Occult Pneumothoraces in Children With Blunt Torso Trauma

Objectives Plain chest x‐ray (CXR) is often the initial screening test to identify pneumothoraces in trauma patients. Computed tomography (CT) scans can identify pneumothoraces not seen on CXR (“occult pneumothoraces”), but the clinical importance of these radiographically occult pneumothoraces in children is not well understood. The objectives of this study were to determine the proportion of occult pneumothoraces in injured children and the rate of treatment with tube thoracostomy among these children. Methods This was a planned substudy from a large prospective multicenter observational cohort study of children younger than 18 years old evaluated in emergency departments (EDs) in the Pediatric Emergency Care Applied Research Network (PECARN) for blunt torso trauma from May 2007 to January 2010. Children with CXRs as part of their trauma evaluations were included for analysis. The faculty radiologist interpretations of the CXRs and any subsequent imaging studies, including CT scans, were reviewed for the absence or presence of pneumothoraces. An “occult pneumothorax” was defined as a pneumothorax that was not identified on CXR, but was subsequently demonstrated on cervical, chest, or abdominal CT scan. Rates of pneumothoraces and placement of tube thoracostomies and rate differences with 95% confidence intervals (CIs) were calculated. Results Of 12,044 enrolled in the parent study, 8,020 (67%) children (median age = 11.3 years, interquartile range [IQR] = 5.3 to 15.2 years) underwent CXRs in the ED, and these children make up the study population. Among these children, 4,276 had abdominal CT scans performed within 24 hours. A total of 372 of 8,020 children (4.6%; 95% CI = 4.2% to 5.1%) had pneumothoraces identified by CXR and/or CT. The CXRs visualized pneumothoraces in 148 patients (1.8%; 95% CI = 1.6% to 2.2%), including one false‐positive pneumothorax, which was identified on CXR, but was not demonstrated on CT. Occult pneumothoraces were present in 224 of 372 (60.2%; 95% CI = 55.0% to 65.2%) children with pneumothoraces. Tube thoracostomies were performed in 85 of 148 (57.4%; 95% CI = 49.0% to 65.5%) children with pneumothoraces on CXR and in 35 of 224 (15.6%; 95% CI = 11.1% to 21.1%) children with occult pneumothoraces (rate difference = –41.8%; 95% CI = –50.8 to –32.3%). Conclusions In pediatric patients with blunt torso trauma, pneumothoraces are uncommon, and most are not identified on the ED CXR. Nearly half of pneumothoraces, and most occult pneumothoraces, are managed without tube thoracostomy. Observation, including in children requiring endotracheal intubation, should be strongly considered during the initial management of children with occult pneumothoraces. Resumen Objetivos La radiografía de tórax simple (RXT) es a menudo la prueba de despistaje inicial para identificar los neumotórax en los pacientes con traumatismo. La tomografía computarizada (TC) puede identificar neumotórax no vistos en la RXT (“neumotórax ocultos”), aunque la importancia clínica de estos neumotórax radiográficamente ocultos en los niños no está muy estudiada. Los objetivos de este estudio fueron determinar la proporción de neumotórax ocultos en los niños accidentados y el porcentaje de tratamiento con tubo de toracostomía en estos niños. Metodología Subestudio diseñado a partir de un gran estudio observacional de cohorte prospectivo multicéntrico de niños menores de 18 años atendidos en los servicios de urgencias (SU) de la Pediatric Emergency Care Applied Research Network (PECARN) que habían sido evaluados por traumatismo torácico cerrado de mayo de 2007 a enero de 2010. Se incluyeron en el análisis los niños en los que la RXT fue parte de la evaluación inicial del traumatismo. Las interpretaciones del radiólogo de las RXT y de cualquier estudio de imagen posterior, incluyendo a TC, se revisaron para la ausencia o presencia de neumotórax. Se definió “neumotórax oculto” como un neumotórax que no fue identificado en la RXT pero que fue posteriormente visualizado en la TC abdominal, torócica o cervical. Se calcularon los porcentajes de neumotórax e inserción de tubo de toracostomía y las diferencias de sus porcentajes con los intervalos de confianza (IC) al 95%. Resultados De los 12.044 incluidos en el estudio principal, se llevo a cabo una RXT en el SU en 8.020 (67%) niños (mediana de edad 11,3 años, rango intercuartílico 5,3 a 15,2), que constituyeron la población de estudio. De estos niños, 4.276 tuvieron una TC realizada en las primeras 24 horas. En 372 de los 8.020 niños (4,6%; IC 95% = 4,2% a 5,1%) se identificó un neumotórax en la RXT y/o la TC. La RXT mostró neumotórax en 148 pacientes (1,8%; IC 95% = 1,6% a 2,2%), incluyendo un falso positivo de neumotórax, que fue identificado en la RXT pero que no fue demostrado en la TC. Los neumotórax ocultos estuvieron presentes en 224 de los 372 niños con neumotórax (60,2%; IC 95% = 55,0% a 65,2%). Se insertaron tubos de toracostomía en 85 de los 148 niños con neumotórax en la RXT (57,4%; IC 95% = 49,0% a 65,5%), y en 35 de los 224 niños con neumotórax oculto (15,6%; IC 95% = 11,1% a 21,1%; diferencia de porcentajes ‐41,8%; IC 95% = ‐50,8 a ‐32,3%). Conclusiones En los pacientes pediátricos con traumatismo torácico cerrado, los neumotórax son poco frecuentes, y la mayoría no son identificados en la RXT en el SU. Casi la mitad de los neumotórax, y la mayoría de los neumotórax ocultos son manejados sin tubo de toracostomía. La observación, incluyendo en los niños que requieren intubación endotraqueal, debería ser especialmente considerada durante el manejo inicial de los niños con neumotórax ocultos.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106913/1/acem12344.pd

Cerebral Metabolic Alterations in Rats With Diabetic Ketoacidosis: Effects of Treatment With Insulin and Intravenous Fluids and Effects of Bumetanide

ObjectiveCerebral edema is a life-threatening complication of diabetic ketoacidosis (DKA) in children. Recent data suggest that cerebral hypoperfusion and activation of cerebral ion transporters may be involved, but data describing cerebral metabolic alterations during DKA are lacking.Research design and methodsWe evaluated 50 juvenile rats with DKA and 21 normal control rats using proton and phosphorus magnetic resonance spectroscopy (MRS). MRS measured cerebral intracellular pH and ratios of metabolites including ATP/inorganic phosphate (Pi), phosphocreatine (PCr)/Pi, N-acetyl aspartate (NAA)/creatine (Cr), and lactate/Cr before and during DKA treatment. We determined the effects of treatment with insulin and intravenous saline with or without bumetanide, an inhibitor of Na-K-2Cl cotransport, using ANCOVA with a 2 x 2 factorial study design.ResultsCerebral intracellular pH was decreased during DKA compared with control (mean +/- SE difference -0.13 +/- 0.03; P < 0.001), and lactate/Cr was elevated (0.09 +/- 0.02; P < 0.001). DKA rats had lower ATP/Pi and NAA/Cr (-0.32 +/- 0.10, P = 0.003, and -0.14 +/- 0.04, P < 0.001, respectively) compared with controls, but PCr/Pi was not significantly decreased. During 2-h treatment with insulin/saline, ATP/Pi, PCr/Pi, and NAA/Cr declined significantly despite an increase in intracellular pH. Bumetanide treatment increased ATP/Pi and PCr/Pi and ameliorated the declines in these values with insulin/saline treatment.ConclusionsThese data demonstrate that cerebral metabolism is significantly compromised during DKA and that further deterioration occurs during early DKA treatment--consistent with possible effects of cerebral hypoperfusion and reperfusion injury. Treatment with bumetanide may help diminish the adverse effects of initial treatment with insulin/saline

Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis

Mutations in the retinoblastoma tumor suppressor gene Rb are involved in many forms of human cancer. In this study, we investigated the early consequences of inactivating Rb in the context of cellular reprogramming. We found that Rb inactivation promotes the reprogramming of differentiated cells to a pluripotent state. Unexpectedly, this effect is cell cycle independent, and instead reflects direct binding of Rb to pluripotency genes, including Sox2 and Oct4, which leads to a repressed chromatin state. More broadly, this regulation of pluripotency networks and Sox2 in particular is critical for the initiation of tumors upon loss of Rb in mice. These studies therefore identify Rb as a global transcriptional repressor of pluripotency networks, providing a molecular basis for previous reports about its involvement in cell fate pliability, and implicate misregulation of pluripotency factors such as Sox2 in tumorigenesis related to loss of Rb function

Existence of the magnetization plateau in a class of exactly solvable Ising-Heisenberg chains

The mapping transformation technique is applied to obtain exact results for the spin-1/2 and spin-S (S=1/2,1) Ising-Heisenberg antiferromagnetic chain in the presence of an external magnetic field. Within this scheme, a field-induced first-order metamagnetic transition resulting in multiplateau magnetization curves, is investigated in detail. It is found that the scenario of the plateau formation depends fundamentally on the ratio between Ising and Heisenbrg interaction constants, as well as on the anisotropy strength of the XXZ Heisenberg interaction.Comment: 16 pages, 10 figures, submitted to J. Phys: Condens. Matte

Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis

Mutations in the retinoblastoma tumor suppressor gene Rb are involved in many forms of human cancer. In this study, we investigated the early consequences of inactivating Rb in the context of cellular reprogramming. We found that Rb inactivation promotes the reprogramming of differentiated cells to a pluripotent state. Unexpectedly, this effect is cell cycle independent, and instead reflects direct binding of Rb to pluripotency genes, including Sox2 and Oct4, which leads to a repressed chromatin state. More broadly, this regulation of pluripotency networks and Sox2 in particular is critical for the initiation of tumors upon loss of Rb in mice. These studies therefore identify Rb as a global transcriptional repressor of pluripotency networks, providing a molecular basis for previous reports about its involvement in cell fate pliability, and implicate misregulation of pluripotency factors such as Sox2 in tumorigenesis related to loss of Rb function

Imaging of ependymomas: MRI and CT

The imaging features of intracranial and spinal ependymoma are reviewed with an emphasis on conventional magnetic resonance imaging (MRI), perfusion MRI and proton magnetic resonance spectroscopy, and computed tomography. Imaging manifestations of leptomeningeal dissemination of disease are described. Finally, salient imaging features obtained in the postoperative period to evaluate completeness of surgical resection, and thereafter for long-term surveillance for disease recurrence, are reviewed

Brain connectivity changes in autosomal recessive Parkinson Disease: a model for the sporadic form

Biallelic genetic mutations in the Park2 and PINK1 genes are frequent causes of autosomal recessive PD. Carriers of single heterozygous mutations may manifest subtle signs of disease, thus providing a unique model of preclinical PD. One emerging hypothesis suggests that non-motor symptom of PD, such as cognitive impairment may be due to a distributed functional disruption of various neuronal circuits. Using resting-state functional MRI (RS-fMRI), we tested the hypothesis that abnormal connectivity within and between brain networks may account for the patients' cognitive status. Eight homozygous and 12 heterozygous carriers of either PINK1 or Park2 mutation and 22 healthy controls underwent RS-fMRI and cognitive assessment. RS-fMRI data underwent independent component analysis to identify five networks of interest: default-mode network, salience network, executive network, right and left fronto-parietal networks. Functional connectivity within and between each network was assessed and compared between groups. All mutation carriers were cognitively impaired, with the homozygous group reporting a more prominent impairment in visuo-spatial working memory. Changes in functional connectivity were evident within all networks between homozygous carriers and controls. Also heterozygotes reported areas of reduced connectivity when compared to controls within two networks. Additionally, increased inter-network connectivity was observed in both groups of mutation carriers, which correlated with their spatial working memory performance, and could thus be interpreted as compensatory. We conclude that both homozygous and heterozygous carriers exhibit pathophysiological changes unveiled by RS-fMRI, which can account for the presence/severity of cognitive symptom