19 research outputs found
Heart Rate-Corrected QT Interval Helps Predict Mortality after Intentional Organophosphate Poisoning
INTRODUCTION: In this study, we investigated the outcomes for patients with intentional organophosphate poisoning. Previous reports indicate that in contrast to normal heart rate-corrected QT intervals (QTc), QTc prolongation might be indicative of a poor prognosis for patients exposed to organophosphates. METHODS: We analyzed the records of 118 patients who were referred to Chang Gung Memorial Hospital for management of organophosphate poisoning between 2000 and 2011. Patients were grouped according to their initial QTc interval, i.e., normal (<0.44 s) or prolonged (>0.44 s). Demographic, clinical, laboratory, and mortality data were obtained for analysis. RESULTS: The incidence of hypotension in patients with prolonged QTc intervals was higher than that in the patients with normal QTc intervals (P = 0.019). By the end of the study, 18 of 118 (15.2%) patients had died, including 3 of 75 (4.0%) patients with normal QTc intervals and 15 of 43 (34.9%) patients with prolonged QTc intervals. Using multivariate-Cox-regression analysis, we found that hypotension (OR = 10.930, 95% CI = 2.961-40.345, P = 0.000), respiratory failure (OR = 4.867, 95% CI = 1.062-22.301, P = 0.042), coma (OR = 3.482, 95% CI = 1.184-10.238, P = 0.023), and QTc prolongation (OR = 7.459, 95% CI = 2.053-27.099, P = 0.002) were significant risk factors for mortality. Furthermore, it was revealed that non-survivors not only had longer QTc interval (503.00±41.56 versus 432.71±51.21 ms, P = 0.002), but also suffered higher incidences of hypotension (83.3 versus 12.0%, P = 0.000), shortness of breath (64 versus 94.4%, P = 0.010), bronchorrhea (55 versus 94.4%, P = 0.002), bronchospasm (50.0 versus 94.4%, P = 0.000), respiratory failure (94.4 versus 43.0%, P = 0.000) and coma (66.7 versus 11.0%, P = 0.000) than survivors. Finally, Kaplan-Meier analysis demonstrated that cumulative mortality was higher among patients with prolonged QTc intervals than among those with normal QTc intervals (Log-rank test, Chi-square test = 20.36, P<0.001). CONCLUSIONS: QTc interval helps predict mortality after intentional organophosphate poisoning
Attenuation of phosphamidon-induced oxidative stress and immune dysfunction in rats treated with N-acetylcysteine
Two cases of acute endosulfan toxicity
Background. Endosulfan is widely used in insect control and is absorbed by both humans and animals through the intestinal tract, the lungs, and the skin. Organochlorine insecticides are highly toxic compounds that are responsible for a number of severe intoxications worldwide, with several deaths. A 9-year analysis by one of Turkey's poison control centers reported that pesticide intoxications accounted for 8.8% of 25,572 poisoning calls, with 80.3% of them relating to insecticides and 19.7% concerning rodenticides. Case Reports. We present two cases of unintentional exposure to endosulfan, one of which presented with neurological manifestations, liver toxicity, and required mechanical ventilation and emergent hemodialysis; the other had only neurological manifestations and liver toxicity. Conclusion. In cases of endosulfan poisoning, physicians must be aware of neurological manifestations, seizures, and severe metabolic acidosis. If severe metabolic acidosis is present, we suggest that hemodialysis may be an important intervention and should be performed early
The prognostic importance of trauma scoring systems for blunt thoracic trauma
Background: Early identification and aggressive management of blunt thoracic trauma are essential to reduce the significant rates of morbidity and mortality. The aim of this study was to evaluate the independent predictive value of 5 different trauma scoring systems (Revised Trauma Score [RTS], Trauma and Injury Severity Score [TRISS], Injury Severity Score [ISS], Lung Injury Scale [LIS], and Chest Wall Injury Scale [CWIS]) with respect to prognostic factors such as tube thoracostomy duration, the need for mechanical support and thoracotomy, the length of hospital and ICU stay, morbid conditions, and deaths of patients with blunt thoracic trauma
Royal jelly can diminish secondary neuronal damage after experimental spinal cord injury in rabbits
PubMed: 22538080The aim of this experimental study was to investigate the neuroprotective effect of Royal jelly (RJ) on traumatic spinal cord injury (SCI). Twenty-one New Zealand male rabbits, weighing between 2.5 and 3.0. kg were divided into three groups: Sham (no drug or operation, n= 7), Control (laminectomy. +. single dose of 1. ml/kg saline orally, after trauma; n= 7) and RJ (laminectomy. +. 100. mg/kg RJ, orally, after trauma, n= 7). Laminectomy was performed at T10 and balloon catheter was applied extradurally for traumatic SCI. Four and 24. h after surgery, rabbits were evaluated according to the Tarlov scoring system. Blood, cerebrospinal fluid and tissue sample from spinal cord were taken for measurements of antioxidant status or detection of apoptosis. Four hours after SCI, all animals in control or RJ treated groups became paraparesic. Significant improvement was observed in RJ treated group, 24. h after SCI, with respect to control. Traumatic SCI led to increase in the lipid peroxidation and decrease enzymic or non-enzymic endogenous antioxidative defense systems, and increase in apoptotic cell numbers. RJ treatment mostly prevented lipid peroxidation and also augmented endogenous enzymic or non-enzymic antioxidative defense systems. Again, RJ treatment significantly decreased the apoptotic cell number induced by SCI. © 2012 Elsevier Ltd.Traumatic SCI was found to lead an increase in the lipid peroxidation and a decrease in enzymatic or nonenzymatic endogenous antioxidative defense systems. Furthermore, it was observed that SCI led to apoptosis in spinal cord tissue. A preliminary study was performed to investigate the neuroprotective effect of Royal jelly in spinal cord injury. This work demonstrates for the first time the effect of RJ on SCI. RJ treatment mostly prevented lipid peroxidation, augmented endogenous antioxidative defense systems and prevented apoptosis or neurodeficite following a traumatic SCI. Thus, neuroprotective effect of RJ in the SCI was supported by behavioral, biochemical and histopathological tests. Inhibition of oxidative stress or apoptosis by RJ may have potential therapeutic benefits for reducing secondary damage and improving the outcome after a traumatic SCI. The authors believe that further studies are necessitated about the effect of different doses of RJ or the effect of RJ at different terms after SCI
Effect of interleukin-10 on pancreatic damage caused by organophosphate poisoning
Organophosphate poisoning is a common cause of severe morbidity and mortality in emergency departments. Acute pancreatitis is a frequently reported consequence of organophosphate poisoning, but preventing this potentially severe complication has not been the subject of much research. We tested whether interleukin-10, a cytoprotective agent, could prevent or diminish pathological signs of acute pancreatitis caused by organophosphate poisoning. Thirty rats were divided into three equal groups. Group 1 did not receive any agent during the experiment. Group 2 received 0.8 g/kg fenthion intraperitoneally, followed by 6 ml/kg intraperitoneal normal saline 30 min and 3 h later. Group 3 received 0.8 g/kg fenthion intraperitoneally, followed by 2 mu g/kg of interleukin-10 intraperitoneally 30 min and 3 h later. All rats underwent laparotomy and thoracotomy while still under anesthesia at 6 h, and tissue samples were obtained from the pancreas. After blood samples were taken by cardiac puncture, the animals were sacrificed. Organophosphate poisoning resulted in significant elevations of serum amylase and glucose. Interleukin-10 significantly reduced pancreatic damage as determined by pathologic scoring, but not by enzyme elevations. Interleukin-10 should be considered for larger studies in other animal models to confirm its ability to decrease pancreatic damage after organophosphate poisoning treatment with interleukin-10. (C) 2005 Elsevier Inc. All rights reserved
BNP shows myocardial injury earlier than Troponin-I in experimental carbon monoxide poisoning
OBJECTIVE: In this study, our purpose was to determine whether plasma BNP level can be useful or not in determining the severity of myocardial injury formed by CO poisoning and to compare plasma BNP level with serum cTnI level
Evaluation of the relationship between heart type fatty acid binding protein levels and the risk of maternal cardiac ischemia in low risk obstetric population during delivery
PMID = 2292636