CHRONIC WOUNDS
Based on a presentation by
Dr. David Thomas
at the AMDA Convention
Four Kinds of Chronic Wounds
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Pressure Ulcer (PU)
Diabetic Ulcer (DU)
Venous Ulcer (VU)
Arterial Ulcer (AU)
Chronic Ulcer Types
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Etiology is different
Treatment is different
Outcome is different
Gestalt is different
Differential Diagnosis
LOCATION
CAUSE
APPEARS
PU Bony Prom
DU Callus
Pressure
Crater
Neuropathy/trauma Borders
distinct
VU Calf/ankle
AU Distal points
Venous Stasis
Inadequate
arterial flow
Irregular
Gangrene
Diagnostic Approach
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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
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DU: no or diminished pain,
sensation
VU: little pain, intact sensation
PU: intermittent pain
AU: constant pain
Pressure Ulcers
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Visible evidence of pathological
interruption of blood flow to dermal tissues
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Chief cause: sustained pressure
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Most commonly over sacrum, hip
Pressure Ulcers:
What Works
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Must relieve pressure or it won’t heal.
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Must use moist dressing or it won’t heal.
Types of Moist Dressings
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Wet to wet: cheapest
Hydrocolloid: for dirty areas
Hydrogel/ Foam/ Alginates/
Biomembranes/ Collagen
Thin Film Polymers: tear off top
layer of cells
Problems
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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
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Zinc paste
Antacid
Gold leaf
Aluminum foil
Topical insulin
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Ultrasound
Lasers
Arginine
Dry dressings
Paraffin
Treatments with No Data
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Magnet therapy
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Honey/ Sugar
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“Skin equivalents”
Treatments With
Very Flawed Data
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Vitamin C
Patient’s serum mixed with
proprietary gel
Vacuum therapy
Electrical stimulation
Topical Phenytoin
Cytokine growth factors
Other Effective Treatments
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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
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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
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Address nutrition
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Promote granulation tissue
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Promote epithelialization
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Prevent contamination
Dressings
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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
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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
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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
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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
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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
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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
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All VU’s are colonized
No evidence that colonization impairs
healing, though may interfere with a graft
Don’t culture VU’s!
Recognition of Infection
in VU’s
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Fever
Increased pain
Increased skin erythema
Lymphangitis
Ulcer rapidly becomes larger
If infected, treat with systemic
AB’s
VU Treatments
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Hydrocolloid dressing
Cadexomer iodine topically
Trental (anticytokine) and
compression
Artificial skin
Skin graft
TGF-B2
Ineffective VU
Treatments (RCT’s)
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Antibiotics, including
Bactroban
Elase
Zinc
Stanozolol
Ifetroban
Silver sulfadiazine
Secondary Prevention
in VU’s
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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
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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
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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
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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
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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
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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
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Orthopedic shoes: drop recurrence
rate from 83% to 17%
Sandals
Splints
Crutches/wheelchairs
Total contact casting
Total Contact Casting
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Worsens the ulcer if not applied perfectly
Need to find a consultant for this task on
whom you can rely
Other Possibly
Helpful Treatments
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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
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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
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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
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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
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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
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Control DM and HTN
Moderate exercise
Smoking cessation
Dry dressings (dry gangrene preferable)
? Pletal, gingko biloba
What Works: AU
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Amputation/revascularization/hospice
if ABI < 0.4
Do not compress if ABI < 0.7