Cases reported "Water Intoxication"

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1/17. 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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2/17. rhabdomyolysis after correction of hyponatremia in psychogenic polydipsia possibly complicated by ziprasidone.

    OBJECTIVE: To report a case of rhabdomyolysis related to correction of hyponatremia secondary to psychogenic polydipsia, possibly complicated by the use of ziprasidone. CASE SUMMARY: A 50-year-old white man treated for 3 weeks with ziprasidone 40 mg twice daily for chronic paranoid schizophrenia was admitted to the intensive care unit after a witnessed generalized seizure. Marked hypotonic hyponatremia was present secondary to psychogenic polydipsia. After correction of hyponatremia with intravenous NaCl 0.9%, he developed a substantial elevation in the creatine kinase level without any evidence of muscle trauma, stiffness, or swelling or any signs of neuroleptic malignant syndrome. Renal failure or compartment syndrome did not complicate the clinical picture. DISCUSSION: It is well known that severe hyponatremia can cause neurologic complications such as stupor, seizures, and even coma. hyponatremia from water intoxication (n = 28) and its correction with intravenous fluids (n = 2) may cause non-neurologic complications such as rhabdomyolysis. An explanation may lie within the calcium-sodium exchange mechanism across the skeletal myocyte or the failure of cell volume regulation secondary to extracellular hypo-osmolality. Neuroleptic medications have been linked to the development of rhabdomyolysis, with antipsychotics being the primary offenders. As of August 2005, there has been only one reported case of rhabdomyolysis related to correction of hyponatremia complicated by an atypical antipsychotic (clozapine). It is possible that ziprasidone, like clozapine, may enhance muscle cell permeability leading to rhabdomyolysis under similar conditions. CONCLUSIONS: Psychiatric patients treated with atypical antipsychotic medications should be closely monitored for rhabdomyolysis during correction of hyponatremia, thus permitting prompt therapy to limit its complications.
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3/17. child abuse: acute water intoxication in a hyperactive child.

    A 4-year-8-month-old boy was brought to our emergency department with coma and seizure. Initial physical examination showed evidence of physical child abuse and sudden body weight gain of 3.4 kg in one day. The laboratory results showed normal renal function with severe hyponatremia and the MRI study showed diffuse brain swelling. All of these findings were compatible with the diagnosis of acute water intoxication. Careful history taking from the boy and his parents separately confirmed the course of chronic polydipsia with acute compulsive water drinking. After clinical assessment and follow-up by psychiatrist, the patient was diagnosed with hyperactivity disorder. We present this case and show the possibility of correlation between compulsive water drinking, child abuse and hyperactivity disorder on acute water intoxication.
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4/17. The water-intoxicated patient.

    In a long-term psychiatric setting, self-induced water intoxication may be a life-threatening situation. At first glance, the symptoms or behaviors of self-induced water intoxication are similar to schizophrenia, i.e., inappropriate behavior, delusions, hallucinations, confusion, and disorientation. In some cases, the symptoms of water intoxication mimic schizophrenia and thus, are disguised as a part of the psychoses. Affected individuals develop polydipsia, which is accompanied by overhydration and dilutional hyponatremia. If untreated, the symptoms may progress from mild confusion to acute delirium, seizures, coma, or death (Ripley, Millson, & Koczapski, 1989). Under normal circumstances there is a delicate balance of water requirement and water intake. If the balance of water is altered, electrolyte imbalance can occur. The recognition of water intoxication or self-induced water intoxication and psychosis among chronic, institutionalized patients may prevent their death or the development of neurological damage (Arieff, 1985). Because self-induced water intoxication often goes unrecognized in its early stages and may have irreversible or fatal complications, early detection is crucial. This article will discuss the etiology, nursing assessment, and interventions associated with patients suffering from self-induced water intoxication.
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5/17. schizophrenia and fatal self-induced water intoxication with appropriately-diluted urine.

    A 31-year-old woman with untreated chronic schizophrenia developed extreme polydipsia which rapidly led to coma and death due to cerebral edema. hyponatremia (120 mEq/liter) and serum hypo-osmolality (260 mOsm/kg) were associated with marked polyuria (up to 1850 ml/hour) and appropriately low urinary osmolality (90 mOsm/kg) which responded to treatment. This case and few qualifying previous reports which are reviewed support the possibility that pure self-induced water intoxication with no major contribution of inadequate release of antidiuretic hormone may occur, and that extreme polydipsia can sometimes overwhelm normal renal diluting capacity in psychotic patients.
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6/17. Acute water intoxication after intranasal desmopressin in a patient with primary polydispsia.

    Only a few cases of severe acute water intoxication (AWI) due to intranasal desmopressin have been reported, none of which occurred in patients with primary polydipsia. We describe a case of AWI with semicoma and convulsions, due to intranasal desmopressin, in a 32-year-old patient with dipsogenic diabetes insipidus. Previous reported cases of AWI due to desmopressin are discussed. The importance of ruling out primary polydipsia when this drug is used, not only for central diabetes insipidus but also for other current indications such as classic hemophilia, is stressed.
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7/17. Altered state of consciousness in a compulsive water drinker.

    A relatively normal 16-year-old Chinese woman with a six-month history of compulsive water drinking resulting in a comatose state is reported. The drinking was perpetuated by an enjoyable altered state of consciousness after ingestion of an average of 20 litres of water per day. Treatment by fluid restriction and, later, simple education was successful. The subjective dimension of an altered state of consciousness may provide an important explanation for the obscure aetiology.
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8/17. water intoxication and Syntocinon infusion.

    A case of severe water intoxication with convulsion and prolonged coma, following the use of a high dose Syntocinon infusion is described. The pathogenesis and treatment of the condition are discussed.
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9/17. Death from self-induced water intoxication among patients with schizophrenic disorders.

    review of 60 consecutive records of patients who died before the age of 53 years in a state mental hospital revealed that 27 of those patients (45%) had a schizophrenic disorder. Of those 27 patients, five (18.5%) died of the complications of self-induced water intoxication and schizophrenic disorders (SIWIS). Clinical, laboratory, and autopsy features of those five SIWIS patients and of an additional five SIWIS cases obtained from the literature include psychosis, polydipsia, polyuria, severe hyposthenuria (specific gravity 1.003 or less), hyponatremia, seizures, coma, and cerebral and visceral edema. SIWIS characteristically develops during Arieti's third or "preterminal" stage (5 to 15 years after onset of psychosis) of schizophrenic disorders and it must be included in the differential diagnosis of unexplained death among psychiatric patients. As there are no pathognomonic SIWIS tissue changes, the pathologist must carefully integrate clinical, laboratory, and autopsy findings to arrive at the proper diagnosis. When premortem findings of polydipsia and hyponatremia are not available, evidence of antecedent severe hyposthenuria and postmortem vitreous humor hyponatremia of less than 120 mEq/1 are strongly supportive of the diagnosis of death due to SIWIS.
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10/17. Fatal water intoxication in a case of psychogenic polydipsia.

    The term "water intoxication" is used to describe a condition of agitation, delirium, convulsion, and coma brought on by excessive intake of water, resulting in severe hyponatremia. Psychogenic polydipsia (compulsive water drinking) has until recently been considered a relatively benign process. Since 1974, however, three fatal cases of water intoxication, resulting from psychogenic polydipsia, have been reported. All three individuals died while hospitalized, thereby permitting performance of blood electrolyte determinations and documentation of the associated electrolyte imbalance. In the authors' case, there was a well-documented prior episode of water intoxication in which serum electrolytes showed a pattern typical of this entity. Death, however, occurred at home, thus preventing valid serum electrolyte determinations to be performed. Analysis of the vitreous humor revealed a severe hyponatremia, thus substantiating the diagnosis of fatal water intoxication. This case, once again, points out the usefulness of electrolyte analyses on the vitreous humor as an aid to establishing a cause of death.
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