A 60-year-old woman presents with a 3-month history of painful ulceration of her lower left leg. She has a history of congestive heart failure, diabetes, and has varicosities on the lower limbs.
Her physical examination is unremarkable except for the presence of a 6-cm2 ulcer over her left medial malleolus. The ulcer is shallow, with a yellowish base and scattered islands of granulation tissue. There is a scaly brown-reddish hyperpigmentation surrounding the ulcer’s borders without signs of infection. The patient’s extremities are cool, with the presence of varicosities and edema of the left extremity making palpation of the dorsalis pedis pulses difficult. Figures 91-1 and 91-2 demonstrate a typical case of venous ulceration that may be misdiagnosed as cellulitis in its earliest stage prior to ulceration. Figures 91-3 and 91-4 illustrate an atypical location of a stasis ulceration that can be located on the lateral or posterior calf.
Venous ulcers affect 500,000 to 600,000 people in the United States every year and account for 80% to 90% of all leg ulcers.1
Venous stasis ulcers are common in patients who have a history of leg swelling, varicose veins, or a history of blood clots in either the superficial or the deep veins of the legs.
Peak incidence occurs in women aged 40 to 49 years and in men aged 70 to 79 years.
ETIOLOGY AND PATHOPHYSIOLOGY
Venous ulcers are chronic nonhealing ulcers that occur in the lower extremities of patients with venous obstruction or valvular incompetence (often caused by a previous venous thrombosis).
Venous ulcers classically develop in regions of dependent swelling and edema.
Comorbidities that aggravate edema (such as heart failure, renal failure, hepatic failure, the use of medications such as calcium channel blockers, nonsteroidal anti-inflammatory drugs, and cyclo-oxygenase 2 inhibitors, and many others) may contribute to the formation of ulcers.
Patients with venous incompetency typically present with unilateral edema or bilateral edema that is worse in one leg.
Dilatation of the capillaries and leakage of plasma proteins and red blood cells are a direct result of venous hypertension and may lead to fibrin deposition and impaired oxygen transport, producing ischemia and hypoxia that results in cell death and ulcerations.2