Isabel C. Valencia

Managing the Patient with Venous Ulcers

A 75-year-old woman presents with a 2-month history of ulceration of her lower right leg. She has a history of congestive heart failure and has varicosities on the lower limbs. She does not drink or smoke. Despite the discomfort from the ulcer on her leg, she feels well overall. Her physical examination is unremarkable except for the presence of a 12-cm 2 ulcer over her right medial malleolus. The ulcer is shallow, with a yellowish base and scattered islands of granulation tissue. There is a scaly brown hyperpigmentation surrounding the ulcers borders. There are no signs of infection. A neurologic examination regarding perception of pain, touch, and pressure was performed and yielded normal results. The patients extremities are cool, and the presence of 2+ edema of the right extremity makes palpation of the dorsalis pedis pulses difficult. Venous ulcers are a major health problem because of their high prevalence and associated high cost of care. The cost of venous leg ulcers is estimated to be

Hypocomplementemic urticarial vasculitis with angioedema, a rare presentation of systemic lupus erythematosus: rapid response to rituximab

1 billion per year in the United States, and the average cost for one patient over a lifetime exceeds

Severe Staphylococcal Cutaneous Infections and Toxic Shock Syndrome

40 000 (1). There is no racial predilection; however, women seem to develop venous ulcers more often than men (2). Venous ulcers are more common with increasing age, with peak prevalence between 60 and 80 years of age (3, 4). However, 22% of persons develop venous ulcers by 40 years of age and 13% do so before 30 years of age, which may represent a substantial effect on work productivity (5, 6). Therefore, proper diagnosis and adequate management are vital when caring for patients with venous leg ulcers to promote faster healing and prevent recurrences. What Are the Potential Causes of This Patients Leg Ulcer? The four most common causes of lower-extremity ulcers are venous insufficiency, arterial insufficiency, neuropathy (often due to diabetes), and ulcers caused by prolonged pressure and ischemia (Table 1). At times, several of these causes may overlap in one patient. Less common causes of lower-extremity ulcers include trauma, inflammatory or metabolic conditions, malignancy, and infections (7). When caring for a patient with lower-extremity ulcers, a provider should identify the underlying cause to determine the management and prognosis. Table 1. Clinical Aspects of the Most Common Types of Ulcers of the Lower Limbs Venous insufficiency is the most common cause of lower-leg ulcers, accounting for nearly 80% of all cases. Of the approximately 7 million people in the United States with venous insufficiency, approximately 1 million develop venous leg ulcers (1). Patients with venous ulcers suffer from ambulatory venous hypertension, which is an abnormally sustained elevation of the venous pressure upon ambulation. The mechanism by which venous hypertension results in ulceration remains unclear. Recently proposed theories, such as pericapillary fibrin cuff deposition, abnormalities of the fibrinolytic system, trapping of growth factors by macromolecules in the dermis, and leukocyte plugging in the vessels of the lower extremities, are some of the consequences of venous hypertension thought to be responsible for the development of venous leg ulcers (8-10). The patient reports occasional leg pain and swelling, especially at the end of the day. She notes that her mother had varicose veins. What Clinical Characteristics Suggest that Leg Ulcers Are Due to Venous Disease? Patients with venous ulcers commonly report swelling and aching of the legs, often worse at the end of the day, which may be exacerbated by dependency and improved by leg elevation (1). A history of ulcer recurrence, particularly at the same location, is characteristic. Recent publications have challenged the assumption that venous ulcers are not painful; as many as three quarters of patients with venous ulcers report pain that adversely affects their quality of life (11, 12). Several risk factors for the development of venous ulcers have been identified. Up to 50% of patients with chronic venous insufficiency have a history of leg injury (13). Obesity, phlebitis, family history of varicose veins, type of employment and lifestyle (activities that require long hours of standing or sitting), deep venous thrombosis, and previous surgery for varicose veins have also been considered important risk factors for venous ulcerations (14, 15). Venous ulcers are characteristically located over the medial malleolus, also called the gaiter area. They may be single or multiple and can involve the entire circumference of the leg if untreated. Venous ulcers usually have irregular, flat, or only slightly steep borders. The ulcer bed tends to be shallow with granulation tissue, as well as some fibrinous material, and the wound surface rarely, if ever, shows necrosis or exposed tendons; their presence should lead a provider to consider another cause (16). Commonly associated findings include dependent edema, varicose veins (ranging from a submalleolar venous flare to various degrees of vessel dilatation), a reddish-brown pigmentation and purpura due to extravasation of erythrocytes, and subsequent hemosiderin deposition. Eczematous changes with redness, scaling, and pruritus, often referred to as venous dermatitis, are also commonly present. This eczematous dermatitis is caused or aggravated by sensitization to applied topical medications, to which patients with venous disease are particularly susceptible (17, 18). Atrophie blanchesmooth, ivory-white atrophic plaques of sclerosis speckled with telangiectasesis described in up to one third of patients with chronic venous insufficiency and, when present in the gaiter area, may point to a venous cause of a lower-extremity ulcer (19). In long-standing venous disease, the skin develops an induration and fibrosis of the dermis and subcutaneous tissue, usually restricted to the medial leg and sharply demarcated from proximal normal skin, resulting in the appearance of an inverted bottle. Lipodermatosclerosis, a term used to describe these clinical findings, suggests a greater impairment of the fibrinolytic system and is highly associated with and usually restricted to the legs of patients with venous insufficiency (17, 20). Other possible causes of lower-extremity ulcers are arterial insufficiency and neuropathy (Table 1) (21-23). The ulcer presented by the patient in this case has a typical presentation of venous leg ulcer with associated venous dermatitis. What Diagnostic Procedures Are Useful in Evaluating Leg Ulcers? In up to three quarters of cases of venous ulcers, diagnosis may be made by clinical criteria alone (21-23). However, 25% of patients will have ulcers with mixed characteristics; therefore, noninvasive methods may aid in an accurate diagnosis, as may anatomic and functional evaluation of the venous system (24, 25). The anklebrachial index (ABI) may aid in detecting peripheral vascular disease. The systolic blood pressure is obtained by placing an appropriately sized cuff around the calf and inflating it so to occlude the pedal arteries. When the sounds are heard with Doppler ultrasonography after deflation of the cuff, the ankle systolic pressure is obtained. This is then compared with the brachial systolic pressure to determine the ABI (value > 1 is normal). Values less than 0.97 identify patients with peripheral arterial disease with a sensitivity of 96% to 97% and a specificity of 94% to 100% (23). Although false-normal results may be observed in patients who are elderly or diabetic, this simple, noninvasive method can be useful in detecting arterial disease. In the elderly and in diabetic patients, a transcutaneous oxygen measurement may be preferred to evaluate arterial flow. This is important since compression therapy, the mainstay of therapy for venous ulcers, can lead to worsening of an arterial ulcer and, at times, gangrene (26). Color duplex ultrasonography is the gold standard in evaluating venous disease. It is accurate, reproducible, and noninvasive and provides anatomic and functional information about both arterial and venous systems (27, 28). With the use of color duplex ultrasonography, veins can be identified and their dimensions measured, as can the velocity and direction of flow. Other examinations, such as photo and air plethysmography, allow the clinician to assess whole-limb venous hemodynamics at rest and after exercise and are adjuncts to duplex scanning. Invasive venography is usually reserved for investigation before surgery, if indicated. If osteomyelitis is suspected, radiography, bone scanning, and bone biopsy should be considered. The incidence of osteomyelitis in chronic venous ulcers is unknown. For diabetic foot ulcers, a prospective trial found that probing of sinuses and deep ulcers was a highly sensitive method of detecting bone infection (29). Therefore, if bone is palpable at the base of an ulcer, with no intervening soft tissue, osteomyelitis is likely and further investigation is warranted. Independent of the suspected cause, if a wound is present for more than 3 months, a biopsy is recommended to rule out malignancy. At that time, an atypical infection can be detected by microscopic examination, as well as tissue culture. Since palpation of the dorsalis pedis pulses on the affected limb is difficult to perform in this patient because of edema, further diagnostic evaluation to rule out an associated arterial insufficiency is warranted. You perform an ABI examination, which yielded a score of 1, and a transcutaneous oxygen measurement was normal. A leg ulcer secondary to venous insufficiency was diagnosed on clinical grounds, and no further venous studies were performed. The patient asks how you will treat her. The goals of treatment for patients with venous ulceration include reduction of edema, improvement of pain and lipodermatosclerosis, ulcer healing, and prevention of recurrence. The simplest method to reverse the effects of venous hypertension is bed rest with leg e

Tissue-Engineered Skin (Apligraf) in the Healing of Patients With Epidermolysis Bullosa Wounds

We report a case of hypocomplementemic urticarial vasculitis and recurrent angioedema in a patient with systemic lupus erythematosus unresponsive to mycophenolate mofetil, high-dose methylprednisolone, and intravenous immunoglobulin that responded rapidly to rituximab. Rituximab is a monoclonal antibody against CD20 transmembrane protein on the surface of mature and malignant B cells. No adverse effects occurred during or after therapy, and the patient was discharged from the hospital for outpatient rituximab infusion and follow-up care.

The Use of Tissue-Engineered Skin (Apligraf) to Treat a Newborn With Epidermolysis Bullosa

S. aureus is a Gram-positive cocci of the Micrococcaceae family. It is one of the most common pathogens in skin and soft-tissue infections, and can cause potentially serious nosocomial infections when acquired in the hospital setting. S. aureus has a diverse arsenal of components and products that contribute to the pathogenesis of infection. The virulence of S. aureus infection is remarkable, given that the organism is a commensal that colonizes the nares, axillae, vagina, pharynx or damaged skin surfaces. Infections are initiated when a breach of the skin or mucosal barrier allows staphylococci access to adjoining tissues or the bloodstream (Fig. 7.1). Whether an infection is contained or spreads depends on a complex interplay between S. aureus virulence determinants and host defense mechanisms [1–3]. Penicillin was introduced in the 1940s as an effective treatment against S.aureus. Methicillin, a semisynthetic penicillin was introduced in 1959 to overcome the resistance to penicillin that developed shortly after its introduction [4]. However, within a year, methicillinresistant Staphylococcus aureus (MRSA) emerged as a hospital-acquired infection, and was fi rst detected in the United Kingdom and later in the United States › Community-acquired Staphylococcus aureus (CA-MRSA) infections have become epidemic in the United States and elsewhere, and represent a threat to the community and to persons without risk factors. › MRSA infection should be suspected in certain patient populations, and in patients not responding to standard β-lactam therapy. › Cultures of wounds should be obtained, and proper antibiotic guidelines should be followed. › Because there are epidemiological and microbiological differences between communityassociated and health care-associated MRSA infections, strategies to prevent and treat these infections likely differ as well. Core Messages