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Use of magnetic resonance imaging (MRI) as a tool to aid in neuroprognostication after cardiac arrest (CA) has been described, yet details of specific indications, timing, and sequences are unknown. We aim to define the current practices in use of brain MRI in prognostication after pediatric CA.A survey was distributed to pediatric institutions participating in three international studies. Survey questions related to center demographics, clinical practice patterns of MRI after CA, neuroimaging resources, and details regarding MRI decision support.Response rate was 31% (44 of 143). Thirty-four percent (15 of 44) of centers have a clinical pathway informing the use of MRI after CA. Fifty percent (22 of 44) of respondents reported that an MRI is obtained in nearly all patients with CA, and 32% (14 of 44) obtain an MRI in those who do not return to baseline neurological status. Poor neurological examination was reported as the most common factor (91% [40 of 44]) determining the timing of the MRI. Conventional sequences (T1, T2, fluid-attenuated inversion recovery, and diffusion-weighted imaging/apparent diffusion coefficient) are routinely used at greater than 97% of centers. Use of advanced imaging techniques (magnetic resonance spectroscopy, diffusion tensor imaging, and functional MRI) were reported by less than half of centers.Conventional brain MRI is a common practice for prognostication after CA. Advanced imaging techniques are used infrequently. The lack of standardized clinical pathways and variability in reported practices support a need for higher-quality evidence regarding the indications, timing, and acquisition protocols of clinical MRI studies.

Background/Objective Multimodality neurologic monitoring (MMM) is an emerging technique for management of traumatic brain injury (TBI). An increasing array of MMM-derived biomarkers now exist that are associated with injury severity and functional outcomes after TBI. A standardized MMM reporting process has not been well described, and a paucity of evidence exists relating MMM reporting in TBI management with functional outcomes or adverse events. Methods Prospective implementation of standardized MMM reporting at a single pediatric intensive care unit (PICU) is described that included monitoring of intracranial pressure (ICP), cerebral oxygenation and electroencephalography (EEG). The incidence of clinical decisions made using MMM reporting is described, including timing of neuroimaging, ICP monitoring discontinuation, use of paralytic, hyperosmolar and pentobarbital therapies, neurosurgical interventions, ventilator and CPP adjustments and neurologic prognostication discussions. Retrospective analysis was performed on the association of MMM reporting with initial Glasgow Coma Scale (GCS) and Pediatric Risk of Mortality III (PRISM III) scores, duration of total hospitalization and PICU hospitalization, duration of mechanical ventilation and invasive ICP monitoring, inpatient complications, time with ICP > 20 mmHg, time with cerebral perfusion pressure (CPP) 20 mmHg, time with CPP

Management after cerebral arteriovenous malformation (AVM) rupture aims toward preventing hemorrhagic expansion while maintaining cerebral perfusion to avoid secondary injury. We investigated associations of model-based indices of cerebral autoregulation (CA) and autonomic function (AF) with outcomes after pediatric cerebral AVM rupture. Multimodal neurologic monitoring data from the initial 3 days after cerebral AVM rupture were retrospectively analyzed in children (

Hyperosmolar agents are cornerstone therapies for pediatric severe traumatic brain injury. Guideline recommendations for 3% hypertonic saline (HTS) are based on limited numbers of patients, and no study to date has supported a recommendation for mannitol.To characterize current use of hyperosmolar agents in pediatric severe traumatic brain injury and assess whether HTS or mannitol is associated with greater decreases in intracranial pressure (ICP) and/or increases in cerebral perfusion pressure (CPP).In this comparative effectiveness research study, 1018 children were screened and 18 were excluded; 787 children received some form of hyperosmolar therapy during the ICP-directed phase of care, with 521 receiving a bolus. Three of these children were excluded because they had received only bolus administration of both HTS and mannitol in the same hour, leaving 518 children (at 44 clinical sites in 8 countries) for analysis. The study was conducted from February 1, 2014, to September 31, 2017, with follow-up for 1 week after injury. Final analysis was performed July 20, 2021.Boluses of HTS and mannitol were administered.Data on ICP and CPP were collected before and after medication administration. Statistical methods included linear mixed models and corrections for potential confounding variables to compare the 2 treatments.A total of 518 children (mean [SD] age, 7.6 [5.4] years; 336 [64.9%] male; 274 [52.9%] White) were included. Participants' mean (SD) Glasgow Coma Scale score was 5.2 (1.8). Bolus HTS was observed to decrease ICP and increase CPP (mean [SD] ICP, 1.03 [6.77] mm Hg; P .001; mean [SD] CPP, 1.25 [12.47] mm Hg; P .001), whereas mannitol was observed to increase CPP (mean [SD] CPP, 1.20 [11.43] mm Hg; P = .009). In the primary outcome, HTS was associated with a greater reduction in ICP compared with mannitol (unadjusted β, -0.85; 95% CI, -1.53 to -0.19), but no association was seen after adjustments (adjusted β, -0.53; 95% CI, -1.32 to 0.25; P = .18). No differences in CPP were observed. When ICP was greater than 20 mm Hg, greater than 25 mm Hg, or greater than 30 mm Hg, HTS outperformed mannitol for each threshold in observed ICP reduction (20 mm Hg: unadjusted β, -2.51; 95% CI, -3.86 to -1.15, P .001;25 mm Hg: unadjusted β, -3.88; 95% CI, -5.69 to -2.06, P .001;30 mm Hg: unadjusted β, -4.07; 95% CI, -6.35 to -1.79, P .001), with results remaining significant for ICP greater than 25 mm Hg in adjusted analysis.In this comparative effectiveness research study, bolus HTS was associated with lower ICP and higher CPP, whereas mannitol was associated only with higher CPP. After adjustment for confounders, both therapies showed no association with ICP and CPP. During ICP crises, HTS was associated with better performance than mannitol.

A dynamic relationship exists between diffuse traumatic brain injury and changes to the neurovascular unit. The purpose of this study was to evaluate vascular changes during the first week following diffuse TBI. It was hypothesized that pathology is associated with modification of the vasculature.Male Sprague-Dawley rats underwent either midline fluid percussion injury or sham-injury. Brain tissue was collected 1, 2 or 7 days post-injury or sham-injury (n = 3/time point). Tissue was collected and stained by de Olmos amino-cupric silver technique to visualize neuropathology or animals were perfused with AltaBlue casting resin before high-resolution vascular imaging. The average volume, surface area, radius, branching and tortuosity of the vessels were evaluated across three regions of interest.In M2, average vessel volume (p0.01) and surface area (p0.05) were significantly larger at 1 day relative to 2 days, 7 days and sham. In S1BF and VPM, no significant differences in the average vessel volume or surface area at any of the post-injury time points were observed. No significant changes in average radius, branching or tortuosity were observed.Preliminary findings suggest gross morphological changes within the vascular network likely represent an acute response to mechanical forces of injury, rather than delayed or chronic pathological processes.

Adenosine triphosphate-binding cassette (ABC) transport proteins ABCC1 and ABCB1 (also known as multidrug resistance-associated protein 1 and p-glycoprotein, respectively), are key membrane efflux transporters of drugs and endogenous substrates, including in the brain. The impact of traumatic brain injury (TBI) on ABCC1 and ABCB1 expression in humans is unknown. We hypothesized that ABCC1 and ABCB1 expression would be altered in brain tissue from patients acutely after severe TBI. Archived TBI samples (n=10) from our Brain Trauma Research Center and control samples (n=7) from our Alzheimer Disease Research Center were obtained under Institutional Review Board approval. Protein was extracted from fresh frozen cortical brain tissue for Western blot analysis and sections were obtained from fixed cortical tissue for immunohistochemistry. Relative abundance of ABCC1 was increased in samples from TBI versus controls (2.8±2.5 fold; p=0.005). ABCC1 immunohistochemistry was consistent with Western blot data, with increased immunoreactivity in cerebral blood vessel walls, as well as cells with the morphological appearance of neurons and glia in TBI versus controls. Relative abundance of ABCB1 was similar between TBI and controls (p=0.76), and ABCB1 immunoreactivity was primarily associated with cerebral blood vessels in both groups. These human data show that TBI increases ABCC1 expression in the brain, consistent with possible implications for both patients receiving pharmacological inhibitors and/or substrates of ABCC1 after TBI.

One of the most opposing barriers—both literally and figuratively—challenging the translational advancement of therapeutics targeting brain trauma involves effective delivery of potentially neuroprotective agents to the damaged brain. Aspects distinguishing delivery of drugs to the injured brain relative to other tissues include: (1) several unique physical features of the blood–brain barrier (BBB) vs. other blood–tissue barriers; (2) added diffusion distance associated with astrocyte swelling (in addition to interstitial edema) away from the therapeutic target; and (3) membrane transporters at both the BBB and blood–CSF barriers (BCSFB), such as ATP-binding cassette (ABC) transporters, organic anion transporters (OAT), and organic anion transporting peptides (OATP) that have the capacity to move drug substrates out of the brain, actively reducing brain bioavailability. While these “barriers” represent unique challenges to the development of efficacious neuroprotective agents for the treatment of traumatic brain injury (TBI), recent pharmacological advancements provide an optimistic outlook for designing strategies that impact outcome for victims of TBI in the near future.

As important mediators of solute transport at the blood-brain and blood-cerebrospinal fluid barriers, ATP-binding cassette (ABC) transporters (including ABCB1, ABCC1, and ABCC2), impact the bioavailability of drugs and endogenous substrates in the brain. While several ABCB1, ABCC1, and ABCC2 single nucleotide polymorphisms (SNPs) have been identified, their impact on outcome after traumatic brain injury (TBI) is unknown.ABCB1, ABCC1, and ABCC2 SNPs are associated with Glasgow Outcome Scale (GOS) score after TBI.DNA samples from 305 adult patients with severe TBI (Glasgow Coma Scale, GCS score ≤ 8) were genotyped for tagging SNPs of ABCB1 (rs1045642; rs1128503), ABCC1 (rs212093; rs35621; rs4148382), and ABCC2 (rs2273697). For each SNP, patients were dichotomized based on presence of variant allele for multivariate analysis to determine associations with GOS assigned at 6 months adjusting for GCS, Injury Severity score, age, and patient sex.For ABCB1 rs1045642, patients homozygous for the T allele were less likely to be assigned poor outcome versus those possessing the C allele [CT/CC; odds of unfavorable GOS = 0.71(0.55-0.92)]. For ABCC1 rs4148382, patients homozygous for the G allele were less likely to be assigned poor outcome versus those possessing the A allele [AG/AA; odds of unfavorable GOS = 0.73(0.55-0.98)].In this single-center study, patients homozygous for the T allele of ABCB1 rs1045642 or the G allele of ABCC1 rs4148382 were found to have better outcome after severe TBI. Further study is necessary to replicate these very preliminary findings and to determine whether these associations are due to central nervous system bioavailability of ABC transporter drug substrates commonly used in the management of TBI, brain efflux of endogenous solutes, or both.

The objectives of this study were to determine the prevalence of clinical findings associated with intussusception based on age and to evaluate the test characteristics of the presence of air in the ascending colon on abdominal radiographs and the effectiveness of ultrasound in diagnosing intussusception.This was a retrospective cohort study via chart review at a tertiary care center from January 2002 to December 2008. All children, aged 0 to 17 years, were identified with intussusception by International Classification of Diseases, Ninth Revision diagnostic coding. Charts were reviewed for clinical signs and symptoms at presentation, and all diagnostic studies were retrieved. A pediatric radiologist reviewed all films and ultrasounds.A total of 219 patients were identified with intussusception. One hundred thirty-two (60%) of patients were male; 127 (60%) were younger than 1 year (median, 7 months), 59 (27%) were 13 to 35 months (median, 23 months), and 33 (15%) were 3 years or older (median, 5 years). Children younger than 12 months were more likely to present with emesis, irritability, and guaiac-positive or grossly bloody stools compared with children older than 12 months (P0.05). In children older than 12 months, abdominal pain was the most common symptom (96%). Plain films were performed in 192 children, and of these, 163 (85%) had no air present in the ascending colon. Abdominal ultrasound was performed on 63 patients, with 58 (92%) having findings consistent with intussusception.Abdominal pain is the most common complaint in all ages for children presenting with intussusception. In children younger than 12 months, the strongest clinical predictors are emesis, irritability, and blood in the stool. For diagnosing intussusceptions, radiographs of the abdomen performed well, but ultrasound performed better, diagnosing intussusception in 92% of the cases.

Background Standard practice has been to admit children for an observation period after enema-reduced intussusception. However, the utility of such routine practice has not been clearly justified. Study Objectives The main objective was to determine the rate and timing of recurrent intussusception after successful enema reduction and describe any associated complications. Methods The study was a retrospective chart review identifying children with enema-reduced intussusception during a 7-year period from 2002 through 2008. Subjects were children ages 0 to 17 years presenting to the Emergency Department (ED) of a tertiary care, free-standing children’s hospital with confirmed and uncomplicated enema-reduced intussusception. Results During the study period there were 98 children with successful enema reduction of intussusception. There were 10 episodes of recurrence in 7 patients, for an overall recurrence rate of 7.1%. Three patients had two recurrences each, and the remainder had single recurrences. Two patients had early recurrences ( 48h) was 5.1%. No adverse events were noted in any of the recurrences. Conclusions Given the low early recurrence rate for enema-reduced intussusception and the minimal risk of adverse outcomes, ED observation for a 6-h period seems to be a safe alternative to inpatient management. These results support previous work and suggest that these patients can be managed on an outpatient basis.