1/155. A case of fatal salt water intoxication following an exorcism session. In response to a recent article published in this review, we present in this paper, an unusual case of fatal salt water intoxication. In this case, we point out three special features, the type of water ingested, the physiopathologic consequences of the ingestion and the very strange context of occurrence. This complex case allows us to point out complications due to salt poisoning and others caused by water intoxication. ( info) |
| 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. ( info) |
| 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. ( info) |
4/155. 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. ( info) |
5/155. 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. ( info) |
6/155. Treatment of psychogenic polydipsia: comparison of risperidone and olanzapine, and the effects of an adjunctive angiotensin-II receptor blocking drug (irbesartan). OBJECTIVE: Our objective was to determine the outcome of novel strategies in managing a case of severe polydipsia. CLINICAL PICTURE: The patient was a 39-year-old male with a 20-year history of paranoid schizophrenia who, despite only mild residual psychotic symptoms, had been hospitalized for the previous 10 years because of severe polydipsic behaviour complicated by water intoxication. TREATMENT: Novel antipsychotic agents, risperidone and olanzapine, as well as the specific angiotensin-II receptor blocking drug, irbesartan were employed at selected intervals in a study lasting nearly 3 years. A strict behavioural management programme was ongoing, in which diurnal weight change and the number of breaches of weight limits, requiring management in a low-stimulus environment, were documented on a daily basis. Summary measures of diurnal weight change and behavioural intervention were charted against changes in treatment. OUTCOME: Polydipsic behaviour improved on risperidone up to 4 mg daily, but was not sustained. Olanzapine was similarly successful in stabilizing polydipsia, and improvement was achieved with the addition of irbesartan. CONCLUSION: We suggest that the D2-sparing profiles of receptor binding achieved with low-dose risperidone and olanzapine may account for this beneficial effect. The benefit derived with irbesartan implicates the involvement of brain angiotensin systems centrally in helping to regulate drinking behaviour. ( info) |
7/155. Cerebral oedema in enuretic children during low-dose desmopressin treatment: a preventable complication. Seven cases of cerebral oedema have been observed in enuretic children during low-dose desmopressin (DDAVP) treatment given in a dose of 7-21 microg daily in the czech republic between 1995 and 1999, after the drug started to be marketed for this indication and delivered in simple bottles with a dropper. All seven children (age 5-11 years, four boys) experienced a period of unconsciousness but all recovered without sequelae. In most cases, safety measures were underestimated and natraemia was not regularly controlled. Two children developed cerebral oedema after excessive water intake in preparation for uroflowmetry, another one drank much during a hot summer day, in one diabetes insipidus was not recognised and two children were clearly non-compliant with reduced fluid intake on a long-term basis. Only in one child, no risk factor was found. Conclusion. Proper selection and instruction of patients is needed to avert cerebral oedema during treatment with desmopressin for nocturnal enuresis. ( info) |
8/155. University of Miami Division of Clinical pharmacology Therapeutic Rounds: the water-intolerant patient and perioperative hyponatremia. Perioperative hyponatremia has been recognized as a serious in-hospital complication for many years. Because the kidney responds to changes in extracellular fluid tonicity by adjusting water excretion, a defect in any of several key elements of water excretion can lead to water retention and hyponatremia. Most cases of hyponatremia are caused by impaired renal water excretion in the presence of continued water intake. For the kidney to excrete excess free water and thereby protect the extracellular fluid against hyponatremia, there must be an adequate glomerular filtration rate (GFR), adequate delivery of glomerular filtrate to the diluting segments of the distal nephron, intact tubular diluting mechanisms, and appropriate inhibition of antidiuretic hormone (ADH) synthesis and release. Virtually all of the clinical disorders producing hyponatremia are based on abnormalities of these few mechanisms of water regulation. Finding the reason for impaired renal water excretion is the key to diagnosing the cause of hyponatremia. Impaired renal water excretion may be caused by impaired GFR (renal failure), impaired water delivery to the diluting segments of the distal nephron because of increased proximal reabsorption (decreased extracellular fluid volume and edematous states), impaired renal diluting mechanism (thiazide diuretics), the syndrome of inappropriate ADH (SIADH) due to a variety of causes including the perioperative state, and hypothyroidism or adrenal insufficiency. Any of the states that impair water excretion can produce hyponatremia in a patient with an initially normal serum sodium concentration if sufficient free water is supplied. Therefore, a patient who has one of the conditions listed above, including the perioperative state, may be considered "water intolerant" even if the serum sodium is normal. Such a patient is at risk for developing severe hyponatremia if given hypotonic IV fluids or a large oral water load. An understanding of the basic mechanisms leading to impaired water excretion and "water intolerance" is therefore an important key to avoiding perioperative hyponatremia. ( info) |
| 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. ( info) |
10/155. hyponatremia associated with overhydration in U.S. Army trainees. This report describes a series of hyponatremia hospitalizations associated with heat-related injuries and apparent over-hydration. Data from the U.S. Army Inpatient Data System were used to identify all hospitalizations for hyposmolality/hyponatremia from 1996 and 1997. Admissions were considered as probable cases of overhydration hyponatremia if this was the only, or primary, diagnosis or if it was associated with any heat-related diagnosis. Seventeen medical records were identified, and the events leading to hospitalization were analyzed. The average serum sodium level was 122 /- 5 mmol/L (range, 115-130 mmol/L). All 17 patients were soldiers attending training schools. Seventy-seven percent of hyponatremia cases occurred in the first 4 weeks of training. Nine patients had water intake rates equal to or exceeding 2 quarts per hour. Most patients were in good health before developing hyponatremia. The most common symptoms were mental status changes (88%), emesis (65%), nausea (53%), and seizures (31%). In 5 of 6 cases in which extensive history was known, soldiers drank excess amounts of water before developing symptoms and as part of field treatment. The authors conclude that hyponatremia resulted from too aggressive fluid replacement practices for soldiers in training status. The fluid replacement policy was revised with consideration given to both climatic heat stress and physical activity levels. Field medical policy should recognize the possibility of overhydration. Specific evacuation criteria should be established for exertional illness. ( info) |