Burst suppression

Clinical - Neurologic

Pharmacologic neuroprotection/burst suppression has been of great interest for decades in the setting of acute cerebral insults. It has been studied in the setting of both global and focal cerebral injury. The interest stems from the knowledge that burst suppression with anesthetic agents (barbiturates, propofol, midazolam, isoflurane) results in a large reduction (approximately 50%) in the cerebral metabolic rate of oxygen(CMRO2) (1-3). Animal models have shown efficacy and this naturally led to human trials (1-3). Anesthetic burst suppression has been studied in comatose survivors of cardiac arrest (3) with no evidence of benefit. Lower level evidence showing no benefit exists for cerebral aneurysm surgery (4). There is insufficient evidence in the setting of stroke or traumatic brain injury to determine benefit or harm (5).

Therapy (barbiturate, propofol, or halogenated anesthetic) is titrated to an electroencephalographic (cEEG) endpoint. Complete pharmacologic suppression results in a flat-line EEG. Typically, a 1:10 burst to suppression ratio is chosen as an arbitrary endpoint, but this is neither evidence based nor a universal practice. In other words, a 10 second screen of EEG would have 1 second of burst activity and 9 seconds of flat-line EEG. Optimal dosing is unknown and there is no evidence base to guide therapy (6).


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    Anesthesiology;2007 Jan;106(1):92-9; discussion 8-10

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    N Engl J Med;1986 Feb 13;314(7):397-403

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    Anesthesiology;2010 Jan;112(1):86-101

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    Cochrane Database Syst Rev. 2012;12:CD000033

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    J Trauma;2010 Aug;69(2):275-83

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    See also Thiopental theraputic coma

    See also Barb coma: EEG endpoint

    See also Monitoring: barbiturate coma