Neurocritical Care

25. Hyponatremia After Subarachnoid Hemorrhage

A 46-year-old woman with history of smoking and hypertension developed a thunderclap headache associated with emesis but no loss of consciousness. On arrival to the emergency department she was mildly confused and had no focal neurological deficits (World Federation of Neurological Surgeons–WFNS–Scale grade I). Head CT scan showed subarachnoid hemorrhage with aneurysmal pattern and mildly dilated ventricles. Her admission serum sodium level was 140 mmol/L. She was admitted to our neurosciences ICU, and a lumbar drain was placed, with resulting improvement of her headache and confusion. The following morning she had a cerebral angiogram, which revealed an anterior communicating artery aneurysm. The aneurysm was coiled without complications. She remained well over the following three days but developed increasing polyuria and a progressive decline in serum sodium. On day four she was still mostly asymptomatic but we noticed subtle new cognitive difficulties. We rechecked a transcranial Doppler and noticed that the mean blood flow velocities in the first segments of both anterior cerebral arteries and the right middle cerebral artery were increased by 30-40% compared with the previous day. Despite consistently receiving 150 cc per hour of 0.9% sodium chloride for the last 2 days, her fluid balance had been negative by 1.5 liters over the preceding 24 hours. Her serum sodium level has declined to 128 mmol/L from 135 mmol/L 8 hours earlier. What do you do now?

What do you do now?

Hyponatremia can occur in nearly half of cases of aneurysmal subarachnoid hemorrhage (aSAH). Serum sodium may decline at any time between 3 and 14 days after aneurysm rupture, but more commonly before the onset of cerebral vasospasm. Symptoms from hyponatremia are generally not severe. Confusion, increased drowsiness, and even seizures can occur when sodium levels are declining rapidly. Focal deficits are not caused by hyponatremia. The appearance of hyponatremia in aSAH should be considered a warning sign indicating the possibility of intravascular volume contraction, which can be particularly concerning in the setting of cerebral vasospasm.

Hyponatremia and volume contraction go hand in hand because the main cause of hyponatremia in aSAH is cerebral salt wasting syndrome. This is a disorder characterized by excessive secretion of natriuretic peptides leading to increased urinary sodium loss. In turn, the increased sodium in the urine drags water with it. The consequences are polyuria and intravascular volume depletion. Patients with aSAH may also have the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), which produces excessive retention of free water at the tubular level and results in dilutional hyponatremia. The problem is that readily available tests of the blood and urine are not very useful to differentiate SIADH (associated with normal or mildly expanded intravascular volume) from cerebral salt wasting (associated with intravascular volume contraction) (Figures 25.1 and 25.2). Cerebral salt wasting typically predominates, as reflected by the frequent improvement of hyponatremia after infusion of isotonic saline in these patients (isotonic fluid administration worsens hyponatremia associated with SIADH).

Determining the volume status of the intravascular compartment in aSAH is extremely difficult and most times it can only be roughly estimated. Monitoring the central venous pressure may help, but the reliability of this measurement is limited. We, like many others, have moved away from using pulmonary artery catheters in most of these patients. Novel noninvasive methods appear promising, but they have not been sufficiently validated. Thus, since there are no ideal ways to gauge the volume status, it is most prudent to assume that polyuric patients with worsening hyponatremia will develop volume contraction.

When treating patients with aSAH we must therefore replace fluid volume and sodium. Hypertonic saline can achieve this goal. We often start with 1.5% sodium chloride, but resort to 3% solution if the hyponatremia is severe or fails to improve with lower concentration of sodium replacement. If hyperchloremic acidosis develops, we switch to sodium acetate, adjusting the concentration to maintain the same tonicity. Our therapeutic goal is to correct the hyponatremia and, most importantly, to maintain euvolemia.


FIGURE 25.1 Differential diagnosis between cerebral salt wasting (CSW) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

Some patients with aSAH become extremely polyuric, and this tends to occur at the peak of cerebral vasospasm. In these situations it is all too common that we get stuck in a vicious circle of giving more crystalloid fluids to compensate for the unrelenting fluid and sodium loss. One must scale back fluid administration to avoid complications such as pulmonary edema or renal medullary washout.

Mineralocorticoids are useful to prevent or ameliorate excessive urinary excretion and hyponatremia in patients with aSAH. Only early initiation (within 72 hours of aneurysm rupture) has been formally tested and proven effective. In placebo-controlled studies, fludrocortisone was associated with fewer side effects than hydrocortisone (which may cause hyperglycemia due to its glucocorticoid activity), but neither medication increased the risk of congestive heart failure. In our practice, we start fludrocortisone (0.2 mg twice daily) early in most patients with aSAH (higher doses of fludrocortisone may be needed in refractory cases).


FIGURE 25.2 Algorithm for the evaluation and management of hyponatremia in a critically ill neurological patient. CSW, cerebral salt wasting; SIADH, syndrome of inappropriate secretion of antidiuretic hormone.

Hypotonic intravenous fluids (Table 25.1) should be avoided in patients with aSAH, not only because hyponatremia is so frequent but also because these patients are at increased risk of intracranial hypertension. In alert patients tolerating an oral diet, the tonicity and sodium concentration of ingested fluids should also be regulated. These patients usually get thirsty as they become polyuric, and abundant ingestion of water may exacerbate the hyponatremia. In these cases, we have patients drink fluids enriched with high concentrations of sodium (attempting to treat hyponatremia with sodium tablets or salty foods is inefficient).

TABLE 25.1 Sodium Content in Common Intravenous Fluid Solutions

Intravenous fluid

Sodium content (mmol per liter)

5% dextrose*


0.45% sodium chloride*


Ringer’s Lactate*


0.9% sodium chloride


1.5% sodium chloride


3% sodium chloride†**


* Not recommended for use in aneurysmal subarachnoid hemorrhage

 Recommended for use in aneurysmal subarachnoid hemorrhage

** Requires central access

We treated our patient with fludrocortisone and increased volume of 1.5% sodium chloride. Her sodium level improved progressively despite persistent polyuria and it returned to normal range 48 hours later. She also developed fluctuating alertness that we attributed to diffuse cerebral vasopasm, which resolved with hemodynamic augmentation therapy (phenylephrine infusion). She was discharged home after 15 days of hospital stay and returned to work 5 weeks later.

Hyponatremia is a common concern in patients with aSAH, and its pathophysiology is not completely understood. It should be considered an indicator of volume contraction, and its treatment is hypertonic saline. Fludrocortisone can help prevent this complication. Fluid restriction may substantially increase the risk of cerebral infarction in patients with hyponatremia and cerebral vasospasm and therefore it should be avoided.


· Hyponatremia is common after aneurysmal subarachnoid hemorrhage and it is often associated with intravascular volume contraction.

· Treatment of the polyuric, hyponatremic patient should include replacement of sodium and fluid volume.

· The goals of fluid management in cases of aneurysmal subarachnoid hemorrhage are maintenance of normonatremia and euvolemia.

· One must replace volume effectively, but being careful not to induce fluid overload.

· Fludrocortisone is useful to ameliorate urinary sodium loss and hyponatremia.

Further Reading

Audibert G, Steinmann G, de Talanc N et al. Endocrine response after severe subarachnoid hemorrhage related to sodium and blood volume regulation. Anesth Analg 2009; 108:1922–1928.

Brimioulle S, Orellana-Jimenez C et al. Hyponatremia in neurological patients: cerebral salt wasting versus inappropriate antidiuretic hormone secretion. Intensive Care Med 2008; 34:125–131.

Hasan D, Wijdicks EF, Vermeulen M. Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage. Ann Neurol 1990; 27:106–108.

Harrigan MR. Cerebral salt wasting syndrome: a review. Neurosurgery 1996: 38:152–160.

Rabinstein AA, Bruder N. Management of hyponatremia and volume contraction. Neuro Crit Care 2011; in press.

Rabinstein AA, Wijdicks EF. Hyponatremia in critically ill neurological patients. Neurologist 2003; 9:290–300.

Rahman M, Friedman WA. Hyponatremia in neurosurgical patients:clinical guideline development. Neurosurgery 2009:65:925–935.

Sterns RH, Hix JK, Silver S. Treatment of hyponatremia. Curr Opin Nephrol Hypertens 2010:19:493–498.

Sterns RH, Silver SM. Cerebral salt wasting versus SIADH: what difference? J Am Soc Nephrol 2008; 19:194–196.

Wijdicks EF, Vermeulen M, Hijdra A, van Gijn J. Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful? Ann Neurol 1985; 17:137–140.

Wijdicks EF, Vermeulen M, ten Haaf JA et al. Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. Ann Neurol 1985; 18:211–216.