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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven patients admitted to hospital during or immediately after status epilepticus or recurrent episodes of grand-mal seizures had very high concentrations of uric acid in their blood at a time when the blood-urea was normal in five of them. The blood-lactic-acid was high in the five patients in whom it was measured. All of the patients developed reversible renal failure, and two required haemodialysis. The blood-uric-acid should be measured in patients who have had prolonged seizures, and the measures which might be taken in hyperuricaemic patients to prevent the development of acute renal failure include rehydration, alkalinisation of urine, and, where alkalinisation is impossible, haemodialysis.
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PMID:Hyperuricaemic acute renal failure after epileptic seizures. 5 Nov 91

A 35-year-old man ingested food contaminated with lindane, an insecticide containing almost pure gamma hexachlorocyclohexane. Grand mal seizures and severe acidemia developed rapidly. The seizures recurred for nearly 2 hours, then ceased. In addition, the patient had muscle weakness and pain, headaches, episodic hypertension, myoglobinuria, acute renal failure and anemia. Pancreatitis developed 13 days after the ingestion of lindane. A muscle biopsy on the 15th day of illness demonstrated widespread necrosis and regeneration of muscle fibres. The patient's condition improved and he was discharged 24 days after the onset of his illness. During the year following the poisoning the patient noted difficulty with recent memory, loss of libido and easy fatigability. One year after lindane ingestion the results of physical examination, including those for muscle power and bulk, were normal.
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PMID:Acute lindane poisoning with development of muscle necrosis. 7 42

Acute renal failure secondary to interstitial nephritis caused by therapeutic ingestion of sodium diphenylhydantoins has been reported recently. The interference of sodium diphenylhydantoins on Vitamin D metabolism causing or aggravating ricketts has also been reported. This communication deals with an infant girl who was admitted to the hospital due to seizures. Four months before, she had convulsions and she was treated with diphenylhydantoins until admission. She was found to have renal failure and ricketts. Histological diagnosis of interstitial nephritis was established by means of percutaneous renal biopsy. Clinical and radiological improvement of ricketts was observed after dehydrotachysterol treatment. Clinical and biochemical alterations of renal failure slowly subsided. She had a clear-cut history of vitamin D defficiency ricketts. Seizures were due to hypocalcemia tetany but was erroneusly treated as "grand mal" epilepsy, with diphenylhydantoins. Interstitial nephritis complicated with acute renal failure was probably caused by diphenylhydantoins administration.
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PMID:[Renal failure and rickets]. 46 92

Our patient was severely injured, and had a prolonged period of hypotension. After operation she received moderate doses of cefazolin, intravenously, in the face of acute renal failure. Seizures associated with a serum cefazolin level of 455 mg/ml were observed. Although a cause and effect relationship between high cefazolin levels and neurotoxicity cannot be proven conclusively, the implication of this relationship exists. The clinician should be aware of the potential neurotoxicity of this commonly used drug. The importance of adjusting the dose in patients with renal failure is re-emphasized.
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PMID:Convulsions associated with sodium cefazolin: a case report. 86 36

We present three cases of fatal hepatic necrosis in patients with epilepsy taking anticonvulsants, in which the terminal illness presented as an unusually severe generalized tonic-clonic seizure with failure to regain consciousness. In two cases acute renal failure also occurred. It is not certain to what extent drug therapy, physiological and metabolic changes consequent on prolonged seizures, hitherto undiscovered infective agents, or a combination of any of these may play in such a process. We suggest, however, that the case against the drugs alone has yet to be proved.
Seizure 1992 Jun
PMID:Fatal liver failure following generalized tonic-clonic seizures. 134 32

The primary dose-limiting adverse effects associated with foscarnet treatment of cytomegalovirus retinitis in patients with AIDS are renal impairment and ionized hypocalcemia. Dose-limiting renal impairment, consisting of significant alterations in serum creatinine levels or creatinine clearance or acute renal failure, has been observed in 10-20% of AIDS patients receiving foscarnet via intermittent i.v. infusion. Nephrotoxicity can be minimized by adjusting dosage according to creatinine clearance and by ensuring that adequate hydration is provided throughout foscarnet therapy. Transient decreases in serum or plasma ionized calcium levels appear to occur in all patients during foscarnet infusion, with these decreases being observed in the absence of changes in total calcium levels. Hypocalcemia produces mild symptoms in some patients and may play a role in unexplained cases of arrhythmia or seizure. Careful attention should be given to levels of total calcium and other minerals during foscarnet treatment, and the occurrence of symptomatic hypocalcemia should prompt evaluation of ionized calcium concentrations and foscarnet dose reduction. Another potentially treatment-limiting effect attributed to foscarnet is penile ulceration, which appears to result from exposure of the glans penis to unchanged foscarnet in the urine.
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PMID:Review of the toxicities of foscarnet. 153 39

A morbidly obese woman [190 kg total bodyweight (TBW)] was admitted to hospital with a rapidly progressing wound infection. Over the next 2 weeks the patient developed congestive heart failure, acute renal failure, septic shock and multiple seizure episodes. Intravenous phenobarbital was added to phenytoin therapy to achieve seizure control. A total loading dose of phenobarbital 3700 mg (19.5 mg/kg TBW) was administered in 3 divided doses. The initial dose of 1100 mg resulted in a serum phenobarbital concentration of 6.3 mg/L 5h postinfusion, a second 1100 mg dose increased the concentration to 13.1 mg/L 1h postinfusion and a final dose of 1500 mg resulted in a 22.5 mg/L concentration at the end of the infusion. A phenobarbital maintenance regimen of 120 mg every 12h was then started. Peak serum concentrations of 19.8 and 17.8 mg/L were measured. All of the available serum phenobarbital concentrations and dosage amounts were fitted with least-squares nonlinear regression analysis to a 1-compartment model. An apparent volume of distribution (Vd) of 154.9L (0.82 L/kg TBW), total body clearance (CL) of 29 ml/min (1.74 L/h) and elimination half-life of 61h were determined. Our case report suggests that the dose of intravenous phenobarbital should be calculated using TBW. Additional studies are needed to precisely define the appropriate dosage weight, serum concentrations and clinical efficacy associated with intravenous phenobarbital in morbidly obese patients.
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PMID:Phenobarbital pharmacokinetics in obesity. A case report. 158 59

Hypovolemic hyponatremia attributable to severe fluid and electrolyte alterations was diagnosed in a foal with diarrhea. Subsequent consumption of water resulted in rapid reduction of serum sodium concentration and serum osmolar depression. Clinical signs of neurologic disease developed including blindness, loss of menace response, and seizures. Treatment of this condition with IV administered fluids included hypertonic saline solution (7.2%; 2 ml/kg of body weight), and frequent monitoring of serum electrolyte concentrations and osmolality resulted in gradual correction of the fluid and electrolyte imbalance and resolution of the neurologic signs. Hyponatremia has been recognized in foals with renal failure, ruptured urinary bladder, and iatrogenic water overload. The key to diagnosis and management of profound hyponatremia is accurate diagnosis of the status of plasma volume and association of the electrolyte imbalance with clinical signs of neurologic disease. This report describes an unusual complication of a commonly encountered problem in equine practice and documents that the severe metabolic and electrolyte abnormalities associated with diarrhea can result in clinical neurologic disease. The differential diagnosis also should include bacterial sepsis, parasitism, thoracic mass, acute renal failure, congenital neurologic deficit, or seizure syndrome. Serum electrolyte disorders should be considered as a potential cause of signs of neurologic disease in foals with diarrhea.
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PMID:Hypovolemic hyponatremia and signs of neurologic disease associated with diarrhea in a foal. 160 18

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

Cocaine abuse is associated with a constellation of serious medical complications. An unrecognized and recently described complication of cocaine use is rhabdomyolysis with acute renal failure. We describe the first patient identified in our institution with this entity, admitted to the medical services with oliguric acute renal failure. Three days prior to admission the patient had a cocaine snorting binge. He presented with bilateral flank pain, gross hematuria, vomiting and chills. No history of crush injury, prolonged immobilization and or seizures was reported. On admission the vital signs were normal, physical exam revealed periorbital edema and marked soft tissue neck swelling. Lab values: Bun 120 mgs%, Creat. 10.7 mgs%, Na 132 meq/lt, Co2 13mq/lt, Cl, 103meq/lt, Co2 13meq/lt, Ca 5.3 mgs%, CPK 30,800 U/L with a MM fraction of 98%, LDH 600 U/L, SGOT 300 U/L. The urine was dark red with a ph of 6.5 and 100 rbc/hpf. The anti-GBM antibody and blood cultures were negative. An abdominal sonogram was normal. He received peritoneal dialysis and was discharged on his 14th hospital day with a CPK of 2,800 U/L and decreasing azotemia. Cocaine associated rhabdomyolysis has only been recently described in the literature (AJM April, 88). Acute myoglobinuric renal failure needs to be added to the growing list of medical complications of cocaine use.
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PMID:Cocaine and rhabdomyolysis: report of a case and review of the literature. 207 48


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