Duration of cardiopulmonary resuscitation and phenotype of post-cardiac arrest brain injury.

BACKGROUND: Patients resuscitated from cardiac arrest have variable severity of primary hypoxic ischemic brain injury (HIBI). Signatures of primary HIBI on brain imaging and electroencephalography (EEG) include diffuse cerebral edema and burst suppression with identical bursts (BSIB). We hypothesize distinct phenotypes of primary HIBI are associated with increasing cardiopulmonary resuscitation (CPR) duration. METHODS: We identified from our prospective registry of both in-and out-of-hospital CA patients treated between January 2010 to January 2020 for this cohort study. We abstracted CPR duration, neurological examination, initial brain computed tomography gray to white ratio (GWR), and initial EEG pattern. We considered four phenotypes on presentation: awake; comatose with neither BSIB nor cerebral edema (non-malignant coma); BSIB; and cerebral edema (GWR ≤ 1.20). BSIB and cerebral edema were considered as non-mutually exclusive outcomes. We generated predicted probabilities of brain injury phenotype using localized regression. RESULTS: We included 2,440 patients, of whom 545 (23%) were awake, 1,065 (44%) had non-malignant coma, 548 (23%) had BSIB and 438 (18%) had cerebral edema. Only 92 (4%) had both BSIB and edema. Median CPR duration was 16 [IQR 8-28] minutes. Median CPR duration increased in a stepwise manner across groups: awake 6 [3-13] minutes; non-malignant coma 15 [8-25] minutes; BSIB 21 [13-31] minutes; cerebral edema 32 [22-46] minutes. Predicted probability of phenotype changes over time. CONCLUSIONS: Brain injury phenotype is related to CPR duration, which is a surrogate for severity of HIBI. The sequence of most likely primary HIBI phenotype with progressively longer CPR duration is awake, coma without BSIB or edema, BSIB, and finally cerebral edema.

Neurological Prognostication After Hypoglycemic Coma: Role of Clinical and EEG Findings.

BACKGROUND: Hypoglycemic coma (HC) is an uncommon but severe clinical condition associated with poor neurological outcome. There is a dearth of robust neurological prognostic factors after HC. On the other hand, there is an increasing body of literature on reliable prognostic markers in the postanoxic coma, a similar-albeit not identical-situation. The objective of this study was thus to investigate the use and predictive value of these markers in HC. METHODS: We conducted a retrospective, multicenter, cohort study within five centers of the Critical Care EEG Monitoring Research Consortium. We queried our electroencephalography (EEG) databases to identify all patients undergoing continuous EEG monitoring after admission to an intensive care unit with HC (defined as Glasgow Coma Scale < 8 on admission and a first blood glucose level < 50 mg/dL or not documented but in an obvious clinical context) between 01/01/2010 and 12/31/2020. We studied the association of findings at neurological examination (Glasgow Coma Scale motor subscale, pupillary light and corneal reflexes) and at continuous EEG monitoring(highly malignant patterns, reactivity, periodic discharges, seizures) with best neurological outcome within 3 months after hospital discharge, defined by the Cerebral Performance Category as favorable (1-3: recovery of consciousness) versus unfavorable (4-5: lack of recovery of consciousness). RESULTS: We identified 60 patients (30 [50%] women; age 62 [51-72] years). Thirty-one and 29 patients had a favorable and unfavorable outcome, respectively. The presence of pupillary reflexes (24 [100%] vs. 17 [81%]; p value 0.04) and a motor subscore > 2 (22 [92%] vs. 12 [63%]; p value 0.03) at 48-72 h were associated with a favorable outcome. A highly malignant EEG pattern was observed in 7 of 29 (24%) patients with unfavorable outcome versus 0 of 31 (0%) with favorable outcome, whereas the presence of EEG reactivity was observed in 28 of 31 (90%) patients with favorable outcome versus 13 of 29 (45%) with unfavorable outcome (p < 0.001 for comparison of all background categories). CONCLUSIONS: This preliminary study suggests that highly malignant EEG patterns might be reliable prognostic markers of unfavorable outcome after HC. Other EEG findings, including lack of EEG reactivity and seizures and clinical findings appear less accurate. These findings should be replicated in a larger multicenter prospective study.

EEG Findings in Coronavirus Disease.

PURPOSE: Neurologic manifestations of coronavirus disease (COVID-19) such as encephalopathy and seizures have been described. To our knowledge, detailed EEG findings in COVID-19 have not yet been reported. This report adds to the scarce body of evidence. METHODS: We identified eight COVID-19 positive patients who underwent EEG monitoring in our hospital system. RESULTS: EEGs were most commonly ordered for an altered level of consciousness, a nonspecific neurologic manifestation. We observed generalized background slowing in all patients and generalized epileptiform discharges with triphasic morphology in three patients. Focal electrographic seizures were observed in one patient with a history of focal epilepsy and in another patient with no such history. Five of eight patients had a previous diagnosis of epilepsy, suggesting that pre-existing epilepsy can be a potential risk factor for COVID-19-associated neurological manifestations. Five of eight patients who underwent EEG experienced a fatal outcome of infection. CONCLUSIONS: Our findings underscore previous observations that neurologic manifestations are common in severe cases. COVID-19 patients with epilepsy may have an increased risk of neurological manifestations and abnormal EEG.

Awakening from post anoxic coma with burst suppression with identical bursts.

BACKGROUND: Electroencephalography (EEG) is commonly used after cardiac arrest. Burst suppression with identical bursts (BSIB) has been reported as a perfectly specific predictor of poor outcome but published case series are small. We describe two patients with BSIB who awakened from coma after cardiac arrest. METHODS: We identified two out-of-hospital cardiac arrest (OHCA) patients with coma and BSIB. We determined the etiology of arrest, presenting neurological examination, potential confounders to neurological assessment, neurodiagnostics and time to awakening. We reviewed and interpreted EEGs using 2021 American Clinical Neurophysiology Society guidelines. We quantified identicality of bursts by calculating pairwise correlation coefficients between the first 500 ms of each aligned burst. RESULTS: In case one we present a 62-year-old man with OHCA secondary to septic shock. EEG showed burst suppression pattern, with bursts consisted of high amplitude generalized spike waves in lock-step with myoclonus (inter-burst correlation = 0.86). He followed commands 3 days after arrest, when repeat EEG showed a continuous, variable and reactive background without epileptiform activity. Case two was a 49-year-old woman with OHCA secondary to polysubstance overdose. Initial EEG revealed burst suppression with high amplitude generalized polyspike-wave bursts with associated myoclonus. She followed commands on post-arrest day 4, when repeat EEG showed a continuous, variable and reactive background with frequent runs of bifrontal predominant sharply contoured rhythmic delta activity. CONCLUSION: These cases highlight the perils of prognosticating with a single modality in comatose cardiac arrest patients.