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Dermal Edema (dermal + edema)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Necrotizing fasciitis: delay in diagnosis results in loss of limb

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2006
Rajat Varma MD
A 58-year-old man presented to the Emergency Room with a 1-day history of severe pain in the left lower extremity preceded by several days of redness and swelling. He denied any history of trauma. He also denied any systemic symptoms including fever and chills. His past medical history was significant for diabetes, hypertension, deep vein thrombosis, and Evans' syndrome, an autoimmune hemolytic anemia and thrombocytopenia, for which he was taking oral prednisone. Physical examination revealed a warm, tender, weeping, edematous, discolored left lower extremity. From the medial aspect of the ankle up to the calf, there was an indurated, dusky, violaceous plaque with focal areas of ulceration (Fig. 1). Figure 1. Grossly edematous lower extremity with well-demarcated, dusky, violaceous plaque with focal ulceration Laboratory data revealed a white blood cell count of 6.7 × 103/mm3[normal range, (4.5,10.8) × 103/mm3], hemoglobin of 11.5 g/dL (13.5,17.5 g/dL), and platelets of 119 × 103/mm3[(140,440) × 103/mm3]. Serum electrolytes were within normal limits. An ultrasound was negative for a deep vein thrombosis. After the initial evaluation, the Emergency Room physician consulted the orthopedic and dermatology services. Orthopedics did not detect compartment syndrome and did not pursue surgical intervention. Dermatology recommended a biopsy and urgent vascular surgery consultation to rule out embolic or thrombotic phenomena. Despite these recommendations, the patient was diagnosed with "cellulitis" and admitted to the medicine ward for intravenous nafcillin. Over the next 36 h, the "cellulitis" had advanced proximally to his inguinal region. His mental status also declined, and he showed signs of septic shock, including hypotension, tachycardia, and tachypnea. Vascular surgery was immediately consulted, and the patient underwent emergency surgical debridement. The diagnosis of necrotizing fasciitis was then made. Tissue pathology revealed full-thickness necrosis through the epidermis with subepidermal splitting. Dermal edema was also present with a diffuse neutrophilic infiltrate (Fig. 2). This infiltrate extended through the fat into the subcutaneous tissue and fascia. Tissue cultures sent at the time of surgery grew Escherichia coli. Initial blood cultures also came back positive for E. coli. Anaerobic cultures remained negative. Figure 2. Necrotic epidermis with subepidermal splitting. Marked dermal edema with mixed infiltrate and prominent neutrophils. Hematoxylin and eosin: original magnification, ×20 After surviving multiple additional debridements, the patient eventually required an above-the-knee amputation due to severe necrosis. [source]

Localized lymphedema (elephantiasis): a case series and review of the literature

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2009
Song Lu
Background:, Lymphedema typically affects a whole limb. Rarely, lymphedema can present as a circumscribed plaque or an isolated skin tumor. Objective:, To describe the clinical and pathologic characteristics and etiologic factors of localized lymphedema. Methods:, Case,control study of skin biopsy and excision specimens histologically diagnosed with lymphedema and presenting as a localized skin tumor identified during a 4-year period. Results:, We identified 24 cases of localized lymphedema presenting as solitary large polyps (11), solid or papillomatous plaques (7), pendulous swellings (4), or tumors mimicking sarcoma (2). Patients were 18 females and 6 males with a mean age of 41 years (range 16,74). Anogenital involvement was most frequent (75%) , mostly vulva (58%), followed by eyelid (13%), thigh (8%) and breast (4%). Causative factors included injury due to trauma, surgery or childbirth (54%), chronic inflammatory disease (rosacea, Crohn's disease) (8%), and bacterial cellulitis (12%). Eighty-five percent of these patients were either overweight (50%) or obese (35%). Compared with a series of 80 patients with diffuse lymphedema, localized lymphedema patients were significantly younger (41 vs. 62 years old, p = 0.0001), had no history of cancer treatment (0% vs. 18%, p = 0.03), and had an injury to the affected site (54% vs. 6%, p = 0.0001). Histologically, all cases exhibited dermal edema, fibroplasia, dilated lymphatic vessels, uniformly distributed stromal cells and varying degrees of papillated epidermal hyperplasia, inflammatory infiltrates and hyperkeratosis. Tumor size significantly and positively correlated with history of cellulitis, obesity, dense inflammatory infiltrates containing abundant plasma cells, and lymphoid follicles (p < 0.05). A history of cellulitis, morbid obesity, lymphoid follicles and follicular cysts predicted recurrent or progressive swelling despite excision (p < 0.05). Conclusions:, Localized lymphedema should be considered in the etiology of skin tumors when assessing a polyp, plaque, swelling or mass showing dermal edema, fibrosis and dilated lymphatics on biopsy. A combination of lymph stasis promoting factors (trauma, obesity, infection and/or inflammatory disorders) produces localized elephantiasis. [source]

Cutaneous histopathological findings of Aicardi,Goutières syndrome, overlap with chilblain lupus

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 8 2008
Athanassios Kolivras
We report a 2-year-old girl with developmental delay who, from the age of 1 year, developed perniotic lesions of the hands and feet initially diagnosed as chilblain lupus. Histological examination showed features of epidermal necrosis with intraepidermal bulla formation, interface dermatitis, lymphocytic vasculitis with fibrinoid necrosis and thrombi formation, both superficial and deep dermal lymphocytic infiltrate, lymphocytic eccrine hidradenitis and absence of marked dermal edema. Subsequent investigations suggested a clinical diagnosis of Aicardi,Goutières syndrome (AGS), a rare genetic leukoencephalopathy. Recently, both AGS and familial chilblain lupus, an autosomal dominant form of systemic lupus erythematosus (SLE), have been shown to be allelic thus suggesting a common pathogenic basis. In addition, a phenotypic overlap is apparent between SLE and AGS. To our knowledge, this is the first comprehensive dermatopathological report of the cutaneous lesions seen in AGS, and our paper highlights the importance of considering AGS in the differential diagnosis of perniosis and chilblain lupus. [source]