Induction of burst suppression or coma using intravenous anesthetics in refractory status epilepticus

Kang, Bong Su; Jung, Keun‐Hwa; Shin, Jeong-Won; Moon, Jang Sup; Byun, Jung-Ick; Lim, Jong-Deock; Moon, Hee Bom; Kim, Youngsoo; Chu, Kon; Lee, Sang Kun

doi:10.1016/j.jocn.2014.11.007

Cited by 32 publications

(37 citation statements)

References 23 publications

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“…Further, benzodiazepines may have an effect on EEG activity: they increase beta (spindle) activity and reduce lower (alpha) frequency activity (Schulte am Esch and Kochs, 1990 ). Very high intravenous doses of benzodiazepines, e.g., as used for drug-induced coma in refractory status epilepticus, can lead to burst suppression EEG (Kang et al, 2015 ). In our study, we predominately used low oral doses of short-acting benzodiazepines.…”

Section: Discussionmentioning

confidence: 99%

Substance-Specific Differences in Human Electroencephalographic Burst Suppression Patterns

Fleischmann

Pilge

Kiel

et al. 2018

Front. Hum. Neurosci.

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Different anesthetic agents induce burst suppression in the electroencephalogram (EEG) at very deep levels of general anesthesia. EEG burst suppression has been identified to be a risk factor for postoperative delirium (POD). EEG based automated detection algorithms are used to detect burst suppression patterns during general anesthesia and a burst suppression ratio (BSR) is calculated. Unfortunately, applied algorithms do not give information as precisely as suggested, often resulting in an underestimation of the patients’ burst suppression level. Additional knowledge of substance-specific burst suppression patterns could be of great importance to improve the ability of EEG based monitors to detect burst suppression. In a re-analysis of EEG recordings obtained from a previous study, we analyzed EEG data of 45 patients undergoing elective surgery under general anesthesia. The patients were anesthetized with sevoflurane, isoflurane or propofol (n = 15, for each group). After skin incision, the used agent was titrated to a level when burst suppression occurred. In a visual analysis of the EEG, blinded to the used anesthetic agent, we included the first distinct burst in our analysis. To avoid bias through changing EEG dynamics throughout the burst, we only focused on the first 2 s of the burst. These episodes were analyzed using the power spectral density (PSD) and normalized PSD, the absolute burst amplitude and absolute burst slope, as well as permutation entropy (PeEn). Our results show significant substance-specific differences in the architecture of the burst. Volatile-induced bursts showed higher burst amplitudes and higher burst power. Propofol-induced bursts had significantly higher relative power in the EEG alpha-range. Further, isoflurane-induced bursts had the steepest burst slopes. We can present the first systematic comparison of substance-specific burst characteristics during anesthesia. Previous observations, mostly derived from animal studies, pointing out the substance-specific differences in bursting behavior, concur with our findings. Our findings of substance-specific EEG characteristics can provide information to help improve automated burst suppression detection in monitoring devices. More specific detection of burst suppression may be helpful to reduce excessive EEG effects of anesthesia and therefore the incidence of adverse outcomes such as POD.

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Section: Discussionmentioning

confidence: 99%

Substance-Specific Differences in Human Electroencephalographic Burst Suppression Patterns

Fleischmann

Pilge

Kiel

et al. 2018

Front. Hum. Neurosci.

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“…A selection of the commonly cited and examined clinical variables in outcome studies for RSE as well as their complex network of potential interactions with the main predictor, [9][10][11][12][13][14][15][16]18,19,30,31 and the primary 32,33 and all secondary outcomes 2,9,34,35 is illustrated in the postulated causal diagram in Figure 2. The selection of variables included in the final multivariable models was based primarily on level of significance in the bivariate analysis.…”

Section: Selection Of Clinical Variables For the Multivariable Modelmentioning

confidence: 99%

“…Two retrospective studies including a recent, multicenter study looking at 362 episodes of SE from two major academic medical centers showed a similar association between the use of TC and these outcomes without an increased risk for mortality. 9,31 Several other studies suggested that TC increases the risk for infections, new disability upon discharge, and mortality. 10,11,13,40,41 Similar to our cohort, the duration of TC in all these studies had a relatively wide range of treatment duration anywhere from 24 to 96 hours.…”

Section: Tc Duration and Outcome Of Rsementioning

confidence: 99%

Duration of therapeutic coma and outcome of refractory status epilepticus

et al. 2019

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Summary Objective: Examine the association of duration of therapeutic coma (TC) with seizure recurrence, morbidity, and mortality in refractory status epilepticus (RSE). Define an optimal window for TC that provides sustained seizure control and minimizes complications. Methods: Retrospective, observational cohort study involving patients who presented with RSE to the University of Alabama at Birmingham or the University of California at San Francisco from 2010 to 2016. Relationship of duration of TC with primary and secondary outcomes was evaluated using two-sample t tests, simple linear regression, and chi-square tests. Multivariable linear and logistic regression models were used to identify independent predictors. Predictive ability of TC for seizure recurrence was quantified using a receiver-operating characteristic curve. Youden index was used to determine an optimal cutoff value. Results: Multivariable analysis of clinical and treatment characteristics of 182 patients who were treated predominantly with propofol as anesthetic agent showed that longer duration of the first trial of TC (27.2 vs 15.6 hours) was independently associated with a higher chance of seizure recurrence following the first weaning attempt (P = 0.038) but not with poor functional neurologic outcome upon discharge, in-hospital complications, or mortality. Furthermore, higher doses of anesthetic utilized during the first trial of TC were independently associated with fewer in-hospital complications (P = 0.003) and associated with a shorter duration of mechanical ventilation and total length of stay. Duration of TC was identified as an independent predictor of seizure recurrence with an optimal cutoff point at 35 hours. Significance: This study suggests that a shorter duration yet deeper TC as treatment for RSE may be more effective and safer than the currently recommended TC duration of 24–48 hours. Prospective and randomized trials should be conducted to validate these assertions.

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“…Because the metabolism of the brain has been significantly altered during a TBI and areas of the brain may lack a sufficient blood flow, coma-inducing drugs are used to profoundly inactivate the brain so that it consumes less oxygen (41). This is especially helpful if blood vessels, stressed by elevated pressure in the brain, are unable to carry the normal amount of nutrients and oxygen to brain cells (42). Although coma-inducing medications protect the brain, the brain as a whole is, by definition, not receiving the blood it needs.…”

Section: Biomarkersmentioning

confidence: 99%

Advances in diagnosis, treatments, and molecular mechanistic studies of traumatic brain injury

Xia

Wang

et al. 2015

BST

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Induction of burst suppression or coma using intravenous anesthetics in refractory status epilepticus

Cited by 32 publications

References 23 publications

Substance-Specific Differences in Human Electroencephalographic Burst Suppression Patterns

Substance-Specific Differences in Human Electroencephalographic Burst Suppression Patterns

Duration of therapeutic coma and outcome of refractory status epilepticus

Advances in diagnosis, treatments, and molecular mechanistic studies of traumatic brain injury

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