Dabney R. Yarbrough

Fatal toxic epidermal necrolysis related to lamotrigine administration.

Toxic epidermal necrolysis (TEN) and Stevens‐Johnson syndrome (SJS) are severe life‐threatening dermatologic conditions. To date, eight cases of TEN and one of SJS related to lamotrigine administration have been reported in the literature. Most patients were also taking concomitant valproic acid. It was hypothesized that valproic acid may interfere with glucuronidation of lamotrigine, leading to increased serum lamotrigine levels, or perhaps alter the drugs metabolism, resulting in accumulation of a toxic intermediate metabolite. Ultimately, this may possibly predispose a patient to increased dermatologic reactions, including TEN. A 54‐year‐old man developed TEN 4 weeks after beginning lamotrigine for complex partial seizures related to a glioblastoma multiforme brain tumor. The patient had also been taking concomitant allopurinol and captopril for more than 4 years with no complications, and valproic acid 3 months before the cutaneous event. Despite aggressive intensive care management, the patient died 17 days from the onset of symptoms due to multiple organ failure. Administration of lamotrigine, especially in combination with valproic acid, may lead to the development of TEN.

Phaeohyphomycosis Due to Curvularia Lunata Involving Skin and Subcutaneous Tissue After an Explosion at a Chemical Plant

Cases of phaeohyphomycosis due to dematiaceous fungi have been reported in increasing numbers and diversity. The optimal roles of antifungal chemotherapy and surgical debridement in the management of these infections have not been determined. A case of acute cutaneous and subcutaneous phaeohyphomycosis due to Curvularia lunata after an explosion at a chemical plant is reported, in which the organisms may have been inoculated into the tissues by the force of the blast. No organisms were found by histopathologic examination or culture of excisional biopsy specimens taken 10 days after initiation of therapy with intravenous amphotericin B; the antifungal therapy may have eradicated the infection.

Blood and Tissue Oxygenation during Hemorrhagic Shock as Determined with Ultramicro Oxygen Electrodes

Recent clinical and laboratory observations in the field of shock have centered attention upon deficits in pulmonary function as one of the major causes of death and morbidity following shock and trauma.1,2,3,4 Following the initial proposal that an oxygen debt was accumulated in hemorrhagic shock,5 other investigators have found that an oxygen deficit indeed did occur irk hemorrhagic shock and appeared to correlate with irreversibility.6,7 Evidence in the literature is scanty concerning direct measurements of tissue pO2 during hemorrhagic shock and is conflicting concerning arterial pO2 measurements in the same condition. The experiments reported here utilize an ultramicro oxygen electrode to determine arterial pO2 and renal and cerebral parenchymal pO2 during a standard episode of hemorrhagic shock.

Immediate Examination and Care of the Emergency Patient

Although the life-threatening emergencies discussed here—interference with oxygenation, circulatory failure, and severe hemorrhage—are most often found in the traumatized patient, they occur in the acutely ill as well. The progressive methods outlined for dealing with them are applicable to any patient with a serious injury or illness, are very flexible, and allow the physician to concentrate on the major injuries yet not ignore other possible injuries.—MSR