Cases reported "Myoglobinuria"

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1/11. rhabdomyolysis and concomitant neurological lesions after intravenous heroin abuse.

    Seven cases of rhabdomyolysis in heroin addicts are presented. All patients showed concomitant neurological symptoms suggesting mononeuropathy, incomplete plexus lesions or myelopathy. In most cases rhabdomyolysis occurred without preceding trauma to the muscles (for example tissue compression or coma). Five patients had a history of recently resumed heroin abuse after prolonged abstinence. An allergic or toxic reaction to heroin or adulterants seems to be more likely than trauma in the pathogenesis of these complications. Severe rhabdomyolysis can occur without visible muscular swelling. Routine screening of creatine kinase is recommended in heroin addicts with neurological complications, as rhabdomyolysis may lead to fatal renal failure and may easily fail to be diagnosed.
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2/11. Hyperosmolal state associated with rhabdomyolysis.

    We report a case of nonketotic hyperosmolal state associated with rhabdomyolysis. None of the known predisposing factors for rhabdomyolysis, e.g. coma, potassium or phosphate depletion, were present in this patient. We propose that severe hyperosmolality per se may represent another predisposing factor for nontraumatic rhabdomyolysis.
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3/11. Exertional rhabdomyolysis associated with decerebrate posturing.

    A case is presented in which decerebrate posturing after a head injury led to rhabdomyolysis and renal failure. Exertional rhabdomyolysis is caused by an energy deficient state in overworked musculature that leads to a loss of integrity of the muscle cell. The resultant myoglobin in serum leads to acute renal failure. This condition should be suspected in a comatose patient with fever, brown discoloration of the urine, and edema of the extremities. Laboratory results will show orthotoluidine positive urine with a clear serum, elevated serum creatine phosphokinase, and serum creatinine elevation out of proportion to blood urea nitrogen. Management consists of fluids and diuretics with dialysis if necessary. rhabdomyolysis with head injury and decerebracy may occur more frequently than has been previously reported.
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4/11. rhabdomyolysis and acute renal failure.

    In order to determine the prevalence of rhabdomyolysis-associated acute renal failure (RM-ARF) and assess the effect of oliguria on biochemical features in this condition, 127 cases of ARF seen over 18 months were reviewed. Eleven cases of RM-ARF were seen, a prevalence of 8.6% of all cases of ARF. There were ten males and one female (age range 15-72 years) with precipitating events being trauma in three, coma in two, infection in two and other causes in five. Ten had concurrent clinical or historical evidence of dehydration, two had mild hypokalemia, and one abused alcohol. serum and urine myoglobin by radioimmunoassay were greater than 800 ng/l in all cases tested. False negative tests for urine myoglobin by o-tolidine reaction after (NH4)2SO4 extraction occurred in four cases. Despite attempted forced saline diuresis and urinary alkalinisation, seven became oliguric and required dialysis for 12-81 days. Initially (pre-dialysis) oliguric patients had significantly higher maximum serum levels of potassium, phosphate, and rate of rise of creatinine, significantly lower trough levels of calcium, and no significant difference in peak creatine phosphokinase or uric acid levels than non-oliguric patients. Two subjects developed recovery phase hypercalcemia, four required fasciotomy for compartment syndromes, three sustained permanent nerve damage, and three required limb amputation. Ten survived, with a mean creatinine clearance of 96 ml/min after nine to 30 months. RM-ARF is common, may be clinically occult and show false negative urine myoglobin tests. hyperkalemia, hyperphosphatemia, and hypocalcemia are more common in oliguric than in non-oliguric RM-ARF, but both have a good prognosis with appropriate medical and surgical management.
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5/11. Hyperthermia and rhabdomyolysis in self-poisoning with paracetamol and salicylates. Report of a case.

    A young women ingested large amounts of different analgesics, mainly salicylate and paracetamol. On admission about 17 hours later, clearly toxic serum levels of both drugs were demonstrated. She was comatose with respiratory failure for 5 days. During the first day there was a period of several hours of therapy-resistant hyperthermia. A severe bleeding tendency was probably related to profound coagulation defects. Persistingly elevated serum levels of ASAT and ALAT for two weeks were presumably caused by a toxic effect of paracetamol on the liver. When consciousness was regained, widespread pareses of skeletal muscles, predominantly of the lower limbs, were demonstrated. These were related to extensive rhabdomyolysis as evidenced by extremely elevated serums levels of CPK for 6 weeks, and by muscle necrosis in biopsy specimens. There was a gradual improvement, but walking disturbances were still present after one year. The hyperthermia was probably related to the cerebral effects of salicylates or the combination of multiple drugs. The rhabdomyolysis might be related to a deleterious effect of hyperthermia on the muscles or to an effect of paracetamol on the skeletal muscles similar to that which might occur in the myocardium, or to a combination of these mechanisms.
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6/11. myoglobinuria and renal failure after status epilepticus.

    Acute renal failure developed in a 28-year-old man after status epilepticus. myoglobinuria was contributed to by convulsions, trauma and coma during status epilepticus, the three mechanisms responsible for this condition.
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7/11. amoxapine-associated rhabdomyolysis and acute renal failure: case report.

    amoxapine, a new tricyclic antidepressant, has been recently released in the united states and europe. There has been limited experience with amoxapine overdose, and no serious reactions or sequelae were observed in the reported cases. A case of amoxapine overdose associated with rhabdomyolysis and acute renal failure is reported. amoxapine overdose could cause convulsions or prolonged coma leading to atraumatic rhabdomyolysis and myoglobinuric renal failure. Direct muscle or renal toxicity from this drug and its metabolites should not be excluded until evidence to the contrary is available. Acute renal failure should be looked for in cases of amoxapine overdose.
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8/11. rhabdomyolysis secondary to drug overdose and prolonged coma.

    Recent research has contributed to the understanding of nontraumatic rhabdomyolysis. In cases associated with coma, the pathophysiology is secondary to local pressure necrosis caused by compression from the patient's own body. The local pressure results in an edema-ischemia cycle concluding with compartmental tamponade and muscle breakdown. Myoglobin released by the damaged muscle indirectly induces the acute renal failure via its breakdown product, ferrihemate, which poisons renal tubular cells. uric acid nephropathy may also play a role. Radionuclide scanning has assumed a significant role as a diagnostic tool to determine the extent of soft tissue injury. Early volume expansion and administration of sodium bicarbonate and mannitol are recommended as prophylaxis against renal failure. Fasciotomy appears to have a role both in the prevention of limb damage and in the diminution of the systemic toxic effects produced by muscle breakdown.
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9/11. amoxapine overdose in a young man: a transient mitochondrial abnormality?

    amoxapine is a second-generation tricyclic antidepressant structurally related to the neuroleptic loxapine. It was previously marketed as an alternative to traditional tricyclic antidepressants because of alleged shorter onset of action and fewer cardiotoxic effects. However, various adverse reactions, including cardiac dysrhythmias, renal failure, coma, seizures, and neuroleptic malignant syndrome, were reported during therapy or after acute overdose. A 14-year-old boy ingested 1900 mg of amoxapine and developed seizures, hypertension, hyperpyrexia, altered mental status, myoglobinuria, renal failure, and transient magnetic resonance imaging (MRI) changes suggestive of hypertensive encephalopathy and neuroleptic malignant syndrome. Since mitochondrial disorders can cause multisystem failure, including encephalopathy, renal tubular dysfunction, and myopathy, a transient, toxic disorder of mitochondrial function was considered as the basis for the patient's clinical and MRI changes.
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10/11. Case report: severe hyponatremia after water intoxication: a potential cause of rhabdomyolysis.

    A 28-year-old woman, treated for schizophrenia, developed severe hypotonic hyponatremia (serum Na: 109 mEq/L) after several days of compulsive water drinking. The patient was admitted in a coma and required intensive supportive therapy. rhabdomyolysis quickly followed with high serum creatine phosphokinase levels and myoglobinuria. A high volume alkaline diuresis was initiated. Renal failure or compartment syndrome did not complicate the clinical picture. The mechanisms causing water intoxication and hyponatremia are discussed as are the possible pathogenetic explanations behind acute hyponatremia and rhabdomyolysis.
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