Endocrine Testing for the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

Review
In: Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000.
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Excerpt

The diagnosis of Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) relies on an adequate assessment of a hyponatremic state (that is a serum sodium level <136 mmol/l) and on the exclusion of other causative conditions leading to an appropriate secretion of antidiuretic hormone (ADH). The understanding of mechanisms involved in pathological ADH secretion is essential for diagnosis and therapy. Although some forms are due to dysregulation in central nervous system regulation, other forms are dependent on diseases in peripheral organs and structures including ADH-producing/secreting neuroendocrine tumors, while others are induced by drugs. ADH regulation is closely linked to other systems such as the sympathetic nervous system via and baroreflex regulation. Patients with hyponatremia should be assessed carefully whether or not neurological symptoms exist. Further, assessment of volume status is needed. Based on symptoms and volume status, the need for intensive-care monitoring is determined. In parallel, laboratory findings of blood and urine must be analyzed appropriately. It is important to demonstrate true hyponatremia, which is paralleled by a decrease in serum osmolality. Mandatory laboratory diagnostic steps comprise the determination of blood and urine electrolytes and serum and urine osmolality, analysis of thyroid, adrenocortical, and kidney function as well as uric acid. Different test results such as a high fractional uric acid excretion may hint to an existing SIADH. Assessment of urine osmolality and urine sodium concentration and intravascular volume level may allow for further discrimination and may be indicative for a specific underlying disorder, causing SIADH. Brain volume changes (“hydrocephalus ex vacuo”) may depend on age rendering the elderly more tolerant to acute or chronic serum sodium changes. The course of incident hyponatremia, if documented, may affect therapy. A serum sodium drop within less than 48 hours is considered acute hyponatremia. A rapid bolus of 100 to 150 ml of intravenous 3% hypertonic saline is appropriate to avoid catastrophic outcomes in severe cases of acute symptomatic hyponatremia. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.

Publication types

  • Review