Citation

Kochanek PM, Herrmann JR, Bleck TP. Crit. Care Med. 2023; 51(5): 677-680.

Copyright

(Copyright © 2023, Society of Critical Care Medicine, Publisher Lippincott Williams and Wilkins)

DOI

10.1097/CCM.0000000000005826

PMID

37052437

Abstract

The first report of the use of ketamine (CI-581) in humans in 1965 described it as a promising dissociative analgesic and anesthetic phencyclidine derivative with less psychotomimetic effects (1). Ketamine rapidly gained increasing use in anesthesia, given its favorable systemic hemodynamic profile. However, beginning in the early 1970s, concerning effects on intracranial pressure (ICP) were reported in both healthy adults undergoing herniorrhaphy and orthopedic surgical procedures, and infants and children anesthetized for ventriculoperitoneal shunt placement, among other studies (2,3). This raised concerns over its use in patients where there might be raised ICP, and thus its utility in patients with acute brain injury. Increases in cerebral blood flow (CBF), possibly mediated in part by increases in Paco2 during anesthesia, were suggested to mediate the increases in ICP (4).

In the 1990s, several studies questioned the concerns regarding the utility of ketamine in patients with severe traumatic brain injury (TBI). Kolenda et al (5), and Albanèse et al (6), reported that continuous infusion or bolus administration of racemic ketamine was associated with improved cerebral perfusion pressure (CPP) and decreased ICP, respectively, in critically ill adults with TBI. The patients in those studies were also sedated with midazolam or propofol infusions and managed with controlled normoventilation. Both studies and others prompted...

Language: en