Fatal water intoxication

Farrell, D J

doi:10.1136/jcp.56.10.803-a

Cited by 46 publications

(31 citation statements)

References 8 publications

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“…The possibility that this relationship may indicate causality is plausible, but cannot be proven with the observational design of this analysis. Patients with severe hyponatremia experience cerebral edema as well as risk for seizures, acute brain injury and death [15,16,17]. However, in this study we found that most hyponatremia was mild to moderate, not generally of a magnitude that would cause harm.…”

Section: Discussioncontrasting

confidence: 54%

Hyponatremia in Community-Acquired Pneumonia

et al. 2007

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Background/Aim: Community-acquired pneumonia (CAP) is a frequent cause for hospitalization and may result in a number of different renal and electrolyte complications. The purpose of this study was to describe the incidence of hyponatremia in CAP and to analyze risk factors for its occurrence. Methods: Records were reviewed for all 342 subjects who participated in the Community-Acquired Pneumonia Standardized Order Set study, a 2-year trial of supplemental treatment tools in hospital pneumonia treatment. Results: Hyponatremia (serum sodium concentration <136 mg/dl) was present at hospital admission in 27.9% of patients. The magnitude was generally mild, only 4.1% of patients had serum sodium <130 mEq/l. Patients with hyponatremia had greater initial heart rate (100.2 vs. 93.2 beats/min, p = 0.03), white blood cell count (15,100 vs. 12,100/µl, p < 0.0001) and pneumonia severity index class 4 or 5 (35.7 vs. 25.1% of patients, p = 0.05). Hyponatremia at admission was associated with greater risk for death and increased length of hospital stay. Hyponatremia developed during the hospitalization in 10.5% of subjects, with most cases being mild, only 2.6% of all patients having serum sodium decrease to <130 mEq/l. Patients developing hyponatremia were more likely to have end-stage renal disease and to have had initial intravenous fluids other than isotonic saline, but had similar severity of illness on admission to those without acquired hyponatremia. Conclusion: Hyponatremia is a common complication present at the time of admission for CAP. It is associated with more severe illness, increased mortality risk and extended hospital stays. Hyponatremia develops less frequently during the hospitalization and is unrelated to severity of illness on admission, but is an iatrogenic complication and thus initial treatment with isotonic saline may reduce the risk of this complication.

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Section: Discussioncontrasting

confidence: 54%

Hyponatremia in Community-Acquired Pneumonia

et al. 2007

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“…Subsequent studies in controlled experimental settings have demonstrated that both the basal impairments in water excretion (Goldman et al, 1988(Goldman et al, , 1996 and their aggravation during acute psychosis are attributable to unexplained increases in vasopressin activity that are not seen in other schizophrenic patients. Although effective treatments for hyponatremia have subsequently been introduced, reports of fatalities from water intoxication continue to accumulate (Farrell and Bower, 2003;Hayashi et al, 2005;Loas and Mercier-Guidez, 2002). The current study establishes a plausible mechanism for the previously unexplained rise in vasopressin activity in hyponatremic schizophrenics: an enhanced neuroendocrine response to psychological stress.…”

Section: Mechanism Of Water Intoxication In Schizophreniamentioning

confidence: 70%

Neuroendocrine Responses to a Cold Pressor Stimulus in Polydipsic Hyponatremic and in Matched Schizophrenic Patients

Goldman

Gnerlich

Hussain

2006

Neuropsychopharmacol

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Schizophrenia, many believe, reflects an enhanced vulnerability to psychological stress. Controlled exposure to stressors, however, has produced inconclusive results, particularly with regards to neurohormones. Some of the variability may be attributable to the nature and psychological significance of the stimulus and failure to control physiologic confounds. In addition, it is possible that the heterogeneity of schizophrenia is an important factor. In a carefully designed study and in a controlled setting, we measured the neuroendocrine response of eight polydipsic hyponatremic (PHS), seven polydipsic normonatremic (PNS), and nine nonpolydipsic normonatremic (NNS) (ie normal water balance) schizophrenic in-patients as well as 12 healthy controls (HC) to two different stressors: one of which appears to influence neuroendocrine secretion through its psychological (cold pressor) and the other (upright posture) through its systemic actions. Subjects in the three psychiatric groups were stabilized and acclimated to the research setting, and all received saline to normalize plasma osmolality. Following the cold pressor, plasma adrenocorticotropin and cortisol levels showed a more prolonged rise in PHS patients relative to PNS patients. NNS patients, in contrast, exhibited blunted responses relative to both of the polydipsic groups and the HC. Peak vasopressin responses were also greater in PHS and blunted in NNS patients. Responses to the postural stimulus were similar across patient groups. These findings provide a mechanism for life threatening water intoxication in schizophrenia; help to reconcile conflicting findings of stress responsiveness in schizophrenia; and potentially identify a discrete patient subset with enhanced vulnerability to psychological stress.

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“…Byramji et al [97] and Ingham and Byard [98] reviewed Unnatural cases of hyponatremia upon autopsy [97,[104][105][106][107][108][109][110][111][112][113] include water intoxication from psychogenic polydipsia, environmental polydipsia, ingestion of dilute infant formulas, beer potomania, endurance exercise, fresh water immersion and iatrogenic causes including drug and parenteral fluid administration and surgical irrigation. If antemortem findings are not available, vitreous sodium levels lower than 120 mmol/l could support the diagnosis of fatal hyponatremia [104].…”

Section: Electrolytesmentioning

confidence: 98%

Postmortem chemistry update part I

2011

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Postmortem chemistry is becoming increasingly essential in the forensic pathology routine and considerable progress has been made over the past years. Biochemical analyses of vitreous humor, cerebrospinal fluid, blood and urine may provide significant information in determining the cause of death or in elucidating forensic cases. Postmortem chemistry may essentially contribute in the determination of the cause of death when the pathophysiological changes involved in the death process cannot be detected by morphological methods (e.g. diabetes mellitus, alcoholic ketoacidosis and electrolytic disorders). It can also provide significant information and useful support in other forensic situations, including anaphylaxis, hypothermia, sepsis and hormonal disturbances. In this article, we present a review of the literature that covers this vast topic and we report the results of our observations. We have focused our attention on glucose metabolism, renal function and electrolytic disorders.

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Fatal water intoxication

Cited by 46 publications

References 8 publications

Hyponatremia in Community-Acquired Pneumonia

Hyponatremia in Community-Acquired Pneumonia

Neuroendocrine Responses to a Cold Pressor Stimulus in Polydipsic Hyponatremic and in Matched Schizophrenic Patients

Postmortem chemistry update part I

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