Of Mice and Men-The Physiology, Psychology, and Pathology of Overhydration.

The detrimental effects of dehydration, to both mental and physical health, are well-described. The potential adverse consequences of overhydration, however, are less understood. The difficulty for most humans to routinely ingest ≥2 liters (L)-or "eight glasses"-of water per day highlights the likely presence of an inhibitory neural circuit which limits the deleterious consequences of overdrinking in mammals but can be consciously overridden in humans. This review summarizes the existing data obtained from both animal (mostly rodent) and human studies regarding the physiology, psychology, and pathology of overhydration. The physiology section will highlight the molecular strength and significance of aquaporin-2 (AQP2) water channel downregulation, in response to chronic anti-diuretic hormone suppression. Absence of the anti-diuretic hormone, arginine vasopressin (AVP), facilitates copious free water urinary excretion (polyuria) in equal volumes to polydipsia to maintain plasma tonicity within normal physiological limits. The psychology section will highlight reasons why humans and rodents may volitionally overdrink, likely in response to anxiety or social isolation whereas polydipsia triggers mesolimbic reward pathways. Lastly, the potential acute (water intoxication) and chronic (urinary bladder distension, ureter dilation and hydronephrosis) pathologies associated with overhydration will be examined largely from the perspective of human case reports and early animal trials.

Recurrent rhabdomyolysis in a teenager with psychosis-intermittent hyponatremia-polydipsia syndrome.

OBJECTIVE: To report a case of recurrent hyponatremia and rhabdomyolysis in a teenager with psychogenic polydipsia. CASE SUMMARY: A 16-year-old boy was admitted with recurrent episodes of hyponatremia and rhabdomyolysis secondary to psychogenic polydipsia. He was treated with hypertonic saline, intravenous fluids, and supportive care. DISCUSSION: Psychogenic polydipsia is a condition characterized by compulsive drinking. Severe hyponatremia is a rare, but serious complication in patients with psychogenic polydipsia. Failure in cell volume regulatory mechanisms, defective osmoregulation, defective urinary dilution, and enhanced secretion of vasopressin are believed to play a role in the development of hyponatremia. Rhabdomyolysis can complicate severe hyponatremia, although the exact mechanism is not known. Antipsychotic drugs are also implicated in rhabdomyolysis. CONCLUSIONS: Severe hyponatremia and rhabdomyolysis can complicate psychogenic polydipsia. Patients receiving antipsychotic drugs with concomitant severe hyponatremia need to be monitored for rhabdomyolysis.

Forensic aspects of water intoxication: four case reports and review of relevant literature.

Water intoxication (WI) is a rare condition that originates from over-consumption of water, with a potentially fatal outcome. Increased water intake (polydipsia) is followed by urination of high amount of diluted urine (polyuria) which are the main initial symptoms of WI. We present four case reports of WI. Two of them are unusual pediatric clinical cases using medical documentation and police case files, one of which is related to child abuse, and the other to a psychiatric disorder. The other two cases are fatal adult cases submitted to autopsy from a psychiatric hospital. Also, we present a diagnostic algorithm for polydipsia and polyuria before death. WI is usually seen in patients with psychiatric disorders, victims of child abuse or torture, drug abusers or it can be iatrogenically induced.

[Fatal aspiration following polydipsia in schizophrenia]. / Polydipsie bei paranoider schizophrenie mit tödlichem ausgang.

OBJECTIVE AND METHODS: Polydipsia with hyponatraemia commonly occurs with chronic psychosis and is associated with a reduced life expectancy for individuals diagnosed with schizophrenia. We describe a 51 years old man who presented with polydipsia during a relapse of paranoid schizophrenia. While treated with Clozapine, and despite regular observation and daily control of creatinine and electrolytes, the man suddenly collapsed and died after drinking huge amounts of water. No sedation from psychotropic medication or drugs and alcohol was present in this case. Sodium levels on the day of death and the day before were within normal range. A post-mortem revealed aspiration of water and gastric content as the cause of asphyxiation and death. A literature search in Medline and Embase did not yield a description of a similar case. RESULTS AND CONCLUSIONS: This case highlights the risk of aspiration associated with polydipsia in chronic schizophrenia. Daily control of electrolytes to identify hyponatremia and regular observation are recommended but may not be sufficient to prevent sudden death from drinking huge amounts of water.

Treatment of psychogenic polydipsia with acetazolamide: a report of 5 cases.

OBJECTIVE: Psychogenic polydipsia occurs frequently in patients with chronic psychiatric illness and is often unmanageable. We herein report 5 patients in whom acetazolamide was trialed for this symptom. METHODS: We encountered a case in which polydipsia improved with incidental administration of acetazolamide. We then used this treatment for 4 additional cases of treatment-resistant psychogenic polydipsia, some of which were accompanied by hyponatremia. RESULTS: Acetazolamide improved polydipsia and/or hyponatremia in 4 of the 5 cases. This treatment was well tolerated and allowed 3 of the patients to permanently leave isolation. CONCLUSION: Acetazolamide appears to have a beneficial effect in psychogenic polydipsia.

The assessment and treatment of water imbalance in patients with psychosis.

Polydipsia and episodic life-threatening water intoxication remain important clinical problems for a significant portion of persons with schizophrenia. The disorders are associated with increased morbidity and mortality from a number of causes. With a basic understanding of the pathophysiology, one can easily diagnose and assess the clinical conditions. We review here the scope and pathophysiology of disordered water imbalance, including both primary and secondary polydipsia and hyponatremia. Reversible factors and possible interventions are reviewed. Treatment options for preventing water intoxication have expanded from discontinuation of offending agents, targeted fluid restriction, and clozapine therapy to the addition of oral vasopressin antagonists. The latter, however, are extremely potent and must be carefully monitored.

Risk factors for rhabdomyolysis in self-induced water intoxication (SIWI) patients.

Self-induced water intoxication (SIWI) patients present with various neurological and non-neurological symptoms. However, it is reported that non-neurological manifestations such as rhabdomyolysis are comparatively rare. The mechanism underlying rhabdomyolysis remains controversial. To investigate this further, we evaluated 22 SIWI patients for rhabdomyolysis. We reviewed the records of 22 patients with SIWI and evaluated their clinical characteristics. These patients were divided into the following two groups: Group A with rhabdomyolysis and Group B without it. We compared these groups to study the risk factors underlying the occurrence of rhabdomyolysis. Furthermore, we compared the complications and the duration of hospitalization between the two groups. The maximum serum sodium correction speed per hour, the increase in the serum sodium level in the initial 24 h, and the duration of hospitalization for group A were faster, higher, and longer, respectively, when compared with those in group B. Only group A patients showed complications. The rapid correction of hyponatremia may possibly trigger rhabdomyolysis in SIWI patients.

Symptomatic hyponatremia after voluntary excessive water ingestion in a patient without psychiatric problems.

Water intoxication usually happens in patients with a psychiatric problem, who are subject to compulsive water ingestion, and during clinical examinations, such as uroflowmetry, and is seldom observed in ordinary people. Here we report a patient with severe hyponatremia due to voluntary water drinking coexisting with no psychiatric problems. The case presented clinically significant hyponatremia 124 mmol/L without any signs of dehydration after voluntary ingestion of 4000 ml of water over 3 hours. She normally responded to ingestion of 1000 ml of water over 20 min after recovery from hyponatremia, and did not meet the diagnostic criteria of SIADH. She was not a compulsive drinker. The present case suggests that one should consider water intoxication as a cause of hyponatremia in a patient without signs of dehydration, even if he/she does not have a history of compulsive water ingestion.

Fatal water intoxication in a schizophrenic patient--an autopsy case.

We report a case of fatal water intoxication due to polydipsia. A 69-year-old schizophrenic male was found dead at his room of the hospital in which he had been admitted. Medico-legal autopsy was carried out to determine the cause of his death. The autopsy revealed no severe trauma leading him to the death. Internally, it was noticed that the stomach was vigorously expanded, including fluid contents. Intracardiac blood, being dark-red in color, seemed to be diluted. The both lungs ballooned aqueously, showing apparently edema. However, there was neither macroscopic nor histopathological lesion, being responsible for his death. Postmortem biochemical analyses revealed severe hyponatremia of 92 mEq/ml. In cases with short postmortem interval, serum sodium level almost similarly reflected antemortem level. According to his psychiatric doctor, he had been diagnosed as water intoxication due to polydipsia. Moreover, at 2 h before the discovery of his body, he had been found to drink much running water. It was concluded the cause of his death as fatal water intoxication.

[Generalized compartment syndrome after excessive drinking. A rare complication of psychological disorders?]. / Das generalisierte Kompartmentsyndrom nach exzessivem Trinken. Seltene Komplikation psychischer Erkrankungen?

Psychogenic polydipsia can lead to compartment syndromes, which is too infrequently considered in psychiatric patients who binge-drink on hypotonic fluids. If masked by the leading clinical presentation of cerebral edema, compartment syndromes of the extremities may be diagnosed too late or remain undetected. Based on a literature review and case report, we discuss additional factors and the specific features of diagnosis and treatment.

Efficacy of clozapine in a non-schizophrenic patient with psychogenic polydipsia and central pontine myelinolysis.

Clozapine is an atypical antipsychotic drug that has been demonstrated to be a highly effective treatment for polydipsia in schizophrenic patients. The authors report the first case of a non-schizophrenic patient affected by polydipsia and central pontine myelinolysis who was successfully treated with clozapine.

[Potomania associated with schizophrenia: a case report]. / La potomanie associee a la schizophrénie: à propos d'un cas.

The potomania or primary polydipsia is associated to schizophrenia in 20% of cases. Authors reports a case of a patient 27 old years, that suffering from hebephrenia who presented potomania. It was necessary to eliminate secondary polydipsia. The main complication resulting from potomania is water intoxication. Neurobiological or psychological hypothesis were suggested related to the etiopathogeny of this association. Some biological or comportemental therapy were effective in this context.

Effects of clonidine in schizophrenic patients with primary polydipsia: three single case studies.

A pilot study was conducted in schizophrenic patients with primary polydipsia to determine the tolerability of adding clonidine to an existing antipsychotic drug regimen and to seek evidence of an antidipsic effect. Three patients with chronic schizophrenia and primary polydipsia underwent open controlled prospective trials of treatment with clonidine in doses of up to 800 microg/day. The trials lasted from 2 to 5 months each, and analysis of variance was used to test for changes in dependent variables on a case-by-case basis. Blood pressure and pulse declined significantly in a dose-dependent manner, but fluid intake, as assessed by measurements of weight and 24-h urine volume, was not affected. Hypotension and bradycardia limited the extent to which the dose of clonidine could be increased. The lack of evident effect of clonidine on polydipsia in this small sample and the inconsistent results of two other recent studies of clonidine in patients with schizophrenia and primary polydipsia provide little overall support for the effectiveness of clonidine treatment in primary polydipsia associated with schizophrenia.