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

Thirty-one patients (26 males, 5 females) with mean age 35 +/- 19 years (range 8 to 85 years) were diagnosed as non-traumatic rhabdomyolysis by clinical findings and elevation of serum creatine kinase (CK) between January 1989 and December 1993. Causes, laboratory measures, clinical courses, and outcome were reviewed retrospectively. Drug abuse, seizure, and excessive activity are the most common etiologies for non-traumatic rhabdomyolysis. Twelve patients presented with muscular pain and seven patients with muscle weakness. Twenty eight patients had urinalysis and five of them (18%) had negative orthotolidine dipstick test. Only seven patients (25%) were detected positive orthotolidine test without microscopic hematuria. Patients with acute renal failure had higher levels of potassium and uric acid. The patients who developed acute renal failure after admission had significantly higher levels of uric acid. The peak levels of CK did not correlate with development of acute renal failure. There was no episode of hyercalcemia. Seventeen patients (55%) had acute renal failure. Hemodialysis was required in nine cases. All survivors recovered with normal renal function except one who needed maintenance hemodialysis after two months follow-up. Two patients died of multi-organ failure and sepsis.
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PMID:Non-traumatic rhabdomyolysis and acute renal failure. 893 69

The clinical course as well as the effects of the treatment in 27 children suffering from IgA nephropathy were followed in this study. The observation period lasted from 1.5 to 15.5 years, mean 9.1. The clinical picture according to changes in urine was the criterion of classification into 4 groups, and was related to the WHO classification of pathomorphological types. Hypertension as well as acute renal failure were observed in each clinical group except the group of children with erythrocyturia and/or haematuria. Depending on the pathomorphological changes in kidneys, different groups of drugs were used, e.g. anticoagulants, corticosteroids and also alkylating agents. In 9 children no treatment was prescribed. Only 6 children showed regression of urine changes: 2 of them with steroid-sensitive nephrotic syndrome and 1 with steroid-resistant nephrotic syndrome. In 12 children, erythrocyturia and proteinuria decreased and the intervals between successive seizures of haematuria became longer. In 3 of 8 children with nephrotic syndrome, chronic renal failure as well as end-stage renal disease were observed. In 2 of them hypertension was present during the entire observation period and it was difficult to achieve control using hypotensive drugs. In the remaining 2 children, regression of nephrotic syndrome was found, but slight proteinuria and hypertension are observed.
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PMID:[Clinical course and treatment results of IgA nephropathy in children]. 897 18

A 24 years old woman with sclerosis multiplex was admitted to our hospital after generalized seizures. In the first days of observation occurred symptoms of acute renal failure and liver damage with hemolysis. The differential diagnosis allowed us to recognize acute renal failure in the course of rhabdomyolysis. After a few hemodialysis normal renal function was achieved.
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PMID:[Acute renal failure in the course of rhabdomyolysis after status epilepticus]. 927 35

A case of acute renal failure due to rhabdomyolysis in a patient who used cocaine on a daily basis is presented. In contrast to many prior reports of renal failure occurring with cocaine-associated rhabdomyolysis, our patient did not use intravenous cocaine and did not have any evidence of trauma, seizure, hypotension, hyperthermia, hyperactivity, or coma. His creatine phosphokinase peaked at 448,000 U/liter. He was treated initially with forced diuresis and i.v. furosemide, but he became oliguric, developed pulmonary edema, and required hemodialysis. He recovered fully after 3 weeks of dialysis. The literature is reviewed in an attempt to delineate a rational approach to evaluating cocaine users at risk for rhabdomyolysis.
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PMID:Severe rhabdomyolysis with renal failure after intranasal cocaine use. 940 1

To explore the natural history of critically ill patients with acute renal failure due to acute tubular necrosis, we evaluated 256 patients enrolled in the placebo arm of a randomized clinical trial. Death and the composite outcome, death or the provision of dialysis, were determined with follow-up to 60 d. The relative risks (RR) and 95% confidence intervals (95% CI) associated with routinely available demographic, clinical, and laboratory variables were estimated using proportional hazards regression. Ninety-three (36%) deaths were documented; an additional 52 (20%) patients who survived received dialysis. Predictors of mortality included male gender (RR, 2.01; 95% CI, 1.21 to 3.36), oliguria (RR, 2.25; 95% CI, 1.43 to 3.55), mechanical ventilation (RR, 1.86; 95% CI, 1.18 to 2.93), acute myocardial infarction (RR, 3.14; 95% CI, 1.85 to 5.31), acute stroke or seizure (RR, 3.08; 95% CI, 1.56 to 6.06), chronic immunosuppression (RR, 2.37; 95% CI, 1.16 to 4.88), hyperbilirubinemia (RR, 1.06; 95% CI, 1.03 to 1.08 per 1 mg/dl increase in total bilirubin) and metabolic acidosis (RR, 0.95; 95% CI, 0.90 to 0.99 per 1 mEq/L increase in serum bicarbonate concentration). Predictors of death or the provision of dialysis were oliguria (RR, 5.95; 95% CI, 3.96 to 8.95), mechanical ventilation (RR, 1.53; 95% CI, 1.07 to 2.21), acute myocardial infarction (RR, 1.95; 95% CI, 1.24 to 3.07), arrhythmia (RR, 1.51; 95% CI, 1.04 to 2.19), and hypoalbuminemia (RR, 0.56; 95% CI, 0.42 to 0.74 per 1 g/dl increase in serum albumin concentration). Neither mortality nor the provision of dialysis was related to patient age. These observations can be used to estimate risk early in the course of acute tubular necrosis. Furthermore, these and related models may be used to adjust for case-mix variation in quality improvement efforts, and to objectively stratify patients in future intervention trials aimed at favorably altering the course of hospital-acquired acute renal failure.
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PMID:Predictors of mortality and the provision of dialysis in patients with acute tubular necrosis. The Auriculin Anaritide Acute Renal Failure Study Group. 955 72

Acute renal failure, disseminated intravascular coagulation, ARDS, hypoglycaemia, coma or epileptic seizures are manifestations of severe Plasmodium falciparum malaria. On the other hand, vivax malaria or benign tertian malaria is usually free from complications. In the present report we describe a case of acute tertian malaria with a severe and complicated course. In this situation bacterial coinfection should always be suspected and treated empirically with broad-spectrum antibiotics, until the results of cultures are available. Mixed plasmodial infection (P. vivax and P. falciparum) must be excluded by repeated and meticulous examination of blood smears. Newer techniques such as PCR processing or ParaSight F Test are mentioned.
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PMID:[ARDS in plasmodium vivax malaria]. 969 37

Rhabdomyolysis is a condition affecting body homeostasis that results from impaired supply of muscles with energy, nutritional factors and blood. Complex pathophysiological mechanism causes that extended myolysis may complicate different clinical conditions, such as: crush syndrome, excessive physical effort (work, seizures), toxic effect of drugs and toxins, water-electrolyte disturbances, congenital enzymatic deficiencies etc. It seems that on the cellular level, essential role is played by excessively high intracytoplasmatic calcium level, which affects metabolic processes. So high calcium level is a consequence of muscular cell injury irrespective to its reason. It manifests clinically as muscular weakness, pal and oedema and laboratory tests reveal elevated CK, GOT, GPT, aldolase and LDH levels as well as dark brown urine colour. Demonstration of elevated serum myoglobin level or its presence in urine directly confirms development of rhabdomyolysis. In unfavorable conditions, rhabdomyolysis may result in acute renal failure. Appropriately early and adequate water supply and alkalization plays an essential role in prevention of impairment in renal function. In advanced phase of renal failure, hemodialysis is a standard treatment.
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PMID:[Rhabdomyolysis: clinical features, causes, complications and treatment]. 974 Nov 96

Rhabdomyolysis results from muscular fibre lysis with release of cellular contents (myoglobin, enzymes, electrolytes) into the plasma. Traumatic (crush syndrome) and non-traumatic rhabdomyolysis have been mostly reported in adults. Traumatic rhabdomyolysis are mostly due to ischemic and reperfusion injuries. Non-traumatic rhabdomyolysis include several factors: muscular compression (comas), cytotoxic injury (infections and poisonings), ischemia (shock, cardiorespiratory arrest) or excessive muscular activity (seizures, strenuous exercise). The main etiologies reported in children are: anoxic-ischemic encephalopathy (including sudden infant death and life threatening events); electrolyte disorders; severe hyperthermia; poisonings; hereditary myopathies. Non-traumatic rhabdomyolysis must be suspected in these circumstances, requiring blood creatinine phosphokinase measurements. Indeed, clinical signs are inconstant and non-specific, and functional signs are difficult to appreciate in children. During the initial phase, the main risk is arrhythmias secondary to hyperkalemia. The two main complications are the compartmental syndrome leading to irreversible vasculo-nervous injuries and acute renal failure. Treatment of traumatic and non-traumatic rhabdomyolysis includes correction of hyperkalemia, active fluid loading in order to prevent acute renal failure and alkalinisation. Prognosis of rhabdomyolysis relates to the aetiology and the presence of acute renal failure.
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PMID:[Acute rhabdomyolysis in the child]. 975 96

Six patients with severe and complicated falciparum malaria (6.7 +/- 2.7 WHO criteria) were admitted to our Intensive Care Unit. All patients acquired the disease while travelling in tropical Africa without appropriate chemoprophylaxis. The clinical manifestations included hyperpyrexia (all patients), chills (4), sweating (2), asthenia (3), anorexia (2), headache (1), arthralgias (1), vomiting (4), diarrhoea or abdominal discomfort (3), jaundice (2) and disturbances of consciousness (4). All patients had anemia, thrombocytopenia, hyponatremia, hypoproteinemia, hypoalbuminemia, hypocalcemia and acute renal failure, in one case associated with anuria. A low grade parasitemia was observed in two patients and a high grade parasitemia (20%-58% of erythrocytes) in four. Exchange transfusion was performed only in high parasitemic patients and all of them survived. All patients were treated with quinine, a sulfonamide and pyrimethamine. Additionally, five patients received oxytetracycline, doxycycline or clindamycin. Three patients required hemodyalisis. Five patients had delirium, coma or seizures. All patients had at least one sign of hepatic impairment: liver enlargement, jaundice or increased bilirubin or aminotransferase levels. Two patients had spleen enlargement. Laboratory findings suggested disseminated intravascular coagulation in four patients. Four patients developed pulmonary changes and three of them required mechanical ventilation. A Swan-Ganz catheter was placed in four patients. In three of them (two with pulmonary edema) the pulmonary capillary wedge pressure was initially increased, which suggested a cardiogenic or hypervolemia mechanism, but soon returned to normal level. One patient with low grade parasitemia died because of adult respiratory distress syndrome after 18 days. In our series, the degree of parasitemia was not related to the severity of the disease.
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PMID:[Severe and complicated malaria. Report of six cases]. 977 80

Falciparum malaria remains a major killer in developing countries, particularly for African children. The sequestration of parasitized erythrocytes in the deep microvasculature is mostly mediated by their cytoadherence to activated endothelium. Proinflammatory cytokines and particularly tumor necrosis factor contribute to severe disease but the pathophysiology of coma remains poorly understood. In young children, features of severe malaria include severe anemia, hypoglycemia and cerebral malaria. Half of the children with neurological impairment actually have raised intracranial pressure, and seizures are extremely common. Clinical respiratory distress usually reflects severe lactic acidosis. In non immune adults, pictures of severe sepsis with shock, acute renal failure and respiratory distress syndrome are common and often associated with bacterial coinfection. Although chemotherapy of malaria is challenged by the continuing evolution of antimalarial resistance, quinine remains the first-line drug for severe disease. The optimization of symptomatic management of severe malaria remains a major concern in developing countries.
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PMID:[Severe malaria]. 978 Oct 74


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