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      Ketamine does not increase intracranial pressure compared with opioids: meta-analysis of randomized controlled trials.

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          Abstract

          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.

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          Management of intracranial hypertension.

          Shankar P. Gopinath, Fiona Robertson, Leonardo Rangel-Castilla (2008)
          Effective management of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased intracranial pressure. When intracranial pressure becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. Medical management of increased intracranial pressure should include sedation, drainage of cerebrospinal fluid, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from traumatic brain injury.
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            Safety of sedation with ketamine in severe head injury patients: comparison with sufentanil.

            Aurélie Bourgoin, Renaud Vialet, Nicolas Wereszczynski … (2003)
            The aim of the study was to compare the safety concerning cerebral hemodynamics of ketamine and sufentanil used for sedation of severe head injury patients, both drugs being used in combination with midazolam. Prospective, randomized, double-blind study. Intensive care unit in a trauma center. Twenty-five patients with severe head injury. Twelve patients received sedation with a continuous infusion of ketamine-midazolam and 13 with a continuous infusion of sufentanil-midazolam. All patients were mechanically ventilated with moderate hyperventilation. Prognostic indicators (age, Glasgow Coma Scale scores, computed tomography diagnosis, and Injury Severity Scale score) were similar in the two groups at study entry. Measurements were carried out during the first 4 days of sedation. The average infusion rates during this time were 82 +/- 25 micro x kg x min ketamine and 1.64 +/- 0.5 microg x kg x min midazolam in the ketamine group and 0.008 +/- 0.002 microg x kg x min sufentanil and 1.63 +/- 0.37 microg x kg x min midazolam in the sufentanil group. No significant differences were observed between the two groups in the mean daily values of intracranial pressure and cerebral perfusion pressure. The numbers of intracranial pressure elevations were similar in both groups. The requirements of neuromuscular blocking agents, propofol, and thiopental were similar. Heart rate values were significantly higher in the ketamine group on therapy days 3 and 4 ( <.05). With regard to arterial pressure control, more fluids were given on the first therapy day and there was a trend toward greater use of vasopressors in the sufentanil group. Sedative costs were similar in the two groups. The results of this study suggest that ketamine in combination with midazolam is comparable with a combination of midazolam-sufentanil in maintaining intracranial pressure and cerebral perfusion pressure of severe head injury patients placed under controlled mechanical ventilation.
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              Sedation for critically ill adults with severe traumatic brain injury: a systematic review of randomized controlled trials.

              J. Roberts, Heidrun H. Krämer, David A Zygun … (2011)
              To summarize randomized controlled trials on the effects of sedative agents on neurologic outcome, mortality, intracranial pressure, cerebral perfusion pressure, and adverse drug events in critically ill adults with severe traumatic brain injury. PubMed, MEDLINE, EMBASE, the Cochrane Database, Google Scholar, two clinical trials registries, personal files, and reference lists of included articles. Randomized controlled trials of propofol, ketamine, etomidate, and agents from the opioid, benzodiazepine, α-2 agonist, and antipsychotic drug classes for management of adult intensive care unit patients with severe traumatic brain injury. In duplicate and independently, two investigators extracted data and evaluated methodologic quality and results. Among 1,892 citations, 13 randomized controlled trials enrolling 380 patients met inclusion criteria. Long-term sedation (≥24 hrs) was addressed in six studies, whereas a bolus dose, short infusion, or doubling of plasma drug concentration was investigated in remaining trials. Most trials did not describe baseline traumatic brain injury prognostic factors or important cointerventions. Eight trials possibly or definitely concealed allocation and six were blinded. Insufficient data exist regarding the effects of sedative agents on neurologic outcome or mortality. Although their effects are likely transient, bolus doses of opioids may increase intracranial pressure and decrease cerebral perfusion pressure. In one study, a long-term infusion of propofol vs. morphine was associated with a reduced requirement for intracranial pressure-lowering cointerventions and a lower intracranial pressure on the third day. Trials of propofol vs. midazolam and ketamine vs. sufentanil found no difference between agents in intracranial pressure and cerebral perfusion pressure. This systematic review found no convincing evidence that one sedative agent is more efficacious than another for improvement of patient-centered outcomes, intracranial pressure, or cerebral perfusion pressure in critically ill adults with severe traumatic brain injury. High bolus doses of opioids, however, have potentially deleterious effects on intracranial pressure and cerebral perfusion pressure. Adequately powered, high-quality, randomized controlled trials are urgently warranted.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): J Anesth
                Title: Journal of anesthesia
                ISSN (Electronic): 1438-8359
                ISSN (Print): 0913-8668
                Publication date (Electronic): Dec 2014
                Volume: 28
                Issue: 6
                Affiliations
                [1 ] Department of Anesthesiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yanchang zhong Road, Shanghai, 200072, China.
                Article
                DOI: 10.1007/s00540-014-1845-3
                PubMed ID: 24859931
                SO-VID: 4a702507-84fe-49de-9349-2cc56dfccaa4
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