Neurocritical Care最新文献

Background: External ventricular drain (EVD)-associated infections (EVDAI) remain a relevant complication of acute hydrocephalus treatment following aneurysmal subarachnoid hemorrhage (aSAH). Whether radiological quantity and anatomical distribution of subarachnoid and ventricular blood impact EVDAI rates has not been thoroughly studied to date.

Methods: This was a retrospective (2009-2023) analysis of patients with aSAH undergoing emergency ventriculostomy. Univariable and multivariable logistic regression analyses were used to assess the association between the Barrow Neurological Institute (BNI) grading scale for subarachnoid hemorrhage and the intraventricular hemorrhage (IVH) score for extent and anatomical distribution of intracerebral bleeding with EVDAI risk. Cox regression analysis was employed to investigate the relationship between hemorrhage extent and the timing of EVDAI onset.

Results: One hundred and ninety-four patients with aSAH received 228 EVDs with a total of cumulative 2,258 EVD days. Overall EVDAI rates were 14% (27/194) per patient and 12% (27/228) per EVD. EVDAI was associated with a larger subarachnoid blood clot (BNI grade 4; odds ratio 6.66, 95% confidence interval 2.04-21.68; p = 0.002) and higher IVH scores (odds ratio 1.33, 95% confidence interval 1.05-1.69; p = 0.02). Intracerebral hemorrhage was more frequently localized in the posterior fossa in the EVDAI group (20% vs. 0%, p = 0.004). Multivariable analysis confirmed a positive independent correlation with larger blood clots. Cox regression demonstrated earlier EVDAI onset in association with higher BNI grades and IVH scores.

Conclusions: Both the quantity and radiological distribution of subarachnoid and ventricular blood positively correlate with EVD-associated nosocomial meningitis, eventually accelerating an earlier infection onset. These findings should help guide future research on EVDAI prevention in patients with aSAH.

Background: Consciousness recovery after severe traumatic brain injury (sTBI) can take minutes to years. Despite this variability, we hypothesized that we could identify subgroups with distinct temporal recovery trajectories and that these subgroups would have distinct clinical features.

Methods: We conducted a retrospective cohort study to analyze recovery trajectories for patients with sTBI (Glasgow Coma Scale [GCS] score ≤ 8) admitted to Stony Brook University Hospital from 2010 to 2019. Patients meeting our criteria for recovery (GCS score ≥ 13) were classified into cohorts using the slopes of their recovery trajectories. We then characterized these groups by their clinical features, neuroimaging, and electroencephalography (EEG).

Results: A total of 501 patients with sTBI (348 men, mean age 51 years) were included in this study. Of these, 299 recovered. After analyzing their recovery rates, two distinct groups emerged, (1) fast recovery (n = 215) and (2) slow recovery (n = 84), with a median recovery time of 6 (interquartile range [IQR] 2-12) vs. 33 (IQR 27-44.75) days. Slow recovery patients had higher Injury Severity Scores (median 30 [IQR 25-41.75] vs. 24 [IQR 16-30]; 95% confidence interval [CI] 4.4495-10.6105; P < 0.001), more thalamic injury on neuroimaging (normalized volume [voxels] - 0.664 vs. 1.74; R² = 0.781; P < 0.016), and impaired interhemispheric connectivity on EEG (phase-locking value 0.35 vs. 0.44; 95% CI 0.055-0.14; P < 0.001).

Conclusions: Recovery after sTBI falls into two broad categories, distinguishable by injury severity, thalamic injury, and disrupted interhemispheric connectivity. This model accounts for heterogeneity in TBI outcomes and represents progress toward identifying targets for future neuromodulatory therapeutic development.

Background: Many traumatic brain injury (TBI) treatment protocols, including the Lund concept, advocate the highest point of the subarachnoid space (typically the vertex) as the zero-reference point for intracranial pressure (ICP) and the level of the right atrium as the zero-reference point for mean arterial blood pressure (MAP). In 2017, at the Department of Neurosurgery in Lund, Sweden, the zero-reference points for ICP and MAP were both changed to the external auditory meatus (EAM), thus altering the calculated cerebral perfusion pressure (CPP) levels. We hypothesized that the ICP and MAP levels obtained from the different zero-reference points resulted in altered neurocritical care management and/or patient outcome.

Methods: We conducted a retrospective analysis of ICP, CPP, MAP, medical management, mortality, and outcome in two different patient cohorts with severe TBI treated at the Department of Neurosurgery, Skåne University Hospital, Lund, Sweden, between 2013 and 2016 and 2018 and 2022.

Results: We collected more than 31,000 measurements from 49 patients between 2013 and 2016 and 53 patients between 2018 and 2022. Age and injury severity were similar in both groups. Mortality and treatment outcome according to the Glasgow Outcome Scale - Extended were similar. Mean ICP levels were higher (p < 0.0001) after the reference point was changed to the EAM. The use of clonidine (65% vs. 49%; p = 0.17) and metoprolol (50% vs. 13%; p = 0.0002) decreased, and the use of norepinephrine increased (42% vs. 98%; p < 0.0001) after changing the reference points.

Conclusions: Higher ICP levels were observed when the reference point was changed to the EAM. The use of metoprolol was reduced, and there was a significant increase in the use of norepinephrine. These results show the impact of zero-reference point placement, which should be reported in TBI studies analyzing ICP and CPP management.

Background: This study aims to explore the predictors of poor outcomes by analyzing the clinical characteristics and prognosis of adult patients with severe forms of autoimmune encephalitis (AE) requiring intensive care unit (ICU) admission.

Methods: A retrospective analysis was conducted on 134 adult patients diagnosed with definite or possible AE and admitted to the neurology ICU between January 2015 and December 2023. Neurological outcomes at 6 and 12 months were assessed using the modified Rankin scale (mRS). The study further analyzed the relationship between their clinical characteristics, auxiliary examinations, and prognosis.

Results: A total of 134 adult patients with AE requiring ICU admission were included. The 6- and 12-month survival rates were 91.8% and 91.5%, respectively. At 6 months, 72.4% (97 of 134) of patients had favorable outcomes (mRS score ≤ 2), whereas 27.6% (37 of 134) had poor outcomes (mRS score ≥ 3). Compared with the favorable group, patients in the poor outcome group were older (42.92 vs. 30.71 years, p = 0.002), had a higher incidence of tumors (24.3% vs. 4.1%, p < 0.001), and were more likely to require mechanical ventilation (67.6% vs. 26.8%, p < 0.001). They also had lower Glasgow Coma Scale scores on ICU admission (p = 0.006), higher Acute Physiology and Chronic Health Evaluation II scores (p = 0.006), elevated cerebrospinal fluid glucose (p = 0.004) and protein levels (p = 0.029), higher autoantibody seronegativity (32.4% vs. 13.4%, p = 0.011), lower glucocorticoid use (p = 0.038), and longer ICU stays (p = 0.031). Multivariate logistic regression identified age (p = 0.001), presence of tumor (p = 0.03), mechanical ventilation (p = 0.025), antibody negativity (p = 0.042), and ICU length of stay (p = 0.000) as independent predictors of poor prognosis.

Conclusions: These factors may help identify high-risk patients with AE early, enabling timely and targeted interventions to improve outcomes.

Background: Most of the sedative and analgesic drugs used in patients with head injury cause a dose-dependent decrease in blood pressure, which may further worsen secondary neurologic injury. The sympathomimetic profile of ketamine, along with its neuroprotectant effect, can have a beneficial effect in these patients.

Methods: A total of 60 adult patients with severe traumatic brain injury were randomized to receive either ketamine infusion at 3 mg/kg/h or normal saline. The study drugs were given by infusion while intracranial pressure (ICP) monitoring was going on. Systemic hemodynamics, arterial blood gas values, ICP, cerebral perfusion pressure (CPP), and jugular venous oxygen saturation were monitored. At the end of 3 months, neurological outcome was recorded by an independent observer using the Glasgow Outcome Scale-Extended.

Results: Baseline values of hemodynamic parameters were comparable in the two groups. In the initial 4-6 h, patients in the ketamine group had a significantly higher level of blood pressure and CPP than patients in the control group, but the effect was not sustained after 6 h. Similarly, a significant reduction in ICP was observed only for a brief period, between the fourth and sixth hours. Vasopressors were more often used in the control group (13 [43.3%] vs. 5 [16.6%]; p = 0.02). There was no difference in the neurological outcome at 3 months in both groups.

Conclusions: There was no significant improvement in neurological outcome with ketamine infusion in patients with severe traumatic brain injury. There was a trend toward better CPP and lower ICP; however, the difference was statistically insignificant. Trial registered at Central Trial Registry of India (CTRI/2018/09/015729) at https://ctri.nic.in/Clinicaltrials/.

Background: The American Heart Association/American Stroke Association recommends achieving systolic blood pressure (SBP) therapeutic targets within 60 min of initiating treatment for intracerebral hemorrhage (ICH), emphasizing avoidance of "overshoot" correction and SBP fluctuations. We evaluated the prognostic value of "SBP reduction with stability," a novel end point combining controlled blood pressure reduction and maintenance, using data from two large multinational clinical trials.

Methods: We analyzed patients with ICH from Antihypertensive Treatment of Acute Cerebral Hemorrhage 2 and Intensive BP Reduction in Acute Cerebral Hemorrhage Trial 2 trials presenting with initial SBP 150-220 mm Hg. SBP reduction with stability was defined as achieving and maintaining SBP between 130 and 150 mm Hg within the first hour after randomization based on consecutive recordings. Outcomes included functional independence (modified Rankin scale 0-2) at 90 days and neurological deterioration within 24 h, adjusted for potential confounders.

Results: Among 3,694 patients with ICH (2,781 patients from Intensive BP Reduction in Acute Cerebral Hemorrhage Trial 2 and 913 patients from Antihypertensive Treatment of Acute Cerebral Hemorrhage 2), 1,061 patients (28.7%) achieved SBP reduction with stability within 1 h. Patients had mean age 63.3 ± 12.9 years, baseline SBP 177.14 ± 18.28 mm Hg, and median hematoma volume of 10.78 mL (interquartile range 5.5-19.16). Achieving SBP reduction with stability significantly improved functional independence odds (odds ratio 1.38, 95% confidence interval 1.16-1.64) and reduced neurological deterioration odds (odds ratio 0.68, 95% confidence interval 0.53-0.88) after adjusting for initial SBP, Glasgow Coma Scale, age, sex, stroke history, hypertension, diabetes mellitus, study, ICH location, hematoma volume, and intraventricular hemorrhage presence.

Conclusions: Only 30% of patients with mild-to-moderate ICH achieved SBP reduction with stability within the first hour. This achievement was associated with improved functional outcomes and reduced early neurological deterioration. These findings suggest that SBP reduction with stability represents a valuable therapeutic target for future clinical trials in ICH management.