Cases reported "Hyponatremia"

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1/69. death from hyponatremia as a result of acute water intoxication in an Army basic trainee.

    Several reports during the past 15 years have described hyponatremia as a result of excessive water intake by athletes during endurance races. The high rates of fluid consumption have been attributed to the desire of athletes to prevent heat injury. The military has adopted guidelines for programmed drinking to maintain performance and minimize the risk of heat casualties. As military personnel increase their fluid intake, their risk of hyponatremia as a result of water overload increases. A potentially life-threatening complication is acute water intoxication. We report the first known death of an Army basic trainee as a result of acute water intoxication. The misinterpretation of his symptoms as those of dehydration and heat injury led to continued efforts at oral hydration until catastrophic cerebral and pulmonary edema developed.
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2/69. Severe hyponatraemia in an amiloride/hydrochlorothiazide-treated patient.

    A 85-year-old woman treated with, among other drugs, a thiazide diuretic presented with a severe hyponatraemia. She met several of the criteria for SIADH and, besides drugs, no cause for SIADH was found. After stopping the thiazide diuretic and restricting fluid intake the patient recovered fully. It was later proved that the thiazide was the cause of the water intoxication by rechallenging the patient with a single dose of amiloride/hydrochlorothiazide 5/50 mg. This "thiazide provocation test" showed its usefulness in the differential diagnosis of suspected SIADH. Moreover, the test demonstrated the paradoxal effect of thiazide diuretics to cause water retention in susceptible patients.
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3/69. Hyponatraemic convulsion secondary to desmopressin treatment for primary enuresis.

    The case of a 6 year old child who presented with convulsions and coma after unsupervised self administration of intranasal desmopressin (DDAVP) for nocturnal enuresis is presented. Children with enuresis can be embarassed by their condition and may believe that multiple doses of their nasal spray may bring about a rapid resolution. water intoxication is an uncommon but serious adverse effect of treatment with intranasal DDAVP. These patients may present with seizure, mental state changes, or both. Basic management consists of stopping the drug, fluid restriction, and suppressive treatment for seizures. Recovery is usually rapid and complete. Administration of the nasal spray in children should be supervised by parents to prevent highly motivated children from accidental overdose. The risks of high fluid intake need to be carefully explained to both parents and children.
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4/69. Fatal child abuse by forced water intoxication.

    BACKGROUND: Although water intoxication leading to brain damage is common in children, fatal child abuse by forced water intoxication is virtually unknown. methods: During the prosecution of the homicide of an abused child by forced water intoxication, we reviewed all similar cases in the united states where the perpetrators were found guilty of homicide. In 3 children punished by forced water intoxication who died, we evaluated: the types of child abuse, clinical presentation, electrolytes, blood gases, autopsy findings, and the fate of the perpetrators. FINDINGS: Three children were forced to drink copious amounts of water (over 6 L). All had seizures, emesis, and coma, presenting to hospitals with hypoxemia (PO2 = 44 /- 8 mm Hg) and hyponatremia (plasma Na = 112 /- 2 mmol/L). Although all showed evidence of extensive physical abuse, the history of forced water intoxication was not revealed to medical personnel, thus none of the 3 children were treated for their hyponatremia. All 3 patients died and at autopsy had cerebral edema and aspiration pneumonia. The perpetrators of all three deaths by forced water intoxication were eventually tried and convicted. INTERPRETATION: Forced water intoxication is a new generally fatal syndrome of child abuse that occurs in children previously subjected to other types of physical abuse. patients present with coma, hyponatraemia, and hypoxemia of unknown etiology. If health providers were made aware of the association, the hyponatremia is potentially treatable.
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5/69. hyponatremia-associated rhabdomyolysis.

    BACKGROUND: hyponatremia is the most frequent electrolyte disorder. However, hyponatremia rarely results from excessive water intake, unless the kidney is unable to excrete free water, such as in patients on thiazide diuretics; in addition, hyponatremia is an uncommon cause of rhabdomyolysis. methods: We present a 51-year-old hypertensive woman on chronic hydrochlorothiazide therapy who developed acute water intoxication and severe myalgias. RESULTS: The patient developed acute hypotonic hyponatremia and subsequent rhabdomyolysis. We discuss the mechanisms responsible for the development of hyponatremia and its association with rhabdomyolysis. CONCLUSION: Muscle enzymes should be monitored in patients with acute hyponatremia who develop muscle pain, and hyponatremia-induced rhabdomyolysis must be considered in patients with myalgias receiving thiazide diuretics.
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6/69. Severe rhabdomyolysis following massive ingestion of oolong tea: caffeine intoxication with coexisting hyponatremia.

    A 36-y-o patient with schizophrenia, who had consumed gradually increasing quantities of oolong tea that eventually reached 15 L each day, became delirious and was admitted to a psychiatric hospital. After abstinence from oolong tea his delirium resolved. He was transferred to our hospital when he was discovered to have acute renal failure with hyponatremia (118 mEq/L) and severe rhabdomyolysis (creatine phosphokinase, 227,200 IU/L). On admission rhabdomyolysis had begun to improve despite a worsening of the hyponatremia (113 mEq/L). With aggressive supportive therapy, including hypertonic saline administration and hemodialysis, the patient fully recovered without detectable sequelae. The clinical course suggests that caffeine, which is present in oolong tea, was mainly responsible for the rhabdomyolysis as well as the delirium, although severe hyponatremia has been reported to cause rhabdomyolysis on rare occasions. We hypothesize that caffeine toxicity injured the muscle cells, which were fragile due to the potassium depletion induced by the coexisting hyponatremia, to result in unusually severe rhabdomyolysis. The possibility of severe rhabdomyolysis should be considered in a patient with water intoxication due to massive ingestion of caffeine-containing beverages.
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7/69. Inappropriate secretion of antidiuretic hormone after cerebral injury.

    A case has been presented in which a patient sustained a closed head injury with concomitant maxillofacial injuries; early signs of water intoxication and ISADH developed six days after injury. This disorder was corrected by restricting free water intake for six days until equilibration occurred. Successful reduction of the facial fractures was accomplished after stabilization of the patient's neurological condition and correction of her metabolic disorder. The ISADH and resulting hyponatremia have been documented in a variety of disease states including trauma to the central nervous system. Disruption or irritation to the hypothalamic-neurohypophyseal system has been proposed as the mechanism of dysfunction after cerebral injury. The results of the secretion of inappropriate amounts of ADH relative to renal function and homeostatis have been discussed. Clinical and laboratory diagnosis as well as the elective and emergency management of ISADH have been reviewed. The fact that the sequelae of this abnormal metabolic state may mimic or mask the neurological deterioration which may follow cerebral injury is significant. This may contribute to the difficulty in making a correct diagnosis and designing proper therapy. The problem is basically one of differentiating a correctable metabolic disorder from a lesion that can be fatal unless surgically removed.
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8/69. Rapid correction of water intoxication by hypertonic saline and frusemide.

    A case of profound hyponatraemia with severe cerebral dysfunction, induced by excess water intake and exacerbated by smoking, is described. Rapid correction with hypertonic saline infusions and frusemide allowed a negative fluid balance and elevation of serum sodium concentration to be achieved without precipitating acute pulmonary oedema.
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9/69. Effect of adjunctive cortisol on serum sodium in a polydipsic hyponatremic schizophrenic patient.

    1. Many polydipsic schizophrenics exhibit enhanced antidiuretic hormone (ADH) activity and thus are hyponatremic and suffer life-threatening water intoxication. Excess cortisol inhibits ADH, while cortisol insufficiency produces impairments in water balance resembling those seen in hyponatremic schizophrenics. Furthermore, hyponatremia normally upregulates cortisol receptors on the neurons which synthesize ADH, which should make them more sensitive to the effects of cortisol. 2. The author treated a hyponatremic schizophrenic, whose water imbalance was unresponsive to standard clinical interventions including clozapine, with a 4-week open trial of 60 mg cortisol daily, followed by a three week taper. 3. Mean serum sodium levels appeared to increase modestly from 114.3 to 118.5 mEq/l while the patient received adjunctive cortisol (P < .06). 4. While a modest effect was seen, the results do not suggest that adjunctive cortisol will reverse hyponatremia, and instead support other data indicating that these patients exhibit a central resistance to glucocorticoid actions.
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10/69. coma and seizures due to severe hyponatremia and water intoxication in an adult with intranasal desmopressin therapy for nocturnal enuresis.

    Desmopressin, a synthetic analogue of the antidiuretic hormone, is an effective medication for primary nocturnal enuresis for both children and adults. Its safety is well established. Although it has a favorable side effect profile, because of its pharmacological effect, intranasal desmopressin can rarely induce water intoxication with profound hyponatremia if given without adequate restriction of water intake. The authors describe an adult patient with water intoxication and severe hyponatremia accompanied by loss of consciousness and seizures after 2-day intranasal administration of desmopressin. The present and the previously reported cases emphasize the need for greater awareness of the development of this serious and potentiallyfatal complication. In addition, to adjust the drug to the lowest required dosage, adequate restriction of water intake is recommended, and serum levels of sodium should be measured periodically to allow for early detection of water intoxication and hyponatremia.
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