Transtentorial herniation: acute unresponsiveness, decline in GCS >=2 pts with uni- or bilateral pupillary dilatation and loss of reactivity to light, and increase in ICP >20mmHg in acomatose patient x 5 mints +/- change in pupillary sie and reactivity.
- 23.4% saline (30-60 mL bolus) over 5-10 minutes
– well-tolerated in renal failure, no observed pulmonary edema or overload despite high incidence of cardiovascular dysfunction in this population (small study)
Proposed Mechanism of Action: hypertonic saline causes osmolar gradient –> to fluid shifts, reduces brain mass, without significant diuresis
- osmotic diuresis
- vasoconstriction resulting in decreased cerebral volume
- reduced blood viscosity
- improved cerebral perfusion from volume expansion
- hypotension – most common adverse event
- pulmonary edema
- rebound ICP elevation
*mechanism for hypotension: ?not clarified yet, small animal study suggests may be mediated by sympathetic neural reflex and not a diuretic effect; others suggest may be due to vasodilatory effect; or maybe due to resolution of Cushing response
Hirsch, Karen G. et al. “Treatment Of Elevated Intracranial Pressure With Hyperosmolar Therapy In Patients With Renal Failure”. Neurocritical Care 17.3 (2012): 388-394.