Cases reported "Rhabdomyolysis"

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1/44. Fatal multi-organ failure after suicidal overdose with MDMA, 'ecstasy': case report and review of the literature.

    A 53-year-old prisoner died of multiorgan failure after a suicidal overdose with 3,4-methylenedeoxymethamphetamine (MDMA, 'Ecstasy'). Twelve hours after ingestion of MDMA, the patient became severely hyperthermic (107.2 degrees F) with evidence of rhabdomyolysis. He subsequently developed acute respiratory distress syndrome (ARDS), disseminated intravascular coagulopathy (DIC) and acute renal failure. At autopsy, plasma concentration of MDMA was 3.05 mg/L. This case shows that MDMA is still abused in our community and clinicians should know the symptoms of MDMA intoxication. In particular, MDMA should be considered when patients have symptoms or signs of increased sympathetic activity. The pathophysiology and treatment of MDMA-induced hyperthermia are discussed.
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2/44. hyponatremia-associated rhabdomyolysis.

    BACKGROUND: hyponatremia is the most frequent electrolyte disorder. However, hyponatremia rarely results from excessive water intake, unless the kidney is unable to excrete free water, such as in patients on thiazide diuretics; in addition, hyponatremia is an uncommon cause of rhabdomyolysis. methods: We present a 51-year-old hypertensive woman on chronic hydrochlorothiazide therapy who developed acute water intoxication and severe myalgias. RESULTS: The patient developed acute hypotonic hyponatremia and subsequent rhabdomyolysis. We discuss the mechanisms responsible for the development of hyponatremia and its association with rhabdomyolysis. CONCLUSION: Muscle enzymes should be monitored in patients with acute hyponatremia who develop muscle pain, and hyponatremia-induced rhabdomyolysis must be considered in patients with myalgias receiving thiazide diuretics.
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3/44. Acute cocaine intoxication in a smuggler. One case report and a review of the literature.

    The smuggling of cocaine into many countries by ingestion of wrapped cocaine packets and gastro-intestinal concealment is a common and well-recognized practice. This is a report of the case of a smuggler carrying 14 ingested packets of cocaine and who presented an acute intoxication with a rare complication, rhabdomyolysis, which were managed medically and the packets removed surgically. A discussion and a review of the literature are undertaken.
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4/44. Severe rhabdomyolysis following massive ingestion of oolong tea: caffeine intoxication with coexisting hyponatremia.

    A 36-y-o patient with schizophrenia, who had consumed gradually increasing quantities of oolong tea that eventually reached 15 L each day, became delirious and was admitted to a psychiatric hospital. After abstinence from oolong tea his delirium resolved. He was transferred to our hospital when he was discovered to have acute renal failure with hyponatremia (118 mEq/L) and severe rhabdomyolysis (creatine phosphokinase, 227,200 IU/L). On admission rhabdomyolysis had begun to improve despite a worsening of the hyponatremia (113 mEq/L). With aggressive supportive therapy, including hypertonic saline administration and hemodialysis, the patient fully recovered without detectable sequelae. The clinical course suggests that caffeine, which is present in oolong tea, was mainly responsible for the rhabdomyolysis as well as the delirium, although severe hyponatremia has been reported to cause rhabdomyolysis on rare occasions. We hypothesize that caffeine toxicity injured the muscle cells, which were fragile due to the potassium depletion induced by the coexisting hyponatremia, to result in unusually severe rhabdomyolysis. The possibility of severe rhabdomyolysis should be considered in a patient with water intoxication due to massive ingestion of caffeine-containing beverages.
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5/44. 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.
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6/44. Severe fenitrothion poisoning complicated by rhabdomyolysis in psychiatric patient.

    Non-traumatic rhabdomyolysis associated with organophosphate intoxication has not been generally reported. We report here in a severe case of fenitrothion poisoning complicated by rhabdomyolysis. A 43-year-old woman ingested approximately 100 ml of fenitrothion emulsion (50%) in an attempt to commit suicide. On day 3 after admission, her creatine phosphokinase (CPK) peaked at 47,762 IU/L. She received supportive treatment included sodium bicarbonate and fluid resuscitation. However, muscarinic symptoms including excessive miosis and salivation developed on day 5 when her CPK levels decreased. The delay in cholinergic symptoms might have been due to the trihexyphenidyl she took with the antipsychotic drugs. Fortunately, the present patient recovered from the acute cholinergic crisis, and acute renal failure was prevented by early diagnosis. This is a case of organophosphate poisoning complicated by rhabdomyolysis in a psychiatric patient. The masking of acute cholinergic symptoms should be taken into consideration in such patients.
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7/44. Fatal rhabdomyolysis after acute sodium monensin (Rumensin) toxicity: case report.

    myoglobinuria or rhabdomyolysis occurs when myoglobin escapes into the blood and then into the urine after acute muscle necrosis. It can be a serious medical condition leading to renal failure and death. There are many causes including exertion, crush syndromes, ischaemia, metabolic disorders, exogenous toxins and drugs, heat stroke and hereditary disorders such as malignant hyperthermia. We report the case of a 17 year-old boy who developed myoglobinuria, renal failure and death 11 days after ingesting sodium monensin, possibly with the intention of developing muscles. Sodium monensin, the active principle of Rumensin(R), is a dietary additive used as a growth promoter for confined cattle. There are no previous reports of human intoxication. Accidental or experimental sodium monensin intoxication in animals produces similar findings to those seen in this case.
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8/44. rhabdomyolysis, acute renal failure, and death after monensin ingestion.

    We report a case of human monensin intoxication; to our knowledge, this is the first reported case in the medical literature. The patient took a dose of monensin three times higher than a dose considered lethal for cattle and developed a clinical picture similar to that reported in veterinary medicine. There was an early and extremely severe rhabdomyolysis followed by acute renal failure, heart failure, and death. The main changes observed at autopsy were extensive skeletal muscle necrosis, complement deposition at the myocardial level, pulmonary edema, and acute tubular damage.
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9/44. subarachnoid hemorrhage and rhabdomyolysis induced acute renal failure complicating organophosphate intoxication.

    Organophosphate is extremely uncommon cause of rhabdomyolysis. This article describe two cases with rhabdomyolysis induced acute renal failure complicating by monocrotophos, an organophosphate compound. First patient had rhabdomyolysis induced acute renal failure and subarachnoid hemorrhage. This is the first reported case of subarachnoid hemorrhage, which may be related with organophosphate intoxication in literature. Second patient described here had rhabdomyolysis induced acute renal failure after organophosphate overdose.
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keywords = intoxication
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10/44. The application of immunohistochemical findings in the diagnosis in methamphetamine-related death-two forensic autopsy cases-.

    Forensic autopsy cases detecting methamphetamine (MA) are usually diagnosed according to its toxicological concentration. It has been reported that the lethal blood concentration of MA is 4.48 microg/ml (3.0 micromol/dl). We autopsied two MA-detected cadavers, and immunohistochemical staining was performed on the skeletal muscle with an anti-myoglobin antibody, and on the kidney with an anti-the 70 kDa heat shock protein (HSP70) antibody. One case showed a high rectal temperature (40 degrees C). The toxicological examination revealed 0.75 microg/ml of MA in the blood, and 16.8 microg/ml in the urine. Myoglobin was negative and HSP70 was positive in the kidney immunohistochemically. From the toxicological and immunohistochemical findings, it was considered that the subject died of hyperthermia and acidosis caused by muscular hyperactivity. In another case, the autopsy revealed highly congested lungs, with dark-red bloody fluid and foam in the trachea and bronchus. MA (17.0 microg/ml) was detected in the blood. HSP70 was negative and myoglobin was positive immunohistochemically. It was thought that the subject died of acute MA intoxication based on the high MA concentration, although rhabdomyolysis was suspected. It is suggested that myoglobin and HSP70 immunostaining are useful to diagnose MA poisoning.
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