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CPTA Annual Conference 9/20/2013

Rose Hamm, PT 1

ACUTE CARE WOUND CARE:UNDERSTANDING WOUND HEALING IN THE ACUTE CARE SETTING

Rose Hamm, PT, DPT, CWS, FACCWS

Assistant Professor of Clinical Physical Therapy

Division of Biokinesiology and Physical Therapy

University of Southern California, Los Angeles

Objectives

• At the end of this presentation the participant will be able to:• Perform a chart review, subjective, and objective assessment of a

patient with a wound.

• Recognize the factors that are impeding wound healing using the common lab values available in the acute setting.

• Diagnose a wound by etiology.

• Stage a pressure ulcer using the NPUAP classification.

• Develop a plan of care for a patient with a wound in the acute care setting.

• Select the appropriate adjunct therapy to facilitate wound healing for a patient in the acute care setting.


Rose Hamm, PT 2

Review of healing response to injuryDermalTendon/ligmt. Muscle Bone

(Bone phases)

Hemostasis

PlateletsEndothelial cells

Platelets and leukocytes; hematoma formation

Inflammation

LeukocytesMonocytesMacrophages

Phagocytes destroy the hematoma

Platelets release fibronectin, PDGF, TGF

(Hematoma formation)

a p agLymphocytes

Proliferation

FibroblastsMacrophagesEndothelial cellsKeratinocytesEpithelial cells

Matrix formation –fibroblasts, myoblasts, endothelial cells

Soft callus formation, angiogenesisHard callus formation/osteoblasts

(Reparative)

(Modeling)

Remodeling

FibroblastsEpithelial cellsMacrophagesLeukocytes

Maturation and contraction of the scar tissue;

Osteoclasts and osteoblasts

(Remodel-ing)

TIME OF NORMAL HEALING PHASES

Phase 1 Phase 2 Phase 3 Phase 4Hemostasis Inflammation Proliferation Remodelinga a a a d g

0---------------------------------REPAIR-----------------------------2 Years

Injury30mins 3-7days------ 21 days---------- 2 Years

Cellular activity levels in wound healing

Out of control cellular activity• No inhibition of cellular response in place• Increased cellular necrosis, increased cellular by-products,

unable to progress healing phases, increased opportunity for infection

U l t d ll l ti itUp-regulated cellular activity• Normal cellular response to injury or bacteria with cells

attracted to area by chemotaxis• Normal sequence of events for wound healing to occur

Baseline• Normal surveillance occurring for injury or bacteria• Normal cell reproduction in response to apoptosis

Cellular activity levels in wound healing

Baseline• Normal surveillance occurring for injury or

bacteria• Normal cell reproduction in response to

apoptosisapoptosis

Senescent• Non-responsive cells, unable to initiate healing response• Altered cell receptor display• Secretion of cell products/gene expression• Metabolic drain- senescent cells consume energy with no

contribution to local cell/tissue health• Resistant to apoptosis• Normal tissue differentiation disrupted Tammy Luttrell, PT,

PhD


Rose Hamm, PT 3

Patient evaluation•Answers two questions:

• Why does this patient have the wound?

• Why is the wound not healing?Why is the wound not healing?

WHY???WHY???

Diagnostic process

• Chart review

• Subjective history

• Objective medical history

• Wound history

• Wound observation

• Wound assessment

• Tests and measures

Diagnostic process

Chart review

Wound assessment

Tests and measures-vascular

Subjective history

Medical history

Wound history

Wound observation Laboratory

tests

Diagnosis

Common diagnoses seen in acute care

• Arterial

• Venous

• Pressure

• Neuropathic

• Burn

• Surgical incision/dehsicence

Wound evaluation by etiologyLocation Tissue Pain Skin Exudate

Arterial Distal digits

Toes or fingers

Dry, necrotic or slough, little or no granulation

Yes!!! May have dependent leg syndrome

Dry, hairless, shiny, thin

None unless infected

Venous Lower 1/3 of the leg (called the gaitor area)

Red or pink, bark texture, yellow slough

Poor granulation

Generally not unless vasculitic

Hemosiderous(dark, brawny appearance)

Atrophie blanche

Varies, may have copious serous drainage

Pressure Over bony prominences

Varies from dark red to eschar

Varies depending on the structures involved

Macerated, wet, erythematous

Varies

Neuro-pathic

Weight bearing surface of the foot or dorsal digits

Callus or blister, slough, may probe to bone, necrotic with PAD

None!!! Until infected, then deep throb

Dry, thick, scaly, hyperkeratotic

Varies, depending on infection

Common causes of non-healing wounds in acute care setting• Infection• Protein energy malnutrition• Diabetes with poorly control blood sugars• Edema• Arterial insufficiency

Medications• Medications• Age• Co-morbidities• History of radiation/chemotherapy• Stress • Obesity• Stress• Social behaviors (smoking, alcohol)• Improper positioning


Rose Hamm, PT 4

Levels of contamination• Normal flora• Contaminated – presence of microbes on the wound bed• Colonized – the microbes are reproducing• Critically colonized – the number of microbes is sufficient

to impede the healing processto impede the healing process• Infected – the number of microbes is more than the host

can deal with; with or without clinical signs of infection (105

organisms/gram of tissue)• Septic – the infection is throughout the body and life-

threatening

Biofilm

• A biofilm is an aggregate of microorganisms in which cells adhere to each other on a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS). Biofilm EPS, which is also referred to as slime(although not everything described as slime is a biofilm), is a ( g y g ),polymeric conglomeration generally composed of extracellular DNA, proteins, and polysaccharides. Biofilms may form on living or non-living surfaces and can be prevalent in natural, industrial and hospital settings. The microbial cells growing in a biofilm are physiologically distinct from planktonic cells of the same organism, which, by contrast, are single-cells that may float or swim in a liquid medium.

Diabetes

• <100mg/dL = normal fasting blood glucose• 100-125mg/dL = prediabetic• >126mg/dL = diagnosis of diabetesg g• <200mg/dL = min. level for protein synthesis

• <150mg/dL = recommended for wound healing

• HbA1c = now the gold standard for diagnosing and

Criteria For Diagnosis of Diabetes & Pre-Diabetes in Adults

Stage Fasting Plasma Glucose Test*

Casual Glucose Test†

Oral Glucose Tolerance Test

Normal <100 mg/dL 2-hr PPG <140 mg/dl

Increased risk -AKA Pre-diabetes

100-125 mg/dL A1C 5 7 6 4%

2-h PPG 140-199 mg/dlAKA Pre diabetes

(impaired glucose tolerace)

5.7-6.4% 199 mg/dl

Diabetes >126 mg/dl >200 mg/dl (plus symptoms)

2-h PPG >200 mg/dl

Diabetes A1C >6.5%

22Diabetes Care January 2011 vol. 34 no. Supplement 1 S11-S61 available at: http://care.diabetesjournals.org/content/34/Supplement_1/S11.full

* Fasting means no calorie intake for 8 hours† Casual means testing any time of day without regard to time since last meal; symptoms are the classic ones of polyuria, polydipsia, and unexplained weight loss.

Poor nutrition

• Protein energy malnutrition• Fewer protein substrates available for new tissue formation• Less energy available for anabolic activity• Decrease in lean body mass

• >10% - wound healing is impaired• >20% - wound healing ceases

• Usually measured by • Albumin (3.5-5.5 g/dL = normal)• Pre-albumin (20-40mg/dL = normal)

Medications

• Steroids• Prednisone• Methotrexate

• NSAIDsh• Cox-2 inhibitors

• Ibuprofen• Naprocin• Aspirin

• Immunosuppressive agents• Anti-rejection medications (Cellcept)• Anticoagulants


Rose Hamm, PT 5

Social factors

• Stress• Hypermetabolism• Increased catabolic activity• Decreased resources for healing and fighting infection

• Smoking/alcohol• Smoking/alcohol• Peripheral vasoconstriction => hypoxia• Decreased fibroblasts, macrophages, cytokines

• Obesity• Decreased vascularity in adipose, poor granulation• Higher frequency of dehisced wounds, infections• Frequently protein energy malnourished• Higher risk for pressure ulcers

Inappropriate dressings• Hydrogen peroxide

• Dakin’s solution (unless infected necrotic tissue)

• Acetic acid (pseudomonas only)

• Betadine

Why is this wound not healing?Time of eval After 2 weeks

After 6 weeks

What is the etiology?

• Arterial

• Neuropathic

• Pressure

• Venous

• Atypical


• Arterial

• Neuropathicp

• Pressure

• Venous

• Atypical


• Arterial

• Neuropathicp

• Pressure

• Venous

• Atypical


Rose Hamm, PT 6


• Arterial

Neuropathic• Neuropathic

• Pressure

• Venous

• Atypical


• Arterial

• Neuropathicp

• Pressure

• Venous

• Atypical


• Arterial

• Neuropathic

• Pressure

• Venous

• Atypical


• Arterial

• Neuropathic

• Pressure

• Venous

• Atypical


• Arterial

• Neuropathic

• Pressure

• Venous

• Atypical


• Arterial

• Neuropathic

• Pressure

• Venous

• Atypical


Rose Hamm, PT 7

Pathophysiology of pressure ulcers

Shear Pressure FrictionShear Pressure Friction

Moisture

Causative factors

Pressure

• Force that is perpendicular to the bony prominence

• Occurs most frequently over areas with little subcutaneous tissuesubcutaneous tissue

• Occurs with bony prominence pushing or resting on a hard surface

Pressure

Pressure against hard surface with

increased interstitial fluid pressure

Capillary collapse, fluid loss, tissue

edema → ischemia

Inflammatory response and

autolysis of dead cells

Decreased nutrients and oxygen to the

tissue

Necrosis and ulceration

Shear

Result is wound with undermining and tracking

i

Tissue anoxia,

inflammatory response,

tissue

Parallel forces break and distort capillaries sinusestissue

necrosiscapillaries

Note discoloration ofSkin that indicates undermining


Rose Hamm, PT 8

Friction

Two surfaces rub against each

other

Abrades the epidermis

Initiates an inflammatory

response

Creates a blister between the

epidermis and dermis

Occurs most frequently at

elbows and heels

Moisture

Decreases the strength and

thickness of the skin

Increases the skin pH,

destroys the acid mantle

Decreases resistance to

bacterai

Increases risk of dermatitis

Creates portal for bacteria to enter the skin

Types of moisture

• Urinary incontinence

• Fecal incontinence

• Wound drainage

• Perspiration

Location, location, location!!!

scapula

elbow

occiput

greater trochanter

ischial tuberosity

medial knee

heel

sacrum, coccyx

Achilles tendon

medial/lateral malleoli

How long does it take???• Intensity versus duration

• Prolonged exposure to mild to moderate increase in forces• Short exposure to moderate to severe increase in forces

Time for pressure ulcer to develop is not the same for every patient!

NPUAP Staging System

• Adopted in 1989 and revised in 2007

• Used ONLY for describing tissue involvement of pressure ulcers

• Required documentation if POA or present on admission; signed by MD within 48 hours of admissiong y

• Is not always easy!!!

• Recommend “two eyes on” policy or

“master stager” consulting

policy within facility


Rose Hamm, PT 9

Stage I

• Intact skin with non-blanchable redness of localized area, usually over bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area.

• Further description: The area may be painful firm softFurther description: The area may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons (a heralding sign of risk).

Stage II

• Partial-thickness loss of dermis presenting as shallow open ulcer with a red-pink wound bed, without slough. May present as an intact or open/ruptured serum-filledblister

• Further description: Presents as a shiny or dry shallowFurther description: Presents as a shiny or dry shallow ulcer without slough or bruising. (Bruising indicates suspected deep tissue injury.) Stage II should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or denudement.

Stage III

• Full-thickness tissue loss. Subcutaneous fat may be visible; bone, tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling.

• Further description: Depth of Stage III pressure ulcer i b t i l l ti Th b id f thvaries by anatomical location. The bridge of the nose,

ear, occiput, and malleolus do not have subcutaneous tissue, and Stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III pressure ulcers. Areas with no subcutaneous fat may be shallow; areas with significant adiposity can be deep. Bone and tendons are not visible or directly palpable.


Rose Hamm, PT 10

Stage IV

• Full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Often includes undermining and tunneling.

• Further description: The depth of Stage IV pressure ulcerFurther description: The depth of Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and Stage III ulcers can be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (eg, fascia, tendon, or joint capsule) making osteomyelitis possible. Exposed bone and tendons are visible or directly palpable.

Suspected deep tissue injury

• Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, and warmer or cooler compared to adjacent tissue.p j

• Further description: Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with treatment.

Unstageable

• Full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Undermining and sinus tracts also may be associated with Stage IV pressure ulcers.

• Further description: Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (dry, adherent, intact without erythema or flutuance) eschar on the heels serves as “the body’s natural (biological) cover” and should not be removed.


Rose Hamm, PT 11

Prevention

• Risk assessment

• Skin care (hydrate, protect)

• Optimize nutrition

• Reposition

• Support surfaces

• Heel protectors (float the heels)

• MOBILIZE!!!

Interventions for the foot

Correct positioning of the foot in a positioner is necessary to prevent ulceration of the metatarsal heads and the Achilles tendon.

Supine positioning

• Weight evenly distributed throughout entire body

• Bed flat as possible

• Head of bed less than 30 degreesg

• Knees elevated slightly to prevent sliding

• Heels off-loaded with pillows

Fowler’s position

30-degree side-lying

150-degree side-lying Prone position


Rose Hamm, PT 12

Treatment of pressure ulcers• Support surfaces• Limit use of linen and bed pads• Reposition with 30-degree side-lying• Avoid donuts and rings• Avoid heat on the pressure ulcer• Avoid head elevation > 30 degrees• Avoid head elevation > 30 degrees• Stage I and II – use protective dressing• Stage III and IV

• Treat infection• Debride moist wound dressings• Electrical stimulation• Ultrasound• Negative pressure wound therapy• Pulsed lavage with suction

Treatment of ICU patients

• Reposition more frequently

• Map pressure for effective pressure redistribution

• Monitor shear when using rotational beds

• Monitor pre-albumin levels carefully

• Float heels at all times

• Use hand-relief of vulnerable areas for reperfusion

Arterial wounds - diagnosisCritical phases of PAD1. Collateral circulation insufficient for metabolic needs => shunting of

blood to muscles where there is less resistance => delayed healing of traumatic wounds

2. Claudication - pain with activity – most effectively treated with exercise

a. thigh and buttock claudication = aortoiliac or iliac involvement

b. calf claudication = femoral or popliteal involvement

3. Rest pain – requires revascularization surgery• Characterized by “dependent leg syndrome”• May be accompanied by signs of ischemia at distal digits

Treatment of claudication

• Differential diagnosis• Arterial insufficiency

• Spinal stenosis

• Progressive exercise program• Establish baseline on treadmill• Establish baseline on treadmill

• Monitor vital signs, pain levels, and rest time for pain to abate

• Perform 3 tasks for each treatment session

• Stress increase in grade rather than speed

• Takes about 3 weeks to have increased function

• Takes about 3 months to have decreased pain levels

Guidelines for establishing plan of care

• Transcutaneous oxygen tension (TcPO2)• Provides information on amount of oxygen available to the tissue

via microcirculation• Used to predict healing potential• Interpretation of readings• Interpretation of readings

• <20 mmHg- healing unlikely• <30 mmHg – delayed healing• <30 mmHg – debridement contraindicated• >40 mmHg – normal

Patients with diabetes may have higher TcPO 2 readings than patients without diabetes, leading to poorer healing results.

Guidelines for establishingplan of care

• Ankle-brachial index• 1.0– 1.2 – Normal

• 0.8-1.0 – Compression for edema control is safe to use.

• 0 5-0 8 – Compression therapy is contraindicated if <0 6; modified• 0.5-0.8 – Compression therapy is contraindicated if <0.6; modified compression is indicated if 0.6-0.8.

• <0.5 – Compression therapy is (almost) always contraindicated.

• <0.2 – Tissue death will occur.


Rose Hamm, PT 13

Prevention of wounds with PAD

• Control blood sugars

• Cease smoking

• Control hypertension, hyperlipidemia, hypercholesterolemiahypercholesterolemia

• Provide proper foot care including shoes that fit and provide pressure relief

• Exercise to build collateral circulation

Treatment before surgery

• Do not debride

• Keep area dry; protect toes with cotton or sterile gauze between toes

• Use foot cradle

• Off-load heels with pillows

• Discourage limb elevation

• Elevate head of bed 5-7 degrees

• Keep extremity warm

• Avoid excessive exercise

Protector

Positioner

Treatment after surgery

• Debride wound of necrotic tissue when granulation tissue is visible at the edges (D. Armstrong)

• Provide moist wound environment with the appropriate advanced dressing

Protect foot with pillows under calves• Protect foot with pillows under calves

• Off-load wound with orthotic, special shoes, assistive device

• Control post-op edema to prevent incisional dehiscence• Cover incision with dry sterile gauze

• Apply short stretch elastic bandage in spiral wrap

• AVOID ELASTIC WRAPS!!!

Dressings


Rose Hamm, PT 14

Shoes/orthotics for arterial wounds

��

Venous wounds – treatment

• Venous wounds• Antibiotics if indicated• Debridement• Absorbent wound dressings• Biological dressings

C i• Compression • Pentoxifylline• Exercise

• Activate the venous pump• Increase ankle range of

motion• Gait training to emphasize

heel/toe sequence

Antibiotics• Systemic

• For overt infection (usually with erythema and warmth 2 cm or more beyond wound margin

• For cellulitis, osteomyelitis

• Topical • For colonization/critical

colonization• For wounds that show no

improvement after 2 wks• For patients with impaired

• Based on culture• Wounds < 1 month

duration: usually gram+• Wounds > 1 month

duration or immunosuppressed pts: broad spectrum Sibbald 2007

p pperfusion with poor delivery of systemic antibiotics (PVD, edema)

• Recommendations:• Low tissue toxicity• Avoid sensitizers that lead

to resistant organisms• Neomycin, bacitracin

Machet 2004

Suggested topical antimicrobials• Purpose

• To restore a balance between bioburden and local immune system• Types of topical antimicrobials that are considered “best practice”

• Ionic silver dressings• Available in a variety of dressings

• Cadexomer iodine• Cadexomer iodine• Iodosorb, Iodoflex

• Polyhexamethylene biguanide compound (PHMB)• XCell antimicrobial

• Acetic acid soaks• For pseudomonads only

Debridement• Types of debridement recommended for venous wounds

• Selective/sharp if pain levels are low• Enzymatic

• Collagenase

• Ultrasound• Ultrasound• Low frequency

• Non-contact: MIST – 40 kHz• Contact – 25-26 kHz

• Soring Sonoca-180 • Arabello


Rose Hamm, PT 15

Absorbent wound dressing

• Purpose• Achieve optimal moisture balance for the wound to heal

• Types• Foams

• Cellulose fiber fillers• Cellulose fiber fillers

• Calcium alginate

• Hydrocolloids

Compression

• Purpose • Augment venous return to central circulation

• Increase interstitial tissue pressures by compressing superficial tissues

• Provide external support (static or dynamic) to the venous• Provide external support (static or dynamic) to the venous pump

• Types• Elastic – multilayered, single layer long stretch, elastic

stockings

• Inelastic – paste, short stretch, orthotic (Circaid)

Traditional Current

Compression for venous wounds

• Unna boot• Semi-rigid

• Requires active gastrocsoleus, ambulation to be

• Multi-layer compression• Is not rigid, conforms to

extremity size and shape

• Effective on an extremity with hypomobile anklea bu a o o be

effective

• Does not shrink as extremity girth decreases

ypo ob e a e

• Provide higher sub-bandage resting pressure

• Shrinks as the extremity girth decreases

Application of multi-layer compression


Rose Hamm, PT 16

Compression Vascular parameters for multilayer compression

• ABI >0.8 – full compression (30-40 mmHg pressure)

• ABI 0.6-0.8 – modified compression (23-27 mmHg pressure)• Examples: short stretch bandages or layers 1,2,4

from the multilayer systems

• ABI <0.5 – static compression contraindicated, may use short stretch bandages.

Exercise!!!• Ankle mobilization

• Joint mobilization• Gastroc stretches

• Exercises to activate the gastrocsoleus musclesA kl• Ankle pumps

• Rocker board• Heel-toe raises in sitting/standing

• Gait training• Progress to heel/toe sequence

during stance phase• Treadmill or bicycle activities

Post-healing• Compression needs to be continued to prevent recurrence. Samson

(1996) reported 79% recurrence in patients who were non-compliant with compression after healing; 4% in those who were compliant.

• Types

• Elastic stockingsElastic stockings• Circaid• Farrow bandages

Post-healing compression

Circaid Farrow bandages

Components of Gait Cycle

Stance 60%

Reference foot is in contact with floor

Swing 40%

Reference foot is not in contact with floor

Single limb support

40%1 limb on ground

Terminal double limb support

10%Both feet on ground

Loading response

10%

Mid-stance

20%Foot flat

Terminal stance20%

Heel off ground

Pre-swing

10%

Initial

13.3%

Mid

13.3%

Terminal13.3%

ROM NEEDED FOR NORMAL GAIT CYCLE

• Ankle

• 0-10 degrees dorsiflexion in stance phase, 0 degrees in swing phase

• 0-20 degrees plantarflexion in stance phase to allow for push offpush-off

• 0-5 degrees eversion at subtalar joint in stance phase

• Metatarsophalangeal joint

• 50-60 degrees of dorsiflexion at the 1st

metatarsalphalangeal joint during push off (deficiency is cause of shear stress in deep tissue)


Rose Hamm, PT 17

GAIT CHANGES IN PATIENTS WITH DIABETES

• Slow speed - Secondary to peripheral effect of DM on other body systems (Brach)

• Prolonged stance phase (associated with slower speed)

• Short stride• Increased step width - May be related to

peripheral nerve motor function or to central influences of the disease (Brach)

• I

central influences of the disease (Brach)• Decreased push off (related to hallux

ROM)• Wider base of support• Greater step time variability on uneven

surfaces (Brach)• Significantly longer activation delays in

the tibialis anterior and vastas lateralis(Sacco and Amadio)

• Increased shear forces between bone and deep tissue OR between shoe material and skin

WALKING FACTS!!!

• Patients with DM take an average of 4548 steps/day, 52% of these steps are in the home!!! Home is not a safe zone! (Armstrong)

• Reaction times are 2x as long in patients with diabetes vs.Reaction times are 2x as long in patients with diabetes vs. age-matched controls (Petrofsky)

ROAD TO NEUROPATHIC WOUNDS

Neuropathy• Sensory• Motor• Autonomic

Foot deformity• Loss of fat pad• Callus

formation

diabetic foot ulcer

NEUROPATHIC ULCERS

• Develop calluses from repeated friction that results in over‐development of the upper most layer of the edipermisp

• Occur under calluses that lead to high pressure points

• Develop due to altered musculoskeletal biomechanics and atrophy of underlying fat pads

100

And the patient does not feel it becauseof the sensory neuropathy!

NEUROPATHIC ULCER APPEARANCE

• Located on weight‐bearing surfaces of the foot or the dorsal toe joints

• Have a pale pink or red wound bed

• Have periwound callus/ hyperkeratotic tissue

• Have slight to minimal drainage

• May be round in shape, especially

101

May be round in shape, especially with arterial component

• Have variable pain pattern based on presence of infection or arterial component

• May have either bounding or diminished pulses

FORCES THAT ARE MEASURED BY FORCE PLATFORM DURING THE STANCE PHASE OF GAIT

• Vertical forces

• Anteroposterior shear

• Mediolateral shear

Shear – what is its effect on deep tissue???


Rose Hamm, PT 18

SHEAR

Is this the same as deep tissue injury???

COMMON CAUSE OF MECHANICAL TRAUMA

Poorly fitting shoes

COMMON CAUSE OF TRAUMA

Walking barefoot

Burns!!

PURPOSE OF FOOTWEAR AND ORTHOTICS

• To reinforce the elements of best practice for each wound type• Neuropathic – off-loading

• Arterial – protection from trauma

• Venous – activate the venous pump and accommodate compression b dbandages

• Pressure – redistribute pressure away from involved area

SHOES FOR ARTERIAL WOUNDS

��


Rose Hamm, PT 19

Shoe to accommodate compression bandages

TYPES OF FOOTWEAR USED TO OFF-L0ADDIABETIC FOOT ULCERS

• The gold-standard – the Total Contact Cast

ALTERNATIVES TO TCC

• Wound healing shoe

• Accommodative dressing

• Football dressing

• Post-op shoe with plastazote inserts

• Non-weight bearing with assistive device

• Wheelchair ambulation only

D’Arco Co.


Rose Hamm, PT 20

Wound bed preparation

• Removal of the barriers to healing so that the wound can progress to the next stage of healing• Static -> inflammatory

• Inflammatory -> proliferation

• Proliferation -> epithelialization

Barriers can be intrinsic,

local, or extrinsic…

Wound bed preparation

D/T debride necrotic tissue

I address inflammation/infection

M maintain moist wound environmentM maintain moist wound environment

E facilitate epithelial migration at the edges

(Sibbald/Falanga)

Debridement

Removal of devitalized tissue

Changes wound into a healthy, positive environment

D th b t i l l dDecreases the bacterial load

Facilitates healing by secondary intention

Changes a chronic wound to an acute wound

Types of debridement• Surgical – non-selective, performed in OR• Sharp – selective, uses sharp instruments or high

powered pulsed irrigation• Autolytic – uses body fluid enzymes to break down

devitalized tissueEnzymatic uses pharmaceutical proteolytic enzymes in• Enzymatic – uses pharmaceutical proteolytic enzymes in a topical dressing

• Mechanical – non-selective, uses physical force to remove necrotic tissue and debris

• Biosurgery – uses sterile maggots, selective.• Hydrosurgical – uses high-powered waterjet (Versajet)• Low-frequency contact ultrasound – uses 40,000 kH

sound waves with built-in saline lavage


Rose Hamm, PT 21

Moist wound dressings• Primary dressing

• Facilitate wound healing• Debridement• Antimicrobial• Maintain moisture balance

Secondary dressing• Secondary dressing• Anchor primary dressing• Protect the wound from mechanical forces• Manage edema

Select the primary dressing based on the wound bed. Select the secondary dressing based on patient’sactivity level.

Dressing SelectionBased on Wound Healing Phase

Inflammatory phaseAntimicrobials

Debriding agentsAbsorbent fillers

Proliferative phase

Remodeling phase

Fillers, foamsHydroactive dressingsHydrogels, biologicals

Silicone-backed foamScar therapy

DIME paradigm for dressing selectionDebridementGels, films Enzymes

Inflammation/infectionAntimicrobialsAlginatesAlginates

Moisture balanceAbsorbent fillersHydroactive dressingsHydrogels

EdgesCollagen Xeroform

(Sibbald)

Dressing selection based on moistureAmount of drainageModerate to copious Cellulose Foams Alginates

Minimal to moderate Cellulose Foams Alginates Hydrocolloids Hydroactive dressings

Scant to minimal Thin foams Hydrocolloids Hydroactive dressings Hydrogels

Maintain moisture balance of wound bed without causing periwound skin maceration.

Biophysical technologies

Pulsed lavage with suction• Post-amputation for removal of coagulum,

bacteria, and exudate

Negative pressure wound therapy• Post-amputation for wound contraction, removal ofPost amputation for wound contraction, removal of

bacteria, stimulation of angiogenesis

Non-contact, non-thermal ultrasound• Superficial wounds for maintenance debridement,

antimicrobial, pain control

Electrical stimulation• Post-amputation for facilitation of

angiogenesis, epithelial migration

NPWT precautions

• Achieve hemostasis before application

• <30% necrotic tissue

• Wound bed moist to wet, not drynot dry

• Intermittent suction preferred for faster granulation

• Protect tendons, bone, muscle with interface


Rose Hamm, PT 22

Tips for NPWT

• Protect edges with Xeroform.

• Cut foam to fit inside wound, not overlapping edges.

• Adjust pressure to manage pain, especially in abdominal wounds.

C b t d l ith dh t h t• Cover bone, tendon, muscle with non-adherent mesh to prevent dessication of the tissue.

• Use thrombin over areas that tend to bleed or produce lymphatic fluids.

• Use topical Lidocaine gel at the edges to reduce pain when removing the dressings.

Case study

Cellulose/saline dressingModified compression

Six days later 4 months later


Rose Hamm, PT 23

References • National Pressure Ulcer Advisory Panel. Pressure Ulcer Prevention and

Treatment. 2010. Available at www.npuap.org.• Holtman D, Gahtan V. Peripheral arterial perfusion: Is it adequate for

wound healing? Wounds. 2008;20(8):230-235.• Bowker JH, Pfeifer JH. Levin and O’Neal’s The Diabetic Foot.

Philadelphia, PA: Elsevier. 2008.• Brach, JS, Talkowski JB, Strotmeyer ES, Newman AB. Diabetes Mellitus y

and gait dysfunction: possible explanatory causes. Physical Therapy 2008;88(11):1365-1374.

• McCulloch JM. Venous insufficiency and ulceration. In McCullocah JM, Kloth LC (Eds.). Wound Healing, 4th edition. Philadelphia, PA: FA Davis, 2010. Pp. 248-255.

• McGuire J. Transitional off-loading: an evidence-based approach to pressure redistribution in the diabetic foot. Advances in Skin and Wound Care 2010;23:175-188.

• Panuncialman J, Falanga V. The science of wound bed preparation. Surgical Clinics of North America. 2009;89(3):611-626.

• Wrobel JS, Najafi B. Diabetic foot biomechanics and gait dysfunction. Journal of Diabetes Science and Technology 2010;4(4):833-845.

Laboratory Values that Indicate Healing Impairments Laboratory Test Normal Range Values Affecting

Wound Healing Clinical

Presentation CBC WBC 4.5 – 11 x 103/mm3 Increased

Decreased

Signs of infection, inflammation, necrosis, trauma or stress Failure to initiate immune response against bacteria

RBC M 4.5-5.5 x 106

/mm3

F 4.1-4.9 x 106/mm3

Decreased Pale or anemic granulation or failure to progress

Hemoglobin M 13.5-18 g/dL F 12-15 g/dL

Decreased Increased

Pale or anemic granulation or failure to progress Failure to progress (patient may show signs of congestive heart failure or COPD)

Hematocrit M 37-50% F 36-46%

Decreased Increased

Pale or anemic granulation or failure to progress Signs of thrombi or emboli

Platelet count 150-400 x 103/mm3 Decreased Increased

Bleeds easily, fatigue Signs of infection or inflammation

Automated Differential

Neutrophil Rel 57-67% of leukocyte count

Increased Bacterial infection Chronic inflammation

Lymphocyte Rel 25-33% of leukocyte count

Increased Decreased

Signs of bacterial infection Opportunistic infections

Monocyte Rel 3-7% of leukocyte Increased Tissue injury

count Early healing response

Eosinophil Rel 1-4% of leukocyte count

Increased Decreased (with corticosteroid use)

Allergic reaction Parasitic infection Delayed inflammatory response

Basophil Rel 0-0.75% of leukocyte count

Increased Allergic reaction

Neutrophil Abs 4,300-10,000 cells/mm3

Increased Signs of infection

Lymphocyte Abs 2500-3300 cells/mm3

2000-2500/µL

Increased Decreased

Signs of bacterial infection Opportunistic infections

Monocyte Abs Eosinophil Abs Basophil Abs 0-1,000 cells/mm3 Increased Allergic reaction Coagulation Studies PT (prothrombin time)

12.3-14.2 sec Increased (>2.5 x reference range)

Bleeds easily

PTT (partial thromboplastin time)

25-34 sec

INR Normal 0.9-1.1 Therapeutic range 2-3 Mechanical heart valves 2.5-3.5

Elevated Bleeds easily Skin bruising

Routine Chemistry Sodium 135-145 mEq/L

Potassium 3.5-5.3 mEq/L Chloride 95-105 mEq/L CO2 22-29 mEq/L

35-45 mmHg (arterial)

Glucose 70-115 mg/dL Decreased (<70) Increased (>200)

Headache, dizziness, altered mental status, malaise Arrested healing processed Signs of infection Increased risk of abscess formation

Calcium 8.8-10.5 mg/dL Phosphate 2.5-5.0 mg/dL BUN 7-18 mg/dL Increased (renal

failure) Decreased (liver failure)

Edema Poor healing Jaundiced skin Yellow fluids

Creatinine 0.1-1.2 mg/dL Increased (renal failure) Decreased

Edema Decreased lean body mass

Albumin 3.5-5.5 g/dL Decreased Increased

Lack of granulation tissue Bilateral edema Muscle wasting Signs of dehydration

Pre-albumin level 15-36 mg/dL Decreased Poor wound healing Lack of granulation formation

Globulin 2.5-3.5 g/dL Fibrinogen 200-400 mg/dL A/G Ratio 1.5:1—2.5:1 Decreased (liver

damage) Increased (iron deficiency)

Bilirubin Total 0.1-1.0 mg/dL Increased Yellow wound fluids Jaundiced skin

Alkaline Phosphate 30-85 U/L Others Hb1AC 4-6% Increased Delayed healing C-reactive protein (CRP)

0-1.0 mg/dL or <10 mg/L

Increased Inflammation Infection

Retinal binding protein

10 mg/L 0.002 g/kg body wt.

Increased Delayed healing due to protein deficits

Magnesium 1.5-2.5 mEq/L Phosphorus Iron Decreased

Increased

Lack of granulation Hemachromotosis

Ferritin Decreased Increased

Anemic granulation Lack of granulation Hemosiderosis

Transferrin 204-360 µg/dL <0.1 g/kg body wt.

Decreased Increased

Delayed wound healing due to protein deficits Iron deficiency

Zinc Decreased Delayed wound healing Lack of epithelialization

Microbology Wound culture Negative Positive Poor wound healing

Wound degradation Blood culture Negative Positive Systemic signs of

infection 1. Goodman CC, Fuller KS, Boissonnault WG. Pathology: Implications for the Physical

Therapist, 2nd Edition. Philadelphia, PA: Saunders. 2003.

2. Huether SE, McCance KL. Understanding Pathophysiology, 4th Edition. St. Louis, MO: Mosby. 2008.

Copyright: Rose L. Hamm, PT, DPT, CWS, FACCWS

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