Neurocritical Care最新文献

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.

Background: Family caregivers of patients with severe acute brain injury (SABI) who commit to tracheostomy and/or percutaneous endoscopic/surgical gastrostomy for the patient often develop chronic emotional distress. To inform future interventions to mitigate this distress, we characterized the stressors and coping strategies of caregivers of patients with SABI with varying levels of emotional distress during the acute and postacute stages of treatment.

Methods: We conducted semistructured interviews with family caregivers of patients with SABI around the time of neurological intensive care unit discharge (T1) and at 2-month follow-up (T2). All caregivers included in this current study completed the Hospital Anxiety and Depression Scale at T1 and/or T2. We then stratified transcripts by caregiver distress level, characterizing caregivers who scored > 11 on at least one Hospital Anxiety and Depression Scale subscale as "high distress" and ≤ 11 as "low distress." We conducted deductive, conceptual content analysis to compare perceived stressors and coping strategies employed at both time points.

Results: Caregivers in both strata reported many similar stressors at each time point, including ongoing uncertainty. However, there were also differences in stressors by level of distress and time point of assessment. At T1, high-distress caregivers reported pronounced stress related to navigating the health care system and communicating with providers, staff, and the patient. At T2, high-distress caregivers noted heightened difficulty with transitioning to long-term caregiving, co-occurring complex emotions, and communication with family and friends. Conversely, low-distress caregivers focused on challenges with team-based medical decision making at T2. Clear differences in coping strategies also emerged, such that high-distress caregivers relied primarily on avoidance at both points, whereas low-distress caregivers incorporated more problem-solving and self-care strategies.

Conclusions: Psychosocial interventions for caregivers of patients with SABI are needed to reduce emotional distress. Skills should be applied to relevant topics based on time since neurological intensive care unit discharge and distress level. Skills should focus on reducing avoidance, promoting active coping, and targeting the perceived stressors specific to high-distress versus low-distress caregivers revealed here.

Background: The objective of this study was to evaluate whether paroxysmal slow wave events (PSWEs) identified in early electroencephalography (EEG) predict posttraumatic epilepsy (PTE) and disability outcomes following severe traumatic brain injury (sTBI).

Methods: A retrospective case-control study included 45 patients with sTBI (17 with PTE and 28 without PTE) matched by age and Glasgow coma scale. Clinical and EEG data were analyzed. Logistic regression and leave-one-out cross-validation (LOOCV) assessed PTE risk and disability. The area under the curve (AUC) measured accuracy.

Results: Patients with PTE had longer time in PSWEs (P = 0.04) and lower median power frequency (MPF) of PSWEs (P = 0.02) on initial EEGs, along with increased time in PSWEs between initial and follow-up EEGs (P = 0.03). Lower MPF was associated with increased PTE risk (odds ratio 5.88; P = 0.04). Multivariate regression identified hemicraniectomy, time in PSWEs, and MPF as PTE predictors (AUC 0.87; P < 0.0001), maintaining strong LOOCV performance (AUC 0.83; P < 0.0001, accuracy 80%). Longer time in PSWEs was observed in patients with severe disability at the 3-, 6-, and 12-month follow-ups compared with moderate-to-good recovery (P = 0.012, 0.006, and 0.04, respectively).

Conclusions: PSWEs predict PTE development and are more prevalent among patients with worse disability after sTBI. Quantitative PSWE analysis may guide preventive and therapeutic strategies for PTE.