Syndrome of Inappropriate Antidiuretic Hormone Secretion

Published on 10/06/2015 by admin

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Last modified 22/04/2025

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Syndrome of Inappropriate Antidiuretic Hormone Secretion

Jonathan P. Wood, MD

Basic Information

Definition

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a dilutional hyponatremia associated with increased renal water retention. It is defined by a plasma sodium level less than 130 mmol/L, plasma osmolality less than 280 mOsm/L, urine sodium level more than 25 mmol/L, urine osmolality greater than the plasma osmolality, absence of edema or volume depletion, and normal renal and adrenal function.

Synonyms

Antidiuretic hormone (ADH) is synonymous with arginine vasopressin (AVP).

ICD-9-CM Code

253.6 Other disorders of neurohypophysis

Epidemiology & Demographics

• Hyponatremia is the most common electrolyte disorder seen in clinical medicine, affecting 15% of hospitalized patients. SIADH is one of the most common causes of euvolemic hyponatremia.
• The most common risk factors in children are central nervous system (CNS) disease, pulmonary disease (especially respiratory viral infection), spinal surgery, and an increasing variety of drugs.
• Nonpulmonary tumors can also lead to SIADH through production of ADH-like substances, although this occurs less commonly in children.

Clinical Presentation

• The hyponatremia of SIADH is usually asymptomatic.
• Symptoms occur most often when the sodium level is less than 120 mEq/L or when a drop in sodium develops rapidly.
• Signs and symptoms include nausea, cramps, lethargy, disorientation, agitation, seizures, and coma.

Etiology

• Excess ADH leads to retention of free water by the kidney, resulting in expansion of the intravascular space and hyponatremia.
• There is no clear unifying cause or pathophysiology.
• Most patients appear to have disordered regulation ADH in response to hypo-osmolality.

Diagnosis

Differential Diagnosis

• Inappropriate intravenous fluid therapy
• Glucocorticoid deficiency
• Water Intoxication
• Hypothyroidism
• Presence of drugs that cause release of ADH or potentiate ADH
• Cerebral salt wasting (CSW), although this is typically a volume-depleted state
• Pseudohyponatremia, caused by a sodium assay idiosyncrasy in hyperglycemic or hyperlipidemic patients

Workup

• Establish hyponatremia.
• Establish that the patient is euvolemic.
• The differential diagnosis of hyponatremia in the dehydrated or edematous patient is different from euvolemic hyponatremia and does not include SIADH.
• Consider other causes of euvolemic hyponatremia (see “Differential Diagnosis”). They need not be ruled out in every patient but should be considered, especially if there is no underlying risk factor for SIADH.
• Evaluate serum and urine levels of sodium and osmolality in the context of urine output.

image Urine output should be significantly reduced in SIADH.
image Decreased serum sodium and osmolality with increased urine sodium and osmolality strongly suggests SIADH.
image In the patient with CNS disease, this combination without reduced urine output suggests CSW. These patients are generally volume depleted, which should also help distinguish SIADH from CSW.

• Ongoing evaluation of serum sodium and urine output is essential.

image SIADH can resolve spontaneously without warning or obvious clinical findings.
image In patients with CNS lesions, SIADH can be followed by diabetes insipidus.

Laboratory Tests

Serum and urine sodium levels and osmolality should be assessed.

Treatment

Nonpharmacologic Therapy

Identify and treat the underlying disease.

Acute General Rx

• Fluid restriction is the mainstay of SIADH treatment. Total fluids should be reduced to two thirds of maintenance levels.
• In the presence of seizures or acute neurologic changes, small volumes of hypertonic (3%) saline may be considered. This therapy must be used with extreme caution and should be aimed at stopping seizures, not normalizing the sodium concentration.
• Rapid correction of hyponatremia, especially in chronic cases, should be strenuously avoided.

Pearls & Considerations

Comments

• Care should be taken in making the diagnosis of SIADH in the presence of diuretic therapy.
• In SIADH, the serum sodium level will not continue to fall indefinitely because of a decline in the renal effect of ADH over time. The reason for this is unclear.
• It is important to distinguish SIADH from CSW because the therapies differ and are counter to each other.
• Most of the drugs associated with SIADH are not commonly used in pediatrics. Notable exceptions are the antineoplastic drugs vincristine and cyclophosphamide. The latter is particularly worrisome in that it is often accompanied by vigorous hydration to avert renal complications.
• Ecstasy use has emerged as a risk factor for SIADH.
• Menstruating women may be more susceptible to long-term neurologic complications from hyponatremia in general. The exact reason for this association is not clear.

Prevention

• There is no role for prophylactic fluid restriction in patients with risk factors for SIADH.
• A reasonable index of suspicion and vigilance in regard to urine output can lead to the diagnosis in time to institute appropriate therapy.

Suggested Readings

Baylis PH. The syndrome of inappropriate antidiuretic hormone secretion. Int J Biochem Cell Biol. 2003;35:1495.

Bussmann C, et al. Hyponatremia in children with acute CNS disease: SIADH or cerebral salt wasting. Childs Nerv Syst. 2001;17:58.

Lieh-Lai 1999 Lieh-Lai MW, et al. Syndrome of inappropriate antidiuretic hormone secretion in children following spinal fusion. Crit Care Med. 1999;27:622.

Palmer BF. Hyponatremia in a neurosurgical patient: syndrome of inappropriate antidiuretic hormone secretion versus cerebral salt wasting. Nephrol Dial Transplant. 2000;15:262.

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