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Petra Klemen - One of the best experts on this subject based on the ideXlab platform.
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glasgow coma scale score and qtc interval in the prognosis of Organophosphate Poisoning
Academic Emergency Medicine, 2004Co-Authors: Stefek Grmec, Stefan Mally, Petra KlemenAbstract:Objectives: The aim of this study was to assess the applicability of the Glasgow Coma Scale (GCS) score and the Q-T interval corrected for heart rate (QTc interval) in predicting outcome and complications in patients with Organophosphate (OP) Poisoning. Methods: This prospective, observational study included 65 patients older than 18 years. In the out-of-hospital setting, the end-tidal carbon dioxide (ETCO2), oxygen saturation (SaO2), QTc interval, and GCS score were monitored in each patient. A statistical comparison was then made between the group with respiratory failure and the group without this complication. Results: The group with complications had significantly different values of measured parameters—a longer QTc interval and a lower GCS score, a higher number of intubations, and worse outcomes (p \ 0.05). The two measures, GCS score and QTc interval, have been shown to be equally good in predicting respiratory failure and hospital mortality in patients with OP Poisoning. Conclusions: In the initial out-of-hospital care of patients with OP Poisoning, it is essential to monitor QTc interval and GCS score. These measures help with prognosis, and may suggest when to initiate precautions to prevent complications (i.e., respiratory failure). The simplicity and promptness of these methods allow providers to perform early and effective triage. Key words: Organophosphate; GCS score; QTc interval; respiratory failure; prognosis. ACADEMIC EMERGENCY MEDICINE 2004; 11:925‐930. The molecular mechanism of Organophosphate (OP) intoxication is well known. The OP first complexes with acetylcholinesterase (AChE), leading to enzyme deactivation by phosphorylation of the serine hydroxyl group located at the active site of AChE. The phosphorylation occurs when an OP leaving the group establishes a covalent bond with AChE. The resultant accumulation of large amounts of acetylcholine causes initial stimulation, then exhaustion of cholinergic synapses. 1‐10 Organophosphate Poisoning is an important cause of worldwide morbidity and mortality. Worldwide studies report mortality rates from 3% to 30%. 3,4,11‐17 The mortality rate for poisoned patients who require ventilation is as high as 50%. 11,15 Poisoning occurs as a result of unintentional ingestion, occupational exposure, and attempted suicide. 3,4,11‐17 Up to 70% of patients with OP Poisoning have a high incidence of respiratory failure 3,11,13,15,16,18 and a prolonged Q-T interval corrected for heart rate (QTc interval). 18‐20 The aim of the present study was to assess the value of the Glasgow Coma Scale (GCS) score and QTc interval in the out-of-hospital setting, and to confirm the applicability of these two methods in predicting outcome and complication rate in cases of OP Poisoning. Our hypothesis was that by observing the QTc interval and GCS score, respiratory failure, and the ultimate prognosis, can be predicted.
W.j Tsai - One of the best experts on this subject based on the ideXlab platform.
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Acetylcholinesterase Inhibition and the Extrapyramidal Syndrome: A Review of the Neurotoxicity of Organophosphate
Neurotoxicology, 2001Co-Authors: B.h Hsieh, J.f Deng, Jiin Ger, W.j TsaiAbstract:Organophosphate Poisonings are not uncommon, and are the leading cause of death in suicide patients in Taiwan. Acute cholinergic crisis caused by the inhibition of synaptic acetylcholinesterase is the major manifestation of Organophosphate Poisoning and may cause death within minutes. Delayed neurotoxicities include intermediate syndrome and delayed polyneuropathy have also been described. However, these symptoms may not characterize the complete picture of Organophosphate Poisoning. Among the 633 patients ever admitted to our hospital with Organophosphate Poisoning, three patients were found exhibiting impermanent neuromuscular dysfunction, including blepharoclonus, oculogyric crisis, intermittent dystonia, rigidity, and tremor, with two of them developing mask face, dyskinesia and akathisia later, following acute cholinergic crisis. The symptoms appeared within 4 days with the duration ranging from 25 days to 2 months. Other causes of the extrapyramidal syndrome noted on these patients have been excluded, and we consider the extrapyramidal syndrome a possible neurotoxic manifestation of Organophosphate Poisoning, which is transient, needs no treatment, and may be missed because of the critical condition, in a minority of patients. The mechanism remains to be identified, but may be related to the impediment of the function of acetylcholinesterase to modify nigrostriatal dopaminergic system, which is independent of hydrolyzing acetylcholine. More detailed observation for Organophosphate poisoned patients and more studies for the biological functions of acetylcholinesterase including the influence on the nigrostriatal dopaminergic system are needed.
Stefek Grmec - One of the best experts on this subject based on the ideXlab platform.
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glasgow coma scale score and qtc interval in the prognosis of Organophosphate Poisoning
Academic Emergency Medicine, 2004Co-Authors: Stefek Grmec, Stefan Mally, Petra KlemenAbstract:Objectives: The aim of this study was to assess the applicability of the Glasgow Coma Scale (GCS) score and the Q-T interval corrected for heart rate (QTc interval) in predicting outcome and complications in patients with Organophosphate (OP) Poisoning. Methods: This prospective, observational study included 65 patients older than 18 years. In the out-of-hospital setting, the end-tidal carbon dioxide (ETCO2), oxygen saturation (SaO2), QTc interval, and GCS score were monitored in each patient. A statistical comparison was then made between the group with respiratory failure and the group without this complication. Results: The group with complications had significantly different values of measured parameters—a longer QTc interval and a lower GCS score, a higher number of intubations, and worse outcomes (p \ 0.05). The two measures, GCS score and QTc interval, have been shown to be equally good in predicting respiratory failure and hospital mortality in patients with OP Poisoning. Conclusions: In the initial out-of-hospital care of patients with OP Poisoning, it is essential to monitor QTc interval and GCS score. These measures help with prognosis, and may suggest when to initiate precautions to prevent complications (i.e., respiratory failure). The simplicity and promptness of these methods allow providers to perform early and effective triage. Key words: Organophosphate; GCS score; QTc interval; respiratory failure; prognosis. ACADEMIC EMERGENCY MEDICINE 2004; 11:925‐930. The molecular mechanism of Organophosphate (OP) intoxication is well known. The OP first complexes with acetylcholinesterase (AChE), leading to enzyme deactivation by phosphorylation of the serine hydroxyl group located at the active site of AChE. The phosphorylation occurs when an OP leaving the group establishes a covalent bond with AChE. The resultant accumulation of large amounts of acetylcholine causes initial stimulation, then exhaustion of cholinergic synapses. 1‐10 Organophosphate Poisoning is an important cause of worldwide morbidity and mortality. Worldwide studies report mortality rates from 3% to 30%. 3,4,11‐17 The mortality rate for poisoned patients who require ventilation is as high as 50%. 11,15 Poisoning occurs as a result of unintentional ingestion, occupational exposure, and attempted suicide. 3,4,11‐17 Up to 70% of patients with OP Poisoning have a high incidence of respiratory failure 3,11,13,15,16,18 and a prolonged Q-T interval corrected for heart rate (QTc interval). 18‐20 The aim of the present study was to assess the value of the Glasgow Coma Scale (GCS) score and QTc interval in the out-of-hospital setting, and to confirm the applicability of these two methods in predicting outcome and complication rate in cases of OP Poisoning. Our hypothesis was that by observing the QTc interval and GCS score, respiratory failure, and the ultimate prognosis, can be predicted.
Jiin Ger - One of the best experts on this subject based on the ideXlab platform.
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Acetylcholinesterase Inhibition and the Extrapyramidal Syndrome: A Review of the Neurotoxicity of Organophosphate
Neurotoxicology, 2001Co-Authors: B.h Hsieh, J.f Deng, Jiin Ger, W.j TsaiAbstract:Organophosphate Poisonings are not uncommon, and are the leading cause of death in suicide patients in Taiwan. Acute cholinergic crisis caused by the inhibition of synaptic acetylcholinesterase is the major manifestation of Organophosphate Poisoning and may cause death within minutes. Delayed neurotoxicities include intermediate syndrome and delayed polyneuropathy have also been described. However, these symptoms may not characterize the complete picture of Organophosphate Poisoning. Among the 633 patients ever admitted to our hospital with Organophosphate Poisoning, three patients were found exhibiting impermanent neuromuscular dysfunction, including blepharoclonus, oculogyric crisis, intermittent dystonia, rigidity, and tremor, with two of them developing mask face, dyskinesia and akathisia later, following acute cholinergic crisis. The symptoms appeared within 4 days with the duration ranging from 25 days to 2 months. Other causes of the extrapyramidal syndrome noted on these patients have been excluded, and we consider the extrapyramidal syndrome a possible neurotoxic manifestation of Organophosphate Poisoning, which is transient, needs no treatment, and may be missed because of the critical condition, in a minority of patients. The mechanism remains to be identified, but may be related to the impediment of the function of acetylcholinesterase to modify nigrostriatal dopaminergic system, which is independent of hydrolyzing acetylcholine. More detailed observation for Organophosphate poisoned patients and more studies for the biological functions of acetylcholinesterase including the influence on the nigrostriatal dopaminergic system are needed.
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the clinical significance of hyperamylasemia in Organophosphate Poisoning
Clinical Toxicology, 1998Co-Authors: Wuichiang Lee, Jiin Ger, Chenchang Yang, Hanchieh Lin, Fullyoung Chang, Joufang Deng, Shoudong LeeAbstract:AbstractObjective: Hyperamylasemia with a presumptive diagnosis of acute pancreatitis has been reported following Organophosphate Poisoning but there are no large-scale studies incorporating more specific diagnostic criteria. Methods; Retrospective review of the medical records of 159 patients with a diagnosis of Organophosphate Poisoning over 3 years. Serum amylase, pancreatic amylase, salivary amylase, lipase and cholinesterase levels, and the clinical manifestations were analyzed. Results; Serum amylase data was available for 121 of the 159 study patients. Hyperamylasemia (amylase ≥ 360 U/L) was found in 44 patients (36%). Lipase was measured in 28 patients with hyperamylasemia; 9 of 28 had hyperlipasemia (lipase ≥ 380 U/L). The finding of hyperamylasemia was closely related to clinical severity and presence of shock. A presumptive diagnosis of painless acute pancreatitis was diagnosed by hyperlipasemia associated with hyperamylasemia, clinical severity, serum LDH, and leukocyte counts. Two patients wi...
T Zilker - One of the best experts on this subject based on the ideXlab platform.
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obidoxime in acute Organophosphate Poisoning 1 clinical effectiveness
Clinical Toxicology, 2009Co-Authors: Florian Eyer, N Felgenhauer, Peter Eyer, Mike Haberkorn, T ZilkerAbstract:Objective. The effects of obidoxime in the treatment of Organophosphate Poisoning were assessed by comparing the clinical course with its effects on laboratory parameters relevant to Poisoning. In this article we report clinical findings and activity of cholinesterase in plasma and acetylcholinesterase (AChE) in red blood cells. In a linked paper we describe changes in neuromuscular transmission and atropine concentrations in the same patient cohort. Methods. We studied 34 atropinized patients with severe parathion, oxydemeton methyl, and dimethoate self-Poisoning who were treated with obidoxime in a standard protocol. We measured the AChE activity in blood and related it to clinical features of Organophosphate Poisoning. Results. Patients poisoned with parathion responded promptly to obidoxime (250 mg bolus followed by continuous infusion at 750 mg/day up to 1 week) with improvement of neuromuscular transmission and increased AChE activity. The effects were only transient in cases with the other poisons....
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obidoxime in acute Organophosphate Poisoning 2 pk pd relationships
Clinical Toxicology, 2009Co-Authors: Horst Thiermann, Franz Worek, N Felgenhauer, Florian Eyer, Peter Eyer, T ZilkerAbstract:Objective. The effects of obidoxime in the treatment of Organophosphate Poisoning were assessed by biochemical and biological effect monitoring. In this article we report effects on neuromuscular function, oxime and atropine concentration, and relate them to acetylcholinesterase (AChE) activity. Methods. We measured the activity of cholinesterase in plasma and AChE in red blood cells (RBC) and related these data with neuromuscular transmission analysis (ulnar nerve stimulation). Concomitantly, poison and oxon along with plasma obidoxime and atropine levels were measured at regular intervals. Results. We found a close correlation between RBC–AChE activity and neuromuscular transmission and a reciprocal correlation between both the atropine maintenance dose and/or its plasma concentration. The steady state of RBC–AChE activity of reactivation and re-inhibition followed the course predicted by laboratory-determined reaction constants. Conclusions. Intense monitoring of Organophosphate-poisoned patients allow...