Open Reduction and Internal Fixation of Pediatric Scapula Fractures: A Report of 2 Cases.

CASE: Two pediatric patients with displaced, extra-articular scapula fractures who underwent surgery because of concerns for persistent deformity and decreased function with continued nonoperative management. CONCLUSION: We advocate careful consideration of all patient factors and treatment options when addressing pediatric scapula fractures. Specific fracture patterns with altered shoulder girdle mechanics may warrant surgical intervention to restore anatomic alignment and stability.

Outcomes research: Mandibular fractures in the diabetic population.

OBJECTIVE: The study aimed to examine the management and outcomes of mandibular fractures in patients with diabetes mellitus by examining the injury modalities, treatment methods, and complications. METHODS: The study conducted was a retrospective case review of patients admitted to Memorial Hermann Hospital from 2007 to 2011 with diagnoses of diabetes mellitus and mandibular fracture. The electronic medical records were reviewed for patient demographics, injury data, surgery methodology, treatment variables, and complications. RESULTS: Out of the 34 diabetic patients, the average age was 52 with the majority of the fractures being the result of falls, 12 (35.3%). Of the 63 total fractures, 24 (38.1%) fractures were repaired through closed reduction and 39 (61.9%) fractures required open reduction with internal fixation. 17 (50.0%) patients had at least one complication following mandibular fracture repair. The most common complications in this sample population included nerve injury, 7 (20.6%), infection, 7 (20.6%), wound dehiscence with or without hardware exposure, 6 (17.7%), and malocclusion, 5 (14.7%). CONCLUSION: When compared to the limited published data our findings imply that diabetic patients with mandibular fractures present as an older population than commonly seen with mandibular fractures and suggest a higher overall rate of complications.

Randomized trial to evaluate nutritional status and absorption of enteral feeding after brain death.

CONTEXT: Catecholamines and inflammatory mediators, with elevated levels after brain death, are associated with reduced function and survival of transplanted organs. Enteral nutrition reduces tissue damage and may benefit organs. OBJECTIVE: To evaluate the effects of immunomodulating enteral nutrition in organ donors. DESIGN: Prospective, randomized, open-label study. SETTING: Intensive care unit. PATIENTS: Thirty-six brain-dead organ donors. INTERVENTIONS: Donors were randomized to receive enteral nutrition containing omega-3 polyunsaturated fatty acid, antioxidants, and glutamine or standard care (fasting). Donors received hormonal replacement therapy of corticosteroid, levothyroxine, dextrose, and insulin. MAIN OUTCOME MEASURES: Gastrointestinal assimilation (measured by 13 carbon-labeled uracil breath analysis), quantity of organs recovered, resting energy expenditure, urine level of urea nitrogen, and serum levels of albumin, prealbumin, interleukin 6, tumor necrosis factor-α, and C-reactive protein were evaluated. RESULTS: Thirteen patients (36%) assimilated 13C-labeled uracil. Resting energy expenditure was significantly higher than predicted between 10 and 14 hours after baseline in 33 donors (P= .007). Other measures were not conclusively different between fed and fasting groups. No adverse events occurred that were related to the enteral feeding. CONCLUSIONS: About 30% of donors metabolized 13C-labeled uracil, although no difference in oxidation rate was found between fasting and fed donors. Corticosteroid administration lowers plasma levels of interleukin 6 and most likely contributes to greater than predicted resting energy expenditure. Thus energy needs may not be met during fasting if hormones are given. Consequences of this possible energy deficit warrant further study.

Human mild traumatic brain injury decreases circulating branched-chain amino acids and their metabolite levels.

The pathophysiology of traumatic brain injury (TBI) is complex and not well understood. Because pathophysiology has ramifications for injury progression and outcome, we sought to identify metabolic cascades that are altered after acute human mild and severe TBI. Because catabolism of branched-chain amino acids (BCAAs; i.e., valine, isoleucine, and leucine) leads to glucose and energy metabolism, and neurotransmitter synthesis and availability, we investigated BCAA metabolites in plasma samples collected within 24 h of injury from mild TBI (Glasgow Coma Scale [GCS] score >12), severe TBI (GCS ≤8), orthopedic injury, and healthy volunteers. We report decreased levels of all three BCAAs in patients with mild TBI relative to healthy volunteers, while these BCAAs levels in patients with severe TBI were further reduced compared with all groups. Orthopedic patients exhibited reductions in BCAA comparable to those in patients with mild TBI. The decrease in patients with mild and severe TBI persisted for derivatives of BCAA catabolic intermediates. Only plasma levels of methylglutarylcarnitine, a derivative of a leucine metabolite, were increased in patients with severe TBI compared with all other groups. Notably, logistic regression combination of three BCAA metabolites whose levels were changed by 24 h post-injury provided prognostic value (area under the curve=0.92) in identifying patients with severe TBI in whom elevated intracranial pressure (≥25 mm Hg) developed. These changes suggest alteration of BCAA metabolism after TBI may contribute to decreased energy production and neurotransmitter synthesis and may contribute to TBI pathophysiology. Supplementation of BCAAs and/or their metabolites may reduce TBI pathology and improve outcome.

Human traumatic brain injury alters circulating L-arginine and its metabolite levels: possible link to cerebral blood flow, extracellular matrix remodeling, and energy status.

Altered cerebral blood flow, cell-matrix interactions, and energy metabolism are secondary pathologies contributing to outcome after traumatic brain injury (TBI). Because L-arginine serves as the precursor for metabolites that are critical to these processes, we measured their plasma levels using LC-MS/GC-MS. Samples were collected from healthy volunteers (n=20), and patients with mild TBI (n=18), severe TBI (n=20), or orthopedic injury without a TBI (n=15), within the first 24 hours of injury. Severe TBI levels of L-arginine, citrulline, ornithine, and hydroxyproline were significantly reduced compared to the other groups. In contrast, the levels of plasma creatine were significantly increased in severe TBI patients compared to healthy volunteers and orthopedic injury subjects. Of interest, the levels of creatine were found to be higher in severe TBI patients (GCS score ≤8) whose intracranial pressure (ICP) remained below 25 mm Hg throughout the 5-day monitoring period, compared to TBI patients (GCS score ≤8) who subsequently developed elevated ICP (≥25 mm Hg). The changes in L-arginine and its metabolite levels were not detected in subjects with mild TBI. The altered levels of arginine and its metabolites may contribute to secondary pathologies following severe TBI, and plasma levels of creatine may have prognostic value in identifying patients at risk for ICP elevation.

Human traumatic brain injury alters plasma microRNA levels.

Circulating microRNAs (miRNAs) present in the serum/plasma are characteristically altered in many pathological conditions, and have been employed as diagnostic markers for specific diseases. We examined if plasma miRNA levels are altered in patients with traumatic brain injury (TBI) relative to matched healthy volunteers, and explored their potential for use as diagnostic TBI biomarkers. The plasma miRNA profiles from severe TBI patients (Glasgow Coma Scale [GCS] score ≤8) and age-, gender-, and race-matched healthy volunteers were compared by microarray analysis. Of the 108 miRNAs identified in healthy volunteer plasma, 52 were altered after severe TBI, including 33 with decreased and 19 with increased relative abundance. An additional 8 miRNAs were detected only in the TBI plasma. We used quantitative RT-PCR to determine if plasma miRNAs could identify TBI patients within the first 24 h post-injury. Receiver operating characteristic curve analysis indicated that miR-16, miR-92a, and miR-765 were good markers of severe TBI (0.89, 0.82, and 0.86 AUC values, respectively). Multiple logistic regression analysis revealed that combining these miRNAs markedly increased diagnostic accuracy (100% specificity and 100% sensitivity), compared to either healthy volunteers or orthopedic injury patients. In mild TBI patients (GCS score > 12), miR-765 levels were unchanged, while the plasma levels of miR-92a and miR-16 were significantly increased within the first 24 h of injury compared to healthy volunteers, and had AUC values of 0.78 and 0.82, respectively. Our results demonstrate that circulating miRNA levels are altered after TBI, providing a rich new source of potential molecular biomarkers. Plasma-derived miRNA biomarkers, used in combination with established clinical practices such as imaging, neurocognitive, and motor examinations, have the potential to improve TBI patient classification and possibly management.

Serum IL-6: a candidate biomarker for intracranial pressure elevation following isolated traumatic brain injury.

BACKGROUND: Increased intracranial pressure (ICP) is a serious, life-threatening, secondary event following traumatic brain injury (TBI). In many cases, ICP rises in a delayed fashion, reaching a maximal level 48-96 hours after the initial insult. While pressure catheters can be implanted to monitor ICP, there is no clinically proven method for determining a patient's risk for developing this pathology. METHODS: In the present study, we employed antibody array and Luminex-based screening methods to interrogate the levels of inflammatory cytokines in the serum of healthy volunteers and in severe TBI patients (GCSor= 25 mm Hg had significantly higher IL-6 levels within the first 17 hours of injury as compared to the patients whose ICP remained 128 pg/ml correctly identified 85% of isolated TBI patients who subsequently developed elevated ICP, and values between these cut-off values correctly identified 75% of all patients whose ICP remained