SIADH Does Not Cause Hypotension
SIADH typically causes euvolemic hyponatremia and does not cause hypotension. 1 In fact, patients with SIADH characteristically maintain normal blood pressure and do not present with edema, which helps distinguish it from other causes of hyponatremia.
Pathophysiology of SIADH
SIADH involves:
- Excessive ADH (vasopressin) secretion that is not suppressed despite low plasma osmolality
- Increased water retention leading to dilutional hyponatremia
- Expansion of both extracellular fluid (ECF) and intracellular fluid (ICF) volumes 1
- Maintained effective circulating volume without hypotension
Volume Status in SIADH vs. Other Hyponatremic States
The volume status in hyponatremia helps distinguish between different etiologies:
| Volume Status | Clinical Signs | Urine Sodium | Likely Causes |
|---|---|---|---|
| Euvolemic | No edema, normal vital signs | >20-40 mEq/L | SIADH, hypothyroidism, adrenal insufficiency |
| Hypovolemic | Orthostatic hypotension, dry mucous membranes, tachycardia | <20 mEq/L | GI losses, diuretics, cerebral salt wasting |
| Hypervolemic | Edema, ascites, elevated JVP | <20 mEq/L | Heart failure, cirrhosis, renal failure |
Diagnostic Criteria for SIADH
SIADH is diagnosed when the following criteria are met:
- Hypotonic hyponatremia
- Continued urinary sodium excretion (natriuresis)
- Urine osmolality exceeding plasma osmolality
- Absence of edema and volume depletion (including absence of hypotension)
- Normal renal and adrenal function 2
Clinical Differentiation from Other Causes of Hyponatremia
SIADH can be distinguished from hyponatremia due to volume depletion or cardiac/hepatic causes:
In SIADH:
- Blood pressure is normal
- No edema is present
- Lower plasma concentrations of urate, creatinine, and urea 3
In hyponatremia due to heart failure or liver cirrhosis:
- Blood pressure may be low
- Edema is typically present
- Plasma measurements of urate, creatinine, and urea are usually elevated 3
Common Causes of SIADH
SIADH is commonly associated with:
- Malignancies (especially small cell lung cancer) 4, 5
- Neurological diseases
- Pulmonary disorders
- Medications (chlorpropamide, carbamazepine, certain antineoplastics)
- Post-operative state with inappropriate hypotonic fluid administration 6, 2
Management Considerations
- The mainstay of treatment is fluid restriction (1,000-1,500 mL/day) 1
- For severe symptomatic hyponatremia: intravenous furosemide and 3% sodium chloride 6
- Vasopressin receptor antagonists (e.g., tolvaptan) for refractory cases 1
- Correction rate should not exceed 8 mEq/L per 24 hours to prevent osmotic demyelination syndrome 1
Common Pitfalls
- Misdiagnosis: Confusing SIADH with hypovolemic hyponatremia can lead to inappropriate fluid administration.
- Inappropriate fluid management: Administering hypotonic fluids to patients with SIADH will worsen hyponatremia.
- Overcorrection: Correcting sodium levels too rapidly can lead to osmotic demyelination syndrome.
- Failure to identify underlying cause: SIADH is often secondary to another condition that requires specific treatment.
Remember that while SIADH patients have euvolemic hyponatremia with normal blood pressure, they may develop neurological symptoms (confusion, seizures, coma) due to hyponatremia itself, not due to hemodynamic compromise.