1/4. Acute hyperammonemic coma with chronic valproic acid therapy.OBJECTIVE: To report a case of dose-related hyperammonemic coma without liver failure in a patient receiving chronic valproate therapy. CASE SUMMARY: A 56-year-old woman with poorly controlled epilepsy, receiving valproate at subtherapeutic levels for 6 years, developed a life-threatening hyperammonemic coma following a moderate dosage increase. DISCUSSION: Hyperammonemic coma without associated liver failure is an extremely rare complication of valproate therapy, described primarily in patients with inborn errors of metabolism and occurring idiosyncratically during initial stages of therapy. In our case, family history was suggestive of an X-linked disorder, raising the possibility that our patient may have been an asymptomatic carrier of a urea cycle enzyme deficiency unmasked by valproate therapy. To our knowledge, as of October 24, 2005, only one prior case of hyperammonemic coma in the context of chronic valproate monotherapy has been described. Application of the Naranjo probability scale score suggests that a causal relationship between valproic acid and hyperammonemic coma was probable. CONCLUSIONS: The widespread use of valproic acid emphasizes the need to maintain a high degree of suspicion with respect to this rare but potentially fatal adverse effect at all times, regardless of therapy duration.- - - - - - - - - - ranking = 1keywords = probability (Clic here for more details about this article) |
2/4. Acute valproate intoxication with fatal outcome in an infant.A healthy twenty-month-old boy ingested a maximal dose of valproate from which about 750 mg/kg were absorbed. Cerebral coma, which lasted for twenty hrs, was followed by an undisturbed period of approximately sixteen hrs. death from cardiorespiratory failure due to severe bronchopneumonia occurred 46.5 hrs after the ingestion of the drug. The serum valproic acid concentration reached a peak of 1061 micrograms/ml within three hours, and fifteen minutes before death it had fallen to 187 micrograms/ml. The half-life of 16.6 hrs was within the range usually found. Metabolic acidosis, hypernatraemia and hyperosmolarity could be corrected, unlike the hypocalcaemia, which developed later. bilirubin, GOT, GPT, gamma-GT, alkaline phosphatase, blood glucose, diastase, urea, creatinine, haemoglobin as well as PT and PTT and the platelet count were all normal. Leucopenia with 1,600 per microliter developed only during the bronchopneumonial stage. The histo-pathological findings were acute hypoxic damage of the myocardium, kidneys and certain neurones of vulnerable areas of the brain (neuronal microvesiculation and tigrolysis) in addition to a severe cerebral oedema in the final stage. A morphological substrate of an acute valproate encephalopathy was not demonstrable. The liver showed no necrosis or cholostasis. The vertebral marrow was inconspicuous. All the results indicate that liver function was not impaired in spite of the initial maximal concentration of valproic acid. In all probability the patient might have survived the acute valproate intoxication had it not been for the bronchopneumonia.- - - - - - - - - - ranking = 1keywords = probability (Clic here for more details about this article) |
3/4. Acute fatty liver of pregnancy--survival despite associated severe preeclampsia, coma and coagulopathy.Acute fatty liver of pregnancy is the least common and most serious cause of jaundice of pregnancy. It is rare, fewer than 100 cases having been reported (Koff, 1981). There is a high probability that it is frequently misdiagnosed and categorized vaguely as some form of variant of 'toxaemia of pregnancy' which is not surprising because of its late-pregnancy onset and the production of multi-system manifestations (Holzback, 1976). In the case reported here, there was associated severe preeclampsia with fetal intrauterine death but maternal survival.- - - - - - - - - - ranking = 1keywords = probability (Clic here for more details about this article) |
4/4. Physical recovery after severe closed head trauma in children and adolescents.Three hundred forty-four patients under 18 years of age with severe closed head injuries, comatose over 24 hours, were followed prospectively for a minimum of one year. motor vehicles were involved in 82% of the injuries. Seventy-three percent of the patients regained independence in ambulation and self-care, 10% remained partially dependent in self-care and achieved only limited ambulation, 9% regained consciousness but were totally dependent, and 8% remained comatose. A favorable prognosis for recovery of motor function can be made if the duration of coma is less than three months. Complications of prolonged hypertension, ventricular enlargement, and seizures significantly decrease the probability of achieving physical independence. Although mortality following severe head injury is decreasing, neurologic sequelae in the survivors are statistically unchanged since 1970. Improved neurosurgical management in recent years has not increased the percentage of severely disabled survivors.- - - - - - - - - - ranking = 1keywords = probability (Clic here for more details about this article) |