What is the relationship between hypernatremia and cerebral vasospasm?

From the Guidelines

Hypernatremia is not directly associated with vasospasm, and the primary concern in the context of aneurysmal subarachnoid hemorrhage (aSAH) is hyponatremia, which has been chronologically associated with the onset of sonographic and clinical vasospasm. The management of hypernatremia is crucial to prevent cerebral edema and other complications, but it is not the primary focus in the context of vasospasm. According to the guidelines for the management of aSAH, hyponatremia can develop from different mechanisms, including cerebral salt wasting, which is produced by excessive secretion of natriuretic peptides and causes hyponatremia from excessive natriuresis 1.

Management of Hyponatremia and Vasospasm

• The diagnosis of cerebral salt wasting is more common in patients with poor clinical grade, ruptured anterior communicating artery aneurysms, and hydrocephalus, and it may be an independent risk factor for poor outcome.
• Uncontrolled studies using crystalloid or colloid agents suggest that aggressive volume resuscitation can ameliorate the effect of cerebral salt wasting on the risk of cerebral ischemia after aSAH 1.
• Two randomized, controlled trials have been performed to evaluate fludrocortisones to correct hyponatremia and fluid balance, and one trial found that it helped to correct the negative sodium balance 1.
• A similar randomized, placebo-controlled trial showed reduced natriuresis and a lower rate of hyponatremia in aSAH patients treated with hydrocortisone 1.

Hypernatremia Management

• Hypernatremia can be managed by correcting the underlying cause, whether it's diabetes insipidus, excessive sodium intake, or inadequate water intake.
• Treatment typically involves administration of hypotonic fluids such as 0.45% saline or 5% dextrose in water, with the specific regimen calculated based on the patient's free water deficit.
• A reduction rate of 10-15 mmol/l/24 h is recommended to prevent cerebral edema and neurological injury 1.

Key Considerations

• Regular monitoring of serum sodium, neurological status, and cerebral perfusion is essential during treatment.
• The underlying cause of hypernatremia or hyponatremia should be identified and addressed to prevent further complications.
• Concurrent vasodilator therapy may be necessary in severe cases of vasospasm, with options including nimodipine, intravenous nicardipine, or milrinone infusion.

From the Research

Hypernatremia and Vasospasm

• Hypernatremia is a disorder of the homeostatic status regarding body water and sodium contents, which may lead to fatal consequences under improper management 2.
• The diagnostic approach to hypernatremia involves eight steps, including excluding pseudohypernatremia, confirming glucose-corrected sodium concentrations, and determining the extracellular volume status 2.
• Hypernatremia can be managed by replacing water deficits, ongoing water losses, and insensible water losses, with six steps to follow, including identifying underlying causes and determining the amount and rate of water administration 2.
• Vasospasm is not directly mentioned in the context of hypernatremia in the provided studies, but fluid management in acute brain injury, which can involve vasospasm, aims to preserve or restore physiology and guarantee appropriate tissue perfusion, avoiding potential iatrogenic effects 3.
• In the management of acute brain injury, intravascular volume management should aim for euvolemia, and isotonic crystalloids should be the preferred agents for volume replacement, while colloids, glucose-containing hypotonic solutions, and other hypotonic solutions or albumin should be avoided 3.
• Hypernatremia is defined as a serum sodium level above 145 mmol/L, and understanding hypernatremia requires a comprehension of body fluid compartments, as well as concepts of the preservation of normal body water balance 4.
• The treatment of hypernatremia should be closely monitored with serial electrolyte measurements, as formulae devised to guide therapy regard the patient as a closed system and do not take into account ongoing fluid losses that are highly variable between patients 5.