Neurocritical Care最新文献

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.

Background: Traumatic brain injury can lead to venous sinus injury and thrombosis, which may be associated with elevated intracranial pressure and poor outcomes. We sought to examine the risk factors, management, and clinical outcomes of traumatic venous sinus thrombosis (tVST).

Methods: We conducted a comprehensive search of our institutional radiology database for final radiology reports from 2013 to 2022 that contained the terms "venous sinus thrombosis," "sinus thrombosis," or "venous occlusion." tVST was detected on computed tomography and confirmed by a board-certified neuroradiologist.

Results: We identified 135 patients on initial screening and entered 112 into our final analysis. Patients were predominantly male (76.8%) and had a mean age of 44 years. Initial Glasgow Coma Scale scores of 13-15, 9-12, and 3-8 were found in 60.7%, 12.5%, and 26.8% of our cohort, respectively. Eighty-nine patients (79.5%) were alive at hospital discharge. Most patients sustained skull fractures (n = 109, 97.3%), including skull base fractures. Seventeen patients required interventions for refractory intracranial hypertension, of whom 16 (94.1%) had multiple tVST. We observed heterogeneity in tVST monitoring and treatment practices. Patients received anticoagulation (AC; 13.4%), antiplatelet (AP; 34.8%), or conservative (no AC or AP; 51.8%) treatment for tVST. Follow-up imaging was available for 52 patients, showing recanalization of venous sinuses in 26 patients (50%) by 6 months post injury. Recanalization rates were higher in the AP group than in the AC group. However, this was likely the result of selection bias, in which patients with mild to moderate injuries were more likely to be assigned to AP therapy. We noted more bleeding complications in AC- and AP-treated patients (20.0% and 12.8%) than in conservatively managed patients (3.4%), even after adjusting for lower survival in the conservative group.

Conclusions: Differences between treatment groups should be cautiously interpreted due to selection bias and confounding by indication. More studies are needed to determine the optimal management of tVST.

Background: Low cerebral perfusion pressure (CPP) has previously been identified as a key prognostic marker after pediatric traumatic brain injury (TBI). Cerebrovascular autoregulation supports stabilization of cerebral blood flow within the autoregulation range. Beyond the upper limit of this range, cerebral blood flow increases with increasing CPP, leading to increased risk of intracranial hypertension and blood-brain barrier disruptions. Based on the hypothesis that children are less sensitive to high CPP, we aimed to characterize the pediatric upper limit of autoregulation and the association between high CPP and outcome.

Methods: Data acquired as part of the "Studying Trends of Autoregulation in Severe Head Injury in Paediatrics" (STARSHIP) study (a prospective, multicenter, observational study that enrolled 135 children with TBI from July 2018 to March 2023) were explored. The association between different levels of CPP and the autoregulation proxy measure, the pressure reactivity index (PRx), were explored visually. The prognostic value of CPP was assessed by exploring overall averages, overall dose, hourly dose, and percentage time spent above specific thresholds. We employed univariable/multivariable (χ² tests, logistic regression, sliding dichotomy) and visual (heatmap) methods.

Results: No clear upper limit of autoregulation could be identified with PRx increasing beyond 0.2 only with CPP values beyond 100 mm Hg. Using iterative χ² testing and logistic regression analyses, similarly, only hourly dose and percentage time beyond CPP of 90 mm Hg displayed a trend toward worse outcome. Using heatmap analyses, regions of CPP with differing risk stratifications could be identified. No difference in CPP could be identified between patients with and without acute respiratory distress syndrome or secondary hemorrhages.

Conclusions: In contrast to the well-established association between low CPP and poor outcome, our findings suggest that exposure to CPP values above those recommended by the Brain Trauma Foundation guidelines may not be associated with worse outcomes in this cohort. However, given the observational nature of the study and potential confounding factors, these results highlight the need for prospective trials to assess the safety and efficacy of targeting higher CPP in pediatric TBI.

Background: Anemia is common after intracerebral hemorrhage (ICH). It has been attributed to inflammation and is associated with poor outcomes. We investigated whether this could be related to the effects of hemoglobin (Hb) on perihematomal edema (PHE).

Methods: We performed an exploratory post hoc analysis of the Intracerebral Hemorrhage Deferoxamine (i-DEF) randomized controlled trial. We included participants with primary supratentorial ICH, available baseline Hb levels, and computed tomography scans at baseline and follow-up after 72-96 h. We investigated the association of Hb and anemia (as continuous and dichotomous exposures, respectively) with edema extension distance (EED) as the main continuous outcome at baseline and follow-up and as its interscan change using Spearman correlation and unadjusted and adjusted linear models. We examined absolute and relative PHE in ancillary analyses.

Results: We analyzed data from 276 of 293 (94%) i-DEF participants. The median age was 61 (interquartile range [IQR] 52-70) years, and 39% of participants were female. The median Hb level was 14.1 (IQR 13-15.2) g/dL, and 41 participants (15%) were anemic. The median EED was 4.4 (IQR 3.5-5.3) mm at baseline and 6.4 (IQR 5.3-7.3) mm at follow-up. Hb was weakly inversely correlated with baseline (ρ =  - 0.12, p = 0.05) and follow-up EED (ρ =  - 0.11, p = 0.07) but not with interscan EED change (ρ =  - 0.01, p = 0.89). Linear models showed similar relationships of Hb with baseline and particularly follow-up EED but not with EED change. In ancillary analyses, absolute and relative PHE showed no clear correlation with Hb but maintained similar relationships with Hb in linear models as in the main analysis.

Conclusions: We identified signals for an association of baseline Hb with PHE after ICH. These findings may warrant further exploration in larger cohorts.

Clinical trial registration: ClinicalTrials.gov identifier: NCT02175225.

Background: Cerebral perfusion pressure (CPP) dose-response on post-traumatic brain injury (TBI) outcome in children remains unknown. This project aimed to produce the first pediatric post-TBI CPP dose-response visualization plot from the international multicenter KidsBrainIT data set.

Methods: Fully anonymized prospectively collected routine minute-by-minute intracranial pressure (ICP), mean arterial blood pressure, and CPP time series data from 104 pediatric patients with TBI were categorized into CPP intensity duration episodes, albeit CPP above or below a range of thresholds. These episodes were then correlated with the 6-month modified Glasgow Outcome Score (GOS) and depicted in 3D color-coded CPP dose-response plots. Additionally, the effects of cerebrovascular reactivity patterns and ICP were examined.

Results: Our pediatric CPP dose-response plots resembled the previously published adult CPP dose-response plots: on the CPP pressure time plots, an exponential "black" transition curve separated CPP episodes associated with poor ("red," GOS < 4) and good ("blue") outcome. Lower and higher ends of CPP intensity were only tolerated for shorter durations. A "safe" CPP zone (56-89 mm Hg) was identified for childhood TBI with active cerebrovascular reactivity pattern and ICP < 20 mm Hg. Passive cerebrovascular reactivity pattern reduced the area of safe CPP doses. ICP levels > 20 mm Hg were associated with worse outcome, irrespective of CPP dose.

Conclusions: The pediatric CPP dose-response on poor outcome was visualized successfully for the first time. Because the "critical" lower CPP limit exceeds the current recommended minimum CPP target for pediatric TBI treatments, there is an urgent need to validate childhood CPP dose-response to provide evidence-based CPP clinical targets in the future.

Background: Pulse shape index (PSI) is a novel artificial intelligence-supported parameter that evaluates the pressure-volume compensatory reserve of the craniospinal system through intracranial pressure (ICP) pulse waveform classification. This study assessed the agreement between PSI derived from invasive ICP monitoring (PSI_ICP) and noninvasive brain4care (B4C) sensor signal (PSI_B4C) and investigated the influence of cranial integrity, age, and internal jugular vein (IJV) compression on PSI values.

Methods: Simultaneous ICP and B4C monitoring was performed in 47 adult patients ( age: 43 (30) years) before and during IJV compression. Patients were grouped by cranial integrity: intact skull bone (n = 17), large skull fractures or craniotomies (n = 17), and craniectomies (n = 13). Pulse waveforms were automatically classified into four classes (from 1 = normal to 4 = pathological) by a neural network, and PSI was calculated as the weighted average of class numbers. Values are presented as median (interquartile range).

Results: Bland-Altman analysis demonstrated good agreement between PSI_ICP and PSI_B4C, with approximately 6% outliers. PSI was significantly higher in patients who underwent craniectomy compared with those with intact skulls (PSI_ICP: 3.5 (0.8) vs. 2.0 (1.2) arbitrary units, p < 0.002; PSI_B4C: 3.0 (0.4) vs. 2.0 (0.6) arbitrary units, p < 0.005) or those with craniotomies or large fractures (PSI_ICP: 3.5 (0.8) vs. 2.0 (2.1) arbitrary units, p < 0.05; PSI_B4C: 3.0 (0.4) vs. 2.0 (2.2) arbitrary units, p < 0.05). IJV compression did not affect PSI. Both PSI_ICP (r_s = 0.35, p < 0.02) and PSI_B4C (r_s = 0.37, p = 0.01) correlated with age.

Conclusions: This study supports the B4C signal's capability to noninvasively reflect ICP waveform morphology via PSI, offering a promising monitoring alternative. PSI appears to be influenced by age and craniectomy but not by a slight, sudden ICP change induced by IJV compression.