One case report of survival after a burst-suppression pattern following cardiac arrest exists ( Becker et al., 2017), but this case had burst suppression following the use and discontinuation of phenobarbital and propofol and may not be comparable to spontaneous burst-suppression patterns.īurst suppression may also be seen in late stages of severe sepsis-associated encephalopathy it portends a poor prognosis in this setting also, with over 70% mortality ( Young, 2013). In one prospective cohort study, burst suppression after cardiac arrest was, without exception, associated with a poor outcome, with 54/54 patients with burst suppression at any time between 6 and 72 h after arrest having poor outcome ( Sivaraju et al., 2015). There are bursts of activity ( arrows) separated by interburst periods of suppression. Burst suppression in a 24-year-old woman following cardiac arrest. 5 Furthermore, proper monitoring of cardiovascular status and maintenance of hemodynamic stability are paramount if barbiturates are to be used.įig. 178 No clear improvement in outcome has been seen in studies involving the use of barbiturate therapy, which has led to the Brain Trauma Foundation stipulating that high-dose barbiturate therapy should only be instituted in cases of treating intracranial hypertension refractory to medical and surgical treatment alternatives. In turn, the significant risk of causing hypotension-a factor known to be a harbinger of poor neurologic outcomes in patients with severe TBI-would offset any beneficial effect seen with ICP reduction. A meta-analysis by the Cochrane group noted that barbiturate infusion was associated with a fall in blood pressure in 25% of patients. 177Ī key side effect to consider prior to barbiturate administration is the potential to precipitate systemic hypotension. Maximal reductions in CBF and cerebral metabolism are seen when electrographic burst suppression of cerebral activity is achieved. 176 illustrated that in the setting of intractable intracranial hypertension, patients whose ICPs were responsive to barbiturate therapy had a significantly reduced mortality.īarbiturates such as pentobarbital are administered concomitant with continuous electroencephalogram monitoring in severe TBI patients with medically refractory intracranial hypertension. Although prophylactic use of barbiturates has no clinical benefit, 137, 175 Eisenberg et al. Studies investigating clinical outcomes in patients who received barbiturate therapy have been inconclusive. 172 The mechanism by which this reduction in ICP occurs is not entirely understood but likely involves mediating cerebral vasoconstriction, 173 reversibly reducing CMRO 2, 174 and preventing the onset of numerous excitatory neurotoxic cascades. The ability of barbiturates to lower ICP has been known since the 1930s.
![burst burst](https://c.tenor.com/3yk1HSkgb18AAAAi/burst-threaten.gif)
Alfredo Quiñones-Hinojosa MD, in Schmidek and Sweet: Operative Neurosurgical Techniques, 2022 Barbiturate-Induced Burst Suppression