DICP : the annals of pharmacotherapy
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The issue of routine anticonvulsant prophylaxis for early and late posttraumatic epilepsy (PTE) has received much attention in the medical literature. Such problems as lack of standard definitions for early and late PTE, the retrospective design of most studies, the wide variability of inclusion and exclusion criteria, and the varied duration of follow-up make this body of literature extremely difficult to evaluate. Severe head trauma appears to cause injured neurons to become hyperexcitable; this in turn brings about the formation of an epileptogenic focus during the time between trauma and seizure occurrence. ⋯ Late PTE incidence after head injuries in the civilian population is less than 5 percent. Risk factors associated with late PTE include loss of consciousness or PTA lasting greater than 24 hours, dural lacerations, depressed skull fractures, and various computerized tomography deficits. These factors vary slightly between the military and civilian populations.(ABSTRACT TRUNCATED AT 250 WORDS)
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Heparin-induced hypoaldosteronism leading to hyperkalemia is an uncommon adverse effect. It appears as though heparin blocks an enzymatic step in the synthesis of aldosterone, and reduced aldosterone levels may be evident as early as four days after initiation of therapy. Although all patients who receive heparin may have reduced aldosterone levels, most are able to compensate through increased renin production and therefore remain asymptomatic. However, patients on prolonged heparin therapy or those unable to adequately increase renin production (e.g., patients with diabetes or renal insufficiency) may exhibit signs of hypoaldosteronism, such as hyperkalemia.