Potential etiologies
(Sterns, 2024) |
- CNS disturbances leading to increased ADH release (stroke, hemorrhage, infection, trauma)
- Malignant tumor production of ADH (common in small cell carcinoma of the lung)
- Drug-related
- Includes but not limited to SSRIs, carbamazepine, chlorpropamide, cyclophosphamide
- Administration of hormones such as vasopressin and desmopressin to treat other medical conditions
- Surgery
- Pulmonary disease
- Pneumonia; less frequently asthma, respiratory failure, atelectasis, pneumothorax
- Hormone deficiency (hypopituitarism, hypothyroidism)
- HIV
- Hereditary
- Idiopathic
NOTE: There is a condition called cerebral salt wasting which may mimic SIADH, but this condition leads to volume depletion, causing a secondary elevation in ADH. |
Clinical manifestations
Signs and symptoms depend on the severity of hyponatremia and the rate at which it develops. If the sodium level has decreased slowly over a long period, the patient may be asymptomatic. |
Hyponatremia
- Severe (Na+ less than 120 mEq/L)
- seizures, poor concentration, weakness, hyperreflexia, headache, speech difficulties, coma, cerebral edema
- Moderate (Na+ 120-129 mEq/L)
- dizziness, gait disturbance, restlessness, headache, confusion, forgetfulness, lethargy, or may present asymptomatic
- Mild (Na+ 130-135 mEq/L)
Note: SIADH may be persistent or transient depending on etiology |
| Common laboratory trends |
- Hyponatremia
- Hypoosmolality (serum osmolality less than 280 mOsm/kg)
- Urine osmolality greater than 100 mOsm/kg
- Urine sodium typically greater than 40 mEq/L
- Serum potassium – normal or low normal
- Acid-base status – normal
- Serum uric acid – low
|
| Treatment |
- Treatment of underlying condition/disease
- Prevent further decline in serum Na+ concentration
- Goals of treatment may vary depending on clinical acuity and co-morbidities
- Key component of treatment is correcting hyponatremia
- Fluid restriction
- Salt administration (increases solute excretion and urine volume leading to increased Na+)
- May be administered with loop diuretics which lowers urine osmolality and increases water excretion
- Vasopressin receptor antagonists
- Saline or hypertonic saline (3%) in severe, symptomatic hyponatremia
- Urea administration (increases solute excretion and urine volume leading to increased Na+)
*Persistent SIADH requires ongoing therapy.
|
| Na+ correction rates |
Hyponatremia MUST be corrected slowly. Rapid correction could lead to cerebral fluid shifts and rarely, a life-threatening complication called osmotic demyelination syndrome (ODS).
- In general, rate of correction should 4-6 mEq/L in the first 24 hours and should always be less than 8 mEq/L during this critical period.
- In those with severe neurologic symptoms, correction rate may be faster, 4-6 mEq/L in the initial 2- to 4-hour period to prevent further neurologic deterioration.
- Na+ should be checked every 2 to 3 hours during initial management an every 4 to 6 hours until NA+ is 130 or greater.
|