Neurocritical Care最新文献

Background: Septic shock is a recognized cause of global mortality in intensive care units. Sedation and analgesia management are essential for patients with sepsis or hemodynamic instability. Although considered safe concerning hemodynamic changes, ketamine use might cause a substantial rise in intracranial pressure (ICP).

Methods: An interventional study was conducted at the intensive care unit of Zagazig University Hospitals from December 2021 to March 2023 and covered 100 adult patients with septic shock requiring mechanical ventilation, sedation, and vasopressors. Patients with acute brain injury were excluded. Noninvasive ICP including ICP derived from pulsatility index, ICP derived from diastolic flow velocity (ICP_FVd), and ICP derived from optic nerve sheath diameter, and hemodynamic monitoring were measured before adjunct low-dosage (0.3 mg/kg/hr) continuous ketamine infusion (T0), after 12 h (T1), and after 24 h of infusion (T2).

Results: Baseline ICP derived from optic nerve sheath diameter, ICP derived from pulsatility index, and ICP_FVd medians were 14.5 (interquartile range [IQR] 7), 16.8 (IQR 0.91), and 13.8 (IQR 9.38) mm Hg, respectively. Only ICP_FVd showed a significant slight increase from 13.75 (IQR 8.5) at T1 to 13.90 (IQR 8.5) at T2 (P value = 0.042). The baseline median noninvasive cerebral perfusion pressure was 74.56 (IQR 12.39) mm Hg without significant change at T1 or T2 (P value = 0.09). The respiratory rate, heart rate, and mean arterial blood pressure showed no significant changes across timepoints (P values = 0.95, 0.86, and 0.14, respectively). The median doses of midazolam, fentanyl, and norepinephrine significantly decreased across the study timepoints, especially at the first 12 h (P value < 0.001 for each).

Conclusions: The present pilot study showed promising results of low-dose continuous ketamine infusion adjunctly on ICP and hemodynamics with a substantial reduction of sedatives and vasopressor dose. Further studies with large sample sizes and longer duration of administration and follow-up are needed to expand the current findings.

Background: Detecting covert consciousness in unresponsive patients is challenging. Although functional magnetic resonance imaging and advanced electroencephalography paradigms can identify volitional brain activity, the limited accessibility of these technologies necessitates alternative approaches. Functional near-infrared spectroscopy may provide a portable solution in the intensive care unit. We assessed the feasibility of functional near-infrared spectroscopy with verbal motor commands to detect volitional brain activity in acute disorders of consciousness (DoC).

Methods: Functional near-infrared spectroscopy recordings and clinical assessments were obtained from 50 patients with DoC with acute brain injury, with data analyzed post hoc and visually at the bedside. Twenty healthy volunteers served as controls.

Results: After quality control, data from 19 controls and 36 patients were analyzed. Cortical activation was detected in 18 (96%) controls and 16 (44%) patients. Among 13 minimally conscious patients, volitional activity was found in 8 (62%), whereas 8 (35%) of 23 clinically unresponsive patients showed activation. Volitional brain activity in the latter was associated with higher odds of command following within a week, although it was not statistically significant (odds ratio 3.1, 95% confidence interval 0.7-15.8; p = 0.14). Visual bedside analysis showed high specificity (90%) but moderate agreement (κ = 0.4) with post hoc computational analysis.

Conclusions: Functional near-infrared spectroscopy with motor commands can detect volitional brain activity in acute DoC, although data quality issues remain a limitation.

We present the case of a 69-year-old woman with acute myeloid leukemia with recurrent transient events characterized by loss of awareness and generalized shaking. The events were initially diagnosed as seizures based on semiology but persisted despite antiseizure medications. The events were recorded using continuous video electroencephalography (EEG) with no epileptiform correlate. However, pertinent changes included diffuse attenuation of fast activity, increase in delta activity, and subsequent attenuation of faster frequencies. Quantitative EEG detected a decrease in fast activity, alpha-delta ratio, and amplitude-integrated EEG. The transient events and EEG findings in the setting of known cancer history raised concern for carcinomatous meningitis despite unremarkable brain imaging. Lumbar puncture showed an elevated opening pressure and cytology confirmed a myeloid blast population consistent with acute myeloid leukemia. The events resolved with serial lumbar punctures supporting the fact that the events were likely secondary to transient elevations in intracerebral pressure. In summary, video EEG with quantitative EEG analysis is a sensitive, non-invasive way to confirm transient elevated intracranial pressure and rule out epileptic activity. This constellation of cancer, clinical symptoms and EEG findings should increase suspicion of carcinomatous meningitis.

Background: Brain magnetic resonance imaging (MRI) has been investigated as a neuroprognostication (NP) test after out-of-hospital cardiac arrest (OHCA); however, most studies have focused on predicting poor neurologic outcomes or death.

Methods: We examined the ability of a composite brain MRI score ("NP score") to predict neurologic outcomes in an OHCA cohort (2017-2023) who underwent brain MRI within 2-7 days post arrest and survived to hospital discharge. NP scores (range 0-214) were calculated from diffusion weighted imaging and fluid attenuated inversion recovery signals in prespecified neuroanatomical regions. We categorized neurologic outcomes as "independent" (Cerebral Performance Categories [CPC] 1-2), "dependent" (CPC 3), and "vegetative state" (CPC 4). We conducted correlation analyses and used computational modeling for probabilities to identify transition points between the outcome categories.

Results: Forty-two OHCA survivors were included (median age 47 years; 74% male, 43% shockable rhythm; 88% underwent targeted temperature management). At hospital discharge, 50% (n = 21) had recovered to independent, 24% (n = 10) were dependent, and 26% (n = 11) remained in a vegetative state. MRIs were obtained at a median of 4 days post arrest, (interquartile range 3-5). NP scores (range 0-136, median 11.5, interquartile range 0-41.5, intraclass correlation coefficient 0.89) strongly correlated with CPC (r_s = 0.69, p < 0.001) and were significantly different between CPC groups (p < 0.001); thresholds of 15 and 54 were identified as transition points between independent-dependent and dependent-vegetative state, respectively. Among survivors with bilaterally intact somatosensory evoked potentials, median NP scores were 0, 29, 68.5 for independent, dependent, and vegetative state patients, respectively.

Conclusions: Quantitative brain MRI-based scoring may predict neurologic outcomes at discharge among OHCA survivors. External validation in larger prospective multicenter cohorts, assessment of long-term outcomes, and examination of the score in deceased patients are needed to establish the prognostic value and address concerns about generalizability.

Transcranial Doppler (TCD) is increasingly used in pediatric acute care with emerging point-of-care ultrasound (POCUS) applications. However, no standardized definition distinguishes POCUS TCD from diagnostic/consultative TCD. This scoping review aims to (1) examine how the terminology "POCUS TCD" is used in pediatric literature, (2) describe physiologic indications driving TCD use in pediatric acute care settings, and (3) compare contexts of performance and operational characteristics across these indications. A comprehensive scoping review was conducted following published guidelines. Databases were searched from inception to June 2024 for studies addressing TCD use in children (≤ 18 years) in emergency departments, inpatient services, or intensive care units. Full-text eligibility and data extraction were performed in duplicate by independent reviewers. Of 4,066 screened studies, 660 full texts were assessed, and 307 studies met eligibility criteria (258 original studies and 49 reviews, guidelines, or surveys). The term "POCUS TCD" was mentioned in only 3% of original studies and 26% of included reviews and guidelines, which were mostly published after 2018. Eleven physiologic indications for TCD use were identified, and specific subtypes of context of use emerged. TCD operational characteristics varied widely and were often incompletely reported. However, notable differences were observed across physiologic indications, particularly in TCD extent, operator type, and use of point-of-care machines. The terminology "POCUS TCD" is infrequently used in current pediatric research, and most studies do not specify the type of TCD performed or intended. Significant differences in the context of performance and operational characteristics across physiologic indications suggest the coexistence of distinct forms of TCD in current clinical practice despite the lack of explicit distinction between POCUS and diagnostic/consultative TCD. Standardizing terminology and improving reporting of operational contexts in future research will be essential to support safe and effective clinical integration of TCD in pediatric critical care.

Background: Measuring reliable intracranial pressure (ICP) is critical for patients with acute brain injuries. The aim of this study was to evaluate zero drift of the intraparenchymal strain gauge Pressio transducer (Sophysa, Orsay, France) in clinical conditions.

Methods: A prospective observational multicenter study was conducted in four French intensive care units of university hospitals. Patients with acute brain injuries were included if they needed ICP measurement using the Pressio transducer. The zero drift was measured at the explantation of the sensor. ICP-related adverse events were also collected.

Results: Between January 1, 2018, and March 31, 2020, 235 patients were included in this study for a monitoring time of 2,180 days. The zero drift assessment was determined in 223 transducers (95%). The median duration of ICP monitoring was 8 days (interquartile range [IQR] 4 to 13 days). The median zero drift was 1 mm Hg (IQR 1 to 3 mm Hg), and a weak correlation was observed between the duration of ICP monitoring and zero drift (ρ = 0.141; P = 0.0357), which lacks clinical significance. Zero drifts higher than 5 mm Hg were found in 10% of transducers. Four patients (1.8%) had ICP-related hematomas, with no clinical impact, and none had ICP-related brain infection. Failures or technical dysfunctions of the monitoring were found in six patients (2.6%).

Conclusions: The Pressio catheter from the Sophysa system exhibited a minor zero drift after a median monitoring period of 8 days. The transducer's precision was comparable to that of other ICP devices using strain gauge technology.

Background: Traumatic brain injury (TBI) is a major life-threatening event. In addition to neurological deficits, it can lead to long-term impairments of cognitive function. The vagus nerve (VN) provides a direct communication conduit between the central nervous system and the periphery, and modulation of the inflammatory reflex via electrical stimulation of the vagus nerve (VNS) shows efficacy in ameliorating pathology in neurodegenerative diseases. Our objective was to investigate the impact and underlying mechanism of VNS for cognitive impairment in a rat model of TBI.

Methods: Male rats were implanted with VNS electrodes on the left VN 1 week prior to controlled cortical impact. Mitochondrial permeability transition pore blocker cyclosporin A (CsA) and stimulator of interferon genes (STING) agonist 2'3'-cGAMP were delivered by intranasal administration or intraventricular injection. Post-VNS assessments included Morris water maze, Nissl staining, hematoxylin and eosin staining, Western blotting, quantitative polymerase chain reaction, mitochondrial membrane potential, and enzyme-linked immunosorbent assay.

Results: We found that VNS treatment significantly improved cognitive impairment, increased mitochondrial membrane potential, reduced accumulation of cytosolic mitochondrial DNA, attenuated cyclic GMP-AMP synthase (cGAS)-STING pathway, suppressed nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome activation, and partially reversed hippocampus neuronal damage and loss caused by TBI. However, 2'3'-cGAMP delivery significantly abrogated these effects of VNS. In addition, CsA also showed neuroprotective effects, including improved cognitive impairment, decreased levels of cGAS, phosphorylated STING, and suppressed the expressions of NLRP3 inflammasome and pyroptosis-pertinent components containing cleaved Caspase-1, ASC, and N-terminal Gasdermin D. CsA also inhibited interleukin-1β and interleukin-18 proinflammatory cytokine concentration.

Conclusions: Stimulation of the VN attenuates the pyroptosis and neuroinflammatory cascades in the rat of the TBI model by regulating the mitochondrial DNA/cGAS/STING /NLRP3 pathway.