Topics: Diuretic, Water intoxication, Hyponatremia Pages: 7 (2372 words) Published: July 5, 2012
INTRODUCTION — In almost all cases, hyponatremia results from the intake (either oral or intravenous) and subsequent retention of water [1]. A water load will, in normal subjects, be rapidly excreted as the dilutional fall in plasma osmolality suppresses the release of antidiuretic hormone (ADH), thereby allowing the excretion of a dilute urine. The maximum rate of water excretion on a regular diet is over 10 liters per day, thereby providing an enormous range of protection against the development of hyponatremia.

Some patients with primary polydipsia retain water and become hyponatremic because they drink such large quantities of fluid that they overwhelm the excretory capacity of the kidney. In almost all cases, however, hyponatremia occurs because there is an impairment in renal water excretion, due most often to an inability to suppress ADH release.

Although the definition may vary among different clinical laboratories, hyponatremia is commonly defined as a serum sodium concentration ≤135 meq/L [2]. An overview of the causes of hyponatremia will be presented here (table 1). Most of the individual disorders are discussed in detail separately, as are issues related to diagnosis and treatment [1,3]. (See "Diagnosis of hyponatremia" and "Overview of the treatment of hyponatremia".) It should also be emphasized that, in selected patients, multiple factors may contribute to the fall in the plasma sodium concentration. Symptomatic infection with human immunodeficiency virus (HIV) is an example of this phenomenon, as volume depletion, the syndrome of inappropriate ADH secretion, and adrenal insufficiency all may be present. (See "Electrolyte disturbances with HIV infection".)

The presence of hyponatremia, even of relatively mild severity, is associated with adverse survival. This includes patients with heart and/or hepatic failure, and/or acute myocardial infarction. (See "Hyponatremia in cirrhosis" and "Hyponatremia in heart failure".) DISORDERS IN WHICH ADH LEVELS ARE ELEVATED — The two most common causes of hyponatremia are effective circulating volume depletion and the syndrome of inappropriate ADH secretion, disorders in which ADH secretion is not suppressed [4]. Effective circulating volume depletion — Significantly decreased tissue perfusion is a potent stimulus to ADH release. This response is mediated by baroreceptors in the carotid sinus, which sense a reduction in pressure or stretch, and can overcome the inhibitory effect of hyponatremia on ADH secretion. Thus, hyponatremia can develop in patients with any of the following disorders. True volume depletion — True volume depletion from gastrointestinal or urinary losses or bleeding will increase ADH and result in hyponatremia if there is adequate water intake. Such patients may also have hypokalemia and azotemia due to decreased renal perfusion. This constellation of findings in patients with a large villous adenoma has been called the McKittrick- Wheelock syndrome.

The replacement of severe diarrheal losses due to cholera (which is associated with a sodium concentration in stool of 120 to 140 meq/L) with an oral rehydration solution with reduced osmolality may result in an increased incidence of hyponatremia as compared to replacement with standard (and higher sodium concentration) oral rehydration therapy [5]. (See "Oral rehydration therapy".)

Exercise-associated hyponatremia — Marathon and ultramarathon runners can develop potentially severe hyponatremia that is primarily due to excessive water intake combined, in many cases, impaired water excretion due to persistent ADH secretion. A similar sequence can occur during military operations and desert hikes. (See "Exercise-associated hyponatremia".) Heart failure and cirrhosis — Even though the plasma volume may be markedly increased in these disorders, the pressure sensed at the carotid sinus baroreceptors is reduced due to the fall in cardiac output in heart failure and to peripheral vasodilatation in cirrhosis...
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