1/5. Successful use of alternate waste nitrogen agents and hemodialysis in a patient with hyperammonemic coma after heart-lung transplantation.BACKGROUND: Lethal hyperammonemic coma has been reported in 2 adults after lung transplantation. It was associated with a massive elevation of brain glutamine levels, while plasma glutamine levels were normal or only slightly elevated. In liver tissue, glutamine synthetase activity was markedly reduced, and the histologic findings resembled those of reye syndrome. The adequacy of therapy commonly used for inherited disorders of the urea cycle has not been adequately evaluated in patients with this form of secondary hyperammonemia. OBJECTIVE: To determine whether hemodialysis, in conjunction with intravenous sodium phenylacetate, sodium benzoate, and arginine hydrochloride therapy, would be efficacious in a patient with hyperammonemic coma after solid-organ transplantation. DESIGN: Case report. SETTING: A children's hospital. PATIENT: A 41-year-old woman with congenital heart disease developed a hyperammonemic coma with brain edema 19 days after undergoing a combined heart and lung transplantation. methods: Ammonium was measured in plasma. amino acids were quantitated in plasma and cerebrospinal fluid by column chromatography. The effectiveness of therapy was assessed by measuring plasma ammonium levels and intracranial pressure and performing sequential neurological examinations. RESULTS: The patient had the anomalous combination of increased cerebrospinal fluid and decreased plasma glutamine levels. To our knowledge, she is the first patient with this complication after solid-organ transplantation to survive after combined therapy with sodium phenylacetate, sodium benzoate, arginine hydrochloride, and hemodialysis. Complications of the acute coma included focal motor seizures, which were controlled with carbamazepine, and difficulty with short-term memory. CONCLUSIONS: The aggressive use of hemodialysis in conjunction with intravenous sodium phenylacetate, sodium benzoate, and arginine hydrochloride therapy may allow survival in patients after solid-organ transplantation. An acute acquired derangement in extra-central nervous system glutamine metabolism may play a role in the production of hyperammonemia in this illness that resembles reye syndrome, and, as in other hyperammonemic disorders, the duration and degree of elevation of brain glutamine levels may be the important determining factors in responsiveness to therapy.- - - - - - - - - - ranking = 1keywords = chromatography (Clic here for more details about this article) |
2/5. Toxicological and histopathological analysis of a patient who died nine days after a single intravenous dose of methamphetamine: a case report.A man in his late twenties collapsed shortly after intravenously injecting himself with methamphetamine (MA). He slipped into a deep coma and remained in this condition for 9 days, until his death. autopsy revealed severe brain edema and localized subarachnoid hemorrhages in the cerebrum and cerebellum. Histopathological examination revealed myocardial necrosis in the left ventricle, rhabdomyolysis and bronchopneumonia. Blood derived from the cadaver was found to have high levels of blood urea nitrogen and creatinine, suggesting he experienced acute renal failure probably due to rhabdomyolysis. Most of the postmortem findings were consistent with MA poisoning. The patient's bronchopneumonia may have represented a hypostatic pneumonia that developed as a result of his deep coma. While the patient's brain edema, myocardial necrosis and rhabdomyolysis were diagnosed soon after admission, his bronchopneumonia and acute renal failure only occurred 6 and 8 days later, respectively. Although MA was not detected in the cadaver's blood, urine or liver, analysis of the decedent's hair using gas chromatography-mass spectrometry confirmed its presence at a concentration of 1.1 ng/mg. Based on these findings, we concluded that the patient's cause of death was multiorganopathy resulting from MA poisoning. This case suggests that the postmortem diagnosis of MA poisoning in patients who survive for relatively longer periods after drug injection should include toxicological hair analysis in combination with histopathological and postmortem physiochemical examination.- - - - - - - - - - ranking = 1keywords = chromatography (Clic here for more details about this article) |
3/5. Clinical experience with the benzodiazepine antagonist flumazenil in suspected benzodiazepine or ethanol poisoning.The clinical efficacy of different doses of the specific benzodiazepine antagonist flumazenil was studied in a total of 72 patients with benzodiazepine or ethanol overdose. In a randomized double-blind study, 18 patients (group 1) and eight patients (group 2) with suspected benzodiazepine overdose received 5 mg (group 1) or 1 mg (group 2) flumazenil or placebo, respectively. The stage of coma, heart rate, blood pressure and respiratory rate were monitored within the following 15 min. If no change in the stage of coma was observed, 5 mg (group 1) or 1 mg (group 2) flumazenil were given, and the stage of coma, heart rate and blood pressure were again monitored. In a similar way, the effect of 5 and 1 mg flumazenil was investigated in 13 patients (group 3) and four patients (group 4) with ethanol intoxication. In an open trial, the clinical efficacy of flumazenil for the diagnosis of benzodiazepine or ethanol overdose was studied in 29 patients (group 5). In all patients, a toxicological screening confirmed benzodiazepine or ethanol overdose. None of the patients receiving placebo showed effects on stage of coma, heart rate, blood pressure or respiratory rate. patients with benzodiazepine overdose who received 5 mg flumazenil regained consciousness about 1-2 min after the end of injection. The effect of 1 mg flumazenil (group 2) on benzodiazepine-induced coma was less pronounced. In patients with ethanol overdose (group 3), ethanol-induced coma was reversed after 5 mg flumazenil more slowly than in patients of group 1. No effect of flumazenil on ethanol-induced coma was observed in group 4. In group 5, flumazenil proved to be useful for diagnosing benzodiazepine or ethanol intoxication. In one patient with coma due to carbamazepine overdose, flumazenil was also found to be effective. Additionally, a possible analytical interference of flumazenil and its metabolites with the identification of other benzodiazepines by a toxicological screening procedure was studied. Even after an oral dose of 200 mg flumazenil, no interference with immunological benzodiazepine assays (EMIT, TDX, and RIA) was found. A metabolite and an artifact of flumazenil could be identified in urine by gas chromatography/mass spectrometry.- - - - - - - - - - ranking = 1keywords = chromatography (Clic here for more details about this article) |
4/5. naloxone-reversible coma unrelated to opiate drugs.A role for endogenous opioids in central nervous system disorders has often been proposed. A case report is presented of a 47-year-old male, medicated only with carbamazepine and lithium, who developed a precipitous alteration of consciousness (Glascow coma scale = 4). An extensive medical workup did not reveal an underlying cause. He exhibited a graded awakening with two intravenous doses of naloxone, which gradually reversed as the last naloxone dose was eliminated. immunoassay and thin-layer chromatography of two urine samples (to evaluate the possibility of a medication error, alcohol ingestion, or illicit drug use) revealed only the presence of carbamazepine. A dysregulation of the endogenous opioid system is believed to underlie this episode.- - - - - - - - - - ranking = 1keywords = chromatography (Clic here for more details about this article) |
5/5. A sudden awakening from a near coma after combined intake of gamma-hydroxybutyric acid (GHB) and ethanol.OBJECTIVE: A case of a sudden awakening from a near coma after combined intake or gamma-hydroxybutyric acid (GHB) (125 micrograms/mL), ethanol (134 mg/dL), and cannabinoids is described. methods: GHB was determined by gas chromatography-mass spectrometry after acetonitrile precipitation and derivation with N-methyl-N-trimethylsilyltrifluoroacetamide, using valproic acid as the internal standard. CONCLUSION: The described case illustrates the consequences of GHB overdose. GHB overdose should be considered in every case of unexplained sudden coma, i.e., without any evidence of head injury, intake of coma-inducing drugs, or increasing intracranial pressure. GHB overdose will be missed by routine toxicological screening.- - - - - - - - - - ranking = 1keywords = chromatography (Clic here for more details about this article) |