1/13. A report of acute ethanol poisoning in a child: mouthwash versus cologne, perfume and after-shave.The ingestion of ethanol-containing products, such as cologne, perfume and after-shave, in children under six years of age is common, but serious poisoning is rarely reported. Thus, it has been recently suggested that children ingesting up to 3.5 ounces of these products may be safely observed at home as long as they remain asymptomatic. While it may be assumed that products with a significantly lower alcohol content represent a much smaller poisoning hazard, mouthwashes are a relatively frequent cause of serious poisoning in children. In the following case report, 75 milliliters of mouthwash caused hypoglycemia, coma and manifestations of tonic seizure activity. Because of the palatable nature of mouthwash, wine and liquor, it appears that children are more apt to drink large quantities, consuming dangerous amounts of ethanol. The apparent safety of cologne, perfume, and after-shave may be due to a lack of palatability as well as the irritant nature of high concentrations of ethanol. This case suggests that consumer items such as mouthwash should be packaged in child-resistant containers.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/13. 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 = 8keywords = coma (Clic here for more details about this article) |
3/13. Fatal thrombosis of the basilar artery due to a minor head injury.A case is reported where a 20-year-old alcohol-intoxicated man was admitted to the hospital after a minor head injury. Initially there was no neurologic disturbances or complaints but after a few hours he became comatose, and he died 4 days later without regaining consciousness. The autopsy revealed no lesions of the upper cervical spine or the vertebral arteries, but the basilar artery was occluded in its entire length. No traumatic lesions could be seen by naked eye examination of the artery, and there was no accompanying subarachnoid haemorrhage. A thorough microscopic examination, however, using step-sectioning technique revealed a significant incomplete arterial rupture with an occluding luminal thrombosis superimposed, consisting predominantly of aggregated platelets. Only the very thin adventitia separated the vascular lumen from the subarachnoid space preventing the more well known fatal complication to a minor head injury: A subarachnoid haemorrhage. To the best of our knowledge, fatal thrombosis of the basilar artery due to a minor head injury has not previously been reported. The pathogenetic mechanism seems to be identical to that underlying fatal subarachnoid haemorrhage following a similar trauma apart from the resulting arterial rupture being incomplete instead of complete.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
4/13. Sleeping beauty: a case of pickwickian syndrome.The patient arriving at the emergency department with somnolence must be evaluated quickly, efficiently, and with a definite goal in mind. head and neck trauma should always be suspected and protective steps taken in the unconscious patient. The coma mnemonic, AEIOU TIPS, (alcohol, epilepsy, insulin, overdose, uremia, trauma, infection, psychiatric, stroke) provides an excellent memory tool for the evaluation of decreased level of consciousness in the emergency setting. Interventions that provide diagnostic and therapeutic results (naloxone and 50% dextrose) should be initiated immediately while blood samples are drawn for pretreatment documentation. Each of the possible causes of lethargy or somnolence needs to be evaluated with the understanding that a multitude of factors may be present in the patient whose condition precludes a thorough history; the depressed diabetic may have taken an overdose of medications in addition to his insulin. Social preconceptions may also effect the outcome. The intoxicated patient described herein was allowed to "sleep it off" in the emergency department under the watchful eyes (and ears) of a nursing staff who faithfully recorded vital signs and pupil reactivity as the patient's blood gas values deteriorated.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
5/13. survival of a child despite unusually high blood ethanol levels.A 30-month-old, 13-kg child reportedly ingested up to 16 ounces of a wine containing 20% ethanol. The child was brought into the emergency department by paramedics, and upon arrival was found to be comatose and unresponsive to deep stimuli but breathing spontaneously. The patient remained unconscious and unresponsive for three hours after admission. Despite an initial blood ethanol level of 98.78 mmol/L (455 mg/dL), recovery was complete without sequelae. Treatment consisted of prompt gastric decontamination and maintenance of adequate hydration and euglycemia. Elimination of ethanol was rapid in this child and appeared to follow first-order kinetics instead of the zero-order kinetics usually observed. To our knowledge, this is the highest initial blood ethanol level reported in a child with survival. Additionally, no significant metabolic or cardiorespiratory derangement occurred. Ethanol toxicity, elimination kinetics, and treatment are discussed.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
6/13. Pitfalls of the alcohol dehydrogenase procedure for the emergency assay of alcohol: a case study of isopropanol overdose.We describe a case of ethanol and isopropanol ingestion that resulted in coma. The concentration of ethanol and isopropanol was 0.90 and 1.65 g/liter in serum and 3.12 and 5.34 g/liter in gastric contents. With an enzymatic (alcohol dehydrogenase) method for ethanol determination we obtained erroneous analytical results. Because of partial cross reactivity with isopropanol, ethanol concentration was overestimated and total alcohol (i.e., the contribution of isopropanol) was underestimated. This was recognized by measuring serum osmolality. Differences between measured and calculated serum osmolality that are not accounted for by the serum ethanol concentration as determined by an enzymatic ethanol method must be further investigated by specific methods to see if other alcohols are present.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
7/13. A case of poisoning by a mixture of methanol and ethylene glycol.A fatal case of poisoning by a mixture of methanol and ethylene glycol is described. A 72-year-old man was hospitalized when he was found stuporous to semicomatose, and despite massive bicarbonate therapy, died 36 hr after the admission. While the presence of numerous oxalate crystals in urine strongly suggested ethylene glycol intoxication, the GC analysis of the liquid the patient ingested revealed that he presumably drunk about 150 to 200 ml of a mixture of methanol (80%) and ethylene glycol (20%), the amount well over the lowest lethal dose when the additiveness of toxicity was considered. Retrospective evaluation of the signs suggested that while some of them such as oxalate crystalluria, elevated CPK, hypocalcemia, renal failure are attributable to the toxicity of ethylene glycol, others including elevated serum amylase and cyanosis are indicative of methanol poisoning. Disturbed consciousness was considered to be of metabolic origin; the high anion gap observed (38.2 mEq/liter) may be due not only to lactic acidosis but also to acidogenicity of the two chemicals ingested. The importance of gas chromatographic analysis for identification of the causative chemical(s) is stressed.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
8/13. Ethanol-induced hypoglycemic coma in a child.Reported is a case of ethanol-induced hypoglycemic coma in a 33-month-old boy after accidental ingestion of ethanol. blood glucose was 10 mg% and blood ethanol was 71 mg%. He responded promptly to an IV bolus of 50% dextrose. The pathophysiology and clinical presentation of this not uncommon metabolic disorder are discussed. A plan for early recognition and management is presented.- - - - - - - - - - ranking = 5keywords = coma (Clic here for more details about this article) |
9/13. Impaired metabolism of methylphenobarbital after a combined drug overdose: treatment by resin hemoperfusion.A 38-yr-old woman who by history ingested 13 g methylphenobarbital, alcohol, and 6 g acetaminophen became comatose slowly over 4 d. Acute hepatic injury appeared to impair the oxidative N-demethylation of methylphenobarbital to its product, phenobarbital. On the eighth day after ingestion she was treated because of protracted coma with Amberlite XAD-4 resin hemoperfusion. hemoperfusion, which removed 0.83 g methylphenobarbital and 2.10 g phenobarbital, led to transient clinical improvement. When supportive patient management fails to produce a satisfactory clinical course in a methylphenobarbital-intoxicated patient, hemoperfusion could be a useful adjunct to therapy.- - - - - - - - - - ranking = 2keywords = coma (Clic here for more details about this article) |
10/13. hypoglycemia following ethanol ingestion in children: report of a case.Ethanol is present in a large number of pharmaceuticals, cosmetics, detergents and beverages. Without adequate safety measures, the accidental ingestion of such products by children is possible. Ethanol ingestion by children is known to cause various metabolic and neurologic disorders, including hypoglycemia, metabolic acidosis, seizures or coma. In taiwan, little information has been published regarding the effects of ethanol ingestion by children. This is a report of a 5-year-old boy who became hypoglycemic after ingestion of rice wine. Admitted in a coma, the boy regained consciousness within 30 min after slow administration of 5% dextrose. His initial plasma glucose level was extremely low and hypokalemia was also found. Blood ethanol was 159 mg/dL, 3 h after the alcohol ingestion. He was discharged in good health the following day. Ethanol-induced hypoglycemia may be easily overlooked as symptoms of adrenaline excess are frequently absent. Prompt recognition and treatment with intravenous glucose are essential and may be life-saving. Pediatricians need to be aware of the devastating impact of ethanol. Preventive measures, such as child-proof packaging and parent education, are required if ethanol intoxication in children is to be avoided.- - - - - - - - - - ranking = 2keywords = coma (Clic here for more details about this article) |
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