Excessive Water Intake Research Articles

Hyponatremic Encephalopathy after Excessive Water Ingestion Prior to Pelvic Ultrasound: Neuroimaging Findings

We report two patients with acute hyponatremic encephalopathy which developed after massive water ingestion for pelvic ultrasound and emphasize the findings of magnetic resonance (MR) imaging including diffusion-weighted imaging (DWI). Both subjects had completely recovered within 24 hours following fluid restriction and salt replacement. MR imaging revealed cortical sulcal narrowing, restricted diffusion and sulcal T2 hyperintensity along with diffuse pial enhancement suggesting diffuse cerebral cortical cytotoxic edema and blood-brain barrier breakdown. In addition to the first illustration of multimodality MR imaging features of water-intoxication, these two cases also highlight the need for standardized practice on the quantity of water intake recommended to distend the bladder for pelvic ultrasound, especially in patients at risk for serum inappropriate ADH syndrome-related hyponatremia.

Extent of the Aral Sea drop in the Middle Age

The landlocked Aral Sea, which is dying off at present (Fig. 1), was a widespread weaksalty basin with abundant life at least in the 1960s. Then its level started to drop rapidly, the area of the lake decreased to a quarter of its former size, and its volume was reduced tenfold. The ecological crisis of the Aral Sea is considered to be the effect of excessive water intake from the feeding tributaries, Amu Darya and Syr Darya, for irrigation. Did a similar catastrophe occur in the past, or is it an exclusively anthropogenic phe� nomenon.

Exercise-Associated Hyponatremia

Disorders of serum sodium occur commonly in athletes participating in endurance sports. The most life-threatening of these is hyponatremia, which can occur in as many as 2% to 7% of participants. Exercise-associated hyponatremia (EAH) is caused by a combination of excessive water or hypotonic fluid intake as well as high levels of arginine vasopressin, which limits the ability of the kidney to excrete water. Other factors in the pathogenesis of EAH include sweat sodium loss, inability to mobilize exchangeable sodium stores, metabolic water production, and impaired renal blood flow and glomerular filtration rate. Most cases of EAH lead to minimal or absent complications and do not require specific therapy other than close monitoring and fluid restriction. However, a small number of athletes may present with severe and life-threatening hyponatremia associated with cerebral edema and possibly noncardiogenic pulmonary edema. Rapid diagnosis and appropriate therapy of these athletes with hypertonic saline is required to prevent severe complications or death.

Clinical Characteristics of Acute Decompensated Heart Failure With Rapid Onset of Symptoms

Background Few reports regarding the definition, epidemiology, and pathophysiology of acute decompensated heart failure (ADHF) are available. The clinical characteristics of 194 consecutive ADHF patients with abrupt onset of symptoms were investigated. Methods and Results Patients with acute coronary syndromes including acute myocardial infarction, acute pneumonia, severe valvular disease, and end-stage renal disease that required dialysis therapy were excluded. Patients were divided into 2 groups: rapid-progression group, onset within 24 hours before admission (n = 78); and gradual-progression group, onset more than 24 hours before admission (n = 52). No significant differences were observed in the age, gender, prescriptions, and hematological data between the 2 groups. The proportion of patients who drank excessive water was higher in the rapid-progression group. Systolic blood pressure, diastolic blood pressure, heart rate, left ventricular ejection fraction, and left ventricular wall thickness were greater in patients in the rapid-progression group. Indexes indicating left ventricular diastolic function were significantly deteriorated in the rapid-progression group. Conclusion Excessive water intake, acute hypertension, and diastolic dysfunction are associated with the pathophysiology of abrupt-onset ADHF. Hypertensive patients with diastolic dysfunction should be treated cautiously to prevent the occurrence of ADHF.

Excessive water ingestion and repeated seizures: the domino effect

Despite variations in sodium and water concentrations, our body relies on several mechanisms to maintain the plasmatic osmolality within the normal range of 275–290 mOsm/L1. Hyponatremia is defined as a reduction in plasma sodium concentration below 136 mmol/L2. It occurs in 12% of the hospitalized patients and in 30% of the patients in the intensive care unit (ICU)3 […] Excessive water ingestion and repeated seizures: the domino effect

Exercise-Associated Hyponatremia

Disorders of serum sodium concentration occur commonly in athletes participating in endurance sports. While hypernatremia is the most commonly seen disorder, hyponatremia can occur in 2% to 7% of participants. Hyponatremia is due to a combination of excessive water or hypotonic fluid intake as well as high levels of arginine vasopressin (or antidiuretic hormone), which limits the ability of the kidney to excrete water. Most of these cases are associated with either no or minimal side effects and do not require specific therapy other than close monitoring and fluid restriction. However, a small number of athletes may present with severe and life-threatening hyponatremia associated with cerebral edema and possibly noncardiogenic pulmonary edema. Rapid diagnosis and appropriate therapy of these symptomatic athletes with hypertonic saline is required to prevent severe complications or death. The ability to have rapid on-site measurement of serum sodium concentration greatly facilitates accurate diagnosis and therapy. Prevention is based on widespread education regarding the risks of overhydration and judicious intake of fluids during endurance events.

Influence of two different diets on fluid and particle retention time Javan langur ( Trachypithecus auratus auratus)

In captivity, langurs (foregut fermenting primates) often suffer from digestive disorders, and in particular display soft stools on diets with a high proportion of fruits, vegetables, and grain products. In this study, we tested whether the improvement in feces consistency expected after an omission of vegetables from a conventional diet was also accompanied by a change in the excretion pattern as measured by the mean retention time (MRT). Two adult Javan langurs were kept together and offered a conventional diet of pellets, browse, vegetables, or a diet consisting of pellets and browse only. MRT were measured with cobalt-EDTA as the fluid and chromium oxide as the particle marker before, during, and after the test diet, collecting the feces of both animals together. MRTs of fluids and particles were longer (47/49 h) on the test diet as compared to the usual diet (42/43 h). Feces consistency improved during the test period. The test period was marked by an increased fiber intake; however, on the conventional diet, dietary water intake exceeded the calculated water flux for these animals distinctively, due to the high proportion of vegetables. Therefore, it cannot be decided whether the increase of fiber level alone or also a reduction of the excessive water intake was responsible for the changes observed. Comparing the results of this study to other studies on ingesta retention in foregut fermenting primates, no correlation between the body mass of the animals and the MRTs measured is evident, which is in accordance with observations in other groups of foregut fermenters.

Scanning sports medicine

An Ultracyclist with Pulmonary Edema During the Bicycle Race Across America A recently published case report in the January 2007 issue of Medicine & Science in Sports & Exercise, the official journal of the ACSM, highlights the pitfalls of overly aggressive sodium intake during an endurance race at altitude. It is well known that multiday ultra-endurance athletic events tax the body’s ability to maintain sodium and water homeostasis. Much focus has been placed on the danger associated with excessive water intake without sodium repletion, namely hyponatremia. This case study presents the risk associated with aggressive sodium intake coupled with heavy exertion at a high altitude. The subject presented is an extremely fit 38-year-old male participant in the Bicycle Race Across America who developed severe pulmonary edema while cycling at an altitude of 2380 meters on the fourth day of his race. His daily sodium intake over the course of the race averaged between 1000 and 1100 mEq and his weight on the day of hospitalization was 2.7 kg greater than his prerace weight. The athlete responded appropriately to standard support for pulmonary edema while in the hospital and he made a full recovery. Later, he underwent testing for cardiopulmonary disease or susceptibility to high-altitude pulmonary edema. The results of the entire work-up were negative. The authors hypothesize that the excessive sodium intake led to an expanded extracellular volume, increased hydrostatic pressure, and decreased oncotic pressure. Racing at high altitudes, where a hypoxia-induced rise in pulmonary artery pressures already exists, may have exaggerated the effects of the changes in hydrostatic and oncotic pressures seen with extracellular volume expansion. This, coupled with ambient hypoxia, elevated cardiac output, and reduced renal perfusion associated with sustained highlevel exercise seems to lead to the development of acute pulmonary edema.

Change of blood viscosity and urinary frequency by high water intake

Physicians recommend a high water intake to prevent cerebral infarction by decreasing blood viscosity. However, there is no evidence that high water intake decreases viscosity, although it increases urinary frequency. Therefore, we investigated the change of blood viscosity and urinary frequency by high water intake. We examined the change of blood viscosity after acute water intake, the circadian rhythm of blood viscosity, and the change of early morning blood viscosity and urinary frequency after high water intake for 1 week in healthy volunteers aged 31-75 years. Blood viscosity decreased transiently by acute water intake, but remained within the range of its circadian rhythm. Morning blood viscosity did not alter by high water intake for 1 week, although urinary frequency increased. Because excessive water intake increases urinary frequency without decreasing blood viscosity, a high water intake should not be recommended in persons with urinary frequency.

Symptomatic Hyponatremia after Voluntary Excessive Water Ingestion in a Patient without Psychiatric Problems

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

Exercise-Associated Hyponatremia

Exercise-associated hyponatremia has been described after sustained physical exertion during marathons, triathlons, and other endurance athletic events. As these events have become more popular, the incidence of serious hyponatremia has increased and associated fatalities have occurred. The pathogenesis of this condition remains incompletely understood but largely depends on excessive water intake. Furthermore, hormonal (especially abnormalities in arginine vasopressin secretion) and renal abnormalities in water handling that predispose individuals to the development of severe, life-threatening hyponatremia may be present. This review focuses on the epidemiology, pathogenesis, and therapy of exercise-associated hyponatremia.

Exercise-induced hyponatremia: causes, risks, prevention, and management.

Exercise-induced hyponatremia is most commonly associated with prolonged exertion during sustained, high-intensity endurance activities such as marathons or triathlons. In most cases, exercise-induced hyponatremia is attributable to excess free water intake, which fails to replete the sometimes massive sodium losses that result from sweating. The risk of hyponatremia can be lowered by strategies to ensure fluid balance during exercise by maintaining the proper volume and type of fluid intake. Treatment of exercise-induced hyponatremia is based on whether the patient is volume-depleted, euvolemic, or fluid-overloaded. Because therapy must be tailored to volume status, physicians must make this determination before initiating therapy. If hyponatremia is life-threatening, hypertonic saline may be warranted to increase sodium in the extracellular fluid compartment and restore the natural balance.

Reproducibility of Contrast Enhanced Magnetic Resonance Renography in Adolescents

We sought to determine the reproducibility of magnetic resonance imaging renography using 3 different mathematical models and 2 different approaches to convert the relative signal intensity into quantitative indices. Furthermore, we wanted to examine the influence of fluid intake on the obtained renal parameters. A total of 10 healthy volunteers 13 to 16 years old were subjected to magnetic resonance imaging 3 times within 10 weeks, including an examination where fluid intake was increased. At each examination 0.1 mmol/kg gadolinium diethylenetriamine pentaacetic acid was administrated intravenously as a rapid bolus during a fast magnetic resonance renography sequence. Images were acquired in the coronal plan, and 1,200 images were recorded during approximately 7 minutes. Cortical data were analyzed to estimate absolute and differential function of renal parameters by converting signal intensities into quantitative units. Using the simple approach that a change in magnetic resonance imaging signal is linearly related to the change in gadolinium diethylenetriamine pentaacetic acid concentration, we found reproducibility in the range of 1% to 5% of all estimations of the differential renal function. The relative glomerular ultrafiltration (ml per minute per cm(3) kidney cortex) was calculated and a reproducibility of 7% was observed for relative glomerular ultrafiltration (using the model based on deconvolution). Increased hydration caused a significant change in most parameters. Contrast enhanced magnetic resonance renography is reproducible in the normal human kidney but excessive water intake has a significant influence on these parameters. Further studies are required to elucidate whether similar measurements can be applied to a kidney with impaired function.

Is polydipsia sometimes the cause of oxcarbazepine-induced hyponatremia?

Hyponatremia is a commonly encountered clinical problem with potentially severe complications. Among the underlying implicated etiologies are medications such as oxcarbazepine, which has been well documented and attributed to the syndrome of inappropriate antidiuretic hormones (SIADH). We report the case of a 28-year-old woman with a diagnosis of secondary antiphospholipid syndrome who presented with asymptomatic hyponatremia secondary to excessive water intake after oxcarbazepine ingestion, suggesting a new mechanism for oxcarbazepine-induced hyponatremia.

An Observational Study On The Spectrum Of Heat-Related Illness, With A Proposal On Classification

During operations in subtropical areas over the summer months of 2001 and 2003 the authors audited 80 patients with heat-related illness, with the intention of defining the nature and distribution...

Current Perspective on the Pathogenesis of Central Diabetes Insipidus

Diabetes insipidus is a heterogeneous condition characterised by polyuria and polydipsia caused by a lack of secretion of vasopressin, its physiological suppression following excessive water intake, or kidney resistance to its action. The clinical and laboratory diagnosis is confirmed by standard tests, but recent advances in molecular biology and imaging techniques have shed new light on the pathophysiology of this disease. In many patients, central diabetes insipidus is caused by a germinoma or craniopharyngioma; Langerhans' cell histiocytosis and sarcoidosis of the central nervous system; local inflammatory, autoimmune or vascular diseases; trauma from surgery or accident; and, rarely, genetic defects in vasopressin biosynthesis inherited as autosomal dominant or X-linked recessive traits. Thirty to fifty percent of cases are considered idiopathic. Tumour-associated central diabetes insipidus is uncommon in children younger than 5 years old. Biopsy of enlarged pituitary stalk should be reserved for patients with hypothalamic-pituitary mass and progressive thickening of the pituitary stalk since spontaneous recovery may occur. Molecular biology in selected patients may identify those with apparently idiopathic diabetes insipidus carrying the vasopressin-neurophysin II gene mutation.

Physiological and pathophysiological influences on thirst

Thirst motivates animals to seek fluid and drink it. It is regulated by the central nervous system and arises from neural and chemical signals from the periphery interacting in the brain to stimulate a drive to drink. Our research has focussed on the lamina terminalis and the manner in which osmotic and hormonal stimuli from the circulation are detected by neurons in this region and how that information is integrated with other neural signals to generate thirst. Our studies of osmoregulatory drinking in the sheep and rat have produced evidence that osmoreceptors for thirst exist in the dorsal cap of the organum vasculosum of the lamina terminalis (OVLT) and in the periphery of the subfornical organ, and possibly also in the median preoptic nucleus. In the rat, the hormones angiotensin II and relaxin act on neurons in the periphery of the subfornical organ to stimulate drinking. Studies of human thirst using functional magnetic resonance imaging (fMRI) techniques show that systemic hypertonicity activates the lamina terminalis and the anterior cingulate cortex, but the neural circuitry that connects sensors in the lamina terminalis to cortical regions subserving thirst remains to be determined. Regarding pathophysiological influences on thirst mechanisms, both excessive (polydipsia) and inadequate (hypodisia) water intake may have dire consequences. One of the most common primary polydipsias is that observed in some cases of schizophrenia. The neural mechanisms causing the excessive water intake in this disorder are unknown, so too are the factors that result in impaired thirst and inadequate fluid intake in some elderly humans.

Self induced Water Intoxication Associated with Routine Employment Drug Screen Leading to Symptomatic Hyponatremia: A Case Report

Acute symptomatic hyponatremia is a rare complication of water intoxication. Excessive water intake alone is unlikely to cause symptomatic hyponatremia unless there is impairment of water excretion. We report a case of hyponatremia associated with non-psychogenic polydipsia and an overdose of an herbal diuretic, uva ursi in preparation for a routine workplace drug screen.

Disorders of Water Metabolism in Children

1. Michael L. Moritz, MD* 2. Juan Carlos Ayus, MD† 1. *Assistant Professor of Pediatric Nephrology, Children’s Hospital of Pittsburgh, Pittsburgh, PA 2. †Professor of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX After completing this article, readers should be able to: 1. Describe the clinical manifestations of hyponatremic encephalopathy. 2. Identify the risk factors for developing hyponatremic encephalopathy. 3. List the risk factors for developing cerebral demyelination following the correction of hyponatremia. 4. Characterize the clinical manifestations of hypernatremia. 5. Identify patients at greatest risk for developing hypernatremia. In conjunction with the tremendous medical advances of the past century, an increasing number of hospitalized patients are dependent on parenteral fluids. Caring for children who have complex medical conditions has resulted in new challenges for prescribing parenteral therapy to maintain sodium and water homeostasis; most electrolyte disturbances occur in the hospital. Although the kidneys play an important role in the development of disorders in water handling, most of the morbidity and mortality results from central nervous system dysfunction (Table 1). This review discusses common disorders of water metabolism, emphasizing the neurologic sequelae. View this table: Table 1. Abnormalities of Water Metabolism Leading to Brain Damage Hyponatremia is defined as a serum sodium level less than 135 mEq/L (135 mmol/L). It is one of the most common electrolyte disorders encountered in hospitals, occurring in approximately 3% of hospitalized children. The cause usually is identified easily, and the condition rarely is fatal, but sometimes the cause can be elusive and mortality can result from inappropriate therapy. ### Pathogenesis Under normal circumstances, the human body can maintain plasma sodium levels within the normal range (135 to 145 mEq/L [135 to 145 mmol/L]), despite wide fluctuations in fluid intake. The body’s primary defense against developing hyponatremia is the kidney’s ability to generate dilute urine and excrete free water. The primary reasons that children develop hyponatremia encompass underlying conditions that impair the kidney’s ability to excrete free water (Table 2). Hyponatremia usually occurs in the setting of excess water intake, with or without sodium losses, in the presence of impaired …

Fatal Water Intoxication of an Army Trainee during Urine Drug Testing

An Army trainee developed acute water intoxication, hyponatremia, pulmonary edema, and fatal cerebral edema. This is the first report of a fatality related to urine drug testing. This resulted from supervised excessive water ingestion in an attempt to induce a sufficient urine specimen for substance abuse testing. To avoid a similar preventable death in the future, we make several recommendations. These include limiting the volume of ingested fluid to eight ounces every 30 to 45 minutes, not to exceed 40 ounces, and providing a relaxed, reassuring environment when obtaining urine specimens for substance abuse detection.