355

Treatment of Ankle Fractures

The A-O group suggests that exact anatomic reconstruction of the ankle mortise is necessary for perfect guidance of the talus. Elegant retrospective studies performed by Bauer indicate supination-eversion stage n fractures with less than 2 mm displacement are stable and do not lead to post-traumatic arthrosis when treated conservatively rather than surgically reduced.

Ankle joint integrity depends upon: I) Correcting length of the fibula in its position within the :fibular notch 2) Integrity of the tibiofibular ligaments

The surgical correction of ankle fractures requires the use of A-O screws, plates and/or tension band principles. Distal fibular fractures may be repaired with lateral buttress plates or posterior anti-glide plate technique. Weber C fractures of the fibula require fixation of the :fibula to the tibia, which facilitates repair of the interosseous membrane.

TIBIAL PLAFOND FRACfURES <PILON FRACTURES)

A pilon fracture is the result of direct impact of the talar trochlea against the distal ubial articular surface. The soft cancellous metaphysis of the distal tIbia is compacted, creating a large void when length is restored.

AlIgower Oassification - based upon the amount of comminution ~ :fissure fracture without significant displacement ~: :fissure fracture with significant articular incongruity Type lli: compression fracture with significant displacement of the weightbearing cancellous segments of the metaphysis

I

\~ ''-OV II ill

356

Treatment of Pilon Fractures Treatment frequently involves a combination of internal and external fixation techniques. The A-O suggest four step

method for adequate surgical reduction--Step 1: reoonstruction of the fibula -Step 2: reoonstruction of the tibial articular swface -Step 3: bone graft the metaphyseal deficit -Step 4: buttress plate the tIbia

PHYSEAL FRACTURES

Physeal fractures are injuries involving the physis or epiphyseal growth plate. These ~juries are often incorrectly referred to as epiphyseal fractures, which descnbe fractures of the epiphysis of the bone.

Anatomy and Physiology Each long bone may be divided into epiphysis, metaphysis and diaphysis. The epiphyseal complex refers to epiphysis and thephysis.

The physis is the radiolucent cartilaginous plate with a characteristic arrangement of cells that progress from resting chondrocytes to ossified bone.

Three zones of the physis: 1. Growth zone

=> most important zone of the physis => relatively strong area aqjacent to the epiphysis => consists of predominantly intercellular matrix with germinal cells or dividing chondrocytes

2. Zone of Cartilage Cell Degeneration (zone of maturation) => h)pertrophy of chondrocytes followed by calcification and degeneration => weakest area of the phyusis because of the loss of inten:ellular matrix and intracellular substance

3. Zone ofPrimaIy Bone Formation (zone of transformation) => vaScuIar ingro\\th occurs followed by ossification and remodeling => adjacent to the metaphysis

Zone ofRanvier: => consists of fibrous tissue and osseous ring of Lacroix (osseous Ring of Lacroix is an extension of the

metaphyseal cortex) => provides structural support to the physis and appositional gro\\th

Blood Supply

Epiphysis: epiphyseal arteries form a vascular plexus and extend to supply the germinal cel1s of the physis Metaphysis: metaphyseal arteries via the nutrient arteries of the diaphysis Perichondrium: perichondral vessels ~supplied by epiphyseal, metaphyseal and perichondral vessels

The result of interruption of the blood supply to the physis will differ according to the vessel damaged. -epiphyseal vessel damage leads to permanent growth disturbance -metaphyseal vessel disruption results in transient slowing of growth -perichondral vessel damage has no adverse effects on longitudinal growth

357

Differences between Child and Adult Injuries

~ The physis is tbe weakest area, relative to bones and ligaments in children. This results in fracture patterns that differ from those in adults.

=;> Ligaments are relatively stronger than bones in children. Therefore, ligamentous injuries in children are uncommon. ~ Certain pbyseal injuries will cause growth disturbance if the germinal cells of the growth zone and/or the epiphyseal

blood supply are damaged

Regarding ankle joint injuries-l. -before 8 years of age the pbysis represents a relatively weak structure that is less resistant to tensile forces,

compared to bone and ligaments ~ separation of the physis is more likely since the ligaments with high tensile strength insert below the physis

of the ankle joint ~ ligamentous or osseous injuries are rdrely seen in this age group

2. -at 10 years of age the union between the epiphysis and metaphysis strengthens. Separation of the physis usually involves a .fracture

3. -after 15 years of age the fracture pattern resembles those occurring in adults

Classification svstems

Epiphvseal Fractures (:fracture of the epipbysis without involvement of the physis) 1. Avulsion at ligament attachment 2. Compression fracture of epiphysis 3. OsteochondIal fracture

Phvseal Injuries The two types of physeal injuries are separation and fracture

1. Separation of physis: ~ Most frequently occurs along the metaphyseal border of the physis in the region of the zone of primary bone

fonnation and the degenerating cartilage cells ~ Qx:urs at the weakest area of the physis and is a result of shear forces => There is no damage to the epiphysis, its blood supply or to the growth zone of the physis and, thus,

prognosis is good 2. Fracture of physis:

~ Involves a fracture at the articular epiphyseal surl3ce that continues through the physis ~ Injury results from axial compression and bending forces ~ Damage occurs to the epiphysis, the growth zone ofphysis and possibly the eipphyseal blood supply. Thus,

prognosis is worse

Complications ofPbyseal Injuries Common complications include:

1. Angular deformity due to premature partial physeal closure 2. Limb-Iength discrepancy due to premature complete physeal closure 3. Joint incongruity with seconda.ty post-tIaumatic osteoarthritis

The most common reason for growth distwbance is bony bridging This callus bridge formation between the epiphysis and metaphysis is the strongest stimulus to premature closure of a growth plate

358

Ao pbyseal iniory classification

T:we A: good prognosis ::::::> NO injury to growth zone of physis ::::::> NO injury to epiphyseal vessels ::::::> good prognosis with adequate

reduction

T:we B: doubtful prognosis ::::::> Injury to growth zone ::::::> Potential injury to epiphyseal vessels ::::::> Usually serious sequelJae if treated

incorrectly

Salter-barris classification of pbyseal injuries Type!: ::::::> sepuation of pbysis without damage to the germinal cells or epiphyseal

blood supply ::::::> results from a shearing force ::::::> diagnosis by clinical suspicion of localized edema and point tenderness

along the physis

Treatment: usually possible to obtain adequate results with closed reduction

TypeR: ::::::> partial separation of physis with a metaphyseal fragment

U C::J

* Thurston-Holland sign=metaphyseal fragment produced by a lateral displacement force

Treatment: usually closed reduction will give adequate alignment * if displacement is unacceptable, ORIF may be needed ie-4.0 cancellous screw parallel to the physis; parallel small smooth k-wires approximately 90 to physis

short leg cast NWB 4'() ,,'eeks

359

TypeID: => fracture of epiphysis with partial physeal separation intra-articular fracture

Treatment: lor 2 screws (4.0 or 3.5 nun) parallel to physis short leg cast NWB 4-6 weeks

Tll.LAUX FRACTIJRE (transitional fracture) => represents a Salter-Harris m of the distal tibia => most commonly occurs at age 13-14 => physiologic closure of the distal tibia physis begins at its midpoint and progresses medially. the lateral

half of the physis closes approxiIuately 18 months later at age 14-18 => external rotatory force may canse AITF ligament to avulse the anterolateral quadrant of tIbia with the

Type IV:

open lateral physis goal is anatomic reduction to restore joint congruency => premature closure of physis is not a concern because there is limited growth potential => only case when a screw may be placed across an open physis => follow ORIF with short leg cast NWB 4-6 ",eeks

=> fracture of epiphysis. partial physeal separation and fracture of metaphysis

Treatment: commonly unstable and will require ORIF to obtain acceptable reduction, smooth joint smface and adequate reduction to prevent bony bridging and growth distwbance

short leg cast NWB 4-6 weeks

TripJane fracture ofjmJde: combination of Salter-Harris n and Salter-Harris ill => fracture lines run in three planes and require multiple x-ray views to clarify fracture pattern => cr scan will help evaluate extent ofinjury and fragmental patterns (2 or 3)

Treatment: same as for Salter-Harris IV injury

360

Type V: => crush injury of the physis => may be misdiagnosed as a Salter-Harris I => prognosis is worse because bony bridging may lead to

partial or complete premature ph~ closure and growth distuIbmce

Type VI: => avulsion of perichondral ring

(modification by Rang)

TypeVll: => avulsion fracture of epiphysis without involvement of

physis (modification by Ogden)

Guide to treatment of pbyseal injuries

Rang Modification

8 1. Bilateral films for comparison to he1p recognize physea1 separation. 2. Multiple views in different planes to avoid missing diffiadt fracture lines which may be obscured by overlapping bones. 3 . X-ray the joint above and the joint below if clinically indicated to rule out additional fractures. 4. <lJtain post-reduction x-rays to assess anatomic position after reduction and to clarify fracture patterns.

<lJtain cr scans to assess artiadar congruency and the extent of injmy. 5. Treatment is determined by:

-type of injury -degree of damage to physis, epiphysis and its blood supply -skeletal age of patient -potential growth ofbone remaining -degree of intra-artiadar damage ~ of closed reduction

6. The key to successful treatment ofphysea1 injuries is dependent on REMODELING Remodeling will generally help:

* child with 2 years or more of growth remaining * fracture near the ends ofbone * deformity in the plane of joint motion

Remodeling will not help: * displaced intra-artiadar fracture * fracture in middle of long bone that is grossly shortened, angu1ated or rotated * displaced fracture with axis of displaacement at right angle to plane of motion * displaced ftacature crossing physis at right angle

7. Generally all physeal injuries should be followed for 6 months to 1 year for potential complications of growth di.stmbance. 8. Effects of compression on the physis:

-increase in pressure along an axis parallel to direction of growth may inhibit or arrest longitudinal growth -screws or threaded pins placed across the physis will cause compression and lead to prematme physeal closure

361

-small smooth k -wires should be placed 90 to the physis or near the margins of the physis to decrease the incidence

of growth disturbance

Summaty of Classification ofPhyseal Injuries

Salter & Harris )1 ( ~I \ ~IIt Av~ )v ~ 1963 t:J ~OO t17t:t

Aitken 1936

A.O.

Rang 1969

Poland 1898

OPEN FRACTURES

Gustillo classification Type I: wound less than I em long

B ffi !;)o

~ ~ C~ ffi~

t3§Gb&

little soft tissue damage; no sign of crushing injury simple. transverse or short oblique fracture with little comminution

Type IT: wound greater than I em long no extensive soft tissue damage; slight or moderate crushing injury moderately comminuted fracture; moderate contamination

Type m: extensive soft tissue damage; high degree of contamination; severely comminuted fracture associated with high velocity trauma

type InA - soft tissue covemge of bone is adequate (despite flaps, lacerations, soft tissue destruction) severely comminuted fracture from high energy trauma

)~

type IIIB - extensive injury to or loss of soft tissue requiring local or free flap for coverage after adequate debridement associated with periosteal stripping and exposure ofOOne, massive wound contamination and fracture comminution

type me - any open fracture associated \\'ith an arterial injury that must be repaired

Open Ii'adures associated with arterial. injuries that DIIL'It be repaired have m amputation rate of25-9O"/o.

362

Absolute indications for primary amputation >Type me injwy acoompanied by disruption of the posterior ubial nerve >Type me iIYmY with loss of soft tissue, massive contamination, severely comminuted segmental fracture or

massive loss ofbone that wiUlikely result in significant impairment offunction Relative indication for amputation

>Type me iIYmY that is untreated for 8 hours or more

Antibiotic therapy Type I: single dose of 2.0 gm cephalosporin on admission and 1.0 gmevery 6-8 hours for 48-72 hours Type n & m: single dose of2.0 gm cephalosporin andanaminoglycoside (1.5 mglkgbodyweight) on admission

continue this regimen of cephalosporin and aminoglycoside (3-5 mgIkg body wt) for 48-72 hrs. add 10 million units Penicillin if fi:mn injwy

According to the liternture, infections are largely due to gram negative bacteria. Previous studies had implicated gram positive Ol"fiInisms-

Treatment Protocol: 1. Initial evaluation in Emergency Department

-history & physical. wound inspection and cultures. tetanus prophylaxis. temporary stabilization 2. Debridement with copious irrigation in OR

a) repeat debridement in 48-72 hours b) debridement may need to be repeated with types IIIB or C to achieve clean. stable wound

3. Stabilization offracture 4. Antibiotic Therapy 5. Coverage and closure ofwound

-delayed primary closure 5-7 days after injury with types I & n

TYPE RAlE OF INFECTION RAlE OF AMPUTATION I 0-2% II 2-7010 IlIA 7010 00/0 IIIB 10-50010 16% me 25-50010 42%

363

Avascular Necrosis

Definition Death of bone marrow and trabecular elements secondary to repeated interruptions or a single massive interruption of the blood supply to the bone.

Etiology • Atraumatic:

- alcoholism - hyperlipidemia - hypercorticalism - hemoglobinopathies - obesity - hyperuricemia - infection - pancreatitis - pregnancy

• Traumatic: - fractures/dislocations - iatrogenic

Signs & Symptoms

• Progressive Acute joint pain Occasional spasm

• • • • • •

Radiographic

Aggravated by weightbearing; relieved by rest Limitation of motion Continuous joint pain Joint destruction

• Not for early diagnosis • Focal subchondral demineralization • Radiolucency surrounded by radiodensity • Subchondral collapse/stress fracture • Total joint destruction

Treatment • Early Stages

• Late Stages

GOAL => prevent subchondral collapse TotalNWB Electrical bone stimulation NSAID's

GOAL => alleviate pain Conservative -- patellar tendon weightbearing brace, NSAID's Surgical - arthrodesis procedures, bone grafting procedures

364

COMPARTMffiNTSYNDROME

*** SOOIo of cases occur in the lower extremity

Etiologies a) fractures b) crush injuries c) musculoskeletal surgeIY

d) hematoma e) arterial emboli (rare) f) infection

Pathogenesis a) increased tissue pressure: increase in net force per unit area on the vessel wa1ls b) increased venous pressure c) decreased arteriovenous gradient d) decreased local blood flow and oxygenation

Diagnosis a) the six P's

I. pain: the most important sign. The pain is usually out of proportion to what one would expect for the clinical situation. This is often one of the first signs since nerves are the most sensitive tissue to ischemia The pain is exacerbated by putting the muscles in the compartment at passive stretch.

2. paresthesias: followed by hypoesthesia and anesthesia; these are reliable indicators. 3. paralysis: a late finding 4. pressure: tenseness of the compartment envelope.

Second most important sign; can be measured via a wick catheter. An intracompartmental pressure of greater than 30 mmHg is considered to be diagnostic of compartment syndrome; however, some believe that irreversible damage doesn't occur until 45 mmHg.

5. pink: routinely have good capillary refill, except in cases of major arterial disease. 6. pulses: routinely present except in cases of pre-existing major arterial disease.

b) timing of signs, symptoms and tissue damage: the disease progresses rapidly, thus patients should be monitored every 30 minutes.

• 30 minutes paresthesias • 2-4hours functional muscle changes • 3 hours post-ischemic swel1ing • 4-12 hours irreversible muscle deterioration begins • over 12 hours contracture formation • 24 hours onset of myoglobinuria

Treatment a) remove all casts and dressings b) keep limb at heart level; do not elevate. Elevation creates more ischemia and interferes with venous

drainage. c) hydration (prevents deleterious effects of myoglobinuria) d) surgical decompression via fasciotomy: individual compartments can be decompressed if not all

compartments are involved Often all four compartments and decompressed The wound is not closed, but packed·open.

I. single incision: through an incision at the peroneal compartment all four compartments can be decompressed

II. double incision: through an anterolateral incision the anterior and lateral compartments can be decompressed Through a posteromedial incision both deep compartments can be decompressed.

365

ill. Four compartments a) anterior: along with the deep posterior compartment are the two compartments most

commonly involved in compartment syndrome. b) lateral c) deep posterior: along with the anterior compartment are the two compartments most

commonly involved in compartment syndrome. d) superficial posterior

Sequela a) Volkmann's contracture of muscle

muscle ischemia muscle necrosis muscle contrncture b) renal fuilure: secondary to myoglobinuria

Osteochondritides

Definition: A group of related disorders, which are thought to be due to a disturbance to the ossification center of the bone. It may affect both the primary and secondary ossification centers during the time of developmental activity.

Clinical Findings: pain swelling symptoms increase with activity

Radiographic Findings: lucency fragmentation collapse of articular surface

Names of Specific Osteocbondritides: Theiman Phalanges Freiberg Metatarsal heads Islen 5th metatarsal base Buschke Cuneiforms Kohler Navicular Lance Cuboid Sever Osgood-Schlatter -Blount Kohler

Calcaneus Tibial tuberosity Tibial epiphysis (proximal) Patella

366

GUNSHOT WOUNDS

Theory of Wounding Capacity Kinetic Energy (KE)

m=mass v=velocity

-velocity is more important than lua:;~ -energy imparted on impact determines extent of injury

High velocity == >2000 ftlsec ==> -requires emergent radical wound debridement ==> -military battlelhuntingaccidents ==> -<:avitation effect

KE==

* energy of bullet exceeds expansile capacity of tissue * a vacuum is created pulling debris into the wound

Low velocity == <2000 ftlsec (majority of pedal gunshot wounds) ==> -consists of bullets weighing 100-300 grains ==> -entry port sometimes not enough energy for exit ==> -occur at short ranges

mv~

2

==> -no cavitation; expaI1Slble capacity of tissue exceeds energy of bullet

Management -A,B,C'sistabilize patient -detailed foot and ankle exam

-Tetanus

-vascular status -neurological status -muscle testing -entry/exit wounds, laceration, skin slough -ROM, pain, crepitus, deformity -presence of foreign bodies -radiographic studies

0.5ml toxoid if previous immunization 250 units of tetanus immunoglobulin + 0.5ml of toxoid if no previous immunization

Fracture -any fracture associated with external environment is considered open -bullet not heat sterilized / wound considered contaminated / potentially infected -adhere to principles outlined by Gustillo for open fractures

-if> 8 hr considered infected -most LV are type I -antibiotic recommended (cephalosporin) for 3 days or until infect. subsides

-open reduction -fractures that require intraarticular reconstruction/rigid fixation to stabilize

Surgery -debridement

-gross contamination/necrosis -intraarticular -neurovascular destruction -compartment syndrome

-prophylactic antibiotics -not essential for wounds not grossly contaminated -determined by clinical appearance of each individual wound

-most L V injuries not cause devitalized tissue at distance from wound tract

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-extreme debridement may not be necessary -cleansing of wound

-3 L saline or 10 % povidine iodine -excise exposed muscle and fascia -avoid probing of missile tract -foreign bodies removed only if excessive dissection not required -bullets not excised unless superficial and palpable -complicated exploration avoided unless vital structure threatened -closure

-depends on degree of surgical intervention -small wounds left open allow to granulate -surgical debridement Gustillo I&II <8m can close primarily -any question leave open until no sign of infection (3-7 days)

SOFT TISSUE TRAUMA(General)

General guidelines for evaluation of lower extremity soft tissue trauma. 1. Primary survey: assess airway, breathing and circulation 2. Secondarv survev: check for life threatening injuries and associated injuries (ie-spinal fractures, etc) 3. Obtain a historv

PMH;. Meds; Allergies; PSH; Family history: Social history Female -last menstrual period tetanus status time food/drink last ingested (in case of emergency surgery) mechanism of injury and time of occurrence estimated blood loss initial treatment

4. Phvsical Examination vitals: temperature, pulse, respiration, blood pressure vascular: pulses; capillary filling time; skin temp; edema

if pulses nonpalpable - Doppler, arteriogram neurologic: sensory; motor, deep tendon reflexes musculoskeletal:

evaluate for muscle or tendon damage ROM; palpation muscle strength testing x-rays if fracture or foreign body suspected

wound evaluation: dimensions (width, depth, length) signs of infection (ie-edema, erythema, calor, pus, etc)

wound classification: clean = less than 6 hours post trauma

contaminated = greater than 6 hours post trauma debris and necrotic tissue present extensive soft tissue damage or loss increases the possibility of infection

infected = clinical signs of infection significant gross contamination

Wound care guidelines for soft tissue trauma 1. Tetanus immunization status 2. Cleanse surrounding skin with betadine or Hibiclens solution 3. Exploration:

• inspect for foreign body and debris • inspect for deep tissue damage (ie-tendon laceration, joint involvement) • inspect for vascular damage

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4. control small vessel bleeding by the following-• apply gentle manual compression • elevation of the limb • electrocoagulation with bovie • band tie or suture ligature • thrombin (protein substance that clots fibrinogen of blood) • SUIgicel® (a sterile absorbable knitted 13bric of cellU1ose~ after saturated with blood, the Surgicel

swells into a ge1atinous mass which accelerntes clotting) • Gelfoam®(absOIbable sterile ge1atin sponge~ absorbs many times its weight in blood within its mesh

and functions as a hemostatic agent) 5. Take deep cultmes (aerobic, anaerobic); gram stain 6. Debridement and IIIigation

• dilute betadine, Hibiclens solution, saline or lactated Ringer's solution • use syringe and blunt needle or N catheter to create pulsating lavage

7. Decision planning for wound closure is guided by: a) contaminated wound versus infected wound

1. signs of infection [clinical infection = >10 -lO orgsIg tissue or one suture+ 10 oq¢g tissue] 2. hours post injury 3. mecbanism of injury and innoculum 4. (ie-rusty, dirty nail puncturing through a sneaker vs. clean kitchen knife vs. animal or human bite) 5. degree of tissue damage or loss

b) natma1 defense mechanisms host resistance depends on medical history (ie-diabetes, long term steroid therapy, etc) immune response (ie-AIDS, leukemia, etc)

c) genemIly primary closure can be performed on clean wounds contaminated wounds converted to clean wounds by copious irrigation and debridement (if questionable, pack wound open)

d) infected wounds require culture and gram stain local wound care with JECking empiric antibiotic theI3py until culture results -evaluate wound in 2-3 days for progress delayed closure when indicated or secondary intention healing

7. Prophylactic vs TheIapeutic Antibiotic TheIapy prophylactic antibiotics should be given within the first 3 hours of contamination for effectiveness -clean and contaminated wounds require adequate debridement and irrigation, not prophylactic antIbiotics -one exception is human bites, which have a high risk of infection

therapeutic antibiotics are indicated for established clinical wound infections 8. Tetanus prophylaxis

tetanus prone wound: greater than 6 hours post injury greater than 1 em depth bum, frostbite, crush or missile injury stellate woWld, abrasion or avulsion of skin devitalized, ischemic tissue contaminants (i~ feces, saliva)

Tetanus Prophylaxis

wound tetanus prone non-tetanus prone

immune status uncertain<5 yrs Td+TIG Td

last tetanus booster 6-lOyrs Td Td no Td

*Td = tetanus and diphtheria toxoid adsorbed dose: 0.5cc 1M

*TIG = tetanus immune globulin (human) dose: 250 U 1M

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CHRONIC REGIONAL PAIN SYNDROME (REFLEX SYMPA mE TIC DYSTROPHY)

Misnomer RSD and Sudeck's atrophy are not interchangeable. Sudeck's atrophy is pathognomonic for the second stage of RSD. which includes specific osteolysis Etiology

• usually triggering factor is trauma • severity of trauma has little correlation to severity of symptoms • ankle sprains, pes valgo planus, neuroma, injections. tourniquets. poliomyelitis. infection

Phases LA,. cold/vasoconstrictive phase (2-6 weeks)

decreased temperature of affected foot hyperalgesia present skin mottled by patches of pallor on a pinkish-blue backdrop

ill: the classically described initial phase; "sweaty-vasodilatory phase" (2-6 months) increased warmth to foot hyperalgesia still present foot color changes to red coloration greatest likelihood of remission in this phase

II: hallmark of Sudeck's atrophy osteoporosis visible radiographically osteolysis is in a "spotty" pattern Sudeck's atrophy die to hyperemia, increased intramedullary pressure, and decreased pH. Not due to disuse! skin is taut and glossy with a brawny coloration poor likelihood of reversing syndrome

ill: dead phase (6-12 months) foot is pale and wax-like marked joint stiffness marked osteoporosis

T reatrnent: • local anesthetic blocks into areas ofpain (trigger points) • 1ENS units • surgical sympathectomy • supportive • physical therapy; analgesics: anti-inflammatories • calcitonin therapy

TRAUMATIC NERVE PATHOLOGY

Nerve Anatomy endoneurium surrounds a single nerve fiber perineurium surrounds a bundle of nerve fibers (fascicle) epineurium surrounds a large nerve (multiple fasciculi)

Seddon Classification of Nerve Injurv Neuropraxia: least severe

nerve contusion/compression conduction deficit without axonal damage

Axonotmesis: Wallerian degeneration (degeneration of axon distal to injury) axon damage without endoneurial tube damage reversible; muscle wasting may occur

Neurotrnesis: most severe partial or complete severance of nerve with complete disruption of endoneuria! tubes irreversible unless surgically repaired

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Feature Neuropraxia Axonotmesis Pathologic

Anatomic continuity Preserved Preserved Essential damage Myelin sheath distortion Wallerian degeneration

with endoneurial tube preservation

Clinical Motor paralysis Complete Complete Muscle atrophy Very little Progressive Sensory paralysis Usually spared Complete Autonomic paralysis Usually spared Complete

Recovery Quality Perfect Perfect Rate of recovery Rapid; days to weeks 1-2 mm/day

March of recovery No order According to order of innervation

Treatment Surgical repair Not necessary Usually not necessary

Seddon "s. Sunderland Classifications SUNDERLAND

Type/Degree First Second Third

SEDDON

Sunderland Classification First degree - equivalent to Neuropraxia.

Neurotmesis

Maybe lost Complete disorganization

Complete Progressive Complete Complete

Imperfect 1 -2 mm/day (if surgically repaired) According to order of innervation

Essential

Fourt h

Fifth

Second degree - corresponds with axontmesis with axon disruption but not endoneurial tube disruption. Third degree - form of axon tmesis or neurotmesis and incorporates axon and endonuiraI tube disruption with intact perineurium. Fourth degree - encompasses physical disruption of fascicles and perineurium with intact epineurium. Fifth degree - true neurotmesis, complete disruption of the nerve trunk

Nerve surgerv • neurolysis: lysis of adhesions • external neurolysis (detach adhesions outside of nerve) • internal neurolysis (enter epineurium to detach adhesions) • neurorrbaphy: resection with end-to-end anastomosis • neurectomy: nerve resection • nerve grafting

37i

Surgical treatment of traumatic neuromas Note: Numerous procedures and devices have been devised to prevent stump neuroma (the most common complication with neurectomy) The follo",ing is a small list of what has been attempted. None have been consistently reliable

Inhibition of Axonal Regrowth PhYsical Containment

+ Chemical Treatment Alcohol Phenol Formaldehyde Nitrogen mustard Pepsin Hydrochloric acid Iodine Gentian violet Steroids

+ Cauterv Electrocoagulation Laser Radiofrequency current Cryosurgery

+ Ligation

Types of Nerve Inju~; Based on Etiology

Cause o/Injury Neuropraxia Cuts and lacerations Fractures Missiles + Traction + Compression + (momentary) Thermal + Ischemia + a+, frequent; ±, occasional: -, infrequent

± + + +

+ Synthetic Containment Silicone caps Rubber Plastic Lucite Polyethylene Collodium Cellophane Metallic foil Tantalum Glass Nerve glue

+ Physiologic containment Epineurorrhaphy Nerve grafting

Translocation away from Painful Stimuli Excision and retraction Implantation into muscle Implantation into bone En bloc translocation

Axonotmesis Neurotmesis +

± + +

+ (prolonged) + + +

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Quantitative Sensory Testing (QST)

• Conceived by neurologists in order to provide a non-painful method to measure peripheral nerve function

• Measures cutaneous pressure perception with the use of a pressure-specifying sensory device (PSSD)

Pressure Specifying Sensory Device (PSSD)

• Designed to measure the threshold for perception of pressure stimuli on the surface of the human body

• Provides a threshold measurement throughout a continuous range of applied pressures • Consists of 2 metal prongs with hemispherical tips that measure the distance between the tips

ofthe prongs as well as the amount of cutaneous pressure required for perception of the tips • Able to measure one-point moving, one-point static, two-point moving, and two-point static

over a particular piece of skin • Pressure threshold measured in g/mm2 • Patient recordings compared to normative data

Indications

• Diabetic neuropathy

• Tarsal tunnel syndrome • Heel pain • Cubital tunnel syndrome • Morton's neuroma • Sural nerve entrapment • Carpal tunnel syndrome

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ACEITLLESTENDONRUPTURE

Diagnosis: • stabbing type pain of posterior ankleJIeg • tenderness and palJXlble defect in the Achilles tendon which increases with dorsiflexion • decreased active plantarflexion and weakness of plantarflexion of the ankle joint against resistance • apropulsive gait with a "ball-like" contracted calf muscle • Thompson's test- with the patient lying in a prone position, the gastroc-soleus complex is squeezed to

assess plantarflexion of the ankle joint •

positive test = decreased to no plantarflexion of the ankle joint relative to the contralateral foot false negative = the long flexors, tibialis posterior and peroneus longus provide motion at the ankle joint

Differential Diagnosis: • achilles tendonitislbursitis

partial rupture of gastrocnemius • mnligonfractwreoftheadcaneus • traumatic hematoma of the lower leg

Pathogenesis: Rupture commonly occurs 2-6 cm proximal to its insertion at an area of decreased vascularity (Lagergren & Lindholm) Predispogng factors: collagen vascular diseases (ie-gout, RA)

• long term systemic steroid therapy • load steroid injection

Treatment Conservative:

• Indicated for partial tears, sedentary older patients and non-surgiad candidates • higher incidence of re-rupture compared to surgiad treatment • gravity equinus casting: • long leg cast with knee flexed at 20 or SLC; ankle joint placed in gravity equinus for 6-8 weeks • followed by SLC weight-bearing with reduced amounts of equinus to eventual heel lift in shoegear

Surgical: a) primary reprir with suturelimplant

I. Ma and Griffith: percutaneous suture reprir with nonabsorbable suture on a straight needle 2. End-~End anastomosis with nonabsorbable suture 3. Implants (absorbable polymer carbon fiber compogte - Parsons et al) 4. Pull-out wire techniques 5. Fascial reinforcement

a. Bugg and Boyd: modified Bunnell pull-out wire suture in combination with three fascia lata strips b. Lynn: reinforcement of end-to-end anastomogs with the plantaris tendon; plantaris is detached

from its insertion and fanned out to form a membrane c. Silverskiold: central strip of gastrocnemius aponeurosis is flapped distally over the defect d Lindholm: two outer strips of gastrocnemius aponeurogs are flapped distally to reinforce the

tendon repair 6. Tendinous reinforcement

a. Bosworth: a strip of gastrocnemius tendon is freed proximally, flapped distally and passed through the proximal and distaI tendon stumps to join the ruptured tendon

b. Teuffer: peroneus brevis is detached from its insertion, placed through a drill hole in the adcaneaI tuberosity and passed proximally along the ruptured tendon for reinforcement; its is also sutured to itself to produce a dynamic loop.

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Achilles Tendon Primary Repair Techniques

MA &: GRIFFITH BUGG&BOYD

SILVERSKIOW UNDHOIM BOSWORTH

LIGAMENTOUS ANKLE INJURIES

Diagnosis a) history

1. what happened? how long ago? 2. where does it hurt? ( point with one finger) 3. what treatment have you done? can you walk on it? 4. mechanism of injury 5. past medical history, social history 6. current medications, if any 7. allergies

b) physical exam 1. vascular status (pedal pulses; cft) 2. senoory/ neurologic status 3. edema, erythema, ecchymosis, calor, dolor 4. palpation

lateral foot dorsolateral foot lateral ankle - anterior talofibular li~ent

calcaneofibular li~ent posterior talofibular li~ent

medial ankle - deltoid li~ents posterior ankle lateral malleolus high fibula (Maisonneuve fracture) medial malleolus

5. radiographic exam DP and oblique of the foot lateral of the foot and ankle AP, mortise, and oblique of the ankle

6. stress inversion normal depends on which study must compare to opposite limb

LYNN

TEUFFER

positive usually greater than lO for double ligament injury (ATF and CF)

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7. anterior drawer greater than 4 mm is positive for ATF tear several ways to measure anterior drawer

8. peroneal tenogram infiltrate dye into peroneal tendon sheath CF lig. in intimate contact with lateral ankle joint capsule and deep aspect of peroneal tendon sheath mortise and lateral ankle x-rays normal study = dye stays within tendon sheath positive study for CF ligament rupture = dye extravagates into the ankle joint

several authors describe a normal communication between peroneal tendon sheath and ankle joint (approx. 2%)

9. ankle joint arthrography dye injected into the ankle joint positive study = dye extravagates into soft tissues

diagnostic for ATF ligament rupture less accurate than tenogram for CF lig. rupture

10. MRI - able to evaluate soft tissues (ie-ligaments)

Associated fractures a) fifth metatarsal base b) anterior process of calcaneus c) dorsal lateral calcaneus (EDB a"u}sion) d) lateral talar process e) Shephard's fracture (posterior talar process) f) osteochondral fracture of the talar dome g) avulsion fracture oflateral malleolus (usually associated with dislocation of peroneal tendons) h) high fibula (Maisonneuve fracture) i) medial malleolus j) Salter-Harris I in children

Oassifications of Lateral Ankle Ligamentous Injuries a) Leach

first degree: partial or complete tear of ATF ligament second degree: partial or complete tear of ATF and CF third degree: partial or complete tear of ATF, CF and PTF ligs

b) O'Donoghue first degree: ligament stretch with minimal disruption second degree: partial ligament disruption with joint instability third degree: complete ligament disruption

c) Dias grade I: tmtial rupture of CF ligament grade 2: ATF ligament rupture grade 3: ATF, CF anellor PTF ligament rupture

d)Henry group 1: tender over A TF lig.; negative anterior drawer:

taIar tilt < 5 group 2: moderate injury; tender over ATF and CF ligs.; negative anterior drawer, talar tilt < 15 group 3: severe injury; lateral ankle swelling and pain; positive anterior drawer, talar tilt > 15 group 4: chronic problem; positive anterior drawer;

talar tilt > 15

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Treatment a) conservative

I. rest, ice, compression. and elevation 2. Unnaboot 3. Gibney boot 4. Jones compressive dressing with -

5. Aircast

posterior splint AO splint eggshell cast

6. degree of weight bearing depends on severity of injury b) surgical

I. primaIy repair of tom ligaments usually reserved for a combined ATF and CF lig. tear

2. lateral ankle stabilization procedures

VASCULAR TRAUMA

Categories a. blunt trauma: artery is crushed or contused resulting in hemorrhage; may cause compartment S)'ndrome b. penetrating tmuma: ie~ep laceration, gunshot wound

Treatment: • stop active bleeding by gentle manual compression; elevation of limb may further compromise the

ischemic foot • assess DP and Pf pulses; if the major vessel in the vicinity of the wound is nonpalpable, you must assume

Vascular injury until proven otherwise • if pulses nonpalpable, auscultate with the Doppler; determine ankle/brachial index

even with pulses the extremity should be monitored for compartment syndrome • if vascular status is compromised or questionable, get a vascular consult; arteriogram may be required to

evaluate the extent of the injury

NAn.. BED INJURIES

All require x-rays to RIO distal phalanx fracture

• Subungual hematoma involving <25% of nail bed

dIain hematoma using #11 scalpel blade, 18 gauge needle, rotary ball burr or sterilized paper clip

involving >25% of nail bed skin p-ep, nail avulsion to RIO nail bed laceration

• Nail bed laceration a. skin prep and nail avulsion b. wound care c. primary repair with absorbable suture within 7 days post injury to avoid scar formation

of nail bed d prevent nail bed and proximal nail fold contact in order to avoid nail deformity, use

Adaptic, Vaseline impregnated gauze or Xeroform to maintain space

*if nail bed laceration noted with underlying phalangeal fracture, treat injury as an open fracture"

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Rosenthal Classification of Digital Injury

Level of tissue loss zone I: distal to bony phalanx zone II: distal to lunula zone III: proximal to distal end oflunula

Plane of tissue loss: dorsal oblique transverse plantar oblique axial (tibial or fibular oblique) central (gouging)

Treatment: zone I:

Rosenthal Classification of Digital hJjuries

~ ~

~ Central

•

• distal digital amputation with nail bed avulsion • ",ithin zone I without exposed bone, allow to granulate in by secondary intention healing • tissue loss> 1 em , skin graft on acute or delayed OOsis (ie-full thickness skin graft on digital tip;

reverse dennal graft to:fill large nail bed avulsion defect)

zone II: • local (adjacent) pedicle flaps are indicated

(ie- Atasoy plantar V-Y advancement graft; Kutler type V-Y advancement graft for toe reconstruction)

zone III:

• nail bed augmentation • ablate remaining nail bed if too much has been lost

• generally not amenable to nail bed reconstruction • primary amputation is usually performed with attempt to preserve distal IPJ and distal tendon

function

PUNCTURE WOUNDS

I. Foreign body injuries a) plantar foot wounds may be contaminated with dirt, grass, sock or shoe material b) pin/needle

diagnosis: standard x-rays removal by the following methods -triangulation with needles placed at 90 angle to isolate the foreign body's depth -visualization under C-arm fluoroscopy -hand held electromagnetic metal locators emit a higher pitch sound wave near metal objects ~on follows clinical signs of inflammation, abscess or hemorrhage

c) wood toothpicks/splinters diagnosis: xeroradiography, standard x-rays, CT (most reliable)

d) glass diagnosis: standard x-ray can pick up tinted or glass containing lead

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2. Complications ofpuncture wounds a) cellulitis: Staph aureus >50% of cases

Staph epi, streptococcus, E. coli b) abscess c) osteomyelitis: Pseudomonas aeruginosa approx. 90 of cases usually wounds 3-4 wks old

3. Treatment of puncture wounds a) tetanus status b) x-rays c) wound care with removal of foreign body; pack wound open

surgical debridement and lavage if it penetrates the joint d) antibiotics if infectedlcellulitic, if deep wound extends to bone or if penetrates the joint e) if infected puncture wound does not respond to anbbiotics, there is probably a foreign body present

BITE WOUNDS

Dog and Cat Bites • common pathogens: Pasturella multicida (facultative gram neg rod)

Staph. aureus, alpha-hemolytic streptococcus treatment:

1. tetanus prophylaxis 2. Rabies prophylaxis

Dog/Cat: >if animal is healthy and available for observation, no treatment unless animal develops rabies >rabid animal, suspected or unknown status: give rabies immune globulin and IIDCV (human diploid ceU vaccine) if animal is negative, stop prophylaxis

3. Wound care: explore to rIo tendon laceration, joint damage 4. Antibiotic therapy: controversial

-some advocate prophylaxis because animal bites are high risk and highly contaminated -recommend Augmentin (ifPCN allergic, give Erythromycin) ~thers only use antIbiotics if clinically infected

Human Bites • Common pathogens: anaerobes (ie-Bacteroides fragilis)

Eikenella corrodens (gram neg rod) Stapha~,Staph~dermidis Treatment:

1. follow guidelines for wound care 2. if injury >6 hours old, pack wound open and foUow-up in 2-3 days 3. AntIbiotics

oral: Augmentin parenteral: Unasyn, Timentin prophylaxis advised because human bites are highly contaminated wounds and at high risk of infection

BURNS

Classification By depth: • first degree = erythema • second degree = blistering • third degree = destruction of epidermis, dennis and skin appendages: anesthetic • fourth degree = destruction of fat, muscle and bone

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Or. partial thickness: first or second degree full thickness third or fourth degree

By extent of bum: o/ototal body surface area (BSA) nile of nines -

head 9% chest/abdomen 18% arm 9% back 18% groin I % leg 18%

Treatment: I. remove burning agent 2. ABC's and treat associated injuries 3. tetanus status 4. assess vascular status.

-observe for vascular compromise with circumferential burns, edema and eschar -circumferential eschars may require escharotomy

5. wound care: immediately cool the area with water or saline

• blister care • debride ruptured blisters • intact blisters may be left undisturbed for 24-36 hours to provide biologic wound coverage and to

prevent tissue necrosis topical agents (for burns >20% BSA)

silver nitrate silver sulfadiazine (Silvadene); bacitracin: neomycin mafenide acetate Xeroform dressing

reconstruction for third or fourth degree burns with skin grafts is indicated 6. Antibiotics

• -prophylactic antibiotics are not recommended because it may result in superinfection with Pseudomonas or yeast

• common pathogens of infected bums Staphylococcus Streptococcus Pseudomonas Proteus

COLD INJURIES

Immersion foot injury to tissue due to a combination of wet and cold

Frostbite injury to tissue due to freezing frostbite classification

L hyperemia 2. blisters 3. necrosis 4. necrosis and tissue loss

treatment tetanus status rewarm limb rapidly at temperature of 104-108 for 15-20minutes: may require narcotic analgesics.

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FROSTBITE L Definitions

A Frostnip: pallor and numbness of the affected tissues; mildest form; warming results in freedom from epidermal or dermal damage

B. Chilblain/pernio: chronic vasculitis of the dermis that is provoked by repeated exposure to cold temperatures above freezing in high humidity

C. Trencbfoot: occurs when feet are exposed to wet conditions and temperatures between 0-20 degrees celsius

D. Frostbite: occurs when skin and subcutaneous tissues exposed to thenna! stress freeze with tempemtures < 2 degrees celsius

II. Who is at risk? -males between ages 20-50 -altered mental status

*psychiatric disorders *alcohol abuse *headinjwy

-homeless

III. Predisposing Factors -environmental temperatures *low tempemtures *moisture *windchill *duration of exposure

-Miscellaneous *motor vehicle problems *improper clothing *fatigue

IV. Pathogenesis Direct freeze

-elderly -malnourished -military personnel -outdoor sports enthusiasts *skiers, runners, climbers

-laborers in cold environment

-host factors *alcohol abuselhomeless *psychiatric illness *malnnourishment *PVD/atherosclerosis *smoking *chronic liver/renal disease *Raynaud's disease

-extracellular ice crystal formation followed by intmcellular ice crystal formation with cell membrnne damage

-increase osmotic pressure in interstitium causing water to be dmwn out of cells, intracellular dehydmtion, and cell death

-denaturing of lipid protein membrnne

Indirect Injwy (vascular and inflanunatory changes) -"Hunting Reaction": alternating vasoconstriction and vasodilation -persistent vasoconstriction leading to hypoxia, acidosis, increased blood viscosity -capillaries, arterioles, and venules thrombose -release of inflammatory mediators: prostaglandin PGF2 and thromboxane A2

-vasoconstriction, platelet aggregation, and blood vessel thrombosis

V. Clinical Presentation Predictors of Poor Outcome: Favorable findings:

-sensation to pinprick -small vessicles with dark blood fluid -skin that indents with pressure -nonblanching cyanosis -normal skin color -skin that feels "wooden" to touch -large blisters filled with clear fluid -skin that does not indent \"ith pressure

-infection -delay in seeking medical attention

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VI. Diagnosis -physical examination -conventional radiography -lxme scintigraphy -angiography -digital plethysmography -doppler flow studies

VII Treatment -University of Chicago Protocol -rapid rewarming in wann water at 104-108 degrees F for 15-30 minutes (patients presenting 24 hours post injury are not rewanned) -white blisters are debrided with application of topical aloe vera every 6 hrs -hemorrhagic blisters are left intact with application of topical aloe vera every 6 hrs -affected part is elevated with splinting as indicated -analgesia as indicated -ASAJibuprofen -daily hydrotherapy -physical therapy

*definitive amputation is delayed until clear demarcation of gangrene (early debridement only indicated with uncontrolled infection)

VIII. Sequelae -cold insensitivity -tissue loss -hyperhydrosis -vasospastic attacks -intrinsic muscle atrophy -hyperesthesias -color changes in integument -chronic pain -arthritis -pinneal calcification -growth plate abnormalities -squamous cell carcinoma

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