1/132. death from hyponatremia as a result of acute water intoxication in an Army basic trainee.Several reports during the past 15 years have described hyponatremia as a result of excessive water intake by athletes during endurance races. The high rates of fluid consumption have been attributed to the desire of athletes to prevent heat injury. The military has adopted guidelines for programmed drinking to maintain performance and minimize the risk of heat casualties. As military personnel increase their fluid intake, their risk of hyponatremia as a result of water overload increases. A potentially life-threatening complication is acute water intoxication. We report the first known death of an Army basic trainee as a result of acute water intoxication. The misinterpretation of his symptoms as those of dehydration and heat injury led to continued efforts at oral hydration until catastrophic cerebral and pulmonary edema developed.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/132. Acute and reversible parkinsonism due to organophosphate pesticide intoxication: five cases.OBJECTIVE: To describe five patients who developed acute and reversible parkinsonism following organophosphate (OP) pesticide exposure, and to consider whether this syndrome represents a rare sequela of such exposure in genetically susceptible individuals. BACKGROUND: Several toxins are known to produce parkinsonism following acute exposure. Although case-control studies have implicated OP pesticides in the etiology of PD, acute parkinsonism following brief pesticide exposure has never been reported. methods: The authors describe the clinical syndrome affecting five patients who presented with recent OP exposure and symptoms of an acute akinetic-rigid syndrome. RESULTS: All patients developed parkinsonism that resembled PD clinically except for poor response to levodopa. Three genetically related patients were exposed to pesticides in a common environment before onset of parkinsonism; other family members remained unaffected. Other secondary causes of parkinsonism were excluded. Four patients recovered completely without treatment, and one patient was lost to follow-up. One patient experienced repeated episodes of parkinsonism with inadvertent reexposure to a pesticide-contaminated environment. CONCLUSION: The clinical course of these five patients suggests their syndrome represents a heretofore undescribed toxic effect of OP pesticides. Our observations strengthen epidemiologic studies implicating OP pesticides in the etiology of PD. A genetic susceptibility to OP pesticide-induced parkinsonism may account for three family members developing this syndrome.- - - - - - - - - - ranking = 0.66666666666667keywords = intoxication (Clic here for more details about this article) |
3/132. Transient amnesia triggered by acute marijuana intoxication.We report an unusual case of sudden isolated transient amnesia triggered by acute marijuana use. The memory disorder, apart from the long duration, had the characteristics of a transient global amnesia-like episode. Acute marijuana intoxication can affect memory more globally and severely than previously reported.- - - - - - - - - - ranking = 0.83333333333333keywords = intoxication (Clic here for more details about this article) |
4/132. Acute dilated cardiomyopathy and central nervous system toxicity following propranolol intoxication.OBJECTIVE: We report a case of a 16-year-old boy who developed central nervous system (CNS) depression and acute dilated cardiomyopathy following ingestion of 3200 mg of propranolol in a suicide attempt. Early echocardiographic findings were the only sign of cardiac toxicity. DESIGN: A case report. SETTING: Pediatric intensive care unit of a teaching hospital. RESULTS: This child developed significant acute dilated cardiomyopathy and severe CNS depression 2 hours after ingesting 3200 mg of propranolol. The child was treated with gastric lavage, activated charcoal, and mechanical ventilation. Following the echocardiographic findings, treatment with isoprenaline hydrochloride and glucagon were given intravenously. Echocardiographic examination 12 hours following treatment showed normal left ventricular size and function. No change in pulse rate or blood pressure was reported on admission and during his hospitalization. DISCUSSION: In the early stages of propranolol and other lipophilic beta-blocker intoxication, severe CNS depression can develop in the absence of clinical signs of cardiac toxicity. Early echocardiographic evaluation is important and may prevent delay in diagnosis and treatment of cardiac toxicity.- - - - - - - - - - ranking = 0.83333333333333keywords = intoxication (Clic here for more details about this article) |
5/132. kerosene-induced severe acute respiratory failure in near drowning: reports on four cases and review of the literature.OBJECTIVE: The purpose of this study is to present an unusual respiratory and cardiovascular course after intoxication and near drowning in a river contaminated with kerosene. DESIGN: case reports and review of the literature. SETTING: intensive care unit of a university-affiliated hospital. patients: Four patients after near drowning. INTERVENTION: Supportive only. RESULTS: The four patients developed acute respiratory failure. Cardiomyopathy was present in three patients and a persistent hypokalemia in two patients. The onset of the symptoms was delayed, which led to underestimation of the severity of their illness. Two of the four patients died. The diagnosis of hydrocarbon intoxication was based on bronchoalveolar lavage results, neutrophilic alveolitis with the presence of lipid-laden macrophages, and evidence of lipoid pneumonia from the autopsy performed on one victim. One patient who clinically deteriorated and another who developed a severe restrictive pulmonary disorder were treated with corticosteroids, which were effective only in the latter patient. CONCLUSIONS: Acute kerosene intoxication in a near-drowning event often results in severe respiratory and cardiac failure, with a high fatality rate. Treatment with corticosteroids may lead to a rapid improvement in lung function.- - - - - - - - - - ranking = 0.5keywords = intoxication (Clic here for more details about this article) |
6/132. Acute isoniazid intoxication: seizures, acidosis and coma.isoniazid (INH) is the most widely used of the antituberculosis drugs. An acute overdose is potentially fatal and is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. The diagnosis of INH overdose should be considered in any patient who presents with an unexplained metabolic acidosis and convulsions. The cornerstone of therapy consists in pyridoxine (vitamin B6) and the dose should be equal to the amount of INH ingested. When conservative therapy fails or in case of renal insufficiency, dialysis must be considered. Severe central nervous toxicity can also be caused by chronic ingestion of higher than therapeutic doses of INH. In those cases pyridoxine-therapy can be useful as well. In the present paper a case of acute overdose of INH is reported, followed by a review of the literature.- - - - - - - - - - ranking = 0.66666666666667keywords = intoxication (Clic here for more details about this article) |
7/132. Acute fish liver intoxication: report of three cases.The livers of some larger fish such as shark, tuna and seabass have been reported to be responsible for a peculiar poisoning causing headaches and desquamation. This type of poisoning can also be induced by ingestion of the livers of the sea whale, the polar bear and the seal. Since these animals contain an extremely large quantity of vitamin a in their livers and the symptoms of poisoning in the patients resembled those of patients with acute hypervitaminosis a, the poisoning was believed to have been caused by excessive vitamin a intake. We observed an episode of acute fish liver intoxication in which 3 man experienced dizziness, headache, blurred vision, nausea, vomiting, fever, and desquamation after ingesting the liver of the grouper fish Cephalopholis boenak (C. boenak). One of the patients had full-blown symptoms and presented with a high fever, headache, dizziness, generalized aching pain, and superficial vesicles and bullae of the skin. The treatment was mainly supportive. In the follow-up period, he subsequently developed hair loss and diffuse peeling of the skin on his palms and soles. Acute fish liver intoxication is rare, especially in subtropical regions. Symptomatologically, the clinical pictures of these patients were comparable to acute hypervitaminosis a or retinoid intoxication. The average vitamin a content in the grouper (C. boenak) is high enough to cause acute vitamin a intoxication. Moreover, ethanol may play a potentiating role in this type of event.- - - - - - - - - - ranking = 1.3333333333333keywords = intoxication (Clic here for more details about this article) |
8/132. Acute encephalopathy due to aluminum toxicity successfully treated by combined intravenous deferoxamine and hemodialysis.Acute aluminum intoxication is uncommon in clinical practice but can be fatal. This limited experience is reflected in the paucity of data assessing a viable approach to the treatment of these patients. In this report, the authors describe the clinical course and successful, pharmacokinetic-based deferoxamine-hemodialysis treatment regimen of a patient with severe aluminum encephalopathy following alum bladder irrigation. The combined use of deferoxamine and appropriately timed hemodialysis appears to be a very reasonable means of treating patients with severe acute aluminum intoxication.- - - - - - - - - - ranking = 0.33333333333333keywords = intoxication (Clic here for more details about this article) |
9/132. Cupric sulfate intoxication with rhabdomyolysis, treated with chelating agents and blood purification.We report a case of cupric sulfate intoxication complicated by hemolytic anemia, hepato-renal damage and acute rhabdomyolysis. The patient was successfully treated with dimercaprol, penicillamine, direct hemoperfusion and hemodiafiltration. We discuss the pathophysiology of cupric intoxication, and propose a treatment combined with chelating agents and blood purification.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
10/132. plasmapheresis in life-threatening verapamil intoxication.verapamil intoxications are life-threatening conditions with a far too often fatal outcome. In 2 patients, severe suicidal intoxication by 2.4 g and 9.6 g of verapamil orally resulted in life threatening hypotension and bradycardia with the need of heart-pacing and resuscitation. plasmapheresis was started within less then 4 hours after intoxication and seemed to reduce the verapamil plasma concentration to less then 40%. A dramatic improvement of cardiovascular stability was already observed during plasmapheresis. In-vitro plasmapheresis was performed to verify the effectiveness of the extracorporeal detoxification. verapamil was removed out of the blood by a clearance of 29.2 ml/min at blood flow of 200 ml/min.In conclusion, severe verapamil poisoning should be treated by early aggressive gut decontamination and an appropriate management of the haemodynamic complications. In case of lack of effectiveness for stabilisation, plasmapheresis can reduce verapamil related life threatening symptoms and bridge the time for the hepatic detoxification.- - - - - - - - - - ranking = 1.1666666666667keywords = intoxication (Clic here for more details about this article) |
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