Delta neutrophil index: A reliable marker to differentiate perforated appendicitis from non-perforated appendicitis in the elderly.

BACKGROUND: Delta neutrophil index (DNI) is a new inflammatory marker and the present study aimed to evaluate the predictive value of the DNI for the presence of a perforation in elderly with acute appendicitis. METHODS: This retrospective observational study was conducted on 108 consecutive elderly patients (≥65 years old) with acute appendicitis treated over a 24-month period. RESULTS: Sixty-nine of the 108 patients (median, IQR: 72, 67-77 years) were allocated to the perforated appendicitis group (63.9%) and 39 to the non-perforated appendicitis group (36.1%). WBC, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio and DNI were significantly higher in the perforated group. In multiple logistic regression analyses, initial DNI was the only independent marker that can significantly predict the presence of perforation in multiple regression [odds ratio 9.38, 95% confidence interval (2.51-35.00), P=.001]. Receiver operator characteristic curve analysis showed that DNI is a good predictor for the presence of appendiceal perforation at an optimal cut-off for DNI being 1.4% (sensitivity 67.7%, specificity 90.0%, AUC 0.807). CONCLUSION: Clinicians can reliably differentiate acute perforated appendicitis from non-perforated appendicitis by DNI level of 1.4 or more in elderly patients.

Delta neutrophil index as an early predictor of acute appendicitis and acute complicated appendicitis in adults.

BACKGROUND: This retrospective study aimed to evaluate the ability of the delta neutrophil index (DNI) to predict histologically normal appendicitis preoperatively and to differentiate between simple and complicated appendicitis. METHODS: The data from 650 patients were divided into positive and negative appendectomy groups (histologically normal appendicitis). The patients in the acute appendicitis group were further sub-divided into simple and complicated appendicitis groups. RESULTS: The DNI was significantly higher in the positive group than in the negative appendectomy group (0.4 vs. -0.4, p < 0.001) as well as in the complicated group compared with that in the simple appendicitis group (1.2 vs. 0.3, p < 0.001). The DNI independently predicted a positive appendectomy and an acute complicated appendicitis in multivariate logistic regression analysis [odds ratio (OR) 2.62, 95% confidence interval (CI) (1.11~6.16), p = 0.028 and odds ratio (OR) 4.10, 95% confidence interval (CI) (2.94~5.80), p < 0.001]. The optimum cut-off for a positive appendectomy and acute complicated appendicitis were 0.2 [area under curve (AUC) 0.709] and 0.6 (AUC 0.727). CONCLUSIONS: We suggest that obtaining a preoperative DNI is a useful parameter to aid in the diagnosis of histologically normal appendicitis and to differentiate between simple and complicated appendicitis.

The association of alcohol consumption with patient survival after organophosphate poisoning: a multicenter retrospective study.

Organophosphate (OP) intoxication remains a serious worldwide health concern, and many patients with acute OP intoxication have also consumed alcohol. Therefore, we evaluated the association of blood alcohol concentration (BAC) with mortality among patients with OP intoxication. We retrospectively reviewed records from 135 patients who were admitted to an emergency department (ED) for OP intoxication between January 2000 and December 2012. Factors that were associated with patient survival were identified via receiver operating characteristic curve, multiple logistic regression, and Kaplan-Meier survival analyses. Among 135 patients with acute OP poisoning, 112 patients survived (overall mortality rate: 17 %). The non-survivors also exhibited a significantly higher BAC, compared to the survivors [non-survivors: 192 mg/dL, interquartile range (IQR) 97-263 mg/dL vs. survivors: 80 mg/dL, IQR 0-166.75 mg/dL; p < 0.001]. A BAC cut-off value of 173 mg/dL provided an area under the curve of 0.744 [95 % confidence interval (CI) 0.661-0.815], a sensitivity of 65.2 %, and a specificity of 81.2 %. A BAC of >173 mg/dL was associated with a significantly increased risk of 6-month mortality in the multiple logistic regression model (odds ratio 4.92, 95 % CI 1.45-16.67, p = 0.001). The Cox proportional hazard model revealed that a BAC of >173 mg/dL provided a hazard ratio of 3.07 (95 % CI 1.19-7.96, p = 0.021). A BAC of >173 mg/dL is a risk factor for mortality among patients with OP intoxication.

Refractory ventricular fibrillation treated with esmolol.

AIMS: This study aimed to evaluate the effects of esmolol treatment for patients with refractory ventricular fibrillation (RVF) in out-of-hospital cardiac arrest (OHCA). METHODS: This single-centre retrospective pre-post study evaluated patients who were treated between January 2012 and December 2015. Some patients had received esmolol (loading dose: 500µg/kg, infusion: 0-100µg/kg/min) for RVF (≥3 defibrillation attempts), after obtaining consent from the patient's guardian. RESULTS: Twenty-five patients did not receive esmolol (the control group), and 16 patients received esmolol. Sustained return of spontaneous circulation (ROSC) was significantly more common in the esmolol group, compared to the control group (56% vs. 16%, p=0.007). Survival and good neurological outcomes at 30 days, 3 months and at 6 months were >2-fold better in the esmolol group, compared to the control group, although these increases were not statistically significant. CONCLUSIONS: The findings of our study suggest that administration of esmolol may increase the rate of sustained ROSC and ICU survival among patients with RVF in OHCA. Further larger-scale, prospective studies are necessary to determine the effect of esmolol for RVF in OHCA.

Plasma neutrophil gelatinase-associated lipocalin as an early predicting biomarker of acute kidney injury and clinical outcomes after recovery of spontaneous circulation in out-of-hospital cardiac arrest patients.

AIMS: To determine whether the level of plasma neutrophil gelatinase-associated lipocalin (NGAL) can predict acute kidney injury (AKI) and clinical outcomes after recovery of spontaneous circulation (ROSC) in patients with out-of-hospital cardiac arrest (OHCA). METHODS: We conducted a prospective observational study of consecutive admitted patients with ROSC after OHCA between January 2013 and March 2015. Plasma was collected within 4h of ROSC to determine the level of NGAL. Outcome variables were AKI, 30-day survival, and good neurological outcome (GNO). We evaluated the association between NGAL and outcomes. RESULTS: Fifty-four patients were included. AKI occurred in 26 (48.0%); 15 (27.7%) survived over 30 days and 8 had GNO (14.8%). NGAL was significantly lower in the group with non-AKI, 30-day survival, and GNO. To predict AKI, 30-day survival, and GNO, the area under the receiver operating characteristic curve for NGAL was 0.810, 0.728, and 0.875, respectively. In a logistic regression model, NGAL >189 ngml(-1) was strongly associated with AKI (odds ratio [OR] 7.01, 95% confidence interval [CI]: 1.89-26.01) in a multivariate model. A lower level of NGAL was strongly associated with 30-day survival (OR 6.12, 95% CI: 1.64-23.42 at NGAL <153.5 ngml(-1)) and GNO (OR 19.83, 95% CI: 2.21-178.32 at NGAL <129.5 ngml(-1)) in a univariate model, but was not significantly associated with outcomes in a multivariate model. CONCLUSIONS: Plasma NGAL is a strong predictor of AKI in patients exhibiting OHCA at ICU admission. Lower levels of NGAL are associated with greater chance of 30-day survival and GNO.

The prognostic value of the grey-to-white matter ratio in cardiac arrest patients treated with extracorporeal membrane oxygenation.

AIM: The grey-to-white matter ratio (GWR) is a reliable predictor of the neurological outcome of out-of-hospital cardiac arrest (OHCA). However, the reliability in patients receiving extracorporeal membrane oxygenation-assisted cardiopulmonary resuscitation (ECPR) remains unknown. We evaluated the utility of the GWR in predicting neurological outcomes in ECPR-treated patients. METHODS: This single-centre retrospective study was conducted from July 2009 to January 2014. Patients who received ECPR for OHCA were classified into two groups: Cerebral performance category(CPC) 1-2 was defined as good, CPC 3-5 as poor outcome. Four GWR (GWR-AV[average], GWR-CO[cortex], GWR-BG[basal ganglia], and GWR-SI [simplified])were evaluated and compared between the groups. RESULTS: Of 38 patients who received ECPR for OHCA, 30 patients were enrolled. Five (16.7%) had a good outcome and 25(83.3%) a poor outcome. All GWR were significantly higher in the good outcome group than in the poor outcome group. ROC curve analysis produced the following areas under the curve: GWR-AV=0.920 (95% CI 0.761 to 0.987), GWR-BG=0.872 (95%CI 0.699 to 0.965), GWR-CO=0.952 (95% CI 0.806 to 0.997), and GWR-SI=0.848(95% CI 0.670 to 0.962). The cut-off value with 100% specificity for the prediction of the poor outcome was 1.23 for GWR-AV (sensitivity: 76%), 1.24 for GWR-BG (sensitivity: 88.0%), 1.22 for GWR-CO (sensitivity: 64%), and 1.21 for GWR-SI (sensitivity: 76%). CONCLUSIONS: In ECPR, GWR of patients with poor outcome was significantly lower than that of patients with good outcome.

Early hyperoxemia may not increase mortality after cardiac arrest: a pilot study.

OBJECTIVE: International Liaison Committee on Resuscitation guidelines advocate an arterial saturation of 94% to 96% after return of spontaneous circulation (ROSC). However, a few clinical trials have investigated the impact of postresuscitative O2 therapy after cardiac arrest. We studied whether early hyperoxemia is associated with a poor post-ROSC outcome after in-hospital cardiac arrest. METHODS: We retrospectively reviewed patients who experienced an in-hospital cardiac arrest from January 2005 to January 2011. Based on the results of the first arterial blood gas analysis (ABGA) within 10 minutes and a second ABGA from 60 to 120 minutes after ROSC, patients were classified into three groups: hyperoxemia (PaO2 ≥ 300 mmHg), normoxemia (300 mmHg > PaO2 ≥ 60 mmHg), and hypoxemia (PaO2 < 60 mmHg or ratio of PaO2 to fraction of inspired oxygen < 300). We examined whether early hyperoxemia was associated with survival and neurological outcome. RESULTS: There were 792 patients who met the inclusion criteria: 638 (80.6%) in the hypoxemia group, 62 (7.8%) in the normoxemia group, and 92 (11.6%) in the hyperoxemia group. Multiple logistic regression analysis showed that hyperoxemia was not associated with survival (odds ratio [OR], 1.07; 95% confidence interval [CI], 0.30 to 3.84) or neurological outcome (OR, 1.03; 95% CI, 0.31 to 3.40). CONCLUSION: Postresuscitation hyperoxemia was not associated with survival or neurological outcome in patients with ROSC after in-hospital cardiac arrest.

Neuronal damage using fluoro-jade B histofluorescence and gliosis in the striatum after various durations of transient cerebral ischemia in gerbils.

Ischemic damage occurs well in vulnerable regions of the brain, including the hippocampus and striatum. In the present study, we examined neuronal damage/death and glial changes in the striatum 4 days after 5, 10, 15 and 20 min of transient cerebral ischemia using the gerbil. Spontaneous motor activity was increased with the duration time of ischemia-reperfusion (I-R). To examine neuronal damage, we used Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining. F-J B positive cells were detected only in the 20 min ischemia-group, not in the other groups. In addition, we examined gliosis of astrocytes and microglia using anti-glial fibrillary acidic protein (GFAP) and anti- ionized calcium-binding adapter molecule 1 (Iba-1), respectively. In the 5 min ischemia-group, GFAP-immunoreactive astrocytes were distinctively increased in number, and the immunoreactivity was stronger than that in the sham-group. In the 10, 15 and 20 min ischemia-groups, GFAP-immunoreactivity was more increased with the duration of I-R. On the other hand, the immunoreactivity and the number of Iba-1-immunoreactive microglia were distinctively increased in the 5 and 10 min ischemia-groups. In the 15 min ischemia-group, cell bodies of microglia were largest, and the immunoreactivity was highest; however, in the 20 min ischemia-group, the immunoreactivity was low compared to the 15 min ischemia-group. The results of western blotting for GFAP and Iba-1 were similar to the immunohistochemical data. In brief, these findings showed that neuronal death could be detected only in the 20 min ischemia-group 4 days after I-R, and the change pattern of astrocytes and microglia were apparently different according to the duration time of I-R.

Ischemia-related changes in naive and mutant forms of ubiquitin and neuroprotective effects of ubiquitin in the hippocampus following experimental transient ischemic damage.

Ubiquitin binds to short-lived proteins and denatured proteins produced by various forms of injury. The loss of ubiquitin leads to an accumulation of abnormal proteins and may affect cellular structure and function. The aim of the present study is to observe the chronological changes in ubiquitin naive form and its mutant form (ubiquitin(+1)) in the hippocampal CA1 region (CA1) after transient cerebral ischemia in gerbils. Delayed neuronal death in the CA1 was confirmed 4 days after ischemic insult with NeuN immunohistochemistry. Ubiquitin immunoreactivity and protein level in the CA1 were lowest at 12 h after ischemia/reperfusion; thereafter, they were increased with time. Ubiquitin(+1) immunoreactivity and protein levels in the CA1 were slightly decreased at 3 h after ischemia/reperfusion, and they were significantly increased 1 day after ischemia/reperfusion. In addition, ubiquitin and ubiquitin(+1) immunoreaction was expressed in astrocytes after delayed neuronal death in the ischemic CA1. To elucidate the protective effect of ubiquitin on ischemic damage, the animals were treated with ubiquitin (1.5 mg/kg body weight) intravenously via the femoral vein. Ubiquitin treatment significantly reduced ischemia-induced locomotor hyperactivity, neuronal death and reactive gliosis such as astrocytes and microglia. In addition, 5 days after ubiquitin treatment in the ischemic group, ubiquitin immunoreactivity was similar to that in the ubiquitin-treated sham group, however, ubiquitin(+1) immunoreactivity was higher than that in the ubiquitin-treated sham group. These findings indicate that the depletion of ubiquitin and the accumulation of ubiquitin(+1) in CA1 pyramidal neurons after transient cerebral ischemia may inhibit ubiquitin proteolytic pathway and this leads to delayed neuronal death of CA1 pyramidal neurons directly or indirectly after transient cerebral ischemia.

Changes in immunoreactivity of HSP60 and its neuroprotective effects in the gerbil hippocampal CA1 region induced by transient ischemia.

Heat shock proteins act as molecular chaperones and are involved in protein folding, refolding, transport, and translocation. In the present study, we observed changes in heat shock protein 60 (HSP60) immunoreactivity and protein level in the gerbil hippocampal CA1 region after 5 min of transient forebrain ischemia and its neuroprotective effect against ischemic damage. HSP60 immunoreactivity in the CA1 region began to increase in the stratum pyramidale at 30 min after ischemia/reperfusion, and peaked 24 h after ischemia/reperfusion. Thereafter, HSP60 immunoreactivity was decreased in the CA1 region with time. Seven days after ischemia/reperfusion, HSP60 immunoreactivity was increased again in the CA1 region: at this time point after ischemia/reperfusion, HSP60 immunoreactivity was expressed in glial cells in the ischemic CA1 region. HSP60 immunoreactive glial cells were astrocytes containing glial fibrillar acidic protein. In contrast, change in HSP60 immunoreactivity in the ischemic CA2/3 region was not significant compared with that in the ischemic CA1 region. In Western blot study, HSP60 protein level in the CA1 region was increased after ischemia/reperfusion and highest 24 h after ischemia/reperfusion. Animals treated with recombinant adenoviruses expressing Hsp60 (Ad-Hsp60) showed the neuroprotection of CA1 pyramidal neurons from ischemic damage. These results suggest that HSP60 may be associated with delayed neuronal death of CA1 pyramidal neurons after transient ischemia, and the induction of HSP60 protects the neurons from ischemic damage.