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An acute reduction in plasma osmolality causes rapid uptake of water by astrocytes but not by neurons, whereas both cell types swell as a consequence of lost blood flow (ischemia). Either hypoosmolality or ischemia can displace the brain downwards, potentially causing death. However, these disorders are fundamentally different at the cellular level. Astrocytes osmotically swell or shrink because they express functional water channels (aquaporins), whereas neurons lack functional aquaporins and thus maintain their volume. Yet both neurons and astrocytes immediately swell when blood flow to the brain is compromised (cytotoxic edema) as following stroke onset, sudden cardiac arrest, or traumatic brain injury. In each situation, neuronal swelling is the direct result of spreading depolarization (SD) generated when the ATP-dependent sodium/potassium ATPase (the Na+/K+ pump) is compromised. The simple, and incorrect, textbook explanation for neuronal swelling is that increased Na+ influx passively draws Cl− into the cell, with water following by osmosis via some unknown conduit. We first review the strong evidence that mammalian neurons resist volume change during acute osmotic stress. We then contrast this with their dramatic swelling during ischemia. Counter-intuitively, recent research argues that ischemic swelling of neurons is non-osmotic, involving ion/water cotransporters as well as at least one known amino acid water pump. While incompletely understood, these mechanisms argue against the dogma that neuronal swelling involves water uptake driven by an osmotic gradient with aquaporins as the conduit. Promoting clinical recovery from neuronal cytotoxic edema evoked by spreading depolarizations requires a far better understanding of molecular water pumps and ion/water cotransporters that act to rebalance water shifts during brain ischemia.

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.

Background: Catatonia is a syndrome of altered motor behavior that is mostly associated with general medical, neurologic, mood and schizophrenia-spectrum disorders. The association of newly onset catatonic symptoms with hyponatremia has been rarely reported in the literature. Case Presentation: We present a rare case of a young female patient with schizophrenia, who presented with catatonic symptoms in the context of hyponatremia due to water intoxication. The symptoms were eliminated with the correction of hyponatremia. There are only a few reports of hyponatremia-associated catatonia in psychiatric and non-psychiatric patients. Sometimes, catatonic symptoms may co-occur with newly onset psychotic symptoms and confusion, suggesting delirium. In several cases, the catatonic symptoms responded to specific treatment with benzodiazepines or electroconvulsive therapy. Conclusion: Hyponatremia may induce catatonic symptoms in patients, regardless of underlying mental illness, but this phenomenon is even more relevant in patients with a psychotic or mood disorder, which may itself cause catatonic symptoms. It is important for clinicians not to attribute newly-onset catatonic symptoms to the underlying psychotic or mood disorder without measuring sodium serum levels. The measurement of sodium serum levels may guide treating psychiatrists to refer the patient for further investigation and appropriate treatment.

Purpose Myocardial opioid receptors were demonstrated in animals and humans and seem to colocalize with membranous and sarcolemmal calcium channels of the excitation–contraction coupling in the left ventricle (LV). Therefore, this study investigated whether blockade of the cardiac opioid system by naltrexone would affect cardiac function and neurohumoral parameters in Wistar rats with volume overload-induced heart failure. Methods Volume overload in Wistar rats was induced by an aortocaval fistula (ACF). Left ventricular cardiac opioid receptors were identified by immunohistochemistry and their messenger ribonucleic acid (mRNA) as well as their endogenous ligand mRNA quantified by real-time polymerase chain reaction (RT-PCR). Following continuous delivery of either the opioid receptor antagonist naltrexone or vehicle via minipumps (n = 5 rats each), hemodynamic and humoral parameters were assessed 28 days after ACF induction. Sham-operated animals served as controls. Results In ACF rats mu-, delta-, and kappa-opioid receptors colocalized with voltage-gated L-type Ca2+ channels in left ventricular cardiomyocytes. Chronic naltrexone treatment of ACF rats reduced central venous pressure (CVP) and left ventricular end-diastolic pressure (LVEDP), and improved systolic and diastolic left ventricular functions. Concomitantly, rat brain natriuretic peptide (rBNP-45) and angiotensin-2 plasma concentrations which were elevated during ACF were significantly diminished following naltrexone treatment. In parallel, chronic naltrexone significantly reduced mu-, delta-, and kappa-opioid receptor mRNA, while it increased the endogenous opioid peptide mRNA compared to controls. Conclusion Opioid receptor blockade by naltrexone leads to improved LV function and decreases in rBNP-45 and angiotensin-2 plasma levels. In parallel, naltrexone resulted in opioid receptor mRNA downregulation and an elevated intrinsic tone of endogenous opioid peptides possibly reflecting a potentially cardiodepressant effect of the cardiac opioid system during volume overload.

Water intoxication is a fatal disorder associated with disturbance in brain function, known as hypo-osmolar syndrome which resulting from an excessive water intake, with dilutional hypernatremia leads to a potentially fatal outcome. A change in the electrolyte equilibrium such as this sudden drop in serum sodium level and then subsequent mortality. With hyponatremia, the plasma osmolality decreased leading to water movement into the brain according to the osmotic gradient, resulting in hyponatremic encephalopathy and cerebral oedema. Increased water intake such as in Psychogenic polydipsia is followed by urination of high amount of diluted urine (polyuria) which are the main initial symptoms of water intoxication with headache, blurred vision, nausea, tremor, and deterioration in psychosis. Other serious symptoms involve muscle spasms, Early detection of seizures and coma are more serious outcomes, Untreated cases may lead to death, Risk factor for water intoxication are Marathon runners, military population and athletes and due to this endurance events, these behaviors encouraging heavy sweating that result in heat exhaustion and consume large volumes of fluid, then hyponatremia developed as a result of excessive fluid substitution. Child abuse is other pediatric clinical cases reported with water intoxication. Psychogenic polydipsia which is psychiatric disorder with obsessive water drinking leading to a serious self-induced water intoxication (SIWI), water is normally metabolized and excreted by different means and it is mainly by kidneys in urine, evaporation through the skin, by respiratory system through the respired water vapor and little quantity of water was lost from the gastrointestinal tract (GI).The LD50 of water is > 90 ml/kg orally in rats. The current review illustrates the Life threatening effects of water when it is aggressively consumed.

Magnetic resonance imaging has been used for evaluating of a brain edema in experimental animals to assess cytotoxic and vasogenic edema by the apparent diffusion coefficient (ADC) and T2 imaging. This paper brings information about the effectiveness of methylprednisolone (MP) on experimental brain edema. A total of 24 rats were divided into three groups of 8 animals each. Rats with cytotoxic/intracellular brain edema induced by water intoxication were assigned to the group WI. These rats also served as the additional control group CG when measured before the induction of edema. A third group (WIMP) was intraperitoneally administered with methylprednisolone 100 mg/kg during water intoxication treatment. The group WI+MP was injected with methylprednisolone 50 mg/kg into the carotid artery within two hours after the water intoxication treatment. We evaluated the results in four groups. Two control groups (CG, WI) and two experimental groups (WIMP, WI+MP). Rats were subjected to MR scanning 24 h after edema induction. We observed significantly increased ADC values in group WI in both evaluated areas – cortex and hippocampus, which proved the occurrence of experimental vasogenic edema, while ADC values in groups WIMP and WI+MP were not increased, indicating that the experimental edema was not developed and thus confirming the protective effect of MP.

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.

The most used experimental mouse model of hyponatremia and elevated intracranial pressure (ICP) is intraperitoneal injection of water in combination with antidiuretics. This model of water intoxication (WI) results in extreme pathological changes and death within 1 hr. To improve preclinical studies of the pathophysiology of elevated ICP, we characterized diuresis, cardiovascular parameters, blood ionogram and effects of antidiuretics in this model. We subsequently developed a new mouse model with mild hyponatremia and sustained increased ICP. To investigate the classical protocol (severe WI), C57BL/6mice were anesthetized and received an intraperitoneal injection of 20% body weight of MilliQ water with or without 0.4 µg·kg-1 desmopressin acetate (dDAVP). Corresponding Sham groups were also studied. In the new WI protocol (mild WI), 10% body weight of a solution containing 6.5 mM NaHCO3, 1.125 mM KCl and 29.75 mM NaCl was intraperitoneally injected. By severe WI, ICP and mean arterial pressure increased until brain stem herniation occurred (23 ± 3 min after injection). The cardiovascular effects were accelerated by dDAVP. Severe WI induced a halt to urine production irrespective of the use of dDAVP. Following the new mild WI protocol, ICP also increased but was sustained at a pathologically high level without inducing herniation. Mean arterial pressure and urine production were not affected during mild WI. In conclusion, the new mild WI protocol is a superior experimental model to study the pathophysiological effects of elevated ICP induced by water intoxication.

A 4-month-old male indoor cat was referred for dyspnea, mental dullness and weakness, which appeared two days earlier. The cat had been adopted at 3 months of age. Physical exam showed cyanosis, dyspnea and mild hypothermia. The “spot test” was supportive of methemoglobinemia. Co-oximetry blood gas analysis revealed severe methemoglobinemia (81.40%), severe hyperchloremia and mild hyponatremia. CBC, biochemistry and urinalysis were within normal limits, blood smear showed the presence of Heinz bodies. Treatment was instituted with oxygen therapy, methylene blue 1% solution, ascorbic acid, intravenous fluid therapy. The clinical course was favorable with rapid improvement of cyanosis and methemoglobinemia (4.2%). Acquired methemoglobinemia was hypothesized. Two weeks after discharge the cat was asymptomatic but mild methemoglobinemia (15.60%) and hyperchloremia were evident. Exposure to oxidants contained in drinking water was suspected so the owners were instructed to use bottled water only. One month later the cat was asymptomatic, and methemoglobinemia and chloremia were within normal limits. Even if a congenital form due to cytochrome b5 reductase deficiency cannot be ruled out, drinking water intoxication is the most likely cause of methemoglobinemia in this cat.

Hypotonic hyponatremia secondary to acute water intoxication is most commonly associated with primary polydipsia in the setting of psychiatric illness. However, in certain circumstances, otherwise healthy individuals can be compelled to consume large enough volumes of water to overwhelm the kidney’s dilutional capacity of urine and cause a potentially life-threatening rapid decline in serum sodium. We present such a case of a 20-year-old basic military trainee with acute symptomatic hypotonic hyponatremia after drinking five to six liters of water prior to urine drug testing. The clinical manifestations of this disorder are non-specific and can be seen with many different pathologic processes, presenting a diagnostic challenge to the emergency clinician. This challenge can be further complicated by unclear or unobtainable history depending on clinical presentation. The authors will discuss key diagnostic and treatment elements of this potentially life-threatening disease to encourage clinicians to utilize social history when evaluating cases of acute water intoxication and resultant symptomatic hypotonic hyponatremia.

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.

The health and performance of ultra-endurance athletes is dependent on avoidance of performance limiting hypohydration while also avoiding the potentially fatal consequences of exercise-associated hyponatremia due to overhydration. In this work, key factors related to maintaining proper hydration during ultra-endurance activities are discussed. In general, proper hydration need not be complicated and has been well demonstrated to be achieved by simply drinking to thirst and consuming a typical race diet during ultra-endurance events without need for supplemental sodium. As body mass is lost from oxidation of stored fuel, and water supporting the intravascular volume is generated from endogenous fuel oxidation and released with glycogen oxidation, the commonly promoted hydration guidelines of avoiding body mass losses of >2% can result in overhydration during ultra-endurance activities. Thus, some body mass loss should occur during prolonged exercise, and appropriate hydration can be maintained by drinking to the dictates of thirst.

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.

Dipsogenic diabetes insipidus (DDI) is a subtype of primary polydipsia (PP), which occurs mostly in healthy people without psychiatric disease. In contrast, PP is characterized by a polyuria polydipsia syndrome (PPS) associated with psychiatric illness. However, the pathogenesis of DDI is not well established and remains unexplored. In order to diagnose DDI, the patient should exhibit excessive thirst as the main symptom, in addition to no history of psychiatric illness, polyuria with low urine osmolality, and intact urine concentrating ability. Treatment options for DDI remain scarce. On this front, there have been two published case reports with successful attempts at treating DDI patients. The noteworthy commonalities in these reports are that the patient was diagnosed with frequent excessive intake of water due to a belief that drinking excess water would have pathologic benefits. It could therefore be hypothesized that the increasing trend of excessive fluid intake in people who are health conscious could also contribute to DDI. Hence, this review provides an overview of the pathophysiology, diagnosis, and treatment, with a special emphasis on habitual polydipsia and DDI.

Hyponatremia is a frequent, yet often unrecognized result of water intoxication caused by psychogenic polydipsia in patients with psychiatric disorders such as schizophrenia and anorexia nervosa. The consequences of hyponatremia may include cerebral edema with tonic–clonic seizures and, in extreme cases, death. In cases of hyponatremia seen in psychiatric practices, the use of psychotropic drugs is often necessary to address both the underlying psychiatric problem and reduce the hyponatremia. Therefore, a patient’s clinical condition, the risk of side effects, the possible effect of the medication on hyponatremia and a history of prior medication use should be considered when selecting appropriate psychotropics. The present clinical case details the beneficial effects of olanzapine and fluoxetine in treating a patient with anorexia nervosa and body dysmorphic disorder experiencing acute hyponatremia, and the stable effect the medications achieved over a period of 2.5 years of maintenance therapy.

Background Primary polydipsia, characterized by excessive fluid intake, carries the risk of water intoxication and hyponatremia, but treatment options are scarce. Glucagon-like peptide-1 (GLP-1) reduces appetite and food intake. In experimental models, they also play a role in thirst and drinking behavior in. The aim of this trial was to investigate whether GLP-1 receptor agonists reduce fluid intake in patients with primary polydipsia. Methods: In this randomized, double-blind, placebo-controlled, 3-week crossover-trial, 34 patients with primary polydipsia received weekly dulaglutide (Trulicity®) 1.5mg and placebo (0.9% sodium chloride). During the last treatment week, patients attended an 8-hour evaluation visit with free water access. The primary endpoint was total fluid intake during the evaluation visits. The treatment effect was estimated using a linear mixed-effects model. In a subset of 15 patients and matched controls, thirst perception and neuronal activity in response to beverage pictures were assessed by functional MRI. Results Median [IQR] total fluid intake was 2250ml [1600-2600] on dulaglutide versus 2400ml [1850-3400] on placebo. Patients on dulaglutide reduced fluid intake by 490ml [95%-CI -780, -199], p=0.002, corresponding to a relative reduction of 17%. 24-hour urinary output was reduced by -943ml [95%-CI -1473, -413]. Thirst perception in response to beverage pictures was higher in patients with primary polydipsia versus controls and lower on dulaglutide versus placebo, but functional neuronal activity was similar between groups and treatments. Conclusion: GLP-1 receptor agonists reduce fluid intake and thirst perception in patients with primary polydipsia and could therefore be a novel treatment option for these patients.

Water intoxication is a life-threatening disorder accompanied by brain function impairment due to severe dilutional hyponatremia. We present a young woman who had multiple emergency admissions with severe dyselectrolytemias involving several electrolytes. Further assessment revealed a long history of chronic polydipsia and episodic water intoxication. Her serum electrolytes were normal after an overnight fluid fast. She had no further admissions after discussion and counseling concerning excessive water drinking. This case emphasizes the importance of obtaining an accurate fluid intake history in cases of hyponatremia and multiple electrolyte disturbances.

Water intoxication often causes hyponatremia. Acute hyponatremia and its rapid correction have been reported to cause rhabdomyolysis. However, little is known about the clinical course of water-intoxication-related rhabdomyolysis. We report a case of self-induced water intoxication resulting in rhabdomyolysis, in which serum creatinine kinase surged rapidly. The appropriate selection of fluid therapy was difficult because of the differences in the standard treatments for each complication. Water restriction is used to treat water intoxication, while the opposite, fluid resuscitation, is used to treat rhabdomyolysis. Close monitoring of serum creatinine kinase was useful in determining fluid management in such a situation.

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.

A woman in her late sixties presented with severe hyponatremia and acute kidney injury (AKI) as consequence of psychogenic polydipsia and acute urinary retention due to urinary tract infection. Urinary catheterization promptly drained 5.5 L of urine with resulting polyuria, leading to an initial swift raise in plasma (P) sodium concentration, disregarding the course of fluid resuscitation. After the polyuric phase, normal range P-sodium levels were reestablished by oral water restriction. Treatment with psychoactive drugs, e.g., zuclopentixol, may have contributed to the severity of the condition. There are few published reports regarding water intoxication and urinary retention, but none reflecting severe hyponatremia precipitated by acute urinary retention in a patient with polydipsia. By this report, we illustrate the detrimental consequences on water and electrolyte homeostasis of urinary retention and polydipsia resulting in acute water intoxication. The purpose of presenting this case is firstly to draw attention to the potentially fatal combination of polydipsia and postrenal acute kidney injury, where the kidneys are unable to correct the enormous excess water, then to focus on the difficulty in correcting hypervolemic hyponatraemia in the context of polyuria after relief of urinary retention, and finally, to point out that patients in treatment with antipsychotics may have further worsening of electrolyte derangement.

Background Primary polydipsia is commonly seen in patients with psychiatric illnesses. Excess water intake is also seen in patient with anorexia and anticholinergic medications. We report a patient who had hyponatraemia and rhabdomyolysis after consuming excess water for ureteric calculus. Case presentation A healthy middle-aged male presented with an episode of generalized tonic-clonic seizure and reduced level of consciousness preceded by consumption of excess water. He was recently diagnosed to have a ureteric calculus and was advised to consume plenty of water. On examination, he was disoriented in place, person and time. Except for the generalized diminished reflexes, other neurological and systemic examinations were normal. He had severe hyponatraemia, mild hypokalaemia and myoglobulinuria. His serum creatinine phosphokinase and aspartate aminotransferase were markedly elevated. The diagnosis of rhabdomyolysis in the setting of acute water intoxication was made. Optimum fluid and electrolyte management achieved a dramatic recovery of consciousness, hyponatraemia and rhabdomyolysis. Discussion The patient has had excess water intake due to a compulsive act in the background fear of ureteric calculus. Such act could lead to severe hyponatraemia and rhabdomyolysis. Therefore, future similar acts could be prevented by proper medical advice. Further, emergency physicians should be vigilant for rhabdomyolysis in patients with hyponatraemia or hypokalaemia.

It is not unusual for those participating in ultra-endurance ( 4 hr) events to develop varying degrees of either hypohydration or hyperhydration. Yet, it is important for ultra-endurance athletes to avoid the performance limiting and potentially fatal consequences of these conditions. During short periods of exercise ( 1 hr), trivial effects on the relationship between body mass change and hydration status result from body mass loss due to oxidation of endogenous fuel stores, and water supporting the intravascular volume being generated from endogenous fuel oxidation and released with glycogen oxidation. However, these effects have meaningful implications during prolonged exercise. In fact, body mass loses well over 2% may be required during some ultra-endurance activities to avoid hyperhydration. Therefore, the typical hydration guidelines to avoid more than 2% body mass loss do not apply in ultra-endurance activities and can potentially result in hyperhydration. Fortunately, achieving the balance of proper hydration during ultra-endurance activities need not be complicated and has been well demonstrated to generally be achieved by simply drinking to thirst and avoiding excessive sodium supplementation with intention of replacing all sodium losses during the exercise.

We do not recommend population screening for diabetes insipidus (DI) (B3). We recommend to perform diagnostic testing for central diabetes insipidus (CDI) in patients who underwent neurosurgery, after skull and brain trauma, subarchnoid hemorrhage (B3). We recommend excluding thirst impairment during all stages of diagnostic assessment (С3). We recommend excluding DI in cases of persistent hypotonic polyuria: excretion of more than 3 L. or more than 40 mL/kg of urine daily; urine osmolality less than 300 mOsm/kg or urinary specific gravity less than 1004 g/L in all urine samples or during Zimnitsky test (В3). After hypotonic polyuria is confirmed, we recommend excluding of the main causes of nephrogenic diabetes insipidus (NDI) (B3). We recommend simultaneous measurement of urine osmolality and blood osmolality/sodium level in order to confirm DI. Blood hyperosmolality (more than 300 mOsm/kg) and/or hypernatremia with low urine osmolality (less than 300 mOsm/kg) confirms DI (B2). If testing does not reveal these findings, we recommend performing a fluid deprivation test to exclude primary polydipsia (PP) (B2). Desmopressin test is recommended to distinguish CDI and NDI (B2). In cases of CDI we recommend to perform head MRI with contrast (B3). In cases of NDI we recommend assessing renal structure and function and possible electrolyte disturbances (C3). In cases of PP we recommend to refer a patient to psychiatrist (B3). We recommend treating CDI with synthetic vasopressin analogue – desmopressin (B1). We recommend an individual approach in choosing desmopressin dosage form (B2). As the initial dose is difficult to predict when starting desmopressin treatment, we recommend titrating the dosage using two approaches: “the average dose” and “as required” (C4). We recommend educating the patients to ensure knowledge of the features of various desmopressin dosage forms (C4). To decrease the risk of water intoxication, we recommend educating the patients to the water intake regimen adherence (С4). When CDI is accompanied by thirst impairment, we recommend titrating the dose in a clinical setting, with assessment of blood sodium, bodyweight and/or urine volume (C4).

Pediatric seizures are a common presentation to the emergency department. It is important to separate non-febrile seizures from febrile seizures, as non-febrile seizures have a much broader differential diagnosis. For infants less than six months of age with a normal exam, hyponatremia is the leading cause of new onset non-febrile seizure. Most commonly, this is secondary to water intoxication from inappropriate feeding practices. This case report will review the initial workup of new onset non-febrile seizures in an infant and treatment recommendations for seizures secondary to hyponatremia.

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.

Background People with schizophrenia and medical comorbidities are often on multiple medications to manage their symptoms. Herein we present a case of drug-drug interaction (meloxicam and desmopressin), in a patient also on clozapine, that ultimately resulted in hyponatremia and seizure. Methods The patient provided consent to have his case published. We searched PubMed and after reviewing 321 articles, 11 were chosen for relevance. Results Meloxicam enhanced the adverse effect (hyponatremia) of desmopressin and was the likely culprit. Conclusions In a patient with higher ADH levels, as in our patient taking desmopressin, the addition of an NSAID could further increase water retention and worsen hyponatremia; indeed, meloxicam was the only new medication added to the patient's regimen, and a drug interaction calculator supports the desmopressin-meloxicam drug-drug interaction as the culprit. We urge clinicians to avoid the use of desmopressin in patients with schizophrenia as this can lead to water intoxication. As meloxicam may worsen desmopressin-induced hyponatremia and could result in seizure, one should avoid using NSAIDs in patients with schizophrenia whom are also prescribed vasopressin/desmopressin. Serum sodium levels should be closely monitored in patients with schizophrenia whose regimen includes desmopressin.

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Vasopressin infusion induced hyponatremia is a rare phenomenon. It occurs especially when vasopressin is utilized as an adjunct vasopressor in non-septic shock states. 1 CASE PRESENTATION: 35-year-old Hispanic female without any comorbidities was hospitalized at our institution at the peak of COVID-19 pandemic in New York due to severe hypoxemic respiratory failure requiring ventilatory support and ultimately had to be placed on VV Extracorporeal membrane oxygen (ECMO) support for refractory ARDS. Patient required high doses of intravenous (IV) sedation while on ECMO, with ketamine, hydromorphone and versed. Subsequently, she developed worsening hypotension requiring vasopressor support with low to medium doses of nor-epinephrine (NE) infusion. Fixed dose vasopressin infusion was started in an effort to wean off NE infusion. Serum sodium trended down from 139 to 123 in following four days. Urine output (UOP) progressively dropped from >125 ml/hour to 1.035;calculated serum osmolarity-258;serum cortisol-4.7 and TSH-T4 of 0.948-0.8. Renal evaluation was obtained, vasopressin infusion was discontinued with a subsequent strong diuretic effect and a rapid correction in serum sodium. Patient was already on antibiotics for ventilator associated pneumonia, but shock was not attributed to sepsis considering patient was afebrile with a downtrend in leukocytosis preceding hyponatremia. DISCUSSION: Vasopressin is widely used for co-administration with catecholamines to obtain a dose sparing effect in septic shock. 1 Vasopressin due to an antidiuretic activity via renal V2 receptors can result in decreased in UOP with a secondary hyponatremic effect by causing a state of iatrogenic SIADH. 2 Developing hyponatremia shortly after vasopressin infusion and an anti-diuretic effect should be considered a strong indicator of vasopressin as an underlying etiology. CONCLUSIONS: Vasopressin use an adjunct vasopressor should be avoided in non-septic shock states to prevent a state of hyponatremia and a state of water intoxication. A state of volume overload may have a secondary negative impact on ventilator weaning. REFERENCE #1: Dunser MW, Mayr AJ, Ulmer H, et al. Arginine vasopressin in advanced vasodilatory shock.Circulation. 2003;107(18):2313-2319. REFERENCE #2: Miguel Salazar, Bee Bee Hu, Joyce Vazquez et al. Exogenous Vasopressin-Induced Hyponatremia in Patients with Vasodilatory Shock: Two Cas Reports and Literature Review. Journal of Intensive Care Medicine 2015;30(5) 253-258. DISCLOSURES: No relevant relationships by Zeeshan Hafeez, source=Web Response No relevant relationships by Sana Shahid, source=Web Response No relevant relationships by Abeer Zeeshan, source=Web Response

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.

Objective. The study is the second part of the literature review on hyponatremia in patients with diagnosed mental disorders. This article focuses on psychogenic polydipsia as, along with the SIADH, one of the two most common causes of hyponatremia in the mentioned group of patients. Method: The literature review was based on searching the Medline, the Google Scholar and the Ebsco databases in Polish and English by entering the following phrases: psychogenic polydipsia, the psychosis – intermittent hyponatremia – polydipsia syndrome, water intoxication. Discussion: Psychogenic polydipsia occurs in up to 25% of patients treated for mental disorders. It most frequently concerns patients with schizophrenia. 30% of patients with psychogenic polydipsia suffer from hyponatremia with or without symptoms of water intoxication. In the etiology of psychogenic polydipsia, the influence of dopaminergic and noradrenergic neurotransmission has been considered, as well as angiotensin, which is claimed to have dipsogenic properties. In order to reduce the severity of the disorder, attempts have been made to administer the following groups of medications: β-blockers, opioid receptor antagonists, angiotensin convertase inhibitors and angiotensin receptor antagonists. Other methods include replacing classic antipsychotic drugs with clozapine. There are also reports of a reduced severity of polydipsia with hyponatremia after introducing risperidone and olanzapine. Preventing episodes of water intoxication in patients with psychogenic polydipsia requires the monitoring of their body weight and a suitable reduction of fluid intake by them. Results: Mentally ill patients, especially those with chronic schizophrenia, should be monitored for psychogenic polydipsia and the concomitant hyponatremia.

Introduction: Transurethral resection of the prostate (TURP) syndrome is iatrogenic state of water intoxication after transurethral resection of the prostate, an endoscopic procedure in urology. Neurological changes, heart failure and respiratory failure, followed with hyper or hypotension and hypoxia and acidemia, are dominant signs in clinical presentation of the TURP syndrome. For the last decade, better understanding of TURP syndrome pathophysiology and development of preventive measures, led to decrease incidence of the TURP syndrome. The present incidence of TURP syndrome is below 1 %. Case report: We are presenting case of severe TURP syndrome developed during endoscopic two hours long urologie procedure. TURP syndrome was manifested with serious neurologic disturbance which has expanded to coma and epileptic seizures, followed with hemodynamic instability requiring inotropic and vasopressor support. Severe hyponatremia (serum Na+102 mmol/l) was dominant biochemical finding. We are presenting therapy approach to the patient with severe form of TURP syndrome followed by patient health condition improvement. Conclusion: TURP syndrome is iatrogenic potentially life threatening condition, which may be presented during or after intervention. With constant patient monitoring symptoms of TURP syndrome can be early recognized and with adequate therapy potential complications can be avoided.

Acute water intoxication (AWI) is a disorder of excess water intake that can manifest in neurological injury and death. We describe a case of a 54-year-old man that presents to the emergency department with a generalized toxic-clonic seizure due to AWI. Initial computed tomography of the brain demonstrated diffuse cerebral edema. However, with correction of serum sodium over the one hospital day, the patient's neurological symptoms and imaging completely resolved. Clinicians should recognize of reversibility of this entity with management of hyponatremia.

PULMONARY OEDEMA/ARDS ulmonary edema is a potential cause of hypoxia in the perioperative patient. The accumulation of excessive alveolar fluid results in hypoxia due to interference with diffusion across the alveolar capillary membrane. Frothy (sometimes blood-stained) sputum may be expectorated or observed in the endotracheal tube. the abnormal accumulation of fluid in the interstitial or alveolar spaces of the lung can be explained on the basis of a disturbance in the normal Starling equation1. It involves changes in hydrostatic or oncotic pressure across the alveolar membrane or in the permeability of the alveolar membrane such that fluid moves across from the capillaries into the alveolar space. P

No specific pathognomonic tissue changes establish death from water intoxication, which makes a postmortem diagnosis of water intoxication difficult. We report an autopsy case of fatal water intoxication in which the postmortem computed tomography (PMCT) examination showed findings suggestive of antemortem excessive water drinking, such as diluted intestinal contents and hemodilution. A 52-year-old man who had schizophrenia was found dead in his house. He frequently complained of polydipsia, and drank a large amount of water and vomited before his death. PMCT findings showed distention of the duodenum with low radiodensity content (7 HU). In addition, the right atrium showed a low radiodensity content (46 HU). Autopsy results showed moderate congestion in all the organs, a large amount of light-brownish liquid in the duodenum and upper jejunum, and aspiration pneumonia. Electrolyte concentrations of sodium in the vitreous humor of the right and left eyes were 105 and 107 mEq/L, respectively, and neither drugs nor alcohol was detected in the blood. On the basis of the autopsy and biochemical findings, we determined water intoxication as the cause of death. An evaluation of PMCT findings of cases of various causes of death indicated that the radiodensities of the right atrium and duodenal content in our case were lower than those of the cases of various causes of death, except for fresh water drowning. The present case showed that PMCT provides supplementary findings regarding antemortem excessive water drinking. In addition, PMCT may provide findings to consider death from water intoxication before autopsy.

Psychogenic polydipsia or self-induced water intoxication is a potentially lethal condition seen in many chronic psychiatric patients. This is a literature review based on therapeutic significance of Naltrexone in improving compulsive water drinking behavior in chronic psychiatrically ill patients with psychogenic polydipsia. Naltrexone is an opioid antagonist approved by FDA for alcohol dependence. Extensive literature search provides a line of evidence that suggests correlation of opioid receptor with compulsive water ingestion in animals. However, there is limited data regarding clinical utility of naltrexone in improving psychogenic polydipsia in human species. This review highlights the necessity for further research and trials to elucidate the role of naltrexone in human psychogenic drinking behavior.

Objective This systematic review aimed to elucidate the relationship between polydipsia and antipsychotics. Methods We systematically searched MEDLINE, Embase, and PsycINFO, and included clinical studies and case reports on polydipsia induced or improved by antipsychotics. Results We identified 61 articles: 1 double-blind randomized controlled trial (RCT), 4 single-arm trials, 1 cross-sectional study, 3 case series, and 52 case reports. The double-blind RCT demonstrated no significant difference in improvement in polydipsia between olanzapine and haloperidol. Two single-arm trials showed that polydipsia improved during clozapine treatment, whereas the other 2 showed that risperidone did not improve polydipsia. The cross-sectional study showed the prevalence of hyponatremia with first-generation antipsychotics (FGAs: 26.1%) and second-generation antipsychotics (SGAs: 4.9%). Two case series reported that clozapine improved polydipsia; the other one indicated that patients with polydipsia who were treated with FGAs had schizophrenia (70.4%) and mental retardation (25.9%). Of 90 cases in the case reports, 67 (75.3%) were diagnosed with schizophrenia. Of 83 cases in which antipsychotic treatment started before the onset of polydipsia, 75 (90.3%) received FGAs, particularly haloperidol (n = 24, 28.9%), and 11 (13.3%) received risperidone. Among 40 cases in which polydipsia was improved following antipsychotic treatment, 36 (90.0%) received SGAs, primarily clozapine (n = 14, 35.0%). Conclusions Although the causal relationship between polydipsia and antipsychotics remains unclear because of the paucity of high-quality studies, antipsychotics with high affinity to dopamine D2 receptors may be associated with an increased risk of polydipsia while clozapine may be effective for treating polydipsia.

Introduction Sporadic laterally spreading nonampullary duodenal adenomas (SLSNDA) are an uncommon incidental finding during oesophagogastroduodenoscopy. Endoscopic mucosal resection (EMR) in the duodenum is challenging due to increased risk of perforation and bleeding. Underwater EMR (UEMR) is a novel and effective endoscopic resection technique performed without submucosal injection. Saline-immersion therapeutic endoscopy (SITE) is an evolution of UEMR and saline solution is used instead of water to minimise the risk of water intoxication. Aims and methods Our aim was to evaluate the efficacy and safety of SITE-EMR for SLSNDA via a retrospective review of SLSNDA resected by SITE-EMR at our institution from May 2017 to October 2018. Demographic, clinical, endoscopic findings and follow-up data were analysed. Results Nine SLSNDA (median size 25 mm) were found in eight patients (4 male, median age: 69 year-old). One was located in D1, 4 in D2 and 4 in D3. En-bloc resection was achieved in two lesions (23%) while wide-field resection was performed in seven lesions (77%). Complete resection was achieved in seven patients (87.5%). A circumferential lesion involving the whole duodenal bulb was found in one case and SITE-EMR technique was not feasible as well as other alternative endoscopic resection techniques due to severe fibrosis; the patient was therefore referred for surgery and excluded from further analysis. Histological results revealed six (75%) tubulo-villous adenomas with low-grade dysplasia and two tubular adenomas low-grade dysplasia (25%). Immediate complications including perforation and bleeding did not occur. One patient (12.5%) presented with delayed GI bleeding 24hours post procedure and was treated successfully with endoclips. Three cases (37.5%) of recurrences were identified at 3 months follow-up requiring further endoscopic treatment. No further recurrence was identified at 6 and 12 months follow-up in any patient. Conclusion SITE-EMR of SLSNDA appears to be a safe and effective management with low recurrence rates at long term follow-up.

Introduction Brain Edema (BE) has been studied in animals using water intoxication (WI). Classical models of WI involve the infusion of 10–20% body weight (BW) distilled water. This induces severe ...

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.

Hyponatremia is the most common electrolyte abnormality. Patho physiologically, hyponatremia are classified into two groups: hyponatremia due to non-osmotic hypersecretion of vasopressin (hypovolemic, hypervolemic, euvolemic) and hyponatremia of non-hyper vasopressinemic origin (pseudo hyponatremia, water intoxication, cerebral salt wasting syndrome). The aim of this study was to identify the incidence of hyponatremia in children with pneumonia and to investigated whether there is a link between hyponatremia and the severity and outcome of pneumonia. The present study was planned on 25 children diagnosed with pneumonia in department of Paediatrics in Nalanda Medical College and Hospital, Patna, from March 2016 to Dec 2016. At the time of admission, the patient’s clinical history was recorded in prefixed proforma. Serum sodium was measured by a process known as potentiometry. This method measures the voltage that develops between the inner and outer surfaces of an ion selective electrode. Based on the above findings it can be concluded that serum electrolytes should be measured in children hospitalized for pneumonia; the appropriate fluid therapy must be carefully arranged in children with hyponatremia, and both serum and urine sodium levels should be closely monitored. Regular follow up of serum sodium level during the period of hospital stay should be considered to pick up the high risk cases at an early stage. Keywords: pneumonia, sodium level, Hyponatremia, etc.

Cerebral edema in ischemic stroke can lead to increased intracranial pressure, reduced cerebral blood flow and neuronal death. Unfortunately, current therapies for cerebral edema are either ineffective or highly invasive. During the development of cytotoxic and subsequent ionic cerebral edema water enters the brain by moving across an intact blood brain barrier and through aquaporin-4 (AQP4) at astrocyte endfeet. Using AQP4-expressing cells, we screened small molecule libraries for inhibitors that reduce AQP4-mediated water permeability. Additional functional assays were used to validate AQP4 inhibition and identified a promising structural series for medicinal chemistry. These efforts improved potency and revealed a compound we designated AER-270, N-[3,5-bis (trifluoromethyl)phenyl]-5-chloro-2-hydroxybenzamide. AER-270 and a prodrug with enhanced solubility, AER-271 2-{[3,5-Bis(trifluoromethyl) phenyl]carbamoyl}-4-chlorophenyl dihydrogen phosphate, improved neurological outcome and reduced swelling in two models of CNS injury complicated by cerebral edema: water intoxication and ischemic stroke modeled by middle cerebral artery occlusion.

Despite the clinical importance of polydipsia, no diagnostic criteria or severity scales that comprehensively assess this condition are available. Thus, we aimed to develop diagnostic criteria and a severity scale for polydipsia based on a systematic review and well-experienced clinicians’ consensus. We performed a systematic review, identified 27 studies related to diagnostic criteria or severity classification for polydipsia, and extracted items used to assess polydipsia in these studies. Ten well-experienced clinicians—5 psychiatrists and 5 nurses—participated in the Delphi method. They evaluated 39 items extracted based on the results of the systematic review regarding (1) their necessity in diagnosing and assessing the severity of polydipsia, and (2) their relative importance rated on 7-point scale among the items included in the severity scale. The Polydipsia Diagnostic Criteria (PDC) included 4 essential items—excessive drinking, low serum sodium level or low serum osmolality, abnormal normalized diurnal weight gain, and low urine specific gravity—based on consensus reached using the Delphi method. The Polydipsia Severity Scale (PSS) included 13 items with a maximum score of 59. The first diagnostic criteria and symptom scale for polydipsia were developed based on the findings of a systematic review and well-experienced clinicians’ consensus.

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