Update on the Management of Subarachnoid Hemorrhage

Katja E Wartenberg

Disclosures

Future Neurology. 2013;8(2):205-224. 

In This Article

Electrolyte Disturbances

Hyponatremia occurs in 20–40% of SAH patients. Hypomagnesemia (40%), hypokalemia (25%) and hypernatremia (20%) are also common after SAH.[156–159] Hyponatremia is usually caused by inappropriate secretion of antidiuretic hormone and free-water retention and/or excessive renal sodium excretion due to increased atrial natriuretic factor, so called 'cerebral salt wasting syndrome'.[159,160] Intravascular volume depletion and sodium loss may increase the risk of DCI and infarction.[84,85] In 124 WFNS grade IV and V patients, hyponatremia (serum sodium <135 mmol/l) developed in 63% of patients, caused by cerebral salt wasting syndrome in 55%. Late-onset hyponatremia (between SAH day 4 and 9) correlated with a higher occurrence of cerebral infarction in this patient population. Nevertheless, hyponatremia did not have an association with poor outcome at 3 months (Glasgow Outcome Scale: 1–3).[161]

Fludrocortisone and hydrocortisone were studied for the prevention of hyponatremia in SAH.[162–166] If started early, the corticosteroids are effective in the prevention of natriuresis and hyponatremia. However, their use was complicated by hyperglycemia and hypokalemia.

Administration of large-volume isotonic crystalloids and restriction of free-water intake should be applied to counteract potential hypovolemia and to prevent inappropriate water retention. Hypertonic saline (3%) may be used to correct hyponatremia.[56,167]

Conivaptan is an arginine vasopressin receptor antagonist (V1A/V2) approved for the treatment of euvolemic and hypervolemic hyponatremia.[168] Initial reports of its use in neurocritical care patients with hyponatremia have yielded promising results.[169] Caution should be taken to avoid hypovolemia with the use of conivaptan.[56]

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