Literature DB >> 10547101

Cerebral hemodynamic effects of pentobarbital coma in head-injured patients.

M Cormio1, S P Gopinath, A Valadka, C S Robertson.   

Abstract

The purpose of this study was to examine the changes in cerebral hemodynamics of head-injured patients undergoing barbiturate treatment of refractory intracranial hypertension. Cerebral blood flow (CBF) and metabolism variables were measured in 67 severely head-injured patients at the following times: before the loading dose of pentobarbital; after the loading dose of pentobarbital (average pentobarbital level 28.1+/-8.3 microg/mL); and 3 days later, when the peak pentobarbital level averaged 42.5+/-17.2 microg/mL. Intracranial pressure (ICP) and mean arterial blood pressure (MAP) were decreased by the loading dose of pentobarbital by an average of 12 and 9 mm Hg, respectively. Cerebral perfusion pressure (CPP) was unchanged when the entire group was analyzed together. CBF, cerebral oxygen consumption (CMR(O)2), and arteriovenous oxygen difference (AVD(O)2) were significantly decreased after the loading dose of pentobarbital, by 20%, 31%, and 11%, respectively. The average cerebrovascular resistance (CVR) was increased by 20%. The change in CMR(O)2 with the loading dose of pentobarbital was closely related to the pretreatment value (n = 67, r2 = 0.65, p < .001). Thirty (45%) of the patients had a "good ICP response," with a reduction in ICP from 34+/-9 to 15+/-5 mm Hg after the initial loading dose of pentobarbital. Twenty-seven (40%) of the patients had a "partial ICP response," with ICP decreasing but still remaining above 20 mm Hg after the loading dose of pentobarbital. In the remaining 10 patients, ICP did not change or even increased after pentobarbital. In the 30 patients with a good ICP response, pretreatment CMR(O)2 and AVD(O)2 were greater before administration of pentobarbital, and CMR(O)2 and AVD(O)2 decreased more with the loading dose of pentobarbital, than in the patients with partial or no ICP response. The outcome was significantly better in the patients with a good or partial ICP response to pentobarbital, with 21% of these patients having a good recovery or moderate disability at 3 months after injury, compared with 100% persistent vegetative state or death in the nonresponders. In summary, barbiturate coma can be a useful treatment modality for acutely reducing ICP in selected patients. Patients with overwhelmingly severe injuries are not likely to benefit, partly because their CMR(O)2 is already markedly reduced by the injury and partly because their outcome is already predetermined by the injury. Patients with systemic hypotension are not likely to have a good response because hypotension limits the amount of barbiturates that can be given.

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Year:  1999        PMID: 10547101     DOI: 10.1089/neu.1999.16.927

Source DB:  PubMed          Journal:  J Neurotrauma        ISSN: 0897-7151            Impact factor:   5.269


  10 in total

1.  A Fatal Adverse Effect of Barbiturate Coma Therapy: Dyskalemia.

Authors:  Hyun Mook Kwon; Jin Wook Baek; Sang Pyung Lee; Jae Ik Cho
Journal:  Korean J Neurotrauma       Date:  2016-10-31

2.  Acute gonadotroph and somatotroph hormonal suppression after traumatic brain injury.

Authors:  Justin Wagner; Joshua R Dusick; David L McArthur; Pejman Cohan; Christina Wang; Ronald Swerdloff; W John Boscardin; Daniel F Kelly
Journal:  J Neurotrauma       Date:  2010-06       Impact factor: 5.269

3.  Global cerebral blood flow and CPP after severe head injury: a xenon-CT study.

Authors:  Arturo Chieregato; Alessandra Tanfani; Christian Compagnone; Claudia Turrini; Federica Sarpieri; Maurizio Ravaldini; Luigi Targa; Enrico Fainardi
Journal:  Intensive Care Med       Date:  2007-03-24       Impact factor: 17.440

4.  An evaluation of three measures of intracranial compliance in traumatic brain injury patients.

Authors:  Tim Howells; Anders Lewén; Mattias K Sköld; Elisabeth Ronne-Engström; Per Enblad
Journal:  Intensive Care Med       Date:  2012-04-18       Impact factor: 17.440

5.  Therapeutic targeting of astrocytes after traumatic brain injury.

Authors:  Jessica Shields; Donald E Kimbler; Walid Radwan; Nathan Yanasak; Sangeetha Sukumari-Ramesh; Krishnan M Dhandapani
Journal:  Transl Stroke Res       Date:  2011-11-09       Impact factor: 6.829

Review 6.  Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature.

Authors:  Shaun E Gruenbaum; Alexander Zlotnik; Benjamin F Gruenbaum; Denise Hersey; Federico Bilotta
Journal:  CNS Drugs       Date:  2016-09       Impact factor: 5.749

7.  Neurointensive care management of raised intracranial pressure caused by severe valproic acid intoxication.

Authors:  Niklas Marklund; Per Enblad; Elisabeth Ronne-Engström
Journal:  Neurocrit Care       Date:  2007       Impact factor: 3.210

8.  Barbiturates use and its effects in patients with severe traumatic brain injury in five European countries.

Authors:  Marek Majdan; Walter Mauritz; Ingrid Wilbacher; Alexandra Brazinova; Martin Rusnak; Johannes Leitgeb
Journal:  J Neurotrauma       Date:  2012-12-06       Impact factor: 5.269

Review 9.  Management of raised intracranial pressure in children with traumatic brain injury.

Authors:  Vinay Kukreti; Hadi Mohseni-Bod; James Drake
Journal:  J Pediatr Neurosci       Date:  2014 Sep-Dec

10.  A novel step-down infusion method of barbiturate therapy: Its safety and effectiveness for intracranial pressure control.

Authors:  Yukako Yamakawa; Motohiro Morioka; Tetsuya Negoto; Kimihiko Orito; Munetake Yoshitomi; Yukihiko Nakamura; Nobuyuki Takeshige; Masafumi Yamamoto; Yasuharu Takeuchi; Kazutaka Oda; Hirofumi Jono; Hideyuki Saito
Journal:  Pharmacol Res Perspect       Date:  2021-04
  10 in total

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