Water intoxication pathophysiology

Jump to navigation Jump to search

Water Intoxication Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Water Intoxication from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Water intoxication pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Water intoxication pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Water intoxication pathophysiology

CDC on Water intoxication pathophysiology

Water intoxication pathophysiology in the news

Blogs on Water intoxication pathophysiology

Directions to Hospitals Treating Water intoxication

Risk calculators and risk factors for Water intoxication pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Physiology

Blood contains electrolytes (particularly sodium compounds, such as sodium chloride) in concentrations that must be held within very narrow limits. Water enters the body orally or intravenously and leaves the body primarily in urine, sweat, and exhaled water vapor. If water enters the body more quickly than it can be removed, body fluids are diluted and a potentially dangerous shift in electrolyte balance occurs. In other words, the body has too much water and not enough electrolytes.

Most water intoxication is caused by hyponatremia, an overdilution of sodium in the blood plasma, which in turn causes an osmotic shift of water from extracellular fluid (outside of cells) to intracellular fluid (within cells). The cells swell as a result of changes in osmotic pressure and may cease to function. When this occurs in the cells of the central nervous system and brain, water intoxication is the result. Additionally, many other cells in the body may undergo cytolysis, wherein cell membranes that are unable to stand abnormal osmotic pressures rupture, killing the cells. Initial symptoms typically include light-headedness, sometimes accompanied by nausea, vomiting, headache and/or malaise. Plasma 19 sodium levels below 100 mmol/L (2.3g/L) frequently result in cerebral edema, seizures, coma, and death within a few hours of drinking the excess water. As with alcohol poisoning, the progression from mild to severe symptoms may occur rapidly as the water continues to enter the body from the intestines or intravenously.

A person with healthy kidneys can excrete about 900ml (0.24 gal)/hr.[1] However, this must be modulated by potential water losses via other routes. For example, a person who is perspiring heavily may lose 1 L/hr (0.26 gal) of water through perspiration alone, thereby raising the amount of water that must be consumed before the individual crosses the threshold for water intoxication. The problem is further complicated by the amount of electrolytes lost in urine or sweat, which is variable within a range controlled by the body's regulatory mechanisms.

Water intoxication can be prevented by consuming water that is isotonic with water losses, but the exact concentration of electrolytes required is difficult to determine and fluctuates over time, and the greater the time period involved, the smaller the disparity that may suffice to produce electrolyte imbalance and water intoxication.

Sodium is not the only mineral that can become overdiluted from excessive water intake. Magnesium is also excreted in urine. According to the National Institutes of Health, "magnesium deficiency can cause metabolic changes that may contribute to heart attacks and strokes."[2] Intravenous magnesium is used in cardiac care units for cardiac arrhythmias.[3]

References

  1. Noakes, T.D. (2001). "Peak rates of diuresis in healthy humans during oral fluid overload". National Center for Biotechnology Information. Retrieved 2007-01-21. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  2. Facts about Dietary Supplements, Office of Dietary Supplements, National Institutes of Health, March 2001.
  3. Jay S. Cohen, MD, Statin Drugs, 2005, page 129, ISBN 0-7570-0257-9.



Template:WS