Neurocritical Care

Consideration of iatrogenic hypernatremia

Decreased secretion of ADH or vasopressin results in decreased retention of water at the renal

distal tubules. Observed in the setting of pituitary or hypothalmic damage (brain tumor, TBI) or

brain death.

Characterized by voluminous (greater than 250 mL/hour), dilute urinary output

Hypotonic solutions for free-water replacement

Dextrose 5% in water

0.45% sodium chloride

Water supplementation orally or by feeding tube

Supplementation of ADH to normal functional concentrations

Titrate therapy to normalized urinary output, serum sodium correction, and urine specific gravity.

Desmopressin

Intravenously or subcutaneously: 0.5–4 mcg every 8–12 hours (usual starting dose 1–2 mcg)

ii.

Intranasally: 10–40 mcg/day divided into two or three doses (usual starting dose 10 mcg)

iii.

Orally: 50–800 mcg divided into two doses (usual starting dose 50 mcg)

iv.

May be dosed as needed, depending on initial laboratory values

Arginine vasopressin – Continuous infusion 1–15 units/hour (usual starting dose 1 unit/hour; titrate to

urinary output of 150–250 mL/hour)

Considerations for rapid correction of hypernatremia

Recommended decrease in serum sodium concentration is 0.5 mEq/L/hour or less.

Too-rapid correction of serum sodium may result in cerebral edema.

In general, neurocritical care patients should receive minimal amounts of dextrose or free water–

containing fluids to avoid the risk of cerebral edema.

consciousness in between seizures (Neurocrit Care 2012;17:3-23)

Generalized convulsive status epilepticus: Generalized convulsions present with onset of seizure

activity – Usually clinically evident

present (seizures noted with electroencephalogram [EEG] monitoring only)

benzodiazepine followed by another anticonvulsant medication)

suppression or termination of continuous EEG seizures