infectionsdm 1999

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Diploma in Medicine

Endocrinology Unit

Dr. Kimberly Oman



“Poorly characterized defects in hostimmunity ... make them more susceptible tocertain types of infections including bacterial

infections of the skin and soft tissue” (CID1997;25:1318) Impaired wound healing in diabetics (ibid) Decreased cell mediated immunity (Mandell

1990 p. 129) Decreased neutrophil chemotaxis and

phagocytosis (Mandell p. 145)



Mild diabetic decompensation

Does not seem to be deleterious to the phagocyticsystem

Severe diabetic decompensation

Poor chemotaxis, ingestion and killing by PMNs (?Partly due to hyperosmolar state)

Staphylococcus aureus in diabetes mellitus (Mandell - 1990 p.1496)

Increased nasopharyngeal colonization of diabetic

patients on insulin ? Increased frequency of infection More likely to be severe and protracted



Crepitant soft tissue wounds (p. 809): non-

clostridial anaerobic cellulitis, necrotizingfasciitis, synergistic necrotizing cellulitis (“Gas gangrene”) Fornier’s gangrene (necrotizing fasciitis of the

male genitals) - “if the abdominal wall

becomes involved in an obese patient withdiabetes, the process can spread like wildfire”(p. 810)



Candida vaginitis (p. 1946) Chronic or persistent bacterial pneumonia (p.

566) Infectious arthritis (p. 912) Rhinocerebral mucormycosis (DM esp.

acidosis, leukemia, renal transplant) : facial

pain, headache, involvement of orbit & brain-treat with radicaldebridement (p.1964) ? Cryptococcosis (fungal meningitis,

pneumonia) p. 1982



Clinical presentation Unwell Minimal or no localizing signs Often confused +/- fever Often high white count

Respond to cloxacillin and gentamicin May do poorly if antibiotics withheld

Not uncommon in Fiji but not described in theliterature



Ischemia

Arterial insufficiency in 60% with non-healing

ulcers and 46% with major amputations Infection

Superficial fungal infections leading to

maceration or broken skin

Increased nasal and skin colonization with

Staphylococcus aureus



Peripheral neuropathy present in over 80% ofdiabetics with foot lesions

Sensory neuropathy Unperceived injury

Motor neuropathy: Gait disturbances, foot deformities (such as claw

toe) Autonomic neuropathy Interference with sweating can lead to dry,

cracked skin



Good glycemic control No smoking

Early detection of loss of protective sensation Vibration

Monofilament testing

Regular foot inspection by clinicians Education in foot care and proper footwear



Wash and dry your feet thoroughly every day,

especially between the toes Inspect your feet daily for blister, skin breaks

and infection Apply cream to the skin Cut your toenails carefully Wear well-fitting shoes that don’t rub or hurt

your feet or cause blisters Don’t go barefoot



Seek medical care if you have an infection or

skin breakdown on your feet. Tell patients that preventing foot problems

and treating foot problems early can preventamputations



Most common Unperceived, excessive and repetitive pressure on

plantar bony prominences such as metatarsalheads

Others Foot deformities (elevated focal pressure) Small foreign bodies in footwear Pressure necrosis from poorly fitting footwear Puncture wounds Pacific Islands: going barefoot



History

Prior ulceration Prior surgery involving the metatarsal bones

Physical findings

Callus or hemorrhagic callus Blister or macerated skin Limited hallux dorsiflexion (<30 degrees)

Prominent metatarsal heads inadequately coveredwith soft tissue Other plantar bony prominences

Radiographic findings: Charcot’s fracture



No apparent infection

(No signs of inflammation or drainage or evidenceof osteomyelitis on plain xray)

Mild infection Superficial, < 2 cm of cellulitis

No serious ischemia

No bone or joint involvement

Patient reliable, good home support



Limb-threatening infections Full-thickness ulcer

>2 cm of cellulitis with or without lymphangitis

Bone or joint involvement

Systemic toxicity

Serious ischemia

Patient unreliable or poor home support Major problem: determining if osteomyelitis

is present



Often difficult / problematic

Early osteomyelitis Similar to soft tissue infection

No changes on radiographs

Hard to distinguish on xray from diabeticosteopathy (Charcot’s changes)



History: Ulcer present for more than one week Previous osteomyelitis

History of other foot complications secondary toperipheral neuropathy

Physical exam: Many are not febrile Increased risk if ulcer over bony prominence

Larger or deeper ulcer Bone visible or can be touched with a sterile blunt

probe



Laboratory tests ESR

▪ >70 mm/hr: 100% have osteomyelitis

▪ >40 mm/hr: 12x risk of osteomyelitis WBC, other tests not helpful

Radiography Findings: focal osteopenia; lucencies in cortex or

medullary bone bony abnormalities not present on plain films for 10-20

days Overseas: bone scans / gallium scans / indium labeled

leukocytes / MRI



Bone culture Sensitivity 95% / Specificity 99% Surgical approach OR Percutaneous through uninfected tissue

Laboratory studies Gram stain and culture Histopathology

Not always done due to expense Some skip if osteomyelitis highly likely Consider for suspected unusual organisms



Similar for soft tissue infection and osteomyelitis Soft tissue cultures often grow different organisms

from bone cultures in the same patient Most infections are polymicrobial

Average: 2.2 pathogens in osteomyelitis, twice that in

soft tissue infections Staphylococcus aureus most common

Other gram +: Streptococcus spp., Enterococcus spp.



Gram negative bacilli

Enterobacteriaceae; Pseudomonas (puncturewound especially with rubber-soled shoes; soaking

feet) Anaerobes

Relatively frequent in serious soft tissue infections Less common in osteomyelitis

More frequent in long-standing infections,infections not eradicated by previous antibiotics ornecrotic tissue / foul odor

? Role of Staph epi and Corynebacterium spp.



Guided by soft tissue or bone cultures Some treat all organisms cultured, others do

not Less serious: anti-Staphylococcal cover is

often sufficient More serious: Staphylococcal, gram negative

and anaerobe cover



Traditional: 4 - 6 weeks IV antibiotics

Basis: animal models and anecdotes No reliable data on:

Duration of antibiotic therapy When to switch to oral agents

Approach (CID 1997;25:1310)

Consider bone biopsy for culture and histopathology

Remove entire section of infected bone plus 2 weeks ofantibiotics

OR 4-6 weeks of culture-guided antibiotic therapywithout bony resection



Approach (NEJM 1994;13:854) Traditional 4 - 6 week IV therapy OR Remove entire section of infected bone plus 2 - 3

weeks of antibiotics - at least one week IV (longer fortarsal or calcaneal bone which must be removedpiecemeal)

Also mentioned (CID and NEJM) 10 - 12 weeks antibiotics without surgical debridement Chronic suppression without cure can be a valid

approach



Probe to bone? - Osteomyelitis Suggestive xray? - Osteomyelitis

Unclear? (Too early for xray changes?) Treat as for soft tissue infection (culture-directed)

for 2 weeks

Repeat xray in 2 weeks to look for osteomyelitis

Soft tissue infections: beware gas gangreneand necrotizing soft tissue infections



Mild to moderate infections (not defined) Metronidazole 400mg po 8/24 PLUS

Flucloxacillin 500mg po 6/24 Severe infections

metronidazole 400mg po 8/24 PLUS cloxacillin 1-2g IV 6/24 PLUS

Gentamicin 80mg IV 8/24 (adjust as needed) Alternative

metronidazole 400mg po 8/24 PLUS cephalothin 1-2 gm IV 4/24



Change to oral therapy when infection isunder control

Duration of treatment depends on response Adjust therapy based on culture results

Surgical debridement is often necessary Surgical advice should be sought (often not

necessary in mild cases) Proper dressings and wound care very

important



Clindamycin (old antibiotic) po/IV

Staphylococcus aureus, other gram positives,

anaerobes, excellent in necrotizing Streptococcalor anaerobic infections

Fluoroquinolones (Ciprofloxacin)

Staphylococcus aureus & gram negatives

Not anaerobes

Newer quinolones cover other gram positives (but

not Ciprofloxacin)



B-lactam / B-lactamase combinations po/IV: gramnegative, S. aureus, anaerobes

Amoxicillin - clavulanate - po Ampicillin - sulbactam - IV Ticarcillin - clavulanate - IV Piperacillin - tazobactam - IV

Cefoxitin or cefotetan (2nd generation cephalosporins) -

IV S. aureus, anaerobes, gram “-” with holes

Carbapenems (imipenem / meropenem) - IV

gram negative, S. aureus, anaerobes



Debridement of infected tissue (“diabetics donot tolerate undrained suppuration”)

Remove infected bone if possible (ie. digitalor ray amputation) When to amputate? Revascularization procedures if needed

(overseas)



2-year mortality rate:

35-50%

1-3 year cumulative amputation rate:

40%



High morbidity and mortality Often hard to distinguish soft tissue infection

from osteomyelitis Little data on optimal duration of treatment Little data on IV vs. oral antibiotics

Many valid approaches Therefore best treatment is still uncertain



Caputo GM, Cavanagh PR, Ulbrecht JS,Gibbons GW, Karchmer AW. Assessment andmanagement of foot disease in patients withdiabetes. N Engl J Med 1994;331:854-60.

Lipsky BA. Osteomyelitis of the foot indiabetic patients. Clin Infect Dis1997;25:1318-26.

MandellGL, Douglas RG, Bennett JE eds.Principles of Infectious Diseases 3rd Edition.Churchill Livingstone: New York; 1990.

infectionsdm 1999

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