Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 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

Disseminated intravascular coagulation is here reported as a complication of status epilepticus. Other features of this case were rhabdomyolysis, hyperthermia, myoglobinuria and renal failure.
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PMID:Disseminated intravascular coagulation in status epilepticus. 57 96

Hyperosmolality complicating the management of burned patients has multiple etiologies. Sepsis, hyperglycemia, renal failure, electrolyte disturbances, shock, and substances absorbed from the burn wound may be contributing factors. Chemicals, such as propylene glycol, within bacteriostatic topicals may also lead to hyperosmolality. This report describes a patient who developed severe hyperosmolality after 5% Betadine-glycerin therapy for a 60% partial-thickness burn. Status epilepticus developed 36 hours later, and triglycerides were 9,700 mg/dl. After Betadine-glycerin was stopped the central nervous system status slowly improved but pre-seizure function was never regained.
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PMID:Hyperosmolality caused by percutaneously absorbed glycerin in a burned patient. 706 13

A large family with medullary cystic disease is described to show that juvenile nephronophthisis and medullary cystic disease should not be differentiated by age of onset and type of inheritance. The age at diagnosis of six family members with medullary cystic disease ranged from 4-32 years, and age at death from renal failure or commencement of dialysis from 7-48 years. A mother of two children with renal failure in early childhood has histological evidence of medullary cystic disease with normal renal function. We suggest that juvenile nephronophthisis and medullary cystic disease are the same conditions and that the disease be classified as medullary cystic disease, autosomal dominant or recessive form. When undertaking genetic counselling in the parents of children with medullary cystic disease, we suggest that renal biopsy may need to be considered even if their renal function is normal. Three patients presented with gout, and the possibility of an association with medullary cystic disease should be considered when more than one member of a family develops gout. Two patients died of status epilepticus, and epilepsy is probably an added association of medullary cystic disease.
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PMID:Juvenile nephronophthisis and medullary cystic disease--the same disease (report of a large family with medullary cystic disease associated with gout and epilepsy). 711 1

Status epilepticus can lead to impaired renal function, which has been attributed to complications of myoglobinuria. We confirmed changes in renal function in the absence of myoglobinuria by measuring renal hemodynamics, fluid and electrolyte excretions, and plasma levels of renin and atrial natriuretic peptide (ANP) before and after a 30-min period of recurrent generalized seizures in anesthetized, paralyzed rats. Renal plasma flow (RPF), renal blood flow (RBF) and glomerular filtration rate (GFR) decreased by approximately 60% after seizures. In contrast, urinary sodium excretion, urine flow, and plasma ANP levels increased approximately threefold. Urinary potassium excretion and plasma renin levels were unchanged. Renal function is profoundly altered after 30 min of seizures, primarily due to intense renal vasoconstriction precipitating a dramatic reduction in GFR. The concomitant increases in sodium and urine excretion may be mediated by the marked increase in plasma ANP levels. The decreases in GFR and RBF might contribute to the renal failure observed in some patients after status epilepticus.
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PMID:Recurrent seizures alter renal function and plasma atrial natriuretic peptide levels in rats. 755 80

A 38-year-old man with chronic low back pain underwent myelography and was inadvertently injected with ionic contrast medium. Within minutes, he started complaining of muscle spasms in his lower extremities, followed by respiratory distress and myoclonus. Immediate intravenous treatment with fluids, antihistamines, and supplemental oxygen was started. Within 1 hour after the myelogram, he was intubated and paralyzed with a neuromuscular blocking agent. Shortly thereafter, he began receiving triple anticonvulsant therapy and a lumbar drain was inserted to allow for the evacuation of cerebrospinal fluid. Electroencephalographic monitoring, which initially showed that the patient was in status epilepticus, subsequently showed no more episodes of seizure activity. Massive rhabdomyolysis, renal failure, and metabolic derangement were prevented. He was then extubated and regained full consciousness. He was discharged on the 13th day of hospitalization with mild amnesia and some cognitive dysfunction. A review of the literature reveals descriptions of 9 of 15 patients who survived similar episodes. We conclude that prompt identification of the contrast medium error and prompt intervention are crucial to increase significantly the chances of survival. Elective paralysis, anticonvulsant therapy, and cerebrospinal fluid drainage are the recommended modes of treatment.
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PMID:Inadvertent use of ionic contrast material in myelography: case report and management guidelines. 773 26

A 23-year-old Japanese man presented with status epilepticus unresponsive to medication, respiratory failure, rhabdomyolysis, myoglobinuria, and irreversible renal failure. Muscle biopsy revealed type 1 fiber atrophy and an increased type 2C fibers (7%). His carnitine palmitoyltransferase (CPT) I and II activities were 0.06 and 0.12 nmol/min/mg protein, as compared with a mean value of 0.22 +/- 0.14 and 0.27 +/- 0.07 nmol/min/mg protein, respectively, in control subjects. This appears to be the first report of this disorder presenting as status epilepticus. Metabolic encephalopathy due to CPT deficiency may have presented as status epilepticus. Seizures in the present case may have resulted from the functional disorder of brain due to CPT deficiency.
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PMID:Atypical presentation of carnitine palmitoyltransferase (CPT) deficiency as status epilepticus. 775 48

Seizures are a recognized complication of human immunodeficiency virus (HIV)-type-1 infection. CNS disease processes in these patients include encephalitis, focal brain lesions, and meningitis. Metabolic causes of seizures have received little attention. In a retrospective study, we selected 68 HIV-seropositive patients with new-onset seizures and information available for specified metabolic factors on the day of the first seizure. We sought an association of metabolic abnormalities with convulsive status epilepticus (CSE), which was the initial seizure in 12 patients, predominantly intravenous (i.v.) drug users. HIV-seropositive patients with new-onset seizures and hypomagnesemia or renal failure appeared to be at increased risk for CSE. All HIV-seropositive patients with new-onset seizures should undergo metabolic screening including renal function and serum magnesium levels.
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PMID:Metabolic abnormalities and new-onset seizures in human immunodeficiency virus-seropositive patients. 782 Dec 71

A five month-old infant presented with gastro-intestinal symptoms followed by a multiple organ failure with: shock, status epilepticus, disseminated intravascular coagulation, hepatic and renal failure. The infant survived with major neurological sequelae. The diagnosis and the actuality of the so-called "hemorrhagic shock and encephalopathy syndrome" are discussed.
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PMID:[Hemorrhagic shock with encephalopathy syndrome or major hyperthermia syndrome?]. 805 39

BACKGROUND--Acute dehydration with hypochloronatremic metabolic alkalosis is a classical complication of cystic fibrosis of the pancreas. Its progressive development as a revealing manifestation of the disease is rare as is its appearance in newborns. Case n. 1.--A 13 month-old girl was admitted because of status epilepticus. She was severely dehydrated (20% weight loss) but had normal diuresis. Investigations showed metabolic alkalosis, hypochloronatremia and hypokalemia. All the manifestations disappeared within 5 days with treatment but three sweat tests were abnormal. Case n. 2.--A 7 month-old girl was admitted because she suffered from progressive loss of weight (10%); she was dehydrated and had metabolic alkalosis plus hypochloronatremia, but her diuresis was normal. Two sweat tests were abnormal. Case n. 3.--A 4.5 month-old boy was admitted because he suffered from severe (12%) weight loss. His diuresis was normal despite dehydration; metabolic alkalosis and hypochloronatremia were found. Two subsequent sweat tests were abnormal. Case n. 4.--A 3 day-old girl was admitted suffering from meconium ileus. Two initial mechanism analysis for protein were abnormal. She had a cardiorespiratory arrest on the 13th day of life, when she had lost 14% of her birth weight; investigations showed metabolic alkalosis, hyponatremia (83 mEq/l), hypochloremia (45 mEq/l); kalemia was 5.9 mEq/l. Peritoneal dialysis was needed to correct hydroelectrolytic changes. A sweat test performed on the 26th day of life was also abnormal. Investigations performed during the periods of dehydration, and repeated later, showed transient functional kidney failure. None of the four patients had any respiratory or gastrointestinal clinical manifestations of cystic fibrosis. CONCLUSION--Metabolic alkalosis with hypochloronatremia plus progressive, severe dehydration in infants whose diuresis is paradoxically normal must be followed by examination for cystic fibrosis.
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PMID:[Cystic fibrosis revealed by dehydration with hypochloronatremic alkalosis in 3 infants and a neonate]. 808 18


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