Summary
Infected venous leg ulcer (VLU) is an open skin lesion of the leg or foot that occurs in an area affected by venous hypertension, often caused by chronic venous insufficiency, that develops an infection causing increased pain, swelling, and color change. It is a chronic condition, with recurrence rate within 3 months after wound closure as high as 70%. Thirty-five percent of people with VLU experience four or more episodes. Venous Leg Ulcers are relatively common, affecting 1% of the population in the U.S.
Chronic VLUs are susceptible to microbial invasion and can lead to serious complications, such as delayed healing, cellulitis, enlargement of wound size, debilitating pain, and deeper wound infections causing systemic illness. Recognition and treatment of the infected VLU is an essential skill set for any physician caring for geriatric patients.
Epidemiology
Incidence: overall incidence rate of venous leg ulcer is 0.76 (95% CI, 0.71, 0.83) for men and 1.42 (1.35, 1.48) per 100 person-years for women. A small percentage of cases involve infection
Prevalence: 2.9 cases per 10,000 people
Risk Factors
- > 50 years, male gender
- History of vascular surgery, trauma, repeat intimal venous damage or varicosities
- Family history of VLU
- BMI > 33 kg/m2 with documented nutritional deficiency
- Multiple pregnancy
Pathophysiology
Chronic venous insufficiency results in venous hypertension (ambulatory venous pressures of up to 60 to 90 mmHg, as opposed to the normal levels of 20 to 30 mmHg), which can happen due to obstruction to venous flow or venous reflux from dysfunction of venous valves, and/or failure of the "venous pump". Changes in shear stress to the vein walls are likely initiating events, leading to activation of adhesion molecules on endothelial cells, and leukocyte activation with attachment and migration into vein wall, microcirculation, and in the interstitial space. The pathology of VLU involves an imbalance of inflammation, inflammatory modulators, oxidative stress, and proteinase activity.
By default, chronic wounds are contaminated by several types of bacteria. Bacterial biofilms are estimated to be present in ~78.2% of chronic wounds. When the host (patient) does not adequately respond to bacterial contamination, this contamination can turn into colonization, which can further turn into infection.
Diagnosis
The diagnosis of VLU is predominantly clinical, however peripheral arterial disease (PAD) needs to be ruled out and venous disease should be documented with duplex ultrasound. PAD can be present in up to 25% of VLU patients and may be ruled out with evaluation of ankle brachial index ratio (ABI) or audible handheld Doppler ultrasound with continuous waveform analysis.
Infection: The NERDS mnemonic (Nonhealing ulcer, increased Exudate, Red-friable tissue, Debris, Smell;) can help identify soft tissue infection. If any 3 NERDS are present, superficial soft tissue infection is likely and topical antimicrobial treatment is justified.
The STONEES mnemonic (Size, Temperature, Os (orifice), New breakdown, Exudate, Erythema + edema (cellulitis), Smell) can help identify systemic infection. ystemic antibiotics and topical antimicrobial treatment are justified if 3 or more of the STONEES signs are present.
Differential Diagnosis
Arterial ulcers, neuropathic ulcers, pressure ulcers/injuries, metabolic (diabetes mellitus, gout, Gaucher disease, etc), hematologic (Sickle cell anemia, thalassemia, polycythemia vera, leucemia), autoimmune (Rheumatoid arthritis, leukocytoclastic vasculitis, polyarteritis nodosa), exogenous, neoplasia, infection, medication, skin disorders
Management
Treatment of venous hypertension includes compression therapy, leg elevation and supervised exercises involving the calf-muscle pump. Compression therapy associated with standard wound care has the potential to heal approximately 50% - 75% of VLUs. As for initial choice of compression therapy to promote VLU healing, we suggest multilayered (multicomponent) compression bandages over single layered compression bandages. Oral pentoxifylline or micronized purified flavonoid fraction may be administered with compression therapy to promote healing of long-standing or large VLUs.
For current infection: manage as appropriate, may apply compression after 24 hours of systemic antibiotics and if afebrile. Consider reducing level of compression if difficult to tolerate. Inspect dressing more frequently to monitor infection
For recurrent infection: examine wound regularly and mitigate factors that may contribute to recurrence.
Use antimicrobial dressings only in cases of clinical infection (e.g. if increasing pain is observed) or if no healing is seen in 4 weeks despite appropriate care.
Antimicrobial dressings (with cadexomer iodine, silver, etc):
- For light exudate: hydrogel or hydrogel colloidal sheet-based
- For moderate, heavy exudate: alginate, hydrofiber, super absorbent
In confirmed clinical infection, prescribe systemic antibiotics guided by culture.