This document discusses how medical comorbidities can impact wound healing. It emphasizes that treating the wound is only part of the story - managing the patient's underlying medical problems is also critical for healing. Several common comorbidities that can impair healing are described in detail, including diabetes, rheumatoid disease, nutritional deficiencies, medications, chemotherapy/radiation, and smoking. A thorough history and physical exam is important for identifying potential impediments to healing from comorbidities.

1. MEDICAL COMORBIDITIES AND
THEIR IMPACT ON WOUND
HEALING
Lee C. Ruotsi, MD, CWS, UHM

2. “CARE FOR THE WOUND IS ONLY
PART OF THE STORY. SUCCESS
DEPENDS ON HOW YOU MANAGE
THE REST OF THE PATIENT’S
PROBLEMS”
2

3. NORMAL WOUND HEALING
3

4. HEMOSTASIS
4

5. PROLIFERATIVE
5

6. INFLAMMATORY
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7. REMODELING
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8. 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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10. “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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12. SYSTEMIC FACTORS
 Diabetes
 Rheumatoid Disease
 Scleroderma
 Lupus SMOKING
 Vasculitis
 Renal Failure
 Chemotherapy
 Radiation
 Unusual

13. A GOOD H & P
 Past Medical History
 Past Surgical History
 Past Wounding History; location, timing,
treatment
 Medications
 Family History
 Review of Systems
 Thorough Exam

14. GENERAL APPEARANCE
 Cushingoid (puffy) appearance
 Rheumatoid joints
 Cachexia
 Scleroderma face
 Abnormal affect and behavior
 Focal neurologic deficit
 Tobacco

15. 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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16. 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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17. 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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18. 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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19. 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

20. RHEUMATOID LEG ULCERS
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21. 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

22. LUPUS RELATED LEG ULCERS
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23. 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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24. 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,
24 PD-5’s, nitrates

25. 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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26. 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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27. 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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28. 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
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29. 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
29D) Dietary: calorie counts, % consumption

30. MEDICATIONS
 Systemic Steroids
 Topical Steroids
 NSAIDS
 Amlodipine/Nifedipine
 Methotrexate
 Warfarin
 Heparin
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31. 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, 1992
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32. 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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33. RADIATION THERAPY
 Impairs vascularity
and depletes cell lines Hypoxic
 Impacts all phases of
wound healing
 Progressive over time
 Good response to
HBOT Hypovascular Hypocellular
 Radiation Proctitis
Clark, Cone et al, 2008
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34. RADIATION RELATED WOUNDS
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35. 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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36. 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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37. ETOH INDUCED LIMO DISEASE
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38. 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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40. 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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