Histidine-rich Glycoprotein Could Be an Early Predictor of Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Cerebral vasospasm (CVS) is a major contributor to the high morbidity and mortality of aneurysmal subarachnoid hemorrhage (aSAH) patients. We measured histidine-rich glycoprotein (HRG), a new biomarker of aSAH, in cerebrospinal fluid (CSF) to investigate whether HRG might be an early predictor of CVS. A total of seven controls and 14 aSAH patients (8 males, 6 females aged 53.4±15.4 years) were enrolled, and serial CSF and serum samples were taken. We allocated these samples to three phases (T1-T3) and measured HRG, interleukin (IL)-6, fibrinopeptide A (FpA), and 8-hydroxy-2’-deoxyguanosine (8OHdG) in the CSF, and the HRG in serum. We also examined the release of HRG in rat blood incubated in artificial CSF. In contrast to the other biomarkers examined, the change in the CSF HRG concentration was significantly different between the nonspasm and spasm groups (p<0.01). The rat blood/CSF model revealed a time course similar to that of the human CSF samples in the non-spasm group. HRG thus appears to have the potential to become an early predictor of CVS. In addition, the interaction of HRG with IL-6, FpA, and 8OHdG may form the pathology of CVS

Indication for mild therapeutic hypothermia based on an initial Glasgow Coma Scale motor score

Although neurological evaluation using the Glasgow Coma Scale motor score is mandatory for post-cardiac arrest patients, further study is required to determine if this score can be used as an indicator for mild therapeutic hypothermia. Although the current study conducted by Natsukawa et al. presents interesting data, there are some critical issues regarding study design, selection bias, and interpretation of study results that should be pointed out

Neurological outcomes associated with prehospital advanced airway management in patients with out-of-hospital cardiac arrest due to foreign body airway obstruction

Objectives: Several studies have examined the association between advanced airway management (AAM) and survival for arrest that is non-shockable, noncardiac in origin, or due to suffocation; however, the efficacy of prehospital AAM compared with no AAM following foreign body removal by emergency medical services (EMS) has not been examined. We aimed to compare neurological outcomes in patients after out-of-hospital cardiac arrest (OHCA) due to foreign body airway obstruction (FBAO) managed with and without AAM after foreign body removal. Methods: This retrospective observational cohort study used all emergency transportation data of Japan and the All-Japan Utstein Registry. We included patients with OHCA aged ≥18 years undergoing resuscitation and removal of airway foreign bodies by EMS from January 2015 to December 2017. The exposure of interest was prehospital AAM by EMS after foreign body removal, and the primary outcome was a favorable neurological outcome at hospital discharge (i.e., a cerebral performance category of 1–2). Results: Overall, 329,098 adults had OHCAs and 23,060 had foreign bodies removed from their airways; 3681 adult patients met our eligibility criteria and were divided as: AAM (2045) and non-AAM (1636) groups. Propensity score matching resulted in 1210 matched pairs with balanced baseline characteristics between the groups. The rate of favorable neurological outcome was significantly lower in the AAM group than in the non-AAM group (OR 0.34, 95% CI 0.19–0.62). However, survival was not significantly different between the two groups (OR 1.08, 95% CI 0.84–1.37). Conclusions: We have not demonstrated the benefit of AAM for patients with OHCA due to FBAO. Further study will be required to confirm the efficacy of AAM for those patients

Association of abnormal carbon dioxide levels with poor neurological outcomes in aneurysmal subarachnoid hemorrhage: a retrospective observational study

Abstract Background In patients with aneurysmal subarachnoid hemorrhage (SAH), an association between hypocapnia and poor clinical outcomes has been reported. However, the optimal arterial carbon dioxide tension (PaCO2) remains unknown. The present retrospective study aimed to examine the association of abnormal PaCO2 levels with neurological outcomes and investigate the optimal target PaCO2 level in patients with SAH. Methods We retrospectively selected consecutive adult patients hospitalized in the intensive care unit (ICU) for SAH between January 2009 and April 2017. Univariate and multivariate analyses were performed to identify the independent predictors of unfavorable neurological outcomes (i.e., modified Rankin scale score of 3–6 on hospital discharge). Results Among 158 patients with SAH, 73 had unfavorable neurological outcomes. During the first 2 weeks in the ICU, the median number of PaCO2 measurements per patient was 43. The factors significantly associated with unfavorable neurological outcomes were age, Hunt and Kosnik grade, maximum lactate levels during the first 24 h, and maximum (odds ratio [OR], 1.12; 95% confidence interval [CI], 1.03–1.21; p < 0.01) and minimum PaCO2 levels (OR, 0.81; 95% CI, 0.72–0.92; p < 0.01). Receiver operating characteristic curve analysis revealed that the cutoff range of PaCO2 was 30.2–48.3 mmHg. Unfavorable neurological outcomes were noted in 78.8% of patients with PaCO2 levels outside this range and in 22.8% of patients with PaCO2 levels within this range. Conclusions Both the maximum and minimum PaCO2 levels during ICU management in patients with SAH were significantly associated with unfavorable neurological outcomes. Further prospective studies are required to validate our findings and explore their clinical implications. Our findings may provide a scientific rationale for these future prospective studies

Additional file 1: of Therapeutic hypothermia in patients with coagulopathy following severe traumatic brain injury

Comparison of platelet counts between the control and MTH groups in patients with coagulopathy. MTH, mild therapeutic hypothermia. Values are presented as median (interquartile ranges, IQRs). (DOCX 13 kb

Therapeutic hypothermia in patients with coagulopathy following severe traumatic brain injury

Abstract Background Coagulopathy in traumatic brain injury (TBI) has been associated with poor neurological outcomes and higher in-hospital mortality. In general principle of trauma management, hypothermia should be prevented as it directly worsens coagulopathy. Therefore, we examined the safety of mild therapeutic hypothermia (MTH) in patients with coagulopathy following severe TBI. Methods We re-evaluated the brain hypothermia (B-HYPO) study data based on coagulopathy and compared the Glasgow Outcome Scale scores and survival rates at 6 months using per protocol analyses. Coagulopathy was defined as an activated partial thromboplastin time (APTT) > 60 s and/or fibrin/fibrinogen degradation product levels (FDP) > 90 μg/mL on admission. Baseline characteristics, coagulation parameters, and outcomes were compared between the control and MTH groups with or without coagulopathy. Results In patients with coagulopathy, 12 patients were allocated to the control group (35.5–37.0 °C) and 20 patients to the MTH group (32–34 °C). In patients without coagulopathy, 28 were allocated to the control group and 59 patients were allocated to the MTH group. In patients with coagulopathy, favorable neurological outcomes and survival rates were comparable between the control and MTH groups (33.3% vs. 35.0%, P = 1.00; 50.0% vs. 60.0%, P = 0.72) with no difference in complication rates. On admission, no significant differences in APTT or FDP levels were observed between the two groups; however, APTT was significantly prolonged in the MTH group compared to the control group on day 3. Discussion Based on our study, MTH did not seem to negatively affect the outcomes in patients with coagulopathy following severe TBI on admission; therefore, the present study indicates that MTH may be applicable even in patients with severe TBI and coagulopathy. Conclusions Our study suggests that in comparison to control, MTH does not worsen the outcome of patients with coagulopathy following severe TBI. Trial registration UMIN-CTR, No. C000000231 , Registered 13 September 2005