Bilateral Leg Ulcers in a Cachectic Man

A 51-year-old man is admitted to the hospital with painful ulcers on both lower extremities, severe anemia, and a 45-kg (100-lb) weight loss over the past year. Pain from the ulcers prevents him from walking. The ulcers developed about 5 years earlier, as a result of his wearing high boots for work; they began as small sores and grew over time.

HISTORY

The patient had varicose vein stripping surgery in his right leg in 1997. He denies alcohol and tobacco use but does report a 30-year history of crack cocaine use; he currently uses cocaine about once a week. He denies melena, hematemesis, hemoptysis, and hematuria. His last primary care visit was 3 years earlier.

PHYSICAL EXAMINATION

This cachectic man appears older than his stated age and is in mild discomfort. Vital signs are normal except for tachycardia (heart rate, 115 beats per minute). His height is 1.93 m (6 ft 5 in), and his weight is 64 kg (142 lb); his body mass index is 16.8. Head, ears, eyes, nose, and throat are normal. He has extremely poor dentition, with few remaining teeth. His neck is supple, without bruits or lymphadenopathy. Chest is clear, and heart rhythm is regular, without murmurs. His abdomen is soft, without masses. Results of a fecal occult blood test are negative.

A 17.5 x 26-cm ulcer is visible over the distal tibia of the right leg. In the left leg, a 16 x 27-cm ulcer is seen over the medial aspect of the distal tibia. Both ulcers are above the malleoli. The ulcers are foul smelling, with a filmy exudate. There is minimal peripheral edema and no evidence of cellulitis. Dry gangrene is evident in the second toe of the right foot. Femoral artery and dorsalis pedis pulses are 2+ bilaterally.

LABORATORY AND IMAGING RESULTS

An initial complete blood cell count reveals a hemoglobin level of 6.6 g/dL, hematocrit of 21.3 mL/dL, and a mean corpuscular volume of 67 fL. The metabolic panel shows a total protein level of 5.6 g/dL, an albumin level of 2.4 g/dL, and a prealbumin level of 10 mg/dL. Total cholesterol level is 90 mg/dL. Hemoglobin A_1c is 6.1%.

An MRI scan of both lower extremities shows no osteomyelitis. A venous duplex scan shows no venous thrombosis or venous valvular incompetency above the knee bilaterally; circulation below the knee cannot be evaluated because of pain. Results of a purified protein derivative tuberculin skin test; tests for HIV infection and hepatitis A, B, and C; measurement of lactate dehydrogenase levels; and testing for antinuclear antibodies and rheumatoid factor are all negative. Blood cultures grow no organisms. Wound cultures grow Proteus vulgaris that is resistant to ampicillin and cefazolin, Proteus mirabilis that is pansensitive, and Staphylococcus aureus that is resistant to ampicillin. The patient refuses colonoscopy and esophagogastroduodenoscopy.

What is the most likely cause of this patient’s ulcers?
A. Arterial insufficiency.
B. Venous insufficiency.
C. Uncontrolled diabetes.
D. Malignancy.

CORRECT ANSWER: B

Seventy percent of lower extremity ulcers are caused by venous insufficiency. ¹ Other causes include arterial insufficiency or a combination of both arterial and venous insufficiency, infection, neuropathy (particularly in the setting of diabetes), and dermatological malignancies. Because the cellular components of venous ulcerations, diabetic ulcers, and acute wounds differ, appropriate diagnosis and treatment of contributing factors are important.

Lower extremity ulcerations have characteristic presentations depending on the cause. Venous insufficiency ulcers tend to be large with irregular borders, painful, exudative, and generally on the medial aspect of the leg. Precursor skin changes that indicate venous insufficiency include edema, bluish discoloration of the skin, and varicosities. Although this man’s ulcers were characteristic of those caused by venous dysfunction, he did not have the skin changes usually noted. However, he had previous vein stripping in his right leg, which suggested that he had a history of venous insufficiency.

Pathophysiology of venous ulcers. The pathogenesis of venous ulceration is still being elucidated, and a combination of factors may be involved. Because of incompetence of the valves of the perforating veins that connect superficial drainage to deep drainage, venous blood pressure in the legs is abnormally high and tissue oncotic pressure and edema are increased. Excessive activity of proteolytic factors and fibrin pathway dysfunction also contribute to the destruction of the skin tissues.² A scleroderma-like precursor stage that precedes ulceration—called lipodermatosclerosis— has also been proposed.

Treatment of venous ulcers. Treatment includes appropriate wound care, compression, and exercise. Leg exercises and walking stimulate the calf muscles to pump blood through incompetent veins, which lessens pooling and edema. Compression treatment has a similar effect and, in patients with intact skin, is best executed with stockings that provide appropriate pressure. However, if ulceration has occurred, a circumferential castlike bandage containing zinc oxide—called an Unna boot—is used instead. The boot is reapplied regularly to maintain cleanliness and pressure.

Adherence to these strategies is not easily achieved. In a study that evaluated physical activity in patients with leg ulcers, 35% of participants walked less than 10 minutes per week.¹ This patient exhibits a similar degree of inactivity. Moreover, only 39% of participants in the same study were adherent to compression therapy.¹

The anabolic phase of wound healing requires multiple nutritional resources, including carbohydrates, amino acids, fats, vitamins, and minerals. Patients with leg ulcers also need a higher caloric intake to satisfy their requirement for adenosine triphosphate, which is used in collagen synthesis. Reducing caloric intake decreases the efficacy of collagen synthesis, configuration, deposition, and remodeling. The absence of fatty acids, particularly the essential linoleic acid, also leads to impaired wound healing.³

Although patients with chronic leg ulcers have diminished levels of multiple nutritional factors, few studies have shown which of these factors need to be maintained or replaced—and in what amounts. There is evidence that vitamins A, B, and C are helpful in wound healing. In addition, it is commonly thought that selenium is useful in wound repair and that a deficiency of this mineral may impair a patient’s immune response to infection. Copper and iron also show some benefit in wound healing.⁴

Because of his history and the uncharacteristic appearance of his ulcers, a full workup was initiated in this patient. The workup revealed severe anemia, hypoproteinemia, and hypocholesterolemia—indications of an extremely malnourished state. The patient reported sitting in his room at home most of the day. Because of the pain in his legs, he could not walk to the kitchen for food and instead went without eating for long periods. He lived alone and did not allow family to help; he thus reached a state of extreme malnutrition. This had complicated and compromised his wound healing.

Outcome of this case. The patient was treated with blood transfusions, improved oral nutrition, and daily wound care with pain control. Debridement under anesthesia showed no malignancy. He was given multivitamins and additional vitamin B and C supplements. Daily wet-to-dry dressings were applied, although these were difficult to manage because of pain with changing. He was discharged to home with arrangements for a home health care aide to come every other day for dressing changes, and frequent monitoring by primary care, dermatology, and vascular surgery. He was encouraged to improve his nutritional intake, avoid use of cocaine, and increase exercise as tolerated. In addition, once pain control is improved, this patient would be a candidate for Unna boot treatment.