Trauma Team Activation for Geriatric Trauma at a Level II Trauma Center: Are the Elderly Under-triaged?

Abstract Geriatric patients often sustain life-threatening injuries from minor trauma. A growing body of research suggests that these patients are often under-triaged in the emergency setting.The purpose of this research was to evaluate whether or not geriatric trauma patients are under-triaged at a community based level II trauma center. 1434 trauma patients over the age of 65 presenting from 2010-2015 were retrospectively reviewed from the Cabell Huntington Hospital trauma registry and analyzed for age, gender, arrival type, ED response, Glasgow Coma Scale (GCS), Injury Severity Score (ISS), injury cause, ICD-9 diagnosis codes, and mortality. Under-triage and over-triage rates were determined using the Cribari method (under-triage = ISS ≥ 16 without full trauma team activation [TTA]; Over-triage = ISS ≤ 15 with full TTA). The under-triage rate was 9.5% (132/1393) with the majority of under-triaged patients having head trauma (n=423). There were 371 head trauma patients with a recorded GCS and analysis shows those with a GCS ≥ 13 had a 1.2% mortality risk (n=326; ISS 10.2), but that risk drastically increases to 60% with GSC ≤ 12 (n=45; ISS 21.5). Of the 45 patients with GSC ≤ 12, only 4% had priority 1 TTA using the current protocol (2/45). The American College of Surgeons-Committee of Trauma (ACS-COT) recommends an acceptable under-triage rate of \u3c 5%. In order to improve geriatric care and reduce under-triage rates, we recommend that an age-based criteria be added to our TTA protocol at our community based Level II trauma center: priority 1 TTA for all patients 65 years or older sustaining head trauma with a GCS ≤ 12 or suspicion of intracranial hemorrhage

Association between molecular subtypes of colorectal cancer and patient survival

BACKGROUND and AIMS: Colorectal cancer (CRC) is a heterogeneous disease that can develop via several pathways. Different CRC subtypes, identified based on tumor markers, have been proposed to reflect these pathways. We evaluated the significance of these previously proposed classifications to survival. METHODS: Participants in the population-based Seattle Colon Cancer Family Registry were diagnosed with invasive CRC from 1998 through 2007 in western Washington State (N = 2706), and followed for survival through 2012. Tumor samples were collected from 2050 participants and classified into 5 subtypes based on combinations of tumor markers: type 1 (microsatellite instability [MSI]-high, CpG island methylator phenotype [CIMP] -positive, positive for BRAF mutation, negative for KRAS mutation); type 2 (microsatellite stable [MSS] or MSI-low, CIMP-positive, positive for BRAF mutation, negative for KRAS mutation); type 3 (MSS or MSI low, non-CIMP, negative for BRAF mutation, positive for KRAS mutation); type 4 (MSS or MSI-low, non-CIMP, negative for mutations in BRAF and KRAS); and type 5 (MSI-high, non-CIMP, negative for mutations in BRAF and KRAS). Multiple imputation was used to impute tumor markers for those missing data on 1-3 markers. We used Cox regression to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations of subtypes with disease-specific and overall mortality, adjusting for age, sex, body mass, diagnosis year, and smoking history. RESULTS: Compared with participants with type 4 tumors (the most predominant), participants with type 2 tumors had the highest disease-specific mortality (HR = 2.20, 95% CI: 1.47-3.31); subjects with type 3 tumors also had higher disease-specific mortality (HR = 1.32, 95% CI: 1.07-1.63). Subjects with type 5 tumors had the lowest disease-specific mortality (HR = 0.30, 95% CI: 0.14-0.66). Associations with overall mortality were similar to those with disease-specific mortality. CONCLUSIONS: Based on a large, population-based study, CRC subtypes, defined by proposed etiologic pathways, are associated with marked differences in survival. These findings indicate the clinical importance of studies into the molecular heterogeneity of CRC

Monoallelic NTHL1 Loss-of-Function Variants and Risk of Polyposis and Colorectal Cancer

Contains fulltext : 228713.pdf (Publisher’s version ) (Open Access

Teen perception of texting and driving in rural West Virginia

In the last decade, texting and driving has evolved into a serious problem among the adolescent population. The goal of this study was to determine if education can effectively raise awareness of the dangers of texting and driving and positively influence the behavior of rural West Virginia teens. A 25 question survey designed to asses teen driving behavior was administered to 143 rural West Virginia high school students before and after and educational session. The educational session was designed to explain how texting and driving impairs driving ability and show graphic images of accidents and injuries that resulted from this behavior. Pre and post-lecture survey responses were then analyzed. The survey results revealed that texting and driving is highly prevalent among rural West Virginia teens, with 57% of teens admitting to this behavior. Around 73% of teens agreed that texting and driving was very dangerous, but many continued to do so regardless. Additionally, 59% admitted to talking on the phone while driving, and 11% admitted to drinking and driving. A single lecture was not observed to reduce texting and driving behavior among the study population. More research is needed to establish an effective method to reduce this dangerous behavior

Circulating 25-Hydroxyvitamin D Concentration and Risk of Breast, Prostate, and Colorectal Cancers: The Melbourne Collaborative Cohort Study.

BACKGROUND: The role of vitamin D in cancer risk remains controversial, and limited data exist on associations between vitamin D and subtypes of specific cancers. We investigated associations between circulating 25-hydroxyvitamin D (25(OH)D) and risk of colorectal, breast, and prostate cancers, including subtypes. METHODS: A case-cohort study within the Melbourne Collaborative Cohort Study included 547 colorectal, 634 breast, and 824 prostate cancers, and a sex-stratified random sample of participants (n = 2,996). Concentration of 25(OH)D in baseline-dried blood spots was measured using LC-MS/MS. Cox regression yielded adjusted HRs and 95% confidence intervals (CI) for each cancer in relation to plasma-equivalent 25(OH)D concentration. Associations by stage and BRAF/KRAS status for colorectal cancer, estrogen receptor status for breast cancer, and aggressiveness for prostate cancer were examined in competing risks models. RESULTS: 25(OH)D concentrations were inversely associated with risk of colorectal cancer [highest vs. lowest 25(OH)D quintile: HR, 0.71; 95% confidence interval (CI), 0.51-0.98], which was limited to women (HR, 0.52; 95% CI, 0.33-0.82). Circulating 25(OH)D was also inversely associated with BRAF V600E-positive colorectal cancer (per 25 nmol/L increment: HR, 0.71; 95% CI, 0.50-1.01). There were no inverse associations with breast cancer (HR, 0.98; 95% CI, 0.70-1.36) or prostate cancer (HR, 1.11; 95% CI, 0.82-1.48). CONCLUSIONS: Circulating 25(OH)D concentration was inversely associated with colorectal cancer risk for women, but not with risk of breast cancer or prostate cancer. IMPACT: Vitamin D might play a role in preventing colorectal cancer. Further studies are required to confirm whether vitamin D is associated with specific tumor subtypes

Colorectal cancer linkage on chromosomes 4q21, 8q13, 12q24, and 15q22

A substantial proportion of familial colorectal cancer (CRC) is not a consequence of known susceptibility loci, such as mismatch repair (MMR) genes, supporting the existence of additional loci. To identify novel CRC loci, we conducted a genome-wide linkage scan in 356 white families with no evidence of defective MMR (i.e., no loss of tumor expression of MMR proteins, no microsatellite instability (MSI)-high tumors, or no evidence of linkage to MMR genes). Families were ascertained via the Colon Cancer Family Registry multi-site NCI-supported consortium (Colon CFR), the City of Hope Comprehensive Cancer Center, and Memorial University of Newfoundland. A total of 1,612 individuals (average 5.0 per family including 2.2 affected) were genotyped using genome-wide single nucleotide polymorphism linkage arrays; parametric and non-parametric linkage analysis used MERLIN in a priori-defined family groups. Five lod scores greater than 3.0 were observed assuming heterogeneity. The greatest were among families with mean age of diagnosis less than 50 years at 4q21.1 (dominant HLOD = 4.51, α = 0.84, 145.40 cM, rs10518142) and among all families at 12q24.32 (dominant HLOD = 3.60, α = 0.48, 285.15 cM, rs952093). Among families with four or more affected individuals and among clinic-based families, a common peak was observed at 15q22.31 (101.40 cM, rs1477798; dominant HLOD = 3.07, α = 0.29; dominant HLOD = 3.03, α = 0.32, respectively). Analysis of families with only two affected individuals yielded a peak at 8q13.2 (recessive HLOD = 3.02, α = 0.51, 132.52 cM, rs1319036). These previously unreported linkage peaks demonstrate the continued utility of family-based data in complex traits and suggest that new CRC risk alleles remain to be elucidated. © 2012 Cicek et al

Clinicopathologic Risk Factor Distributions for MLH1 Promoter Region Methylation in CIMP-Positive Tumors

The CpG Island Methylator Phenotype (CIMP) is a major molecular pathway in colorectal cancer (CRC). Approximately 25% to 60% of CIMP tumors are microsatellite unstable (MSI-H) due to DNA hypermethylation of the MLH1 gene promoter. Our aim was to determine if the distributions of clinicopathologic factors in CIMP-positive tumors with MLH1 DNA methylation differed from those in CIMP-positive tumors without DNA methylation of MLH1