The Incidence and Relevance of Hematochezia in the Interstage Congenital Heart Population.

Necrotizing enterocolitis (NEC) increases morbidity and mortality for infants with single ventricle heart disease (SVHD). While hematochezia often proceeds NEC not all hematochezia progresses to NEC. We aimed to examine the incidence, risk-factors, and outcomes associated with hematochezia and NEC for infants with SVHD. A single-center cohort study including SVHD patients requiring Stage I palliation from 12/2010 to 12/2015 was performed. Demographic, clinical, and outcome measures during the interstage period were abstracted from medical records. We defined hematochezia as blood in the stool without alternative etiology and NEC as systemic or intestinal signs concurrent with hematochezia and/or the presence of radiographic pneumatosis. Clinical characteristics and outcome measures were compared between patients with/without hematochezia and with/without NEC. Of 135 patients, 59(44%) had hematochezia and 20(15%) developed NEC. Demographic and operative factors were similar between patients with and without hematochezia. Patients with NEC were more often premature (15% vs 0%, p = 0.04), have lower birth weight (3.0 ± 0.6 vs 3.3 ± 0.5 kg, p = 0.03), longer cardiopulmonary bypass time (median 131 vs. 90 min, p = 0.02) and more often underwent unplanned cardiac catheterization (20% vs 3%, p = 0.04). Patients with hematochezia had more line days (p < 0.0001) and longer post-Stage-I length of stay (p < 0.0001) than those without hematochezia, and those with NEC had more line days than those without NEC (p = 0.02). Hematochezia is frequent following Stage-I palliation, however only one third of these patients develop NEC. Non-NEC Hematochezia is associated with a similar increase in line and hospital days. Further research is needed to identify methods to avoid over treatment.

Microglial depletion after brain injury prolongs inflammation and impairs brain repair, adult neurogenesis and pro-regenerative signaling.

The adult zebrafish brain, unlike mammals, has a remarkable regenerative capacity. Although inflammation in part hinders regeneration in mammals, it is necessary for zebrafish brain repair. Microglia are resident brain immune cells that regulate the inflammatory response. To explore the microglial role in repair, we used liposomal clodronate or colony stimulating factor-1 receptor (csf1r) inhibitor to suppress microglia after brain injury, and also examined regeneration in two genetic mutant lines that lack microglia. We found that microglial ablation impaired telencephalic regeneration after injury. Microglial suppression attenuated cell proliferation at the intermediate progenitor cell amplification stage of neurogenesis. Notably, the loss of microglia impaired phospho-Stat3 (signal transducer and activator of transcription 3) and ß-Catenin signaling after injury. Furthermore, the ectopic activation of Stat3 and ß-Catenin rescued neurogenesis defects caused by microglial loss. Microglial suppression also prolonged the post-injury inflammatory phase characterized by neutrophil accumulation, likely hindering the resolution of inflammation. These findings reveal specific roles of microglia and inflammatory signaling during zebrafish telencephalic regeneration that should advance strategies to improve mammalian brain repair.

Volumetric quantification of aneurysmal subarachnoid hemorrhage independently predicts hydrocephalus and seizures.

OBJECTIVE: Hydrocephalus and seizures greatly impact outcomes of patients with aneurysmal subarachnoid hemorrhage (aSAH); however, reliable tools to predict these outcomes are lacking. The authors used a volumetric quantitative analysis tool to evaluate the association of total aSAH volume with the outcomes of shunt-dependent hydrocephalus and seizures. METHODS: Total hemorrhage volume following aneurysm rupture was retrospectively analyzed on presentation CT imaging using a custom semiautomated computer program developed in MATLAB that employs intensity-based k-means clustering to automatically separate blood voxels from other tissues. Volume data were added to a prospectively maintained aSAH database. The association of hemorrhage volume with shunted hydrocephalus and seizures was evaluated through logistic regression analysis and the diagnostic accuracy through analysis of the area under the receiver operating characteristic curve (AUC). RESULTS: The study population comprised 288 consecutive patients with aSAH. The mean total hemorrhage volume was 74.9 ml. Thirty-eight patients (13.2%) developed seizures. The mean hemorrhage volume in patients who developed seizures was significantly higher than that in patients with no seizures (mean difference 17.3 ml, p = 0.01). In multivariate analysis, larger hemorrhage volume on initial CT scan and hemorrhage volume > 50 ml (OR 2.81, p = 0.047, 95% CI 1.03-7.80) were predictive of seizures. Forty-eight patients (17%) developed shunt-dependent hydrocephalus. The mean hemorrhage volume in patients who developed shunt-dependent hydrocephalus was significantly higher than that in patients who did not (mean difference 17.2 ml, p = 0.006). Larger hemorrhage volume and hemorrhage volume > 50 ml (OR 2.45, p = 0.03, 95% CI 1.08-5.54) were predictive of shunt-dependent hydrocephalus. Hemorrhage volume had adequate discrimination for the development of seizures (AUC 0.635) and shunted hydrocephalus (AUC 0.629). CONCLUSIONS: Hemorrhage volume is an independent predictor of seizures and shunt-dependent hydrocephalus in patients with aSAH. Further evaluation of aSAH quantitative volumetric analysis may complement existing scales used in clinical practice and assist in patient prognostication and management.

Normal cerebral ventricular volume growth in childhood.

OBJECTIVE: Normal percentile growth charts for head circumference, length, and weight are well-established tools for clinicians to detect abnormal growth patterns. Currently, no standard exists for evaluating normal size or growth of cerebral ventricular volume. The current standard practice relies on clinical experience for a subjective assessment of cerebral ventricular size to determine whether a patient is outside the normal volume range. An improved definition of normal ventricular volumes would facilitate a more data-driven diagnostic process. The authors sought to develop a growth curve of cerebral ventricular volumes using a large number of normal pediatric brain MR images. METHODS: The authors performed a retrospective analysis of patients aged 0 to 18 years, who were evaluated at their institution between 2009 and 2016 with brain MRI performed for headaches, convulsions, or head injury. Patients were excluded for diagnoses of hydrocephalus, congenital brain malformations, intracranial hemorrhage, meningitis, or intracranial mass lesions established at any time during a 3- to 10-year follow-up. The volume of the cerebral ventricles for each T2-weighted MRI sequence was calculated with a custom semiautomated segmentation program written in MATLAB. Normal percentile curves were calculated using the lambda-mu-sigma smoothing method. RESULTS: Ventricular volume was calculated for 687 normal brain MR images obtained in 617 different patients. A chart with standardized growth curves was developed from this set of normal ventricular volumes representing the 5th, 10th, 25th, 50th, 75th, 90th, and 95th percentiles. The charted data were binned by age at scan date by 3-month intervals for ages 0-1 year, 6-month intervals for ages 1-3 years, and 12-month intervals for ages 3-18 years. Additional percentile values were calculated for boys only and girls only. CONCLUSIONS: The authors developed centile estimation growth charts of normal 3D ventricular volumes measured on brain MRI for pediatric patients. These charts may serve as a quantitative clinical reference to help discern normal variance from pathologic ventriculomegaly.