The objective was to systematically review the medical literature and comprehensively summarize clinical research performed on biomarkers for pediatric traumatic brain injury (TBI) and to summarize the studies that have assessed serum biomarkers acutely in determining intracranial lesions on CT in children with TBI. The search strategy included a literature search of PubMed,(®) MEDLINE,(®) and the Cochrane Database from 1966 to August 2011, as well as a review of reference lists of identified studies. Search terms used included pediatrics, children, traumatic brain injury, and biomarkers. Any article with biomarkers of traumatic brain injury as a primary focus and containing a pediatric population was included. The search initially identified 167 articles. Of these, 49 met inclusion and exclusion criteria and were critically reviewed. The median sample size was 58 (interquartile range 31-101). The majority of the articles exclusively studied children (36, 74%), and 13 (26%) were studies that included both children and adults in different proportions. There were 99 different biomarkers measured in these 49 studies, and the five most frequently examined biomarkers were S100B (27 studies), neuron-specific enolase (NSE) (15 studies), interleukin (IL)-6 (7 studies), myelin basic protein (MBP) (6 studies), and IL-8 (6 studies). There were six studies that assessed the relationship between serum markers and CT lesions. Two studies found that NSE levels ≥15 ng/mL within 24 h of TBI was associated with intracranial lesions. Four studies using serum S100B were conflicting: two studies found no association with intracranial lesions and two studies found a weak association. The flurry of research in the area over the last decade is encouraging but is limited by small sample sizes, variable practices in sample collection, inconsistent biomarker-related data elements, and disparate outcome measures. Future studies of biomarkers for pediatric TBI will require rigorous and more uniform research methodology, common data elements, and consistent performance measures.

This study assessed whether cytoskeletal protein alpha-II spectrin breakdown products (SBDP150, SBDP145, and SBDP120) would identify the presence of aSAH and be associated with severity (GCS score, WFNS grade and survival to hospital discharge). This prospective case-control study, conducted at a tertiary care Level I trauma center, enrolled adult patients with angiography confirmed aSAH who underwent ventriculostomy placement for cerebrospinal fluid (CSF) drainage. There were 40 patients enrolled in the study, 20 with aSAH and 20 control subjects. Patients with aSAH were a mean age of 54 (SD15) and 75% were female. There were significant differences in SBDP150, SBDP145, and SBDP120 CSF levels between patients with and without aSAH (p < 0.001), even in those presenting with a GCS Score of 15 and a WFNS Grade 1. The AUC for distinguishing aSAH from control subjects was 1.0 for SBDP150 and SBDP145, and 0.95 for SBDP120. SBDP150 and SBDP145 both yielded sensitivities and specificities of 100% and SBDP120 was 90% and 100% respectively. Moreover, there were significantly higher levels of SBDP150 and SBDP145 in the non-survivors than in the survivors (p < 0.001). This study demonstrates the potential that SBDP’s have as biomarkers for recognition and severity of aSAH. A larger prospective study is warranted.

Saddle pulmonary embolism are visible thromboembolus straddling the bifurcation of the main pulmonary artery trunk with a 2 week mortality of 5.8% if not treated. At times, saddle pulmonary embolisms can be associated with a wide range of clinical presentations and hemodynamic instability can be relatively uncommon. Our patient is a 50 year old male with no significant past medical history who presented with heartburn and several months of indigestion, early satiety, decrease appetite, and weight loss. CT abdomen/pelvis was performed which showed severely distended stomach secondary to gastric outlet obstruction caused by mass lesion in the pylorus vs duodenal bulb, with bulky lymph nodes at the root of mesentary and retroperitoneum suspicious for metastatic disease. Patient was taken for endoscopy and biopsy. Biopsy was significant for poorly differentiated signet ring cell adenocarcinoma. CT chest/abd/pelvis done for staging and noted bilateral pulmonary filling defects consistent with saddle embolism (Figure1, 2, and 3). Patient was taken for EKOS and put on heparin drip, then bridged to warfarin. Patient was then started on chemotherapy and follows up at the FAU clinic for continuity of care. Incidental PE have been suspected to occur most commonly in patient with brain, ovarian, gastric and pancreatic cancers with the highest risk within 3-6 moths after initial diagnosis. Despite being a rare occurrence in patient's with signet ring cell adenocarcinoma, some studies have shown patient with cancer have more than 4-fold increase risk of dying after an acute thrombotic event than patient with out. Although treatment for Incidental PE is still not clear, most recommend LMWH for 3-6 months. Even so, most studies show no difference in 6 month mortality between cancer patient with IPE and cancer patient diagnosed with PE based on symptoms along with risk of major bleeding or reoccurrence when on treatment. Despite this, IPE, especially when they become symptomatic, are associated with a poor prognosis in cancer patient's. With such uncertainty and potential risk, further research should be addressed with either earlier direction of VTEs or more appropriate management especially in cancers with high risks of developing VTE.

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