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

A retrospective review of all cases of eclampsia diagnosed at 3 obstetric teaching hospitals in Melbourne from January, 1978 to December, 1992 was undertaken. Ninety cases were identified; there were 5 maternal deaths and 17 perinatal deaths. Severe maternal morbidity such as pulmonary oedema, acute renal failure or HELLP syndrome was found in 26%. Significant maternal thrombocytopenia (< 100 x 10(9)/L) was found in 50% and 35% had abnormal maternal liver function tests. Forty six women received magnesium sulphate for treatment of eclampsia and of these 3 had further seizures compared to 4 of 18 who received phenytoin (odds ratio 0.24 (0.04-1.52) X2, p = 0.09). Eclampsia remains a significant complication of pregnancy with high maternal and perinatal mortality and morbidity. Results of this study show a trend that is in agreement with recent randomized controlled trials which demonstrate a reduced incidence of seizures and maternal and fetal complications with the use of magnesium sulphate. The results of these recent trials suggest that magnesium sulphate should be the drug of choice in the prevention and treatment of eclampsia.
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PMID:A review of eclampsia in Melbourne: 1978-1992. 888 47

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

Recovery from prolonged cold water submersion is well documented in children but rare in adults. In the few adult cases reported, significant body cooling occurred (rectal temperature ranging from 22 degrees to 32 degrees C) and the victims were relatively young (< 40 years). We report a case of a 62-year-old man who was submersed in 2 degrees to 3 degrees C water for 15 minutes (time from initial submersion to intubation = 22 minutes). At the time of rescue, he had no vital signs, received prehospital Advanced Life Support, and was transported to hospital. On arrival at hospital, the patient remained in full cardiopulmonary arrest with an agonal ECG rhythm and had an initial pH of 6.77. Initial rectal temperature was near normal (36 degrees C) but subsequently dropped to 33 degrees C. The patient was resuscitated, rewarmed by forced-air warming, and treated for acute myocardial infarction, pulmonary edema, and generalized seizures. He was discharged after 27 days with minor neurologic abnormalities. Given the near-normal initial rectal temperature, preferential brain cooling may have been at least partially responsible for the positive neurologic outcome.
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PMID:Recovery of a 62-year-old man from prolonged cold water submersion. 943 57

The efficacy and safety of the angiotensin converting enzyme inhibitor enalapril in dogs with naturally acquired class III or class IV heart failure was evaluated in this study. Eighteen small-breed dogs with insufficiency of their mitral valves, but without other diseases were included in this study over a period of six months. When necessary due to massive pulmonary edema or high serum potassium concentrations, furosemide was added to the therapy with enalapril. No other drugs, including digitalis, were used in this study. The treatment was followed by anamnesis, clinical examinations, electrocardiography, radiography, echocardiography and laboratory diagnosis. Examinations were performed before treatment and after one week, after six weeks and after six months of treatment. 72% of the dogs improved in NYHA classification until the end of the study (p < 0.05). The incidence of seizures due to syncopes or severe respiratory distress decreased during this study (p < 0.01). For 28% of the dogs this treatment was not successful. In the electrocardiographic, radiographic and laboratory examinations statistically significant changes could not be recorded. The decrease in heart rate did not reach statistical significance. The echocardiographic investigation evaluated a significant decrease in fractional shortening and in the diastolic diameter of the left ventricular wall (p < 0.05 respectively p < 0.01), but no significant change in the diastolic or systolic diameter of the interventricular septum. The average oral dose of enalapril was 0.38 mg/kg body weight b.i.d., the average dose of furosemide was 0.37 mg/kg body weight b.i.d. in the first week of the study and was raised to 0.74 mg/kg body weight b.i.d. until the end of the study. Side effects like diarrhea, vomiting or reduced appetite did not increase during the course of the study. However one dog was excluded from the study because of repeated vomiting after six weeks of treatment. This study shows the beneficial clinical and hemodynamic effects and the security of the therapy with enalapril for dogs with heart failure due to mitral insufficiency.
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PMID:[Treatment of mitral valve insufficiency in dogs with the ACE inhibitor enalapril. A clinical progress study]. 953 70

Neurogenic pulmonary edema is a rare and serious complication in patients with head injury. It also may develop after a variety of cerebral insults such as subarachnoid hemorrhage, brain tumors and after epileptic seizures. Thirty six patients with severe head injury and four patients with cerebrovascular insults treated in Intensive Care Unit of HC-UNICAMP from January to September 1995 were evaluated. In this period there were two patients with neurogenic pulmonary edema, one with head injury and other with intracerebral hemorrhage. Diagnosis was made by rapid onset of pulmonary edema, severe hypoxemia, decrease of pulmonary complacence and diffuse pulmonary infiltrations, without previous history of tracheal aspiration or any other risk factor for development of adult respiratory distress syndrome. In the first case, with severe head trauma, neurogenic pulmonary edema was diagnosed at admission one hour after trauma, associated with severe systemic inflammatory reaction, and good outcome in three days. The second case, with hemorrhagic vascular insult, developed neurogenic pulmonary edema the fourth day after drainage of intracerebral hematoma and died.
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PMID:[Neurogenic pulmonary edema. Report of 2 cases]. 962 92

A severely hypocalcaemic, hypomagnesaemic lactating bitch exhibited clinical signs of pulmonary oedema, paresis, dementia, gastrointestinal ileus and urinary bladder atony. The total calcium, ionised calcium and magnesium levels were extremely low. The clinical picture was very different from the one typically encountered in canine lactation tetany, and instead resembled bovine postparturient paresis. Muscle tremors, rigidity and seizures were not part of the acute clinical picture, but rather atony, weakness and paresis. General muscle dysfunction probably resulted from the extremely low ionised calcium levels in combination with very low levels of magnesium and possibly potassium. Heart failure and atony of the urinary bladder and intestines were probably a result of the severe hypocalcaemia. The alteration in calcium to magnesium ratio may have depressed neuromuscular transmission, leading to paresis and atony. The unusual electrocardiogram possibly also resulted from abnormal magnesium and calcium cation levels.
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PMID:Paresis and unusual electrocardiographic signs in a severely hypomagnesaemic, hypocalcaemic lactating bitch. 967 8

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

We report two cases with complex partial and secondarily generalized seizures, both on oxcarbazepine and vigabatrin, with additional lamotrigine in one case. Both died in a manner resembling SUDEP, i.e. suddenly, unexpectedly, probably following a seizure with pulmonary oedema at autopsy. Both had SIADH. A number of drugs may cause SIADH, among them carbamazepine and oxcarbazepine. A search for SIADH in patients on carbamazepine and oxcarbazepine, and in cases of sudden death in epilepsy, is recommended.
Seizure 1998 Oct
PMID:Sudden death in two patients with epilepsy and the syndrome of inappropriate antidiuretic hormone secretion (SIADH). 980 22

We describe a five-week-old boy who had seizures and extreme hypernatraemia secondary to ingesting an improper home-made formula. Initial sodium concentration was 211 mmol.l-1. Other clinical and biological features were moderate dehydration and renal insufficiency with generous urine output and high urinary sodium concentration. Fluid therapy with hypotonic dextrose solution corrected the volume deficit in 48 h and progressively decreased the serum sodium concentration. During ICU stay the patient developed recurrent episodes of seizures and pulmonary oedema requiring mechanical ventilation for five days. Recovery was complete with no abnormal sequelae after a ten-month follow-up. Salt poisoning is in unusual cause of extreme hypernatraemia. It can be safely managed with fluid therapy alone if urine output is preserved, with progressive decrease of serum sodium as target. If this condition is recognized, outcome should be favourable.
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PMID:The management of extreme hypernatraemia secondary to salt poisoning in an infant. 1071 47

The diagnosis 'tonic clonic seizure' is frequently established by emergency physicians on scene. In patients with epilepsy mortality due to accidents, asphyxia, cardiac arrhythmias or postictal neurogenic pulmonary oedema (NPO) is twice as high as in the general population. We report a case of acute pulmonary oedema after a tonic clonic seizure. Following this event, the patient developed respiratory insufficiency and evidence of pulmonary oedema not associated with the classic aetiologies of congestive heart failure, aspiration or toxic exposure. The patient survived the incident after aggressive prehospital treatment, long-term intensive care and subsequent rehabilitation. A systematic case analysis and an introduction to the pathophysiology of NPO are presented. We recommend a positive approach to the management of NPO consisting primarily of interventions to stabilize vital functions, decrease intracranial pressure and normalize vegetative dysregulation. Emergency physicians need to consider the possibility of NPO in all cases of pulmonary oedema of unknown origin.
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PMID:Neurogenic pulmonary oedema after generalized epileptic seizure. 1040 21


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