Which Statements About SIADH Are Correct?
The correct answers are (b) SIADH is a common cause of hyponatremia and (d) CNS infections are among the causes of SIADH. Options (a), (c), and (e) are incorrect based on the diagnostic criteria and pathophysiology of this syndrome.
Analysis of Each Statement
Statement (a): "Low sodium concentration in urine" – INCORRECT
SIADH is characterized by inappropriately HIGH urinary sodium concentration (>20 mEq/L), not low. 1 This occurs because the excessive water retention from inappropriate ADH secretion leads to dilutional hyponatremia, which triggers a physiologic natriuresis where the kidneys excrete sodium to maintain fluid balance at the expense of plasma sodium. 2 The combination of hyponatremia with elevated urinary sodium (>20-40 mmol/L) and inappropriately concentrated urine (osmolality >500 mOsm/kg) is a cardinal diagnostic feature that distinguishes SIADH from hypovolemic causes of hyponatremia, where urinary sodium would be <20 mEq/L. 3, 1
Statement (b): "Common cause of hyponatremia" – CORRECT
SIADH is the most frequently recognized cause of hyponatremia among hospitalized patients. 4 Approximately 30% of hospitalized patients develop hyponatremia, and SIADH represents the most common cause of euvolemic (normovolemic) hyponatremia. 5, 2 The syndrome accounts for a substantial proportion of hyponatremia cases encountered in clinical practice, making it essential to recognize and diagnose appropriately. 6
Statement (c): "Arterial hypertension due to vasoconstrictive action" – INCORRECT
SIADH does not cause arterial hypertension through vasoconstrictive mechanisms. While arginine vasopressin (AVP) does have vasoconstrictive properties at high concentrations (hence its alternative name "vasopressin"), the levels of AVP in SIADH are typically not sufficient to cause clinically significant vasoconstriction or hypertension. 2 The primary pathophysiology involves water retention through the antidiuretic effect on renal collecting ducts, leading to dilutional hyponatremia in a euvolemic state—patients characteristically have no edema, no orthostatic hypotension, and normal blood pressure. 1, 5 The absence of volume depletion or volume overload (euvolemia) is actually one of the five cardinal diagnostic criteria for SIADH. 2
Statement (d): "CNS infections are among the causes" – CORRECT
Central nervous system infections are well-established causes of SIADH. 7, 2 CNS disorders—including meningitis, encephalitis, brain abscesses, and other space-occupying lesions—disrupt normal hypothalamic-pituitary function and ADH regulation, leading to inappropriate secretion. 7, 8 In pediatrics, SIADH is most commonly seen in patients with meningitis. 8 The major etiologic categories of SIADH include: (i) neoplasia, (ii) neurological diseases (including CNS infections), (iii) lung diseases, and (iv) various drugs. 2
Statement (e): "Treatment is with desmopressin" – INCORRECT
Desmopressin is contraindicated in SIADH—it would worsen the condition. 3 Desmopressin is a synthetic ADH analog that mimics the antidiuretic action of vasopressin; administering it to a patient with SIADH (who already has excessive ADH activity) would exacerbate water retention and worsen hyponatremia. 3 The correct treatment approach for SIADH includes: (1) identifying and treating the underlying cause, (2) fluid restriction to 1 L/day as first-line therapy for mild-to-moderate cases, (3) oral sodium chloride supplementation if fluid restriction fails, and (4) hypertonic saline (3%) only for severe symptomatic hyponatremia with neurological symptoms. 1, 6, 4, 5 Pharmacologic options for refractory cases include vasopressin receptor antagonists (vaptans), demeclocycline, or urea—all of which counteract ADH effects rather than augment them. 1, 4
Common Diagnostic Pitfalls
Confusing SIADH with cerebral salt wasting (CSW): Both present with hyponatremia and elevated urinary sodium in neurosurgical patients, but CSW shows true hypovolemia (low CVP <6 cm H₂O) requiring volume replacement, while SIADH is euvolemic and requires fluid restriction. 1, 5 Using fluid restriction in CSW can be hazardous and worsen outcomes. 5
Failing to exclude other causes: Before diagnosing SIADH, hypothyroidism, adrenal insufficiency, and volume depletion must be ruled out, as these can present similarly. 5, 2
Overcorrection of chronic hyponatremia: Sodium correction should never exceed 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome. 1, 5