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Essentials of Diagnosis

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  • Hyponatremia develops due to an excess of total body water in relation to total body sodium.
  • Determination of extracellular volume status and urinary indices aids in the classification of hyponatremia.

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General Considerations

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Hyponatremia is present when the serum sodium concentration falls below 135 mEq/L. In healthy subjects, the sodium concentration is closely regulated to remain between 138 and 142 mEq/L despite wide variations in water intake (Figure 3–1). When excess water is ingested, the normal kidney dilutes the urine, excretes excess water, and prevents the development of hyponatremia. Hyponatremia develops when the intake of water exceeds the ability to excrete it leading to dilution of total body sodium.

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Figure 3–1.
Graphic Jump Location

Normal control of plasma osmolality.

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Pathogenesis

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Sodium concentration is the major determinant of plasma osmolality, therefore hyponatremia usually indicates a low plasma osmolality. Plasma osmolality can be estimated by the following equation:

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Low plasma osmolality rather than hyponatremia, per se, is the primary cause of the symptoms of hyponatremia. Hyponatremia not accompanied by hypoosmolality does not cause signs or symptoms and does not require specific treatment.

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The limitation in the kidney's ability to excrete water in hyponatremic states is, in most cases, due to the persistent action of antidiuretic hormone (ADH, vasopressin). ADH acts at the distal nephron to decrease the renal excretion of water. The action of ADH is, therefore, to concentrate the urine and, as a result, dilute the serum. Under normal circumstances, ADH release is stimulated primarily by hyperosmolality. However, under conditions of severe intravascular volume depletion or hypotension, ADH may be released even in the presence of serum hypoosmolality. Disease states characterized by a low cardiac output or systemic vasodilation result in “effective” intravascular volume depletion and may also stimulate ADH release.

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Importantly, ADH alone is not sufficient to cause hyponatremia. Only when the intake of water exceeds its excretory capacity can hyponatremia result. In some cases, massive water ingestion or a defective urinary concentrating mechanism can cause hyponatremia despite the complete absence of circulating ADH.

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Clinical Findings

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Symptoms and Signs

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The symptoms and signs of hyponatremia most likely result from cellular and cerebral edema. Headache, lethargy, confusion, weakness, psychosis, ataxia, seizures, and coma can all occur. Although no consistent correlation between the degree of hyponatremia and neurologic manifestations exists, patients with seizures and altered sensorium generally have serum sodium concentrations less than 120 mEq/L.

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Understanding the physiology of water movement is essential to understand the symptomatology and proper treatment of the disorders of water balance. In hyponatremia, the fall in plasma osmolality causes osmotic movement of water from the hypotonic extracellular compartment into relatively hypertonic cells. When ...

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