Chronic Wounds and Delayed Healing Risk
- Tue, 6/8/10 - 3:08pm
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Dear Readers:
Forewarned is forearmed. Knowing a chronic wound is at risk of being delayed or nonhealing helps wound care providers improve healing outcomes.1 Knowing and helping patients address risk factors for delayed or nonhealing wounds can also help define the limits of patient risk, patient, caregiver, and provider responsibility, and legal liability.
Below are some surprising and some familiar risk factors for delayed and nonhealing wounds. If you recognize any of these risk factors in a patient, consider what you might do to optimize the patient and wound outcomes: Check causes of tissue damage? Change to a more effective treatment? Refer to a specialist?
Recognizing Venous Ulcers at Healing Risk
Reference: Milic DJ, Zivic SS, Bogdanovic DC, Karanovic ND, Golubovic ZV. Risk factors related to the failure of venous leg ulcers to heal with compression treatment. J Vasc Surg. 2009;49(5):1242–1247.
Rationale: Venous ulcer (VU) healing rates range from 40%–95% with compression. Factors predicting compromised VU healing include longer ulcer duration; larger surface area; more than 50% of the ulcer surface covered with fibrin, and an Ankle/Brachial Systolic Blood Pressure Index (ABI) of < 0.85, signifying ischemia as a potential cause of tissue damage. What other risk factors predict nonhealing for a well-compressed VU?
Objective: An open, prospective, single-center study determined risk factors associated with healing delay and nonhealing of VUs treated with a multilayer high compression bandaging system for 52 weeks.
Methods: For 189 subjects with a VU at least 5 cm2 in area and 3 months in duration, factors were explored as predictors of either delayed or nonhealing during 52 weeks of treatment with multilayer high compression bandaging. Venous ulcer factors that were studied included surface area, coverage with > 50% fibrin slough, depth > 2 cm, history of surgical wound debridement, and time since ulcer onset. Patient factors that were tested included gender, age, history of deep vein thrombosis or surgery, body mass index (BMI), calf circumference reduction during the first 50 days of treatment, daily walking distance, calf/ankle circumference ratio < 1.3, and fixed ankle joint status.
Results: During 52 weeks of appropriate compression, 87.3% of the chronic VUs healed. Healing was predicted by ulcer duration < 12 months, area < 20 cm2, and during the first 50 days of treatment, new epithelium on > 10% of ulcer surface and/or a decrease in calf circumference > 3 cm. Predictors of delayed VU healing were initial ulcer depth > 2 cm, patient BMI > 33 kg/m2, walking < 200 m/day, and history of surgical wound debridement. The only independent predictors (P < 0.001) of nonhealing were calf/ankle circumference ratio < 1.3, fixed ankle joint, or reduced ankle range of motion.
Authors’ Conclusions: Failure of VUs to heal during 1 year of treatment with multilayer high compression is associated with failure to resolve lower limb edema related to impaired calf muscle pump function.








Chronic wounds are failures of renewed adequate cellular respiration that all living cells depend upon. Therefore, oxygen deficient wound tissue must be treated with combinations of supplemental O2 supplies (open wounds lack impermeable stratum corneum and accept topical exposure), stimulation of enzyme-catalyzed O2 use biochemically ('respiratory burst'/collagen synthesis), improved O2 diffusion (with heating, pressure, etc.), O3 infection control (thereby adding more O2) and all other standard wound hygiene and tissue optimization methods. The cited evidence of inherent cell self stimulation of neovascularization markers due to O2 is of great relevance and significance and is most physiologically demonstrative. Excellent investigation!
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