A 40-year-old woman presents with a sudden, severe, thunderclap headache. A CT scan and a CT angiogram are obtained which reveal diffuse subarachnoid hemorrhage due to rupture of an anterior communicating artery aneurysm. The aneurysm is successfully coiled. Five days later, the patient becomes progressively confused. Transcranial Doppler sonography is within normal limits, and a repeat CT angiogram is negative for any significant vessel narrowing suggestive of vasospasm. Laboratory tests reveal a serum sodium concentration of 128 mEq/L. Salt tablets are initiated and titrated higher, but the patient’s sodium remains mildly low. A continuous infusion of 3% sodium chloride is begun, and the patient’s sodium normalizes. Within several days, she is weaned from the continuous infusion and is subsequently discharged home with salt tabs and a scheduled taper.
Name an endocrinopathy frequently encountered in the neurologic intensive care unit (NeuroICU)
Patients with aneurysmal subarachnoid hemorrhage (SAH) often develop neuroendocrine dysfunction—the “classic” finding being dysregulated salt and water balance, specifically hyponatremia. The hyponatremia generally begins in a delayed fashion, lasting for days to weeks—a temporal course mirroring the cerebral vasospasm window. In one study of 316 patients with SAH, 179 (56.6%) developed hyponatremia, including 62 (19.6%) with severe hyponatremia.1 There is considerable controversy regarding the pathophysiology of hyponatremia in SAH. Posited mechanisms include cerebral salt wasting and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion, though relative adrenal insufficiency and even inappropriate IV fluid resuscitation may contribute.2,3 In one prospective study of low-grade SAH patients with hyponatremia, SIADH was determined to be the etiology of hyponatremia in 71.4% of patients.4 Others have suggested hyponatremia in SAH that may be due to both disordered arginine vasopressin secretion and exaggerated natriuresis; the predominant clinical presentation would depend on the intensities of each as well as the effects of concomitant therapy (eg, IV fluids, sodium repletion).5
Understanding the volume status of the patient may help distinguish the underlying etiology (SIADH vs cerebral salt wasting) and is critical for the general management of the patient. Cerebral salt wasting is defined by salt loss accompanied by a reduced effective arterial blood volume, whereas the hyponatremic patient with SIADH is generally euvolemic. In cerebral salt wasting, treatment focuses on replenishing both salt and volume. This can be achieved with agents such as fludrocortisone, salt tablets, or hypertonic sodium chloride infusions (Table 58-1). On the other hand, SIADH is theoretically treated with fluid restriction. Fluid restriction may not be appropriate in those SAH patients concurrently demonstrating signs of cerebral vasospasm, as fluid restriction in this setting could precipitate infarction.
Table 58-1.Pharmacologic Treatment of Hyponatremia in SAH Patients ||Download (.pdf) Table 58-1. Pharmacologic Treatment of Hyponatremia in SAH Patients