MEDICAL COMORBIDITIES AND THEIR IMPACT ON WOUND

HEALING

Lee C. Ruotsi, MD, CWS, UHM

“CARE FOR THE WOUND IS ONLY PART OF THE STORY. SUCCESS

DEPENDS ON HOW YOU MANAGE THE REST OF THE PATIENT’S

PROBLEMS”

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NORMAL WOUND HEALING

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HEMOSTASIS

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PROLIFERATIVE

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INFLAMMATORY

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REMODELING

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ABNORMAL WOUND HEALING

Failure to progress through normal orderly stages of wound healing.

Chronicity typically defined by failure to progress normally over a 30 day period.

Most common “hangup” appears to be in the inflammatory phase.

Visually; inadequate granulation, persistent or excessive exudate, deficient wound contraction and/or absence of neo-epithelialization.

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“A chronic wound is an acute wound with an impediment”

T.K Hunt, M.D.

“The impediment may be the treating physician”

Harriett Hopf, M.D.

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SYSTEMIC FACTORS Diabetes

Rheumatoid Disease Scleroderma

Lupus SMOKING

Vasculitis Renal Failure

Chemotherapy Radiation

Unusual

A GOOD H & P

Past Medical History Past Surgical History Past Wounding History; location, timing,

treatment Medications Family History Review of Systems Thorough Exam

GENERAL APPEARANCE

Cushingoid (puffy) appearance Rheumatoid joints Cachexia Scleroderma face Abnormal affect and behavior Focal neurologic deficit Tobacco

DIABETES MELLITUS 20.8 mil (7% of pop.) 6.2 mil undiagnosed! 800,000 new cases per year (120,000 DFU’s) Lifetime risk of ulceration 15% Complex multifactorial effect of DM on micro and

macro-vascular complications Reduced flexibility and resistance of tissues to

tensile compression and shear forces Strong evidence through DCCS and UKPDS that

tight control delays onset of both primary and secondary complications

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NEUROPATHY

MOTOR

Anterior tibial weakness Pedal muscle atrophy

Fat pad atrophy Digital instability and

deformities Increased peak pressures

due to deformities Ulcerations over

deformities

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NEUROPATHY

SENSORY

Diabetic sensory polyneuropathy

Peri-nerve edema Increased wounding risk

due to loss of protective sensation (L.O.P.S.)

Unable to feel pressure or pain over prominences or

with trauma

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NEUROPATHY

AUTONOMIC

Faulty sweat gland activity

Dry, fissured skin leads to infection and ulceration

Uncontrolled vasodilatation due to

decreased arteriolar tone

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RHEUMATOID DISEASE Systemic autoimmune disorder of unknown etiol. Leg ulcerations in 8 – 9% of patients Ulcer is smooth, irregularly shaped and painful Felty’s Syndrome; Combination of RA,

splenomegaly, granulocytopenia and leg ulcers Systemic Treatment: High dose steroids,

cyclophosphamide, Dapsone, disease modifying agents

Wound treatment: Standard wound care, bioengineered skin

RHEUMATOID LEG ULCERS

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SYSTEMIC LUPUS (SLE) Systemic autoimmune disease of unknown etiology Incidence of leg ulcers 2 – 8% Ulcers typically over pre-tibial areas and extremely

painful Characterized by well defined wound margins, purulent

bed and varying amount of granulation Surrounding skin may be normal or erythematous with

evidence of atrophie blanche Treatment is challenging; topical retinoic acid,

intralesional steroids

LUPUS RELATED LEG ULCERS

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SCLERODERMA

Autoimmune disorder of unknown etiology

Ulcers usually over digits and bony prom.

Epithelialization usually difficult

C.R.E.S.T. Syndrome Occlusive dressings

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RAYNAUDS

Intermittent, severe ischemia of fingers/toes

May be precipitated by cold or localized trauma

Sympathetic mediation Soft tissue atrophy and

non-healing ulcerations Vasodilators, platelet

agents, Pentoxyfilene, PD-5’s, nitrates

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VASCULITIS

Inflammation of blood vessel of ? Etiology

Male = Female Prevalent in elderly Flat, red nodules

macules or purpura Lesions frequently

ulcerate and are difficult to heal

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FACTOR V LEYDEN

Protein C resistance Increased risk of

thrombosis, venous > arterial

Progressive thrombotic occlusion leads to poor blood supply and wounding

Difficult to heal

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RENAL FAILURE

Foot ulceration 5x higher in stage 4 & 5 CKD

2x higher prevalence of amputation, PAD, neuropathy

Dialysis is independent risk factor for ulceration

Multifactorial proposed etiologies

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PROTEIN ENERGY MALNUTRITION Rapid and insidious onset Populations at risk – elderly and poor Albumin, fibrinogen and globulin all important Indices: albumin, transferrin, TLC, pre-albumin Hyperglycemia delays wound healing Variety of supplements available B & C vits: immunity, inflammation and collagen D,E,A,K vits: clotting, healing and anti-oxidants Fe, Zn, Cu: small amounts but critical

ABC’S OF NUTRITION ASSESSMENT

A) Anthropometrics: Ht, wt, skinfolds

B) Biochemical: alb, pre-alb, transferrin, TLC,

minerals, BUN/Cr, hgb, hct

C) Clinical signs: skin – pale, dry, scaly, swollen

hair – thin, dull, changed texture

eyes – sunken, scleral yellowing

mouth – cheilosis, tongue color,

missing teeth, gums

D) Dietary: calorie counts, % consumption

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MEDICATIONS

Systemic Steroids Topical Steroids NSAIDS Amlodipine/Nifedipine Methotrexate Warfarin Heparin

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CHEMOTHERAPY

49 pts with stage II – III breast cancer received 3 drug chemo with vinorelbine, cisplatin and 5-FU for up to 6 cycles and up to 30 minutes pre-op. No wound infections or delays in healing noted

Colleoni, et al, 2003

100 pts treated with multi-agent platinum based chemo following surgery for ovarian ca had no increase (11%) in wound complications compared to those receiving no chemo

Kolb, et al, 199231

CHEMOTHERAPY Bevacizumab (Avastin) - Monoclonal antibody

against VEGF inhibits angiogenesis in tumor and healthy tissue alike

Cetuximab (Erbitux) - Monoclonal antibody against EGFR. Led to slightly prolonged hospital stays and drain removals

Harari, et al, 2003

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RADIATION THERAPY

Impairs vascularity and depletes cell lines

Impacts all phases of wound healing

Progressive over time Good response to

HBOT Radiation Proctitis

Clark, Cone et al, 2008

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Hypoxic

HypocellularHypovascular

RADIATION RELATED WOUNDS

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PYODERMA GANGRENOSUM

Non-infectious neutrophilic dermatosis

Painful ulcers of varying depth and size

Violaceous borders Most commonly

associated with underlying disease

Pathergy !

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FACTITIOUS DISORDER

Accompanies various psychiatric disorders

Lesions in various stages of healing

Usually sharp borders Tend to be in

accessible areas, usually sparing mid-back

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ETOH INDUCED LIMO DISEASE

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SMOKING

Impairs wound healing via local hypoxia, endothelial and vasomotor dysfunction, atherosclerosis, platelet activation and inhibition of collagen synthesis

Increased risk of post-op infection and wound rupture compared to non-smokers

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SUMMARY Careful H&P History of prior wounding Lifestyle and mobility questions Nutritional assessment Wound characteristics Prior treatment; successes and failures

Pay attention:

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