Ketamine does not increase intracranial pressure compared with opioids: meta-analysis of randomized controlled trials
- 1.7k Downloads
Ketamine is traditionally avoided in sedation management of patients with risk of intracranial hypertension. However, results from many clinical trials contradict this concern. We critically analyzed the published data of the effects of ketamine on intracranial pressure (ICP) and other cerebral hemodynamics to determine whether ketamine was safe for patients with hemodynamic instability and brain injuries.
We systematically searched the online databases of PubMed, Medline, Embase, Current Controlled Trials, and Cochrane Central (last search performed on January 15, 2014). Trial characteristics and outcomes were independently extracted by two assessors (Xin Wang, Xibing Ding). For continuous data, mean differences (MD) were formulated. If the P value of the chi-square test was >0.10 or I 2 <50 %, a fixed-effects model was used; otherwise, the random effects model was adopted.
Five trials (n = 198) met the inclusion criteria. Using ICP levels within the first 24 h of ketamine administration as the main outcome, the use of ketamine leads to the same ICP levels as opioids [MD = 1.94; 95 % confidence interval (95 % CI), −2.35, 6.23; P = 0.38]. There were no significant differences in mean arterial pressure values between the two groups (MD = 0.99; 95 % CI, −2.24, 4.22; P = 0.55). Ketamine administration was also comparable with opioids in the maintenance of cerebral perfusion pressure (MD = −1.07; 95 % CI, −7.95, 5.8; P = 0.76).
The results of this study suggest that ketamine does not increase ICP compared with opioids. Ketamine provides good maintenance of hemodynamic status. Clinical application of ketamine should not be discouraged on the basis of ICP-related concerns.
KeywordsKetamine Opioids Intracranial pressure Hemodynamic instability Brain injuries
We are grateful for the support from the National Natural Science Foundation. We also thank all authors of the publications included in this study for contributing information as requested.
- 7.Flower O, Hellings S. Sedation in traumatic brain injury. Emerg Med Int. 2012;10:1155–66.Google Scholar
- 9.Bowies ED, Gold ME. Rethinking the paradigm: evaluation of ketamine as a neurosurgical anesthetic. AANA J. 2012;80:445–52.Google Scholar
- 11.Filanovsky Y, Miller P, Kao J. Myth: Ketamine should not be used as an induction agent for intubation in patients with head injury. Can J Emerg Med. 2010;12:154–201.Google Scholar
- 24.Schmittner MD, Vajkoczy SL, Horn P, Bertsch T, Quintel M, Vajkoczy P, Muench E. Effects of fentanyl and S(+)-ketamine on cerebral hemodynamics, gastrointestinal motility, and need of vasopressors in patients with intracranial pathologies. J Neurosurg Anesthesiol. 2007;19:257–62.PubMedCrossRefGoogle Scholar
- 38.Bhutta AT, Schmitz ML, Swearingen C, James LP, Wardbegnoche WL, Lindquist DM. Ketamine as a neuroprotective and anti-inflammatory agent in children undergoing surgery on cardiopulmonary bypass: a pilot randomized, double-blind, placebo-controlled trial. Pediatr Crit Care Med. 2012;13:328–37.PubMedCrossRefGoogle Scholar
- 43.Pfenninger E, Reith A, Domino EF. Status of ketamine in anaesthesiology. Ann Arbor: NPP Books; 1990. p. 109–81.Google Scholar