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Summary A 38-year-old female was initially seen in the intensive care unit after severe postpartum hemorrhage. She was initially diagnosed to have Sheehan’s syndrome and after discharge, she was diagnosed to have a vesicovaginal fistula which initially caused a delay in diagnosing diabetes insipidus in the patient because she was having urinary incontinence. The patient had the vesicovaginal fistula repaired and was on replacement with levothyroxine, prednisone, and desmopressin. Years after her diagnosis, the patient experienced recurrent episodes of hyponatremia in the setting of desmopressin therapy. This case highlights the challenges of diagnosing diabetes insipidus in a patient with Sheehan’s syndrome and a vesicovaginal fistula, as well as the long-term management of central diabetes insipidus in a resource-limited setting. Learning points Sheehan’s syndrome is rarely associated with diabetes insipidus, and in our patient, it was initially missed due to a vesicovaginal fistula which caused urinary incontinence. Water intoxication is more common in young children and older adults but can occur years after initiating treatment with desmopressin in adults and should be kept in mind when treating patients with hyponatremia who have hypopituitarism associated with diabetes insipidus. Water intoxication is much more common in patients with diabetes insipidus being treated with intranasal desmopressin than in those using the oral preparations.

International audience; Nephrogenic diabetes insipidus due to the inability of the kidneys to concentrate urine is frequently observed during lithium therapy. Lithium concentrates into principal cells in collecting ducts in the kidney and downregulates aquaporin 2 expression, which reduces renal reabsorption of water. This disease is characterized by polyuria - polydipsia leading to intracellular dehydration and hypernatremia. Water deprivation test is performed to confirm insipidus diabetes. The desmopressin permits to distinguish nephrogenic from cranial insipidus diabetes. We report the case of a 64 years old women who presented with global dehydration and severe hypernatremia. Four years ago, she was hospitalized for nephrogenic diabetes insipidus related to a self-induced lithium intoxication. Persistent nephrogenic insipidus diabetes after cessation of lithium therapy are described in literature, and this hypothesis may be consistent with this case report.

Introduction. Water intoxication is a well-recognized cause of symptomatic hyponatremia, whose often fatal consequences are described in a wide variety of conditions such as psychiatric disorders, metabolic dysfunctions, child abuse, drug abuse and several medical procedures. The case. We here report a rare case of a 67-year-old woman with severe acute hyponatremia due to an excessive voluntary water intake – 14 litres in two days – following a chiropractic prescription. The patient developed sudden severe symptoms, including water retention, sensory alteration, altered mental status and tonic-clonic seizures. She was thus admitted to the Intensive Care Unit with a diagnosis of coma due to electrolyte alterations following water intoxication. Conclusion. The evaluation, in the present case, of the medicolegal implications related to malpractice involving a practitioner of Complementary and Alternative Medicine, led to the admission of a professional liability of the chiropractor.

Rationale: Cardiac arrest caused by water intoxication syndrome following hysteroscopic surgery is a rare but life-threatening occurrence. Extracorporeal membrane oxygenation (ECMO) is rarely used to treat water intoxication syndrome in hysteroscopic surgery. Here, we successfully treated a patient with water intoxication syndrome following hysteroscopic surgery with ECMO. Patient concerns: We report a rare case of cardiac arrest during hysteroscopic surgery treated with veno-venous (VV) ECMO. Diagnosis: Water poisoning syndrome was diagnosed by electrolyte examination, the lowest value of serum sodium was 110.7 mmol/L. Interventions: VV-ECMO was prescribed as a measure after traditional cardiopulmonary resuscitation. Results: ECMO was successfully evacuated on day 5 and the patient was discharged on day 45. Conclusion: Mastering the hysteroscopic operative techniques and using a bipolar hysteroscopic generator, isotonic fluid, perfusion pressures less than 100 mm Hg, and local anesthesia may reduce the risk of hysteroscopic water intoxication syndrome. During hysteroscopic surgery, patients may experience cardiac arrest and fatal water intoxication syndrome. Even when traditional cardiopulmonary resuscitation is successful, VV ECMO may contribute to the recovery of brain function if oxygenation is not maintained.

Adolescents with eating disorders (EDs) may present not only with abnormal eating behaviors but also with abnormal drinking behaviors varying widely. These behaviors include water loading to cheat on weight measurements, to feel full and suppress appetite and/or to induce vomiting; as well as restricting fluid intake in addition to food. We present a 16-year-old female adolescent with anorexia nervosa restrictive type and major depressive disorder who was hospitalized due to acute food refusal and developed generalized seizures due to dilutional hyponatremia in consequence of consuming excessive amount of water. Psychiatric diagnoses were made according to ‘The Diagnostic and Statistical Manual of Mental Disorders’ (5th ed.; DSM–5) criteria. After starting nutritional rehabilitation with a low calorie meal plan to avoid refeeding syndrome, a weight gain of 2 kg was noted in the second day of hospitalization. At the bedside visit, she was observed in a disoriented manner and consecutively in seconds, lost consciousness with a generalized tonic–clonic seizure lasting 2 min. Her serum sodium level was measured as 116 mEq/L, which was normal at the time of admission. It was later learned that she secretly ingested 19 L of water in a short amount of time. She regained consciousness and no further seizures were observed after intravenous sodium deficit correction and fluid restriction therapy. Her serum sodium level was normalized (137 mEq/L) within 12 h. A thorough clinical assessment of hydration and drinking behaviors as well as eating behaviors is essential for patients with EDs to avoid serious medical complications with high mortality and morbidity during follow-up. It is interesting that this amount of fluid consumption in such a short period of time did not present to the clinic with vomiting, gastric dilatation or bowel irrigation symptoms in a case with acute food refusal and restriction for a year, instead absorbed very quickly causing acute and severe symptomatic hyponatremia with generalized seizures.

Purpose Anorexia nervosa is a chronic disease which may result in various complications. In pediatric clinical practice, it is common to observe complications related to progressive cachexia caused by malnutrition; however, cases of severe complications, like electrolyte disorders, which represent a direct threat to life, due to polydipsia, are rarely observed. The purpose of this study is to highlight that excessive drinking is of primary importance in anorexia nervosa patients, as it can result in severe medical complications, including increased risk of death. Methods We report the case of a 13-year-old girl with anorexia nervosa, who was referred to hospital with seizures, disorders of consciousness, and cardiorespiratory failure. Results The unstable condition of the patient was attributed to hyponatremia (119 mmol/l), decreased serum osmolality (248 mmol/kg), and decreased urine osmolality (95 mmol/kg) caused by polydipsia (water intoxication) and persistent vomiting. The presented girl was drinking large amounts of water prior to a weigh-in to falsify her low body weight. Conclusions Polydipsia is a common problem reported by patients with eating disorders, but one which rarely leads to serious clinical complications, due to severe hyponatremia. This case underscores the importance of careful evaluation of fluid intake and the need for regular monitoring of serum electrolytes in patients with anorexia nervosa. All clinicians treating patients with such disease, as well as the parents of sick children, should be familiar with this life-threatening condition. Level IV Evidence obtained from multiple time series with or without the intervention, such as case studies.

Misguided encouragement to consume large volumes of water during labour for pain relief results in dilutional hyponatraemia in mothers and their babies presenting with neurological dysfunction. We report three babies who were encephalopathic with seizures in the background of hyponatraemia secondary to maternal ingestion of large volumes of water and mild perinatal asphyxia. All babies underwent therapeutic hypothermia in addition to sodium supplementation with fluid restriction. Their neurodevelopment was appropriate for age. This case series highlights the dilemma that could arise with hyponatraemic encephalopathy and mild perinatal asphyxia in the first 6 hours of life, which is the window of opportunity for therapeutic hypothermia for hypoxic-ischaemic encephalopathy. It is important to educate pregnant mothers in labour on the adverse effects of excessive fluid ingestion.

The antidiuretic attribute of oxytocin can cause many side effects. Water intoxication is one of the most serious complications. The authors describe a case of water intoxication with neurological symptoms and severe hyponatraemia in the course of natural labor stimulated by oxytocin in a low-dose regimen.

Hyponatremia during labor and delivery may result in severe maternal and neonatal sequelae. Our aim was to describe the direct effect of hyponatremia in labor on pregnancy outcome.A case series of parturients diagnosed with hyponatremia during labor and their neonates. Clinical presentation, laboratory workup, and maternal and neonatal outcomes are presented.Four parturients and their corresponding six neonates were diagnosed with hyponatremia. Of these, two cases were caused by water intoxication and two were preeclampsia induced. While two were identified due to maternal or neonatal symptoms, two were diagnosed by routine laboratory testing. In all cases, low maternal sodium resulted in similarly low neonatal sodium. Neonatal symptoms included respiratory distress syndrome (RDS), lethargy, and jaundice.Psychogenic drinking during labor and preeclampsia may predispose to maternal hyponatremia, resulting in neonatal hyponatremia. Early recognition and treatment can prevent further maternal deterioration and adverse neonatal sequelae.

Overhydration is a frequent complication in dialysis patients. It has been linked with hypertension, left ventricular hypertrophy, arterial stiffness, atherosclerosis uremic cardiomyopathy, and all-cause mortality or cardiovascular morbidity. In addition, predialysis underhydration is also associated with increased risk of death in ESRD patients. In this context, the optimal evaluation of hydration status is a must. However, this mission is not easy or accurate. In the last 10 years, several new methods have been tested in dialysis patients, particularly bioimpedance and lung ultrasonography. The precise clinical value of these techniques in the daily care of hemodialysis patients is not obvious yet. Sodium is also an important piece of this puzzle. Salt intake and/or removal of sodium during dialysis are essential determinants of optimal hydration status. Recent studies have revealed that salt and water homeostasis is also dependent of tissue sodium storage-increased in hemodialysis patients. However, the significance of increased sodium tissue storage as a cardiovascular risk factor and the relationship between tissue sodium content and hard CV endpoint have not yet been elucidated yet.

A 33-year-old woman in her first pregnancy with no significant medical history had a tonic–clonic seizure one hour after delivery due to acute hyponatraemia caused by excess intake of fluids. She was admitted to a birthing centre as a low-risk labourer where she spent 19 hours including 4 hours in the second stage of labour. Throughout the labour, she was encouraged to drink as per her own initiative and thirst. However, there was no monitoring of fluid intake. In spite of initial confusion about the cause of the seizure, a multidisciplinary approach helped with diagnosis of an underlying pathology and allowed timely treatment to avoid adverse outcomes in this patient. We would like to increase awareness of a possibility, however rare, of water intoxication due to fluid overconsumption by patients in labour and encourage production of information guidance for monitoring of fluid intake of women in labour.

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.

Background Dysnatremias are common electrolyte disturbances with significant morbidity and mortality. In chronic dysnatremias a slow correction rate ( 10 mmol/L/24 h). The median time of correction was 1 day in patients with hypo- and 2.5 days in patients with hypernatremia. The mortality was 7% in patients with hypo- and 29% in patients with hypernatremia. Interpretation Severe acute dysnatremias have significant mortality and require immediate treatment. A rapid correction rate may be lifesaving and is not associated with neurological complications. Chronic dysnatremias, on the other hand, are often compensated and thus less severe. In these cases a rapid correction rate may lead to severe cerebral complications.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with an unknown cause and invariably fatal outcome. We sought to evaluate a correlation between motor neuron disease (MND) mortality rates and residential radon levels that was previously reported for counties in the United Kingdom. We examined the relationships between age-adjusted MND mortality rates in U.S. states with residential radon levels, well water use, and other variables using structural equation modeling. We observed a significant correlation between MND mortality rates and radon levels. However, in structural equation models, radon did not have a significant, direct effect on MND mortality rates. Conversely, MND mortality rates were significantly and directly predicted by race and by the percentage of the population of each state using well water (p

Background Acute water intoxication after hysteroscopy is a rare, life-threatening condition, often accompanied with delayed diagnosis owing to masked symptoms because of general anesthesia. Case presentation Herein we presented a 39-year-old female who presented with cardiac arrest after hysteroscopic myomectomy because of acute water intoxication and survived after extracorporeal membrane oxygenation, continuous venous–venous hemofiltration, and aggressive high sodium fluid resuscitation. Conclusion Failure to recognize and treat this condition appropriately may lead to potentially lethal cardiopulmonary complications.

Cerebral edema leading to elevated intracranial pressure (ICP) is a fundamental concern after severe traumatic brain injury (TBI), stroke, and severe acute hyponatremia. We describe a swine model of water intoxication and its cerebral histological and physiological sequela. We studied female swine weighing 35–45 kg. Four serum sodium intervals were designated: baseline, mild, moderate, and severe hyponatremia attained by infusing hypotonic saline. Intracranial fluid injections were performed to assess intracranial compliance. At baseline and following water intoxication wedge biopsy was obtained for pathological examination and electron microscopy. We studied 8 swine and found an increase in ICP that was strongly related to the decrease in serum sodium level. Mean ICP rose from a baseline of 6 ± 2 to 28 ± 6 mm Hg during severe hyponatremia, while cerebral perfusion pressure (CPP) decreased from 72 ± 10 to 46 ± 11 mm Hg. Brain tissue oxygen tension (PbtO2) decreased from 18.4 ± 8.9 to 5.3 ± 3.0 mm Hg. Electron microscopy demonstrated intracellular edema and astrocytic foot process swelling following water intoxication. With severe hyponatremia, 2 cc intracranial fluid injection resulted in progressively greater ICP dose, indicating a worsening intracranial compliance. Our model leads to graded and sustained elevation of ICP, lower CPP, and decreased PbtO2, all of which cross clinically relevant thresholds. Intracranial compliance worsens with increased cerebral swelling. This model may serve as a platform to study which therapeutic interventions best improve the cerebral physiological profile in the face of severe brain edema.

The authors report a case of a 15-year-old girl with hypopituitarism due to pituitary stalk interruption syndrome diagnosed in the neonatal period. The patient was admitted to the emergency room with impaired consciousness and hypoglycaemia. The day before, she increased her water intake to about 1.5 L to perform a pelvic ultrasound. In the following hours, she developed vomiting and food refusal. Blood analysis revealed hypoglycaemia, hyponatraemia, decreased serum osmolality and normal urinary density. Hyponatraemia and adrenal crisis were managed with a gradual but slow resolution of consciousness and electrolytic balance. This case describes an episode of iatrogenic water intoxication in a patient under desmopressin treatment. Although uncommon, dilutional hyponatraemia is the main complication of desmopressin treatment. We reinforce the importance of patients and caregivers’ long-life education for the potential complications of an increase in fluid intake in patients treated with desmopressin.

Image 1Contribution to Emergency Nursing Practice: •Forced water intake with subsequent hyponatremia is a potentially fatal form of child abuse. •Health care workers should consider forced water intoxication in the differential diagnosis of otherwise unexplained hyponatremia. •Hyponatremic encephalopathy can usually be reversed if proper treatment is initiated promptly.

Objective Hyponatremia due to excessive fluid intake (i.e. primary polydipsia (PP)) is common. It may culminate in profound hyponatremia—carrying considerable risk of morbidity. However, data on patients with PP leading to hyponatremia is lacking. Herein, we describe the characteristics of polydiptic patients hospitalised with profound hyponatremia, and assess one-year outcomes. Design Substudy of the prospective observational Co-MED Study. Patients Patients with an episode of profound hyponatremia (≤125mmol/l) due to PP in the medical emergency were eligible and classified into psychogenic polydipsia (PsyP), dipsogenic polydipsia (DiP), and beer potomania (BP). Measurements Symptoms, laboratory findings, and factors contributing to hyponatremia (comorbidities, medication, and liquid intake) were assessed. A one-year follow-up was performed to evaluate recurrence of hyponatremia, re-admission rate, and mortality. Results 23 patients were included (median age 56 years [IQR 50-65], 74% female), 7 had PsyP, 8 DiP, and 8 BP. Median serum sodium of all patients was 121mmol/l (IQR 114-123), median urine osmolality 167mmol/l (IQR 105-184), and median copeptin 3.6mmol/l (IQR 1.9-5.5). Psychiatric diagnosis, particularly dependency disorder (43%) and depression (35%), were highly prevalent. Factors provoking hyponatremia were found in all patients (e.g. acute water load, medication, stress). During the follow-up period, 67% of patients were readmitted, 52% of these with re-hyponatremia, and 3 patients (38%) with BP died. Conclusion Patients with PP are more likely to be female, and have addictive and affective disorders. Given the high recurrence, re-hospitalisation, and mortality rate, careful monitoring and long-term follow-up including controls of serum sodium, education and behavioural therapy is needed. This article is protected by copyright. All rights reserved.

Healthcare professionals frequently advise patients with simple infective illness to drink more fluids. Here, a 59-year-old woman with a urinary tract infection followed such advice resulting in hospital admission with symptomatic acute hyponatraemia. Water intoxication is well recognised as a cause of symptomatic hyponatraemia in endurance sports, MDMA use and psychogenic polydipsia. It has rarely been described outside of these circumstances. With normal renal function, it is difficult to overwhelm the excretory capacity for water. However, in infective illness, increased levels of antidiuretic hormones (which may be secreted both appropriately to correct volume status and inappropriately as a feature of disease) reduce renal excretion of water. In this scenario, could increased administration of oral hypotonic fluids lead to hyponatraemia, with associated morbidity and mortality, than has previously been recognised? There is a need for more research to qualify our oft-given advise to drink more fluids.

Studies to date have only investigated primary polydipsia in hospitalized psychiatric patient populations, where rates range from 3% to 25%. The objective of the present study was to determine the occurrence of primary polydipsia in a psychiatric outpatient population, and to determine the perceptions of outpatients with self-induced water intoxication regarding reasons for drinking excess fluids, health risks, and insight into their behavior. All 115 psychiatric outpatients from a Community Outreach Program in Kingston, Ontario, were invited to participate in this study. Of these, 89 (77.4%) were enrolled. Data collection included chart reviews, structured interviews, weight measurements, and urine collection. The incidence of primary polydipsia was found to be 15.7%. One-half of the polydipsic people presenting with medical complications suggestive for water intoxication had cigarette smoking as a strong correlate. There were interesting answers to the self-induced water intoxication questionnaire. These showed a lack of knowledge related to the normal quantity of fluids necessary daily and about healthy behaviors. Excessive drinking occurs in psychiatric patient populations outside of institutional/hospital settings. Patients have limited awareness of the severity and possible complications from their problem. Given the prevalence of polydipsia, more effort should be put into identifying and treating this problem.

Water intoxication is a common disorder in calves and is usually characterized by transient hemoglobinuria. In contrast, the condition is very rare in adult cattle, with few reports on naturally occurring cases. In the present report, four female Japanese Black cattle, aged 16-25 months, showed neurological signs when they drank water following a water outage. Hemoglobinuria was not grossly observed, while severe hyponatremia was revealed by laboratory tests. Autopsy indicated cerebral edema with accumulation of serous fluid in expanded Virchow-Robin spaces. These results indicate the possibility of water intoxication associated with cerebral edema due to severe dilutional hyponatremia in adult cattle.

Hyponatraemia is the most common electrolyte disturbance encountered in clinical practice. Several causes of hyponatraemia are recognised and in many patients the aetiology may be multifactorial. An important cause is water intoxication and this is often iatrogenic. We present three patients, all of whom suffered from multiple myeloma, who illustrate different aspects of hyponatraemia, its causes and management.

Two female patients aged over 80 years developed central nervous symptoms after drinking large amounts of water (more than 3 l per day).Both had a hypoosmolar hyponatremia that was induced by concomitant treatment with hydrochlorothiazid (HCT) in the one case and in the other case relied on a distal tubular damage due to reflux nephropathy.Hyponatremia was corrected after withdrawal of HCT and fluid restriction and central nervous symptoms disappeared rapidly.Distal tubular urinary dilution can be disturbed by HCT and parenchymal renal disease and can result in symptomatic hyponatremia after drinking large amounts of water.

Recreational drug use is a significant societal issue and remains a clinical challenge in emergency and critical care departments. We report on a 19-year-old woman admitted to hospital semiconscious and with severe hyponatraemia. Urinalysis was positive for methamphetamine and supported a diagnosis of hyponatraemia related to ecstasy use together with a syndrome of inappropriate antidiuretic hormone secretion (SIADH). The woman was transferred to an intensive care unit, where a hypertonic saline infusion was started. Three hours postadmission she developed polyuria. Follow-up urinalysis at this point was consistent with water intoxication. This case is a reminder that hyponatraemia is a potentially fatal complication after the ingestion of 3,4-methylenedioxymethamphetamine, illustrates the sequential nature of an SIADH and water intoxication and highlights the importance of considering the sequence of onset of hyponatraemia, as the patient may be admitted at any stage.

Polydipsia and water intoxication (PWI) are relatively frequent among schizophrenic subjects, particularly in institutional settings and may lead to severe complications. However, little is known on their association with other characteristics of psychosis. Hence, we took advantage of a cohort of 114 subjects extensively assessed on natural history and clinical variables to examine the correlates of PWI in chronic schizophrenia. We randomly sampled DSM-IV schizophrenic subjects from: i) a lower functioning subgroup, i.e., long-term psychiatric wards or highly structured group housing facilities; and ii) a higher functioning subgroup, i.e., patients living in the community without supervision. Subjects were assessed from multiple sources for lifetime severity of positive, disorganisation, negative and depressive symptoms, premorbid adjustment, age of onset, level of functioning, comorbid diagnoses of substance abuse and lifetime history of PWI. Twelve subjects (10.5%) met our PWI criteria. We observed more severe psychotic symptoms, earlier onset, poorer current adjustment and more frequent prior alcohol use disorder in PWI subjects. When restricting comparisons to patients living in institutional setting, differences on clinical and natural history variables vanished but the association between PWI and prior alcohol abuse persisted (72.7% in PWI vs. 21.4% in non-PWI subjects, p

P-glycoprotein (P-gp), which is coded by the MDR1 gene, in the brain capillary endothelial cell limits the entry of many drugs including antipsychotics into the brain. The aim of this study is to examine whether a functional polymorphism, a C to T substitution at position 3435 in exon 26 of the MDR1 gene, is associated with susceptibility to polydipsia-hyponatremia in schizophrenia (SCZ) in a Japanese case-control sample. It has been reported that individuals homozygous for this polymorphism had significantly lower MDR1 expression levels and dysfunction of MDR1 (PNAS 97:3473-3478, 2000). Furthermore, the brain entry of risperidone and 9-hydroxyrisperidone has been shown to be greatly limited by P-gp (Int J Neuropsychopharmacol 7:415-419, 2004). In order to our knowledge, this is the first association study between the MDR1 polymorphism and polydipsia-hyponatremia in SCZ. Our sample includes 331 patients with SCZ (DSM-IV) (84 with polydipsics and 247 non-polydipsic controls). The common C3435T polymorphism of the MDR1 was genotyped for both groups and differences in genotype and allele frequency between cases and controls were evaluated using the chi(2)-test. A significant association between the MDR1 C3435T polymorphism and polydipsia was found (chi(2) = 4.43, d.f. = 1, P = 0.035; OR = 1.46; 95%CI = 1.03-2.07). Our results suggest that the MDR1 C3435T polymorphism may confer susceptibility to polydipsia in SCZ.

Aquaporin-4 (AQP4) is a water transport protein expressed in glial cell plasma membranes, including glial cell foot processes lining the blood-brain barrier. AQP4 deletion in mice reduces cytotoxic brain edema produced by different pathologies. To determine whether AQP4 is rate-limiting for brain water accumulation and whether altered AQP4 expression, as occurs in various pathologies, could have functional importance, we generated mice that overexpressed AQP4 in brain glial cells by a transgenic approach using the glial fibrillary acid protein promoter. Overexpression of AQP4 protein in brain by approximately 2.3-fold did not affect mouse survival, appearance, or behavior, nor did it affect brain anatomy or intracranial pressure (ICP). However, following acute water intoxication produced by intraperitoneal water injection, AQP4-overexpressing mice had an accelerated progression of cytotoxic brain swelling, with ICP elevation of 20 +/- 2 mmHg at 10 min, often producing brain herniation and death. In contrast, ICP elevation was 14 +/- 2 mmHg at 10 min in control mice and 9.8 +/- 2 mmHg in AQP4 knock-out mice. The deduced increase in brain water content correlated linearly with brain AQP4 protein expression. We conclude that AQP4 expression is rate-limiting for brain water accumulation, and thus, that altered AQP4 expression can be functionally significant.

Water supply is a basic public problem. In modern science, three periods with different approaches to define recommended water intake in adults can be distinguished. Pediatricians agree that hydration in children may be optimal only in breastfed infants. More data are required on the health effects of different hydration states and varying water intakes in particular age and gender groups to define optimal ranges of water intake. The fetus grows in an exceptionally well-hydrated environment. Water metabolism shows several peculiarities in preterm and term infants. Infant diarrhea remains a major topic of basic and clinical research. Water intoxication in infants, toddlers, and children is rare and can only be found in exceptional circumstances. Hydration status characterized by hyponatremia may play a role in the pathogenesis of febrile convulsions in toddlers. There is increasing indirect evidence that spontaneous drinking behavior of a population may be fixed and anchored in the age range of toddlers. Sex differences in hydration status are common, but not obligatory. What causes theses differences? What is behind the various circadian rhythms of urine osmolality in children? At what age and in what quantities can alcohol and caffeine consumption be tolerated? How can individual susceptibility be defined? Reflecting on the modern epidemic of obesity in children and adolescents, a public consensus concerning use and misuse of sweetened drinks seems mandatory. Dietary reference intakes of water refer to 24-hour intake. In nutritional counselling, food and meal-based dietary advice is primarily given. Young parents are confronted with a flood of advice of varying quality. Recommendations on fluid consumption should be collated and revised.

A 66-year-old woman was admitted to our hospital because of vomiting and appetite loss. For the 2 days prior to admission, she had a cold, which had developed into acute viral bronchitis on admission. Because laboratory data on admission showed hyponatremia, intravenous infusion of Ringer's lactate solution was started. However, generalized seizures appeared, and she developed a coma on the day of admission. Her plasma antidiuretic hormone (ADH) level was high in the context of a low serum osmolality on the second hospital day. The infusion rate was increased, and the patient's consciousness level returned to normal. However, her normalized serum Na level declined again as she drank much water to reduce throat discomfort. As the throat discomfort caused by the throat inflammation improved with azulene gargling, her water intake was reduced, and the serum Na concentration returned to normal. Thus, polydipsia caused by a throat inflammation partially contributed to hyponatremia in this patient. We note that increased ADH secretion has been reported in adults with acute respiratory infection. Therefore, we concluded that polydipsia caused by the throat inflammation, plus increased ADH secretion, resulted in hyponatremia in this patient. We should pay attention to the behavior of drinking extra fluid in patients with acute respiratory infections.

Objective Growth hormone (GH)-deficiency is associated with a reduced extracellular volume (ECV), whereas GH replacement may cause fluid retention. We have tested a simple method to assess hydration in GH-deficient patients (GHD) based on concomitant measurements of body resistance by bioelectrical impedance analysis (BIA), and arm muscle area (AMA). Design We prospectively followed 130 patients (54 females, 76 males) with adult-onset GHD before and during 1–5 years GH replacement therapy. Methods Concomitant measurements of body resistance and AMA were done on four occasions: before treatment, after one month and one year of treatment, and at the most recent visit. Based on normative data obtained in 142 women and 84 men an inverse relationship was documented between body resistance and AMA. Assuming that linear height and the concentration of electrolytes remain constant, body resistance at a given AMA will reflect specific hydration. Results In the patients a gender-specific inverse correlation between body resistance and AMA existed, which was different from the control group and changed during GH replacement. A deviation between predicted (based on normative data) and measured body resistance at a given AMA was recorded in the patients before and during therapy compatible with relative dehydration in the untreated state followed by an increase in hydration during therapy. Conclusions Concomitant measurements of BIA and AMA in GHD patients may provide a non-invasive and simple means to estimate hydration before and during GH replacement.

Diminished hippocampal volume occurs in the anterior segment of some schizophrenic patients, and in the posterior segment in others. The significance of hippocampal pathology in general and these segmental differences in specific is not known. Several lines of evidence suggest anterior hippocampal pathology underlies the life-threatening hyponatremia seen in a subgroup of patients with schizophrenia; therefore our goal was to determine if this region was preferentially diminished in hyponatremic patients. We studied seven polydipsic hyponatremic, ten polydipsic normonatremic, and nine nonpolydipsic normonatremic schizophrenic inpatients, as well as 12 healthy controls. All underwent structural scanning on a high resolution (3.0 T) magnetic resonance imaging (MRI) scanner. Hippocampal formation, amygdala, and third ventricle volumes were manually traced in each subject. The hippocampus was divided at the posterior extent of the uncus, and all structural volumes were corrected for whole brain volume and other significant recognized factors (i.e., age, gender, height, parental education). Despite being overhydrated, anterior hippocampal formation volume was diminished in those with polydipsia and hyponatremia relative to each of the other three groups. Third ventricle volume was larger in this group than in healthy controls but similar to the two patient groups. Posterior hippocampal and amygdala volumes did not differ between groups. Other potential confounds (e.g., water imbalance) either had no effect or accentuated these differences. We conclude the anterior hippocampal formation is smaller in hyponatremic schizophrenic patients, thereby linking an important and objective clinical feature of schizophrenia to a neural pathway that can be investigated in animal models. The findings strengthen the hypothesis that anterior hippocampal formation pathology disrupts functional connectivity with other limbic structures in schizophrenia.

Acute symptomatic hyponatremia after thiazide diuretic initiation is a medical emergency. Here we describe the case of a flight attendant who developed acute hyponatremia during a flight and the potential risk factors for developing this condition. A 57-year-old flight attendant with history of essential hypertension was recently started on a thiazide diuretic. As she did routinely when working, she increased her water intake during a flight from London to Mexico City. She complained of nausea and headache during the flight. Upon arrival, she developed severe disorientation and presented to the hospital emergency room (ER) with a Glasgow scale of 12, hypoxia, and a generalized tonic clonic seizure. Her laboratory results on arrival were consistent with severe hyponatremia (serum Na 116 mEql/L) and severe cerebral edema by CT scan. She was treated with hypertonic saline, with complete resolution of the neurologic symptoms. We describe high water intake and hypoxia related to decreased partial pressure of oxygen in the cabin as the two main risk factors for thiazide-induced acute hyponatremia in this case.

Neurogenic stunned myocardium is a rare disease entity that has been typically described as a consequence of subarachnoid hemorrhage and, less commonly, seizures. Here we describe a case of a healthy young woman who drank excessive free water causing acute hyponatremia complicated by cerebral edema and seizure, leading to cardiogenic shock from neurogenic stunned myocardium. Two days later, she had complete return of her normal cardiac function.

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.

Desmopressin has been used extensively for primary nocturnal enuresis and it is associated with a low incidence of adverse effects. The only reported serious side effect is seizure or altered levels of consciousness resulting from water intoxication, which has been reported for the nasal spray. We describe 18 children with clinical symptoms of water intoxication due to the prolonged bioactivity of desmopressin nasal spray.We evaluated 18 patients with clinical suspicion of prolonged desmopressin bioactivity during treatment with intranasal desmopressin for primary nocturnal enuresis. The control group consisted of 50 children with primary nocturnal enuresis and proven nocturnal polyuria who were treated with the same desmopressin regimen.All patients had prolonged maximal urinary concentration capacity and delayed restoration of daytime diluting capacity (p0.01). Of the patients 15 had the characteristic clinical symptoms of water intoxication with vomiting, headache, decreased consciousness and hyponatremia. We suspect that these symptoms are secondary to prolonged desmopressin bioactivity.Prolonged desmopressin bioactivity may increase the risk of water intoxication.

Dipsogenic diabetes insipidus is a syndrome of disordered thirst, in patients without psychiatric disease, which may be confused with partial central diabetes insipidus. Distinguishing these entities involves monitored water testing. Therapy with antidiuretic hormone in patients with dipsogenic diabetes insipidus is thought to be contraindicated for fear of inducing water intoxication. We report a case of a 26-year-old woman without psychiatric illness referred for longstanding polyuria and polydipsia. Otherwise healthy, she complained of near-constant thirst and frequent urination, causing severe disruption of her personal and professional life. She had been consistently eunatremic and polyuric, with low urine osmolality. Results of extensive water testing revealed intact urinary concentrating and diluting capacity, physiologic though blunted antidiuretic hormone (ADH) release, and an abnormally low thirst threshold, consistent with the diagnosis of dipsogenic diabetes insipidus. To control her polyuria we initiated treatment with intermittent, low-dose, intranasal desmopressin and strict water restriction during drug dosing. In follow-up she reported excellent control of polyuria and significant functional improvement. The reviewed literature demonstrates a limited number of reports about dipsogenic diabetes insipidus, and no prior report of a similar treatment strategy. Dipsogenic diabetes insipidus is an uncommonly (and not universally) recognized disorder, requiring monitored testing in order to distinguish it from incomplete forms of central diabetes insipidus. Though therapy with desmopressin cannot be recommended based on the results of a single case, the outcome presented here is intriguing and suggests that larger studies in such patients is warranted to assess the broader application of such an intervention.

Purpose: Desmopressin is widely used in primary nocturnal enuresis, bleeding disorders, central diabetes insipidus and diagnostic urine concentration testing. Hyponatremic hypervolemia leading to seizures has been reported as a rare but potentially life threatening side effect of desmopressin therapy. We sought to identify factors that predispose patients to hyponatremia and to find predictive factors associated with increased risk of water intoxication. Materials and Methods: We report 13 novel cases of desmopressin associated water intoxication and review the literature. A total of 93 instances of symptomatic hyponatremia during desmopressin treatment in children were identified. Specific data were reported in 58 of 93 cases. These 58 cases, in addition to our 13 novel cases, were further analyzed. Results: All children were treated with intranasal or intravenous desmopressin. No patient received oral desmopressin. Younger children are at greater risk for water intoxication than older children. The risk is particularly high at the beginning of desmopressin therapy. A total of 45 patients (63%) had prodromal symptoms, eg nausea, vomiting and headache. In 10 cases (14%) desmopressin was prescribed without an evident need. Conclusions: Based on this analysis, we conclude that the use of desmopressin should be cautiously considered, careful monitoring should be performed during the initiation of therapy, and particular care should be taken when treating young children and when prodromal symptoms such as nausea, vomiting and headaches occur.

SummaryBetween 1986 and 1998, a review of 61 records of patients who died before the age of 53 years in eight psychiatric departments whose catchment area had a total population of 559,429 inhabitants revealed that 24 (39.3%) of those patients had a schizophrenic disorder. Of those 24 patients, one (4.17%; 95% CI: 0–21%) died from complications of self-induced water intoxication (SIWIS). Among the 37 remaining patients, two (5.4%; 95% CI: 0–18%) died from complications of SIWIS.

A variety of evidence suggests that endogenous opioid peptides play a role in the short-term control of eating. More recently, opioid receptor antagonists like naltrexone have been approved as a treatment for alcohol dependence. Here we review the evidence for a role of opioid peptides in both normal and abnormal eating and drinking behaviours and in particular try to identify the nature of the role of opioids in these behaviours. Particular attention is paid to the idea that opioid reward processes may be involved both in the short-term control of eating and hedonic aspects of alcohol consumption, and parallels are drawn between the effects of opiate antagonists on food pleasantness and the experience of drinking alcohol. The review also explores the extent to which data from studies using opiate antagonists and agonists provide evidence for a direct role of endogenous opioids in the control of ingestive behaviour, or alternatively whether these data may be better explained through non-specific effects such as the nausea commonly reported following administration of opiate antagonists. The review concludes that the present data suggests a single opioid mechanism is unlikely to explain all aspects of ingestive behaviour, but also concludes that opioid-mediated reward mechanisms play an important control in hedonic aspects of ingestion. The review also highlights the need for further empirical work in order to elucidate further the role of opioid peptides in human ingestive behaviour.

A 14-year-old girl developed dental pain and was treated for acute infected pulpitis of her right upper lateral incisor with drilling and filling. The pain continued and was helped by analgesia, sucking ice cubes and drinking cold water. Forty-eight hours later, she became confused and disoriented. She started to vomit and complained of headache. Investigations revealed hyponatraemia with normal serum potassium levels and initially normal urinary sodium excretion. Over the next 24 hours, she passed 5.45 L of urine and her serum sodium rose from 125 to 143 mmol/L. Self-induced water intoxication has been described during drinking games and initiation ceremonies, but this would appear to an unusual cause. Conservative management proved successful in allowing this girl to recover without sequelae.

We report a case of a mandibular dentoalveolar fracture caused by severe iatrogenic hyponatremia-induced grand mal seizure in a 31-year-old pregnant lady who underwent normal vaginal delivery. She had oxytocin augmentation of her labor, and the seizure happened in the immediate postpartum period. The seizure was thought to be because of severe hyponatremia and prompt management controlled the metabolic disorder. The fracture was reduced and fixed successfully, and she was discharged after 48 hours, healing was uneventful.

Objective: To compare the demographic and clinical factors and familial psychopathology of chronic psychiatric inpatients with, and without, polydipsia. Method: We undertook a case-control study of chronic psychiatric inpatients both with, and without, polydipsia. Clinical and demographic data were gathered using a predesigned questionnaire, the Positive and Negative Syndrome Scale (PANSS), the Abnormal Involuntary Movement Scale (AIMS), the Mini-Mental State Examination Scale (MMSE), and the Family History–Research Diagnostic Criteria (FH-RDC). Results: The prevalence rate of polydipsia was 20.2%. The group with polydipsia was significantly younger, both at the time of their first-ever psychiatric and current psychiatric admissions, compared with the group without polydipsia. The 2 groups were similar in terms of their illness characteristics and psychiatric diagnoses. In the group with polydipsia, alcohol abuse predated the psychotic illness by a mean of 10.5 (SD 4.4) years, compared with 4.8 (SD 1.6) years for the same period in the unaffected group. The 2 groups did not differ significantly regarding the antipsychotic medication dosage, the proportion on concomitant anticholinergic medicaton, the documented previous response to antipsychotic medication, or past treatment with electroconvulsive therapy (ECT). First-degree relatives of patients with polydipsia were found to have significantly higher rates of alcohol dependence. Conclusion: This study provides further evidence for the higher rate of polydipsia among chronic psychiatric patient populations and for high rates of alcohol-related problems among their first-degree relatives.

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.

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.

To understand the increased susceptibility of the development of serious complications to hypoosmotic hyponatremia in young females, we examined the resistance of blood brain barrier (BBB) permeability to water along with the synaptosomal Na(+),K(+)ATPase activity in both sexes of rats during acute water intoxication. Four groups of rats were used: Group I and II were normal female and male rats injected with only Evans-blue. Group III and IV were water intoxicated female and male rats respectively. BBB permeability in female rats was found to be increased following acute water intoxication. In contrast, synaptosomal Na(+),K(+)ATPase activities in both water intoxicated male and female rats were found significantly lower than those in control rats. But inhibition in enzyme activity in synaptosomes from water intoxicated female rats was more pronounced than those of corresponding male rats. Our results concluded that female sex steroids may be responsible for the highly significant decrease in synaptosomal Na(+),K(+)ATPase activity and increased BBB permeability in female rats following water intoxication.

Two cases of rheumatoid arthritis, who developed severe hyponatremia after treatment with non-steroidal anti-inflammatory drugs (NSAID) are presented. Early diagnosis was followed by rapid correction with hypertonic saline. It is suggested that NSAIDs, like piroxicam, diclofenac and indomethacin, may be added to the list of drugs which can induce syndrome of inappropriate antidiuretic hormone (SIADH). Language: en