Rotational thromboelastometry (ROTEM) can only detect high-degree hyperfibrinolysis (HF), despite being frequently used in trauma patients. We investigated whether considering FIBTEM HF (the presence of maximal lysis (ML) > 15%) could increase ROTEM-based HF detection’s sensitivity. This observational cohort study was performed at a level 1 trauma centre. Trauma patients with an Injury Severity Score (ISS) > 15 who underwent ROTEM in the emergency department between 2016 and 2017 were included. EXTEM HF was defined as ML > 15% in EXTEM. We compared mortality rates between EXTEM HF, FIBTEM HF, and non-HF patient groups. Overall, 402 patients were included, of whom 45% were men (mean age, 52.5 years; mean ISS, 27). The EXTEM HF (n = 37), FIBTEM HF (n = 132), and non-HF (n = 233) groups had mortality rates of 81.1%, 22.3%, and 10.3%, respectively. The twofold difference in mortality rates between the FIBTEM HF and non-HF groups remained statistically significant after Bonferroni correction (P = 0.01). On multivariable Cox regression analysis, FIBTEM HF was independently associated with in-hospital mortality (adjusted hazard ratio 2.15, 95% confidence interval 1.21–3.84, P = 0.009). Here, trauma patients with FIBTEM HF had significantly higher mortality rates than those without HF. FIBTEM be a valuable diagnostic method to improve HF detection’s sensitivity in trauma patients.

Introduction: Chlorfenapyr is a pyrrole-based pro-insecticide. The main activity of this agent is the inhibition of adenosine triphosphate synthesis, and it is used in agriculture to control several insects and mites resistant to carbamate, organophosphate and pyrethroid insecticide. The World Health Organization classifies this agent as a class II toxin (moderately hazardous). Case presentation: All previously reported cases of chlorfenapyr poisoning in humans occurred following oral ingestion except one case involving exposure to chlorfenapyr vapour. Discussion: In this report, we describe a case of chlorfenapyr intoxication after skin exposure in a 49-year-old patient who died 5 days after exposure. Conclusion: This case demonstrates that similar to oral ingestion, dermal absorption of chlorfenapyr may also be fatal.

We aimed to examine the utility of the Poison Severity Score (PSS) and Sequential Organ Failure Assessment (SOFA) score as early prognostic predictors of short-term outcomes in patients with carbon monoxide (CO) poisoning. We hypothesized that both the PSS and the SOFA score would be useful prognostic tools. This was retrospective observational study of patients with CO poisoning who presented to the emergency department and were admitted for more than 24 hours. We calculated PSS, the initial SOFA score, a second (2^nd) SOFA score, and a 24-hour delta SOFA score. The primary outcome was reported as the cerebral performance category (CPC) scale score at discharge. We classified those with CPC 1–2 as the good outcome group and those with CPC 3–5 as the poor outcome group. This study included 192 patients: 174 (90.6%) belonged to the good outcome group, whereas 18 (9.4%) belonged to the poor outcome group. The PSS (1.00 [0.00, 1.00] vs 3.00 [3.00, 3.00], p < 0.001), initial SOFA (1.00 [0.00, 2.00] vs 4.00 [3.25, 6.00], p < 0.001), 2^nd SOFA score (0.00 [0.00, 1.00] vs 4.00 [3.00, 7.00], p < 0.001), and 24-hour delta SOFA score (-1.00 [-1.00, 0.00] vs 0.00 [-1.00, 1.00], p = 0.047) of the good outcome group were significantly higher than those of the poor outcome group. The areas under the receiver operating characteristic curve for PSS and the initial SOFA and 2^nd SOFA scores were 0.977 (95% confidence interval [CI] 0.944–0.993), 0.945 (95% CI 0.903–0.973), and 0.978 (95% CI 0.947–0.994), respectively. The PSS, initial SOFA score, and 2^nd SOFA score predict acute poor outcome accurately in patients with CO poisoning.

It is known that an excess or deficiency of selenium (Se) causes abnormalities in hair. We evaluated changes in the hair follicles associated with Se imbalance in a C57BL/6 mouse model to better understand the role of Se in hair growth. Fifteen C57BL/6 mice were assigned to diets providing excessive, adequate, or deficient amounts of Se. Alopecia with poliosis was observed in the groups receiving either excessive or deficient selenium. Skin biopsy from alopecia patches showed increased telogen hair follicles with epidermal atrophy. There was a significant decrease of anti-apoptotic Bcl-2 and an increase of pro-apoptotic Bax in the excessive-Se group compared with the adequate group. We suggest that alopecia with poliosis is caused by changes in the hair follicle cycle due to the imbalance of Se and partially influenced by the decrease of the ratio of Bcl-2/Bax, which is associated with induction of apoptosis of keratinocytes.