[Treatment of freezing injury]. / Zur Therapie der Erfrierungen.

Report on therapeutic procedures in patients with second and third degree congelations (frostbite) on the feet. Two mechanisms of tissue damage caused by exposure to cold temperature will be discussed pathophysiologically: direct freezing injuries and cell death through intra and extracellular ice crystal formation as well as transient and finally irreversible tissue damage due to decreased perfusion. The condition of decreased perfusion results from persistent vaso-constriction induced by cold temperature, increased blood viscosity, sludge phenomenon and occlusion by platelet thrombi in the microvasculature. Frostbite beyond the erythematous stage should be treated primarily with a parenteral therapy in order to improve the hemorrheologic parameters, in particular within the micro-vascular compartment. Colloidal plasma volume expander such as 10% dextran solution is used to increase the intravascular volume. This solution (with its coating effect) and pentoxifyllin lowers the aggregation of erythrocytes and platelets. The latter will also be favourably influenced by the use of iloprost or acetylsalicylic acid. Iloprost as a stable metabolite of prostacyclin is a powerful vasodilator which attenuates the peripheral vascular resistance and activates fribrinolysis. Pentoxifyllin is considered to lower pathologically increased levels of fibrinogen. Both drugs may protect against damage of the vascular endothelium. Based on their pharmacological effects the above-mentioned drugs may improve tissue perfusion and therefore tissue damage caused by frostbite can be limited. However, an important factor is to strictly avoid bacterial infections in the cold-damaged tissue.

Verrucous carcinoma of the skin: long-term follow-up results following surgical therapy.

BACKGROUND: Owing to the benign appearance and slow growth of verrucous carcinoma of the skin, its diagnosis and therapeutic management still pose problems. OBJECTIVE: This study was undertaken to point out clinical and histopathologic features of verrucous carcinoma of the skin and to provide diagnostic and therapeutic guidelines on the basis of the long-term results from 20 patients. METHODS: A retrospective study of the long-term results of 20 patients treated surgically for verrucous carcinoma of the skin is presented. In 16 cases, a wide resection with histopathologic examination of the margins was possible. Two tumors were shaved; 1 case required below-knee amputation and 1 patient refused primary amputation. In April 1999, 9 of the 10 surviving patients underwent physical examination, ultrasonography of the regional lymph nodes and the abdomen, and chest X-ray. The protocols of autopsies or postmortem examinations of the deceased patients were consulted. RESULTS: The deceased patients achieved an average tumor-free survival period of 86.1 months; eight of the surviving patients had an average tumor-free follow-up of 127.4 months. Two patients suffered recurrences. CONCLUSION: Curative treatment can be achieved by timely and complete resection of verrucous carcinoma of the skin, even in advanced cases.

UV light-induced linear IgA dermatosis.

Various exogenous factors (eg, drugs, dietary antigens, trauma, infections, radiographs, and UV radiation) are known to induce or aggravate skin diseases. UV radiation in particular is known to induce or aggravate the autoimmune bullous diseases of pemphigus foliaceus, pemphigus vulgaris, and bullous pemphigoid. Its role in linear IgA dermatosis, however, is not well recognized. We report the second case of linear IgA dermatosis induced by intense sun exposure in which blistering was induced by UVA radiation. Furthermore, a review of the literature on photoinduced autoimmune bullous diseases and the wavelengths responsible for the induction of blistering is presented and several proposed mechanisms of action for the blister induction, including release or unmasking of antigens, promotion of antibody fixation by UV radiation, and launching of an inflammatory process, are discussed. We conclude that linear IgA dermatosis should be added to the list of autoimmune bullous diseases induced and/or aggravated by UV radiation.