Severe overhydration leads to hyponatremia and potentially fatal cerebral edema.
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Peer-reviewed literature and reference materials report that excessive fluid intake or overhydration results in dilutional hyponatremia, which can progress to severe neurological complications and potentially fatal cerebral edema.
<h4>Background</h4>Hyponatremia has emerged as an important cause of race-related death and life-threatening illness among marathon runners. We studied a cohort of marathon runners to estimate the incidence of hyponatremia and to identify the principal risk factors.<h4>Methods</h4>Participants in the 2002 Boston Marathon were recruited one or two days before the race. Subjects completed a survey describing demographic information and training history. After the race, runners provided a blood sample and completed a questionnaire detailing their fluid consumption and urine output during the race. Prerace and postrace weights were recorded. Multivariate regression analyses were performed to identify risk factors associated with hyponatremia.<h4>Results</h4>Of 766 runners enrolled, 488 runners (64 percent) provided a usable blood sample at the finish line. Thirteen percent had hyponatremia (a serum sodium concentration of 135 mmol per liter or less); 0.6 percent had critical hyponatremia (120 mmol per liter or less). On univariate analyses, hyponatremia was associated with substantial weight gain, consumption of more than 3 liters of fluids during the race, consumption of fluids every mile, a racing time of >4:00 hours, female sex, and low body-mass index. On multivariate analysis, hyponatremia was associated with weight gain (odds ratio, 4.2; 95 percent confidence interval, 2.2 to 8.2), a racing time of >4:00 hours (odds ratio for the comparison with a time of <3:30 hours, 7.4; 95 percent confidence interval, 2.9 to 23.1), and body-mass-index extremes.<h4>Conclusions</h4>Hyponatremia occurs in a substantial fraction of nonelite marathon runners and can be severe. Considerable weight gain while running, a long racing time, and body-mass-index extremes were associated with hyponatremia, whereas female sex, composition of fluids ingested, and use of nonsteroidal antiinflammatory drugs were not.
This report describes a series of hyponatremia hospitalizations associated with heat-related injuries and apparent over-hydration. Data from the U.S. Army Inpatient Data System were used to identify all hospitalizations for hyposmolality/hyponatremia from 1996 and 1997. Admissions were considered as probable cases of overhydration hyponatremia if this was the only, or primary, diagnosis or if it was associated with any heat-related diagnosis. Seventeen medical records were identified, and the events leading to hospitalization were analyzed. The average serum sodium level was 122 +/- 5 mmol/L (range, 115-130 mmol/L). All 17 patients were soldiers attending training schools. Seventy-seven percent of hyponatremia cases occurred in the first 4 weeks of training. Nine patients had water intake rates equal to or exceeding 2 quarts per hour. Most patients were in good health before developing hyponatremia. The most common symptoms were mental status changes (88%), emesis (65%), nausea (53%), and seizures (31%). In 5 of 6 cases in which extensive history was known, soldiers drank excess amounts of water before developing symptoms and as part of field treatment. The authors conclude that hyponatremia resulted from too aggressive fluid replacement practices for soldiers in training status. The fluid replacement policy was revised with consideration given to both climatic heat stress and physical activity levels. Field medical policy should recognize the possibility of overhydration. Specific evacuation criteria should be established for exertional illness.
Acute water intoxication is an uncommon but potentially fatal condition characterized by excessive water consumption over a brief period. It results in dilutional hyponatremia. The condition is frequently associated with psychiatric disorders, endurance athletics, or iatrogenic causes. Early recognition and prompt treatment are crucial for preventing serious complications and ensuring favorable outcomes. A 38-year-old male patient presented to the emergency department exhibiting sudden loss of consciousness followed by altered mental status, confusion, and an episode of seizure. The history revealed ingestion of approximately 8 liters of water within a three-hour period while waiting for uroflowmetry testing. Initial laboratory tests indicated severe hyponatremia with serum sodium of 120 mEq/L. He was diagnosed with acute water intoxication with dilutional hyponatremia. Management involved fluid restriction, electrolyte monitoring, and gradual correction of sodium levels utilizing 3% hypertonic saline. The patient's neurological status improved progressively, and he was discharged after five days. This case highlights the significance of identifying acute water intoxication as a potential etiology of dilutional hyponatremia, particularly in patients presenting with neurological symptoms and a history of excessive fluid intake. Expeditious diagnosis and appropriate management are essential to prevent severe complications such as cerebral edema and permanent neurological damage.
The hyponatremia of exercise.
The hyponatremia of exercise may exist in symptomatic and asymptomatic forms. Symptomatic hyponatremia is usually characterized by severe alterations in cerebral function including coma and grand mal seizures; it develops especially in less competitive athletes who have maintained high rates of fluid intake during endurance events lasting at least 5 hours. The hyponatremia becomes symptomatic when the volume of excess fluid retained exceeds 2 to 3 liters. The etiology of the condition is unknown. Possibly as many as three or more pathologies (abnormal fluid retention possibly due to inappropriate ADH secretion, abnormal regulation of the extracellular fluid volume, translocation of sodium into a "third space") must be present for symptomatic hyponatremia to develop. The avoidance of overhydration would appear to be the only certain way that susceptible individuals can prevent symptomatic hyponatremia. Sodium chloride containing solutions ingested in physiologically significant concentrations would likely prevent a possible "third space" effect.
Published in International journal of sport nutrition (1992)
also known as water poisoning, hyperhydration, overhydration, or water toxemia, is a potentially fatal disturbance in brain functions that can result
Water intoxication, also known as water poisoning, hyperhydration, overhydration, or water toxemia, is a potentially fatal disturbance in brain functions that can result when the normal balance of electrolytes in the body is pushed outside safe limits by excessive water intake.
In normal circumstances, accidentally consuming too much water is exceptionally rare. Most deaths related to water intoxi
Water intoxication, also known as water poisoning, hyperhydration, overhydration, or water toxemia, is a potentially fatal disturbance in brain functions that can result when the normal balance of electrolytes in the body is pushed outside safe limits by excessive water intake.
In normal circumstances, accidentally consuming too much water is exceptionally rare. Most deaths related to water intoxication in healthy individuals have resulted either from water-drinking contests, in which individuals attempt to consume large amounts of water, or from long bouts of exercise during which excessive amounts of fluid were consumed. In addition, water cure, a method of torture in which the victim is forced to consume excessive amounts of water, can cause water intoxication. Excess body water can also result from medical conditions or improper treatments, such as those causing hyponatremia.
Although water is considered one of the least toxic chemical compounds, with an LD50 exceeding 90,000 mg/kg (90 g/kg) body weight in rats, it can be considered a poison when over-consumed in a brief period; drinking six liters in three hours has caused the death of a human.
Mild intoxication may remain asymptomatic and require only fluid restriction. In more severe cases, treatment consists of:
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