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

The effects of acute changes in plasma magnesium concentration on the threshold for lidocaine-induced seizures were evaluated in mechanically ventilated rats receiving 70% nitrous oxide and 30% oxygen. In experiment 1, male rats were intravenously administered either 0.9% sodium chloride (group I) or 5.0% magnesium sulfate to elevate plasma magnesium levels to 5.8 +/- 0.1 (group II) or 10.5 +/- 1.0 mg/dl (group III). In experiment 2, pregnant rats were intravenously administered either 0.9% sodium chloride (normomagnesemia) or magnesium sulfate, resulting in a plasma magnesium concentration of 7.8 +/- 1.4 mg/dl. Thirty minutes later, a continuous intravenous infusion of lidocaine (2.3 mg/kg per minute) was begun in both experiments. Biparietal electroencephalographic activity was monitored continuously. At the onset of electroencephalographic seizure activity, arterial plasma magnesium and lidocaine concentrations were measured. In groups I and III (experiment 1), brain parenchymal magnesium was also assayed. There were no differences in plasma lidocaine concentrations (in experiments 1 or 2) between saline solution and hypermagnesemic groups at onset of seizures. Brain magnesium level was unaltered by magnesium sulfate infusion. We conclude that acute administration of magnesium sulfate alters neither brain magnesium level nor the plasma lidocaine concentration associated with onset of electroencephalographic seizures.
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PMID:Effects of acute hypermagnesemia on the threshold for lidocaine-induced seizures in the rat. 199 23

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.
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PMID:Hypernatremia. 264 64

The etiology, pathophysiology, clinical features, diagnosis, and medical treatment of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are reviewed. SIADH is a common cause of hyponatremia in hospitalized patients. Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Symptoms generally occur only when hyponatremia is severe (less than or equal to 125 meq/L) and may include anorexia, vomiting, and confusion, followed by seizures, coma, and death. SIADH may result from a variety of diseases, as well as from the use of drugs such as chlorpropamide, carbamazepine, diuretics, and some antineoplastic agents. Diagnosis of SIADH is confirmed by demonstration of a high urine osmolality with a low plasma osmolality, in the absence of diuretic use. Immediate treatment of the symptomatic patient with SIADH includes intravenous furosemide and 3% sodium chloride injection to produce a negative free-water balance. If the underlying cause of SIADH cannot be corrected, the treatment of choice for chronic SIADH is fluid restriction. If this is not tolerated by the patient, demeclocycline can be used to induce a negative free-water balance. Urea, lithium, phenytoin, and loop diuretics have been reported to be effective, but there are few data to support their use. Future research into the treatment of SIADH must be directed at developing effective antagonists of ADH. Treatment of SIADH consists of elimination of underlying causes and restriction of fluid intake; if these measures are unsuccessful or poorly tolerated, long-term drug therapy may be indicated.
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PMID:Management of the syndrome of inappropriate secretion of antidiuretic hormone. 312 Dec 40

The safety and efficacy of administering individualized phenytoin sodium loading doses by intravenous infusion were studied on 40 occasions in 37 adult patients having seizures. Doses were calculated based on an average volume of distribution (0.75 L/kg) and desired plasma phenytoin concentration. Total and free phenytoin concentrations were determined before and after the infusion. Phenytoin sodium doses of 225-1300 mg were administered by intravenous infusion at a rate of 40 mg/min after dilution in 0.9% sodium chloride injection to concentrations ranging from 4.5 to 13.5 mg/mL. Infusion rates were reduced if adverse effects occurred. The dosing method accurately achieved desired phenytoin concentrations (predicted mean +/- S.D. concentration, 18.3 +/- 1.6 micrograms/mL; observed mean concentration, 17.4 +/- 2.5 micrograms/mL). Postinfusion concentrations of free phenytoin ranged from 0.8 to 3.6 micrograms/mL (mean +/- S.D., 1.7 +/- 0.6 micrograms/mL). Of 21 patients evaluated for efficacy, 16 responded. A total of 45% of patients experienced pain at the infusion site, which diminished when the infusion rate was reduced. No serious cardiovascular or neurological toxicities occurred. The intravenous infusion method of administration is safe and effective and is useful for rapid achievement of therapeutic phenytoin concentrations in the emergency room setting.
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PMID:Efficacy of individualized phenytoin sodium loading doses administered by intravenous infusion. 335 18

Hyponatremia is always present in patients with water intoxication and accounts for many of the life-threatening symptoms and signs found in this population. In schizophrenic patients, water restriction, a cornerstone in the treatment of water intoxication, may be impossible to implement over the course of long-term management. The use of oral sodium chloride administration in such patients and its short-term efficacy in preventing major motor seizures are described.
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PMID:Oral sodium chloride in the management of schizophrenic patients with self-induced water intoxication. 396 38

The use of rapid intravenous infusions of phenytoin sodium to achieve prompt plasma therapeutic concentrations of phenytoin was studied in adult epileptic patients. Six adult patients who experienced recent tonic-clonic seizures were selected for study. Four of them had not been treated with phenytoin before the study; two were on chronic phenytoin therapy but had subtherapeutic serum levels. A leading dose of phenytoin sodium (15 mg/kg in 100 ml of 0.9% sodium chloride injection) was infused at 30-50 mg/min. Blood samples were drawn before phenytoin administration, every five minutes during the infusion, and at 1, 2, 4, 8, 12, 18, and 24 hours after completion of the infusion. Adverse effects were monitored during the infusion. Pharmacokinetic variables were calculated. Patients received from 750 to 1500 mg phenytoin sodium (mean +/- S.D. = 1040.8 +/- 297.3 mg). From 5 to 30 minutes were required to reach therapeutic (10-20 micrograms/ml) serum phenytoin concentrations; concentrations peaked at 31.1 +/- 10.0 micrograms/ml. Four of the six patients had therapeutic serum concentrations at 18 hours after completion of the infusion. Adverse effects were minimal and not severe; no cardiotoxicities were noted. Phenytoin half-life was 31.2 +/- 8.4 hours, total plasma clearance was 47.2 +/- 10.7 ml/kg/hr, and volume of distribution was 1.96 +/- 0.46 liters/kg. It is concluded that rapid intravenous infusion of phenytoin appears to be a reasonably safe and effective method of rapidly reaching therapeutic phenytoin concentrations.
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PMID:Rapid infusion of phenytoin sodium loading doses. 722 48

The treatment of status epilepticus can be improved by using recent developments in the pharmacokinetics and method of intravenous (IV) administration of phenytoin sodium. While diazepam, administered IV, remains the drug of choice for the short-term control of seizures associated with compromised respiratory exchange, phenytoin is effective in preventing recurrence of such seizures and in treating most other forms of status epilepticus. A loading dose of 18 mg/kg given by IV infusion in either 0.45% or 0.9% sodium chloride at a rate no greater than 50 mg/min results in therapeutic serum levels for up to 24 hours in most patients. Maintenance therapy with phenytoin should start at 4 to 7 mg/kg/day and be adjusted to both clinical response and serum levels.
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PMID:Status epilepticus. The role of intravenous phenytoin. 742 Jun 42

A 4-year-old boy was treated with oxybutinine and desmopressine because of bladder instability associated with secondary enuresis. He was admitted with obnubilation, vomiting and experienced two seizure episodes concomitantly with hyponatremia and hypoosmolality. The child healed promptly under water restriction and intravenous administration of sodium chloride. This case report suggests that desmopressine may be responsible for severe side-effects. This drug should not be widely used and its indications should be restricted to patients with proven antidiuretic hormone secretion abnormalities.
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PMID:[Desmopressin and water intoxication. Apropos of a case treated for enuresis]. 801 69

Serious neurological symptoms are common in patients with a serum sodium concentration below 115 mmol l-1. The treatment is controversial and the most adequate rate of sodium correction to avoid both morbidity due to residual hypo-osmolality and therapy-induced neurological sequelae is debated. The management of symptomatic hyponatraemia is discussed here against the background of two cases and a literature review. It is concluded that the treatment should be based on whether the electrolyte disturbance is acute (< 24-36 h) or has developed insidiously. Slow sodium correction (< 0.5 mmol l-1 h-1) in patients with chronic hyponatraemia and rapid correction (1-2 mmol l-1 h-1) to a moderately hyponatraemic level in those with an acute development are recommended. If available data do not permit differentiation between the two conditions in a patient with seizures or in coma, rapid correction with sodium chloride and furosemide for 3-4 h followed by slow correction therapy is suggested.
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PMID:Management of symptomatic hyponatraemia: dependence on the duration of development. 818 9

The association of severe hyponatremia and the ingestion of large quantities of beer, termed beer potomania, has been known for several years. We report two new cases, and review 20 others from the medical literature. These patients usually have a history of binge beer drinking, poor dietary intake, and then present with severe hyponatremia and various mental status changes or seizures. Typical laboratory findings include hyponatremia, hypokalemia, and a very dilute urine. The patients respond quickly to the administration of sodium chloride containing i.v. fluids. We propose that the pivotal pathophysiologic mechanism in beer potomania syndrome is the minimal intake of solute and the hypoosmolality of the beer ingested. This will lead to the inability to excrete sufficient amounts of free water to keep up with the ingestion of large quantities of the hyposmolar beer. Treatment with isotonic sodium chloride results in the rapid clearance of the accumulated excess free water.
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PMID:Beer potomania: two cases and review of the literature. 934 99


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