CHRONIC WOUNDS

Based on a presentation by

Dr. David Thomas at the AMDA Convention

Four Kinds of Chronic Wounds

Pressure Ulcer (PU) Diabetic Ulcer (DU) Venous Ulcer (VU) Arterial Ulcer (AU)

Chronic Ulcer Types

Etiology is different Treatment is different Outcome is different Gestalt is different

Differential Diagnosis

LOCATION CAUSE APPEARS

PUDU

Bony PromCallus

PressureNeuropathy/trauma

CraterBorders distinct

VUAU

Calf/ankleDistal points

Venous StasisInadequate arterial flow

IrregularGangrene

Diagnostic Approach

Wound over bony prominence (PU,DU)

DM with neuropathy, recurrent trauma, surrounding callus (DU)

PVD, wet or dry gangrene (AU) Signs of venous stasis/calf or

ankle (VU) Other causes possible, but rare

Pain in Chronic Ulcers

DU: no or diminished pain, sensation VU: little pain, intact sensation PU: intermittent pain AU: constant pain

Pressure Ulcers

Visible evidence of pathological interruption of blood flow to dermal tissues

Chief cause: sustained pressure

Most commonly over sacrum, hip

Pressure Ulcers:

What Works

Must relieve pressure or it won’t heal.

Must use moist dressing or it won’t heal.

Types of Moist Dressings

Wet to wet: cheapest Hydrocolloid: for dirty areas Hydrogel/ Foam/ Alginates/

Biomembranes/ Collagen Thin Film Polymers: tear off

top layer of cells

Problems

Most doctors treat few pressure ulcers.

Very few good studies; none for most treatments.

Treatment modalities for pressure ulcers are considered devices: only safety, NOT efficacy, must be proved.

Treatments Proven NOT to Work

Zinc paste Antacid Gold leaf Aluminum foil Topical insulin

Ultrasound Lasers Arginine Dry dressings Paraffin

Treatments with No Data

Magnet therapy

Honey/ Sugar

“Skin equivalents”

Treatments With Very Flawed Data

Vitamin C Patient’s serum mixed

with proprietary gel Vacuum therapy Electrical stimulation Topical Phenytoin Cytokine growth factors

Other Effective Treatments

Sheng-ji-san (SJS) Whirlpool Any kind of pressure relieving

bed Debridement of necrotic

tissue: surgical (required if infected), autolytic, enzymatic

Pearls from Dr. Thomas

Hydrocolloid dressings are impervious to urine and feces but cannot change dressing.

Heel ulcers have a very thin layer of tissue underneath: debridement exposes bone. Debride only if tissue is infected; otherwise form crust with betadyne and use boots.

Pressure Ulcer Guidelines

Address nutrition

Promote granulation tissue

Promote epithelialization

Prevent contamination

Dressings

Stage I: Thin film polymer Stage II: Moist gauze (wet-to-wet) or

hydrocolloid Stage III/ IV with dead space/

exudate: hydrogel, wet-to-wet, or hydrocolloid with synthetic absorption dressing below.

Stage III/ IV with necrosis: debride, then treat as III/ IV above.

Nursing Home Pearl

Home health nursing and nursing home care plans of ulcers tend to call for improved nutrition and healing; if pressure ulcers have occurred because the patient is dying/ not eating, make sure the care plan reflects that (for liability and survey purposes).

Venous Stasis Ulcers

An area of discontinuity of the epidermis, persisting for 4 weeks or more, occurring as a result of venous hypertension and calf muscle pump insufficiency.

Must exclude arterial disease, neuropathy, diabetes, rheumatoid arthritis, hemoglobinopathies, and carcinoma.

Biopsy if long-standing or looks weird.

Diagnosis of Venous Ulcers

Location on the calf Bronzing (lipodermatosclerosis) Exclusion of arterial insufficiency by

bounding DP pulses, or ABI > 0.8 Tend to be slow-healing (~90% heal

by one year), irregular, and associated with edema and sloughing

Treatment of VU:What Works

Must compress the calf, or it won’t heal

However, arterial insufficiency is an absolute contraindication to compression therapy

Must carefully assess for arterial flow

Compression Options for VU

ACE wrap: useful for removing edema Unna boot: works via muscle

contraction against the hard shell; will not work in a nonambulatory patient

Venous support hose: comes 25 to 35 mmHg, but 35 needed to work

All compression must be wrapped tight enough to be effective

Infection in VU

All VU’s are colonized

No evidence that colonization impairs healing, though may interfere with a graft

Don’t culture VU’s!

Recognition of Infectionin VU’s

Fever Increased pain Increased skin erythema Lymphangitis Ulcer rapidly becomes larger If infected, treat with

systemic AB’s

VU Treatments

Hydrocolloid dressing Cadexomer iodine

topically Trental (anticytokine)

and compression Artificial skin Skin graft TGF-B2

Ineffective VU Treatments

(RCT’s) Antibiotics, including

Bactroban Elase Zinc Stanozolol Ifetroban Silver sulfadiazine

Secondary Prevention

in VU’s

Recurrence in ~57% Reflux in deep veins in 50 to 71% Prior DVT causes 95% of DV reflux Venous support hose may reduce

recurrence rate (unpublished data)

Treatment Guidelines--VU

Use moist wound dressings Use a compression bandage system Don’t use AB’s/antiseptics unless

infected Use grafting/artificial skin only if all

other treatments have failed—very expensive, and high recurrence rate

Diabetic Ulcers

Chronic ulcer in a diabetic patient, not primarily due to other causes

Extrinsic causes: smoking, friction, burn

Intrinsic causes: neuropathy, macrovascular and microvascular disease, immune dysfunction, deformity, reopened previous ulcer

Neuropathy in DU

Use monofilament for 5 seconds or less, to avoid triggering propioceptors

Also assess temperature sensation—may use reflex hammer

Can test pinprick and 2-point discrimination

Co-Morbidity in DU

Peripheral vascular disease occurs in 11% of diabetic patients

Peripheral neuropathy occurs in 42% of diabetic patients

PVD is associated with delayed ulcer healing and increased rates of amputation

Treatment of DU:

What Works

Must surgically debride ulcer to allow healing: the wound edges are dead

Weekly debridement down to healthy bleeding tissue gives best results

Must keep pressure off the ulcers to allow healing

Pressure Reduction Off DU

Orthopedic shoes: drop recurrence rate from 83% to 17%

Sandals Splints Crutches/wheelchairs Total contact casting

Total Contact Casting

Worsens the ulcer if not applied perfectly

Need to find a consultant for this task on whom you can rely

Other PossiblyHelpful Treatments

Moist dressings (clearly better than dry) Hyperbaric O2 Dermagraft (cultured skin—human) Platelet-derived growth factor Antibiotics (ineffective if

uncomplicated) Questionable effectiveness: U/S,

electrical stimulation

Pathogens in DU Infections

Mild severity: tend to be Staph and Strep Moderate severity (i.e. non-limb

threatening): Staph, Strep, and gram neg Severe/limb-threatening: usually 5 to 6

organisms, including Staph, Strep, E. coli, Enterobacter, Bacteroides, Proteus, Pseudomonas, and MRSA

Dx of Osteomyelitis in DU Pearl: A steel probe contacting

bone, especially if consistency of bone is crumbly, has PPV 89% and NPV 56%

MRI best imaging modality; serial films also of some benefit

Bone scan non-specific Bone biopsy gold standard Effective treatment: amputation

Arterial Ulcers--AU

Tend to occur on distal areas Diminished/absent pulses Punched-out appearance, or

gangrene Requires either salvage

revascularization, or amputation—usually the latter

Diagnosis: ABI

ABI= LE systolic BP/Brachial art syst BP ABI < 0.7 abnormal; < 0.4 unlikely to heal Can perform in FMC Values: 0.9-1.30 normal; 0.7-0.89 mild;

0.4-0.69 moderate; < 0.4 severe

Medical Treatment of AU

Control DM and HTN Moderate exercise Smoking cessation Dry dressings (dry gangrene

preferable) ? Pletal, gingko biloba

What Works: AU

Amputation/revascularization/hospice if ABI < 0.4

Do not compress if ABI < 0.7