Scalp edema: don't forget sunburn in children.

2012

Shah B, Yavuz ST, Tekşam O.

Source

Department of Pediatrics, Hacettepe University Faculty of Medicine, Ankara, Turkey.

Abstract

Scalp edema is an uncommon and striking finding in children that may alarm both parents and physicians. The objectives of this case report were to raise awareness among pediatric emergency physicians of the unusual presentation of sunburn as scalp edema. We present the case of an eight-year-old boy with sunburn of the head, presenting with scalp and face edema. Pitting edema and erythema were dominant on the forehead. Shaving of the boy's head the day before the symptoms was the most striking issue, and the sunburn healed gradually without any complications. Healthcare professionals should be aware of this condition, and the diagnosis of sunburn must be kept in mind in otherwise healthy-looking patients with a unique history.

PubMed

Purinergic 2Y1 Receptor stimulation decreases cerebral edema and reactive gliosis in a Traumatic Brain Injury Model.

Oct 2012

Watts LT, Sprague S, Zheng W, Garling RJ, Jimenez D, Digicaylioglu M, Lechleiter JD.

Source

University of TExas Health Science Center at San Antonio, Department of Cellular and Structural Biology, 7703 Floyd Curl Drive, San Antonio, Texas, United States, 78229, 210-567-8186, 210-567-8152; wattsl@uthscsa.edu.

Abstract

Traumatic brain injury (TBI) is the leading cause of death and disability in children and young adults. Neuroprotective agents that may promote repair or counteract damage following injury do not currently exist. We recently reported that stimulation of the purinergic receptor subtype P2Y1R using 2-methylthioladenosine 5' diphosphate (2MeSADP) significantly reduced cytotoxic edema induced by photothrombosis (Zheng et al., 2010). Here, we tested whether P2Y1R stimulation was neuroprotective following TBI. A controlled closed head injury model was established for mice using a pneumatic impact device. Brains were harvested at 1, 3 or 7 days post-injury and assayed for morphological changes by immunocytochemistry, western blot analysis and wet/dry weight. Cerebral edema and expression of both aquaporin type 4 (AQ4) and glial fibrillary acidic protein (GFAP) were increased at all time points examined. Immunocytochemical measurements in both cortical and hippocampal slices also revealed significant neuronal swelling and reactive gliosis. Treatment of mice with 2MeSADP (100 µM) or MRS2365 (100 µM) thirty minutes after trauma significantly reduced all post-injury symptoms of TBI including edema, neuronal swelling, reactive gliosis and AQ4 expression. The neuroprotective effect was lost in IP3R2-/- mice treated with 2MeSADP. Immunocytochemical labeling of brain slices confirmed that P2Y1R expression was defined to cortical and hippocampal astrocytes, but not neurons. Taken together, the data show that stimulation of astrocytic P2Y1Rs significantly reduces brain injury following acute trauma and is mediated by the IP3-signaling pathway.

Mary Ann Liebert

Nitric Oxide-Associated Pulmonary Edema in Children With Pulmonary Venous Hypertension.

Oct 2012

Baird JS, Havalad V, Aponte-Patel L, Ravindranath TM, October TW, Starc TJ, Smerling AJ.

Source

College of Physicians and Surgeons, Children's Hospital of New York-Presbyterian, Columbia University, 3959 Broadway, CHN 10-24, New York, NY, 10032, USA, jsb106@columbia.edu.

Abstract

Nitric oxide (NO)-associated pulmonary edema is rarely reported in children; in adults, it is often associated with left-sided heart failure. We report a case series of children with NO-associated pulmonary edema, which was defined as new multilobar alveolar infiltrates and worsening hypoxemia within 24 h of initiation or escalation of NO and radiologic or clinical improvement after NO discontinuation. We identified six patients (0.4-4 years old) with ten episodes of NO-associated pulmonary edema. Diagnoses included atrioventricular canal defect with mitral valve disease (n = 2), pulmonary atresia and major aorta-pulmonary collateral arteries (n = 2), total anomalous pulmonary venous return (n = 1), and pulmonary veno-occlusive disease (n = 1). All patients had evidence of pulmonary venous hypertension, and two had mitral valve disease resulting in clinical evidence of left-sided heart failure. Pulmonary edema improved or resolved within 24 h of discontinuing NO. At cardiac catheterization, mean left atrial pressure was <15 artery="artery" disease="disease" in="in" mitral="mitral" mmhg="mmhg" nbsp="nbsp" none="none" occlusion="occlusion" of="of" patients="patients" pressure="pressure" pulmonary="pulmonary" three="three" valve="valve" was="was" whereas="whereas" with="with">15 mmHg in two of five patients. In conclusion, we describe six young children with NO-associated pulmonary edema and pulmonary venous hypertension. Only two of these children had left-sided heart failure: Left atrial pressure as well as pulmonary artery occlusion pressure may not be helpful in identifying children at risk for NO-associated pulmonary edema.

Springerlink