Role of 3% Hypertonic Saline in Subarachnoid Hemorrhage
3% hypertonic saline is reasonable for correcting hyponatremia in SAH patients and may augment cerebral blood flow in poor-grade SAH, but it should not be used for volume resuscitation or as prophylaxis in normonatremic patients. 1
Primary Indication: Hyponatremia Correction
The use of hypertonic saline is reasonable for correcting hyponatremia after SAH (Class IIa, Level of Evidence B). 1 Hyponatremia occurs in 10-30% of SAH patients and is more common in those with poor clinical grade, anterior communicating artery aneurysms, and hydrocephalus. 1
- Retrospective evidence suggests 3% saline effectively corrects hyponatremia in this setting. 1
- Hyponatremia may be an independent risk factor for poor outcome and is chronologically associated with vasospasm onset. 1
- The mechanism involves cerebral salt wasting from excessive natriuretic peptide secretion causing natriuresis and volume contraction. 1
Administration Protocol for Hyponatremia
- Administer 3% hypertonic saline as continuous infusion targeting serum sodium of 145-155 mmol/L. 1
- Measure serum sodium within 6 hours of initiation and monitor every 6 hours thereafter. 2
- Do not exceed sodium levels of 155-160 mmol/L to prevent complications. 2
- Avoid rapid correction exceeding 10 mmol/L per 24 hours to prevent osmotic demyelination syndrome. 2
Cerebral Blood Flow Augmentation in Poor-Grade SAH
In poor-grade SAH patients, 23.5% hypertonic saline bolus (2 ml/kg) significantly augments cerebral blood flow and improves cerebral oxygenation. 3, 4
- Increases CBF by 20-50% in ischemic regions with maximum effect at 30-60 minutes. 3, 4
- Significantly improves brain tissue oxygen (PbO2) and decreases lactate-pyruvate ratio, indicating improved cerebral metabolism. 3
- Dose-dependent effect on favorable outcome (mRS 1-3) demonstrated on xenon-CT scanning. 4
- Effects include increased cerebral perfusion pressure by 21.2% and decreased ICP by 93.1%. 4
Critical Volume Management Principles
Administration of large volumes of hypotonic fluids and intravascular volume contraction should generally be avoided after SAH (Class I, Level of Evidence B). 1
- Fluid restriction has been associated with increased delayed ischemic deficits. 1
- Volume contraction is linked to symptomatic vasospasm. 1
- Treat volume contraction with isotonic fluids, not hypertonic saline. 1
- Monitoring volume status using central venous pressure, pulmonary artery wedge pressure, fluid balance, and body weight is reasonable (Class IIa). 1
Comparison with Alternative Agents
- Fludrocortisone acetate is also reasonable for correcting hyponatremia, with RCT evidence showing reduced need for fluids and improved sodium levels. 1
- 5% albumin may be effective as a volume expander, though no clear superiority over crystalloids exists. 1
- For ICP management specifically, hypertonic saline produces more rapid ICP reduction than mannitol at equiosmolar doses. 2, 5
Evidence for 3% Concentration in SAH
A retrospective study of 29 hyponatremic SAH patients with symptomatic vasospasm showed 3% sodium chloride/acetate continuous infusion resulted in higher central venous pressures, positive fluid balance, and increased serum sodium without metabolic acidosis or complications. 6
- No reports of congestive heart failure, pulmonary edema, coagulopathy, intracranial hemorrhages, or central pontine myelinolysis occurred. 6
- A comparative study found 160 mL of 3% HSS equivalent to 150 mL of 20% mannitol for ICP reduction in aneurysmal SAH, with no difference in extent or duration of action. 7
Common Pitfalls to Avoid
- Do not use hypertonic saline for volume resuscitation in hemorrhagic shock. 2
- Do not use prophylactically in normonatremic patients without documented intracranial hypertension. 5
- Do not combine with hypotonic solutions (Ringer's lactate, 5% dextrose, 0.45% saline, Hartmann's solution) as these worsen cerebral edema. 2
- Monitor for hypernatremia and hyperchloremia, especially with continuous infusions. 1, 5
Critical Limitation
Despite effectiveness in correcting hyponatremia and augmenting CBF, there is no RCT evidence that hypertonic saline improves neurological outcomes or survival in SAH patients. 2, 5 The evidence for CBF augmentation and outcome improvement comes from uncontrolled studies and retrospective analyses. 3, 4