Objective
To provide evidence that early electroencephalography (EEG) allows for reliable prediction of poor or good outcome after cardiac arrest.
Methods
In a 5‐center prospective cohort study, we ...included consecutive, comatose survivors of cardiac arrest. Continuous EEG recordings were started as soon as possible and continued up to 5 days. Five‐minute EEG epochs were assessed by 2 reviewers, independently, at 8 predefined time points from 6 hours to 5 days after cardiac arrest, blinded for patients’ actual condition, treatment, and outcome. EEG patterns were categorized as generalized suppression (<10 μV), synchronous patterns with ≥50% suppression, continuous, or other. Outcome at 6 months was categorized as good (Cerebral Performance Category CPC = 1–2) or poor (CPC = 3–5).
Results
We included 850 patients, of whom 46% had a good outcome. Generalized suppression and synchronous patterns with ≥50% suppression predicted poor outcome without false positives at ≥6 hours after cardiac arrest. Their summed sensitivity was 0.47 (95% confidence interval CI = 0.42–0.51) at 12 hours and 0.30 (95% CI = 0.26–0.33) at 24 hours after cardiac arrest, with specificity of 1.00 (95% CI = 0.99–1.00) at both time points. At 36 hours or later, sensitivity for poor outcome was ≤0.22. Continuous EEG patterns at 12 hours predicted good outcome, with sensitivity of 0.50 (95% CI = 0.46–0.55) and specificity of 0.91 (95% CI = 0.88–0.93); at 24 hours or later, specificity for the prediction of good outcome was <0.90.
Interpretation
EEG allows for reliable prediction of poor outcome after cardiac arrest, with maximum sensitivity in the first 24 hours. Continuous EEG patterns at 12 hours after cardiac arrest are associated with good recovery. ANN NEUROL 2019;86:203–214
A trial involving comatose survivors of cardiac arrest tested whether aggressively treating rhythmic and periodic EEG activity would improve neurologic outcomes. Despite suppression of abnormal EEG ...activity, the incidence of a poor neurologic outcome did not differ significantly from that with standard care, and mortality was high.
Summary Background Magnesium sulphate is a neuroprotective agent that might improve outcome after aneurysmal subarachnoid haemorrhage by reducing the occurrence or improving the outcome of delayed ...cerebral ischaemia. We did a trial to test whether magnesium therapy improves outcome after aneurysmal subarachnoid haemorrhage. Methods We did this phase 3 randomised, placebo-controlled trial in eight centres in Europe and South America. We randomly assigned (with computer-generated random numbers, with permuted blocks of four, stratified by centre) patients aged 18 years or older with an aneurysmal pattern of subarachnoid haemorrhage on brain imaging who were admitted to hospital within 4 days of haemorrhage, to receive intravenous magnesium sulphate, 64 mmol/day, or placebo. We excluded patients with renal failure or bodyweight lower than 50 kg. Patients, treating physicians, and investigators assessing outcomes and analysing data were masked to the allocation. The primary outcome was poor outcome—defined as a score of 4–5 on the modified Rankin Scale—3 months after subarachnoid haemorrhage, or death. We analysed results by intention to treat. We also updated a previous meta-analysis of trials of magnesium treatment for aneurysmal subarachnoid haemorrhage. This study is registered with controlled-trials.com (ISRCTN 68742385) and the EU Clinical Trials Register (EudraCT 2006-003523-36). Findings 1204 patients were enrolled, one of whom had his treatment allocation lost. 606 patients were assigned to the magnesium group (two lost to follow-up), 597 to the placebo (one lost to follow-up). 158 patients (26·2%) had poor outcome in the magnesium group compared with 151 (25·3%) in the placebo group (risk ratio RR 1·03, 95% CI 0·85–1·25). Our updated meta-analysis of seven randomised trials involving 2047 patients shows that magnesium is not superior to placebo for reduction of poor outcome after aneurysmal subarachnoid haemorrhage (RR 0·96, 95% CI 0·84–1·10). Interpretation Intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended. Funding Netherlands Heart Foundation, UK Medical Research Council.
Hemorrhagic complications during extracorporeal membrane oxygenation are frequent and have a negative impact on outcome. We studied the association between activated partial thromboplastin time or ...platelet count and the occurrence of hemorrhagic complications. The secondary objective was to determine risk factors for hemorrhagic complications.
Retrospective cohort study in a single-center Dutch university hospital. We included all adult patients on extracorporeal membrane oxygenation admitted to the intensive care unit between 2010 and 2017.
We included 164 consecutive patients of which 73 (45%) had a hemorrhagic complication. The most prevalent hemorrhagic complications were surgical site (62%) and cannula site bleeding (18%). Survival to discharge was 67% in the patients without a hemorrhagic complication and 33% in the patients with hemorrhagic complications (p < .01). A higher activated partial thromboplastin time in the 24 h prior was associated with the occurrence of hemorrhagic complications (adjusted hazard ratio per 10 s increase 1.14; (95% CI 1.05–1.24). Venoarterial extracorporeal membrane oxygenation, duration of support, and higher activated partial thromboplastin time were risk factors for the occurrence of hemorrhagic complications.
Higher activated partial thromboplastin time is associated with the occurrence of hemorrhagic complications.
•Hemorrhagic complications during extracorporeal membrane oxygenation occur frequent.•Most prevalent hemorrhagic complications were surgical site bleedings in our cohort.•A higher aPTT was associated with the occurrence of hemorrhagic complications.
Spreading depolarizations may contribute to delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage, but the effect of spreading depolarizations on brain lesion progression after ...subarachnoid hemorrhage has not yet been assessed directly. Therefore, we tested the hypothesis that artificially induced spreading depolarizations increase brain tissue damage in a rat model of subarachnoid hemorrhage. Subarachnoid hemorrhage was induced by endovascular puncture of the right internal carotid bifurcation. After one day, brain tissue damage was measured with T2-weighted MRI, followed by application of 1 M KCl (SD group, N = 16) or saline (no-SD group, N = 16) to the right cortex. Cortical laser-Doppler flowmetry was performed to record spreading depolarizations. MRI was repeated on day 3, after which brains were extracted for assessment of subarachnoid hemorrhage severity and histological damage. 5.0 ± 2.7 spreading depolarizations were recorded in the SD group. Subarachnoid hemorrhage severity and mortality were similar between the SD and no-SD groups. Subarachnoid hemorrhage-induced brain lesions expanded between days 1 and 3. This lesion growth was larger in the SD group (241 ± 233 mm3) than in the no-SD group (29 ± 54 mm3) (p = 0.001). We conclude that induction of spreading depolarizations significantly advances lesion growth after experimental subarachnoid hemorrhage. Our study underscores the pathophysiological consequence of spreading depolarizations in the development of delayed cerebral tissue injury after subarachnoid hemorrhage.
•We studied the effects of propofol on the postanoxic EEG using visual and quantitative analysis.•Propofol reduced amplitude, continuity, and dominant frequency and increased amplitude ...fluctuations.•Propofol did not affect the reliability of EEG-based outcome predictions.
To quantify the effects of propofol on the EEG after cardiac arrest and to assess their influence on predictions of outcome.
In a prospective multicenter cohort study, we analyzed EEG recordings within the first 72 h after cardiac arrest. At six time points, EEGs were classified as favorable (continuous background), unfavorable (generalized suppression or synchronous patterns with ≥50% suppression), or intermediate. Quantitative EEG included measures for amplitude, background continuity, dominant frequency, and burst-suppression amplitude ratio (BSAR). The effect of propofol on each measure was estimated using mixed effects regression.
We included 496 patients. The EEG after propofol cessation had no additional value over EEG-based outcome predictions during propofol administration at 12 h after cardiac arrest. Propofol was associated with decreased EEG amplitude, background continuity and dominant frequency, and increased BSAR. However, propofol did neither increase the chance of unfavorable EEG patterns (adjusted odds ratio (aOR) 0.95 per increase of 2 mg/kg/h, 95%-CI: 0.81–1.11) nor decrease the chance of favorable EEG patterns (aOR 0.98, 95%-CI: 0.89–1.09).
Propofol induces changes of the postanoxic EEG, but does not affect its value for the prediction of outcome.
We confirm the reliability of EEG-based outcome predictions in propofol-sedated patients after cardiac arrest.
Background
Despite systemic anticoagulation and antithrombotic surface coating, oxygenator dysfunction remains one of most common technical complications of Extracorporeal membrane oxygenation ...(ECMO). Several parameters have been associated with an oxygenator exchange, but no guidelines for when to perform an exchange are published. An exchange, especially an emergency exchange, has a risk of complications. Therefore, a delicate balance between oxygenator dysfunction and the exchange of the oxygenator exists. This study aimed to identify risk factors and predictors for elective and emergency oxygenator exchanges.
Methods
This observational cohort study included all adult patients supported with veno-venous extracorporeal membrane oxygenation (V-V ECMO). We compared patients’ characteristics and laboratory values of patients with and without an oxygenator exchange and between an elective and emergency exchange, defined as an exchange outside office hours. Risk factors for an oxygenator exchange were identified with cox regression analyses, and risk factors for an emergency exchange were identified with logistic regression analyses.
Results
We included forty-five patients in the analyses. There were twenty-nine oxygenator exchanges in nineteen patients (42%). More than a third of the exchanges were emergency exchanges. Higher partial pressure of carbon dioxide (PaCO2), transmembrane pressure difference (ΔP), and hemoglobin (Hb) were associated with an oxygenator exchange. Lower lactate dehydrogenase (LDH) was the only risk factor for an emergency exchange.
Conclusion
Oxygenator exchange is frequent during V-V ECMO support. PaCO2, ΔP and Hb were associated with an oxygenator exchange and lower LDH with the risk of an emergency exchange.
Abstract
Background
Thrombocytopenia, hemorrhage and platelet transfusion are common in patients supported with venoarterial extracorporeal membrane oxygenation (VA ECMO). However, current literature ...is limited to small single-center experiences with high degrees of heterogeneity. Therefore, we aimed to ascertain in a multicenter study the course and occurrence rate of thrombocytopenia, and to assess the association between thrombocytopenia, hemorrhage and platelet transfusion during VA ECMO.
Methods
This was a sub-study of a multicenter (
N
= 16) study on transfusion practices in patients on VA ECMO, in which a retrospective cohort (Jan-2018–Jul-2019) focusing on platelets was selected. The primary outcome was thrombocytopenia during VA ECMO, defined as mild (100–150·10
9
/L), moderate (50–100·10
9
/L) and severe (< 50·10
9
/L). Secondary outcomes included the occurrence rate of platelet transfusion, and the association between thrombocytopenia, hemorrhage and platelet transfusion, assessed through mixed-effect models.
Results
Of the 419 patients included, median platelet count at admission was 179·10
9
/L. During VA ECMO, almost all (
N
= 398, 95%) patients developed a thrombocytopenia, of which a significant part severe (
N
= 179, 45%). One or more platelet transfusions were administered in 226 patients (54%), whereas 207 patients (49%) suffered a hemorrhagic event during VA ECMO. In non-bleeding patients, still one in three patients received a platelet transfusion. The strongest association to receive a platelet transfusion was found in the presence of severe thrombocytopenia (adjusted OR 31.8, 95% CI 17.9–56.5). After including an interaction term of hemorrhage and thrombocytopenia, this even increased up to an OR of 110 (95% CI 34–360).
Conclusions
Thrombocytopenia has a higher occurrence than is currently recognized. Severe thrombocytopenia is strongly associated with platelet transfusion. Future studies should focus on the etiology of severe thrombocytopenia during ECMO, as well as identifying indications and platelet thresholds for transfusion in the absence of bleeding.
Trial registration
: This study was registered at the Netherlands Trial Registry at February 26th, 2020 with number NL8413 and can currently be found at
https://trialsearch.who.int/Trial2.aspx?TrialID=NL8413.
BACKGROUND AND PURPOSE—Induced hypertension is widely used to treat delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage, but a literature review shows that its presumed ...effectiveness is based on uncontrolled case-series only. We here report clinical outcome of aneurysmal subarachnoid hemorrhage patients with DCI included in a randomized trial on the effectiveness of induced hypertension.
METHODS—Aneurysmal subarachnoid hemorrhage patients with clinical symptoms of DCI were randomized to induced hypertension or no induced hypertension. Risk ratios for poor outcome (modified Rankin Scale score >3) at 3 months, with 95% confidence intervals, were calculated and adjusted for age, clinical condition at admission and at time of DCI, and amount of blood on initial computed tomographic scan with Poisson regression analysis.
RESULTS—The trial aiming to include 240 patients was ended, based on lack of effect on cerebral perfusion and slow recruitment, when 21 patients had been randomized to induced hypertension, and 20 patients to no hypertension. With induced hypertension, the adjusted risk ratio for poor outcome was 1.0 (95% confidence interval, 0.6–1.8) and the risk ratio for serious adverse events 2.1 (95% confidence interval, 0.9–5.0).
CONCLUSIONS—Before this trial, the effectiveness of induced hypertension for DCI in aneurysmal subarachnoid hemorrhage patients was unknown because current literature consists only of uncontrolled case series. The results from our premature halted trial do not add any evidence to support induced hypertension and show that this treatment can lead to serious adverse events.
CLINICAL TRIAL REGISTRATION—URLhttp://www.clinicaltrials.gov. Unique identifierNCT01613235.
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