Neurocritical Care

Potential for coagulopathy

(MacLaren 2024).

Histamine-2 receptor antagonists (H2RAs) have traditionally been the preferred agents.

Proton pump inhibitors (PPIs) also raise gastric pH, permit hemostasis in areas of gastritis, and are

associated with reduced clinically relevant important upper GI bleeding.

Recent meta-analyses have suggested that PPIs are superior to H2RAs, but a well-powered clinical

trial has not been completed in the ICU or the neurologic ICU population.

Medications taken at home before admission

ii.

Presence of GI bleeding on admission

Glycemic Control

Hyperglycemia is associated with increased mortality in TBI.

Glucose toxicity in neurons

Surrogate for severity of injury

Exacerbation of cerebral edema

Avoid administering dextrose 5% and other hypotonic glucose-containing fluids.

Glycemic goals

Prevent hyperglycemia (greater than 180 mg/dL)

140–180 mg/dL seems reasonable to avoid hypoglycemia.

Caution should be used with glucose values in the low-normal range because of the risk of

hypoglycemia.

Glucose obligate substrate for neurons

ii.

Threshold for glucose needs may be altered in TBI.

iii.

May increase seizure risk

High-dose methylprednisolone plays no role in the treatment of inflammation or edema associated with

TBI.

Altered volume of distribution: Patients with a TBI have increased volume of distribution because of

the following:

Fluid resuscitation

Reduced plasma protein binding (particularly with albumin as a negative acute-phase reactant)

Transient increased permeability of blood-brain barrier

TBI increases hepatic metabolic capacity (extent to which is likely proportional to severity of

injury).

Results in more effective clearance of hepatically metabolized medications

Increased dosing requirement for commonly used agents such as phenytoin, midazolam