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.

Assuming it is not an iatrogenic hypernatremia (eg, the patient was administered hypertonic saline for elevated intracranial pressure or the patient has a significant free water deficit due to dehydration), the diagnosis of diabetes insipidus (DI) should be considered. In healthy adults, arginine vasopressin binds to V2 receptors in the renal collecting tubule, stimulating water reabsorption to maintain salt and water homeostasis. In patients with central DI, there is a failure of antidiuretic hormone (ADH) release from the posterior pituitary, resulting in polyuria and hypernatremia. Large volumes of dilute urine will be excreted, typically > 2.5 mL/kg body weight per hour. Polyuria to this degree can also be caused by hyperglycemia (as glucosuria results in an osmotic diuresis), mannitol administration, or aggressive intravenous hydration, though in these circumstances, a patient’s serum sodium concentration is typically not elevated.

In the NeuroICU, central DI classically develops in 3 patient populations: (1) the patient with an acute traumatic brain injury (TBI), (2) patients who have undergone transsphenoidal surgery for sellar or parasellar pathology, and (3) patients who are brain dead (or progressing to brain death). DI is a well-recognized complication of TBI, with a reported incidence in the medical literature of 3% to 26%.⁶ Clinical features associated with the development of DI in TBI patients include severe TBI (Glasgow Coma Scale < 8), craniofacial trauma and skull fractures (particularly with cranial nerve pathology), and cardiopulmonary arrest. There is a fairly strong correlation of hypernatremia with mortality in this patient population; therefore, it is essential to accurately diagnose and treat DI in TBI patients.⁷ In regards to postoperative patients, 18% to 31% of transsphenoidal surgery patients will develop early postoperative DI (often during the first 24 to 48 hours after pituitary surgery).⁸ Risk factors for DI in this patient population include young age, male gender, and resultant CSF leak, and if there is a craniopharyngioma, Rathke-cleft cyst, or adrenocorticotropic hormone (ACTH)-secreting adenoma, resection.