Severe Acute Organophosphate Poisoning Research Articles

Development of a practical prediction scoring system for severe acute organophosphate poisoning.

Acute organophosphorus poisoning (AOPP) is a serious public health issue, especially in the rural areas. This study was designed to establish a scoring system to assess the risk of cases with severe AOPP. A retrospective cohort study was conducted at two independent hospitals. The derivation cohort included 444 patients with AOPP and the validation cohort included 274 patients. A risk score for patients with severe AOPP was developed. The rates of severe AOPP cases were 20.7% and 20.1% in the derivation and validation cohorts, respectively. A scoring system for severe AOPP risk was developed that included: (1) age >50 years, (2) white blood cell count of >15 × 109 /L, (3) plasma cholinesterase of <360 U/L, (4) plasma albumin of <35 g/L, (5) blood pH <7.3, and (6) lactic acid >3.0 mmol/L. The predicted score in severe cases of AOPP had good accuracy in both the derivation (area under the receiver operating characteristic curve [AUC] 0.88, 95% confidence interval [CI], 0.85-0.92) and validation cohorts (AUC 0.83, 95% CI, 0.77-0.90). A practical bedside prediction scoring system was developed for patients with severe AOPP. The routine use of this scoring system could rapidly assist in identifying patients at higher risk who require more intensive care or transfer to a larger better-equipped hospital.

Usefulness of serum lactate as a predictor of successful discontinuation of continuous atropine infusion in patients with severe acute organophosphate poisoning

ObjectiveIn severe organophosphate (OP) poisoning, administration of atropine via continuous intravenous infusion is typically considered. To date, there have been no studies on predicting successful atropine discontinuation through plasma cholinesterase (PChE) and serum lactate levels, which are monitored during critical care in severe acute OP poisoning. Therefore, we retrospectively evaluated the usefulness of serum lactate and PChE as predictors of successful discontinuation of atropine infusion.MethodsThis retrospective observational study was performed on consecutive adult patients treated for severe acute OP poisoning between March 2011 and December 2016. We sequentially evaluated serum lactate and PChE levels on emergency department arrival and before a discontinuation trial of atropine infusion. Discontinuation of atropine intravenous infusion was attempted in patients after clearance of respiratory secretions and cessation of bronchoconstriction. Discontinuation of atropine infusion attempts were divided into successful and failed trials.ResultsA total of 95 trials were conducted in 62 patients. Serum lactate levels before trials were significantly different between patients with successful and failed trials. The area under the curve for prediction of successful atropine discontinuation using serum lactate levels before trial discontinuation were 0.742 (95% confidence interval, 0.638 to 0.846). PChE level was not significantly different between two groups.ConclusionSerum lactate levels before the discontinuation trial of atropine infusion served to predict successful discontinuation in severe acute OP poisoning.

Acute severe organophosphate poisoning in a child who was successfully treated with therapeutic plasma exchange, high‐volume hemodiafiltration, and lipid infusion

Acute severe organophosphate poisoning is a serious complication seen in developing and agricultural countries. Pralidoxime and high dose atropine are the standard treatments. There is no consensus about acute severe organophosphate poisonings that are unresponsive to pralidoxime, atropine, and supportive therapies. We report a case of acute severe organophosphate poisoning that was unresponsive to standard treatments and successfully treated with high-volume continuous venovenous hemodiafiltration and therapeutic plasma exchange combined with lipid infusion. J. Clin. Apheresis 31:467-469, 2016. © 2015 Wiley Periodicals, Inc.

Therapeutic Effectiveness of Sustained Low‐Efficiency Hemodialysis Plus Hemoperfusion and Continuous Hemofiltration Plus Hemoperfusion for Acute Severe Organophosphate Poisoning

There is no report on the effects of sustained low-efficiency dialysis (SLED) plus hemoperfusion (HP) (SLED + HP) in patients with acute severe organophosphate (OP) poisoning (ASOPP). This study was designed to compare the therapeutic effectiveness between SLED + HP and continuous hemofiltration (CHF) plus HP (CHF + HP) in patients with ASOPP. In order to assess the two treatment methods, 56 patients with ASOPP were divided into CHF + HP group and SLED + HP group. The biochemical indicators, in-hospital duration, hemodynamic parameters, Acute Physiology, and Chronic Health Evaluation (APACHE II) score, and survival and mortality rates were compared. In both groups after treatment, the levels of serum creatine kinase isozyme MB, creatine kinase, creatinine, glutamic-oxalacetic transaminease, and glutamate-pyruvate transaminase, and the APACHE II scores on the first, second, and seventh day decreased (P < 0.05), whereas the levels of serum acetylcholinesterase increased. The two groups showed no statistical differences in in-hospital duration, biochemical indicators, APACHE II score, hemodynamic parameters, survival rate, or the mortality rate (P > 0.05). In conclusion, SLED has similar hemodynamic stability to CHF and the two treatment methods have similar effects on ASOPP patients. More importantly, SLED plus HP is relatively economical and convenient for patients with ASOPP in clinical practice.

Meta-analysis of the effectiveness of plasma exchange in treatment of severe and acute organophosphate poisoning

To discuss the effectiveness of severe and acute organophosphate poisoning (AOPP) treated with plasma exchange in China. Researches about effectiveness of severe AOPP treated with plasma exchange were analyzed by Review Manager 4.2 and fixed effect model of meta-analysis method were used. Six trials including 433 patients were identified. Treatment group including 211 patients adopted traditional physician therapy plus plasma exchange, and control group including 222 patients received physician therapy only. The case-fatality rate of the treatment group was lower than the control one [RR=0.30, 95%CI (0.19-0.49), P<0.01]. Plasma exchange can improve the cure rate of severe AOPP.

Parkinsonism Complicating Acute Organophosphate Insecticide Poisoning

Organophosphate insecticides have a triphasic effect on the central nervous system, namely acute cholinergic crisis, intermediate syndrome and delayed polyneuropathy. Although acute organophosphate poisoning is relatively common, case reports describing parkinsonism as a neurological complication following an acute intoxication are limited. 1 We report a case of parkinsonism noted on day 24 of admission following an acute severe organophosphate poisoning which was successfully treated with benzhexol and levodopa. Previously, response to levodopa was reported to be poor in 3 patients studied by Bhatt et al 1whereas amantidine, dopamine agonist and bipiriden have been shown to be helpful. 2To the best of our knowledge, this is the fi rst case of parkinsonism complicating organophosphate poisoning which responded to levodopa and benzhexol therapy.

Timing of tracheal intubation impact on the therapeutic effect of acute severe organophosphate poisoning patients

Objective To evaluate timing of tracheal intubation impact on the therapeutic effect of acute severe organophosphate poisoning( ASOPP) patients. Methods Retrospectively analyze 82 ASOPP patients with respiratory failure ( RF). The patients were divided into timely tracheal intubation group(n = 42) and delay tracheal intubation group (n =40) ,and compare the therapeutic effect of these two groups. Results Compared with timely tracheal intubation patients and delay tracheal intubation patients,total time of mechanical ventilation,hospital day decreased significantly (P 0.05). Conclusion It was exact that the therapeutic effect of timely tracheal intubation on rescuing the ASOPP patients, and the best time to tracheal intubation was in RF early period. Key words: Poisoning; Insecticide, orgnaophosphorus; Ventilators, mechanical; Intubation, intratracheal

Brain injury due to acute organophosphate poisoning: Magnetic resonance imaging manifestation and pathological characteristics

Background Acute organophosphate poisoning can cause injuries of multiple visceras; especially, central nervous system injury can increase risk factors of patients with severe acute organophosphate poisoning. An application of modern image may increase diagnostic rate of brain injury in an earlier period and provide evidences for clinical treatment. Objective To reveal imaging manifestations, pathological characteristics and multi-ways injured mechanism of brain injury due to acute organophosphate poisoning. Design Contrast observational study. Setting Department of Medical Image, the Second Hospital of Hebei Medical University. Materials The experiment was carried out in the Department of Nerve Molecule Imaging Medicine and Laboratory of Neurology, the Second Hospital of Hebei Medical University from August 2003 to February 2004. A total of 30 healthy cats weighing 2.8–3.5 g and of both genders were selected from Animal Experimental Center of Hebei Medical University. Methods Thirty healthy cats were randomly divided into control group ( n =5) and intoxication group ( n =25). Cats in the control group were subcutaneously injected with 0.3 mL/kg saline at four points; while, cats in the intoxication group were subcutaneously injected with 400 g/L 0.3 mL/kg O,O-dimethyl-S-(methoxycarbonylmethyl) thiophosphate at four points. Two minutes after intoxication, cats received muscular injection with 0.5 mg/kg atropine sulfate, and then, brain tissues were collected from parietal lobe, basal ganglia, hippocampus, cerebellum and brain stem were observed at 3, 6, 24 hours, 3 and 7 days after intoxication respectively under optic microscope and electron microscope and expressions of acetylcholinesterase (AChE), choline acetyltransferase (ChAT), glial fibrillary acidic protein (GFAP), glutamic acid (Glu) and γ-amino butyric acid after immunohistochemical staining. Main outcome measures Results of MRI examinations; histological changes under optic microscope and electron microscope; expressions of AChE, ChAT, GFAP, Glu and γ-amino butyric acid after immunohistochemical staining. Results All 30 healthy cats were involved in the final analysis. ▪ Imaging and pathological observation: Image manifestations of brain injury induced by acute organophosphate poisoning showed as cerebral edema and symmetry signal abnormality of bilateral basal ganglia; while, pathological manifestations also showed as cerebral edema. ▪ Observation of immunohistochemical staining: As compared with the control group, after organophosphate poisoning, area of AChE immune-positive cells was decreased obviously ( P < 0.01), but area of ChAT immune-positive cells was not changed ( P > 0.05); in addition, positive cells of GFAP were increased remarkably ( P < 0.01), positive cells of γ-amino butyric acid in cerebral cortex were increased obviously ( P < 0.05), but numbers of positive cells of Glu were not changed ( P < 0.05). Conclusion Multi-ways injured mechanism invovled in acute organophosphate poisoning. An application of modern image can increase diagnostic rate of brain injury in an earlier period and provide evidences for clinical treatment.

Progression of Type I to Type II paralysis in acute organophosphorous poisoning: Is oxidative stress significant?

Organophosphorous poisoning is a common method of deliberate self-harm in countries where the pesticides are readily available and can result in type I, II and/or III paralysis. The in-hospital morbidity and mortality of the poisoning are mostly associated with type II paralysis (intermediate syndrome). The aim of this study was to determine the role of oxidative stress in relation to the severity of poisoning and development of type II paralysis in patients suffering from acute organophosphate poisoning. This prospective study was carried out at the Christian Medical College Hospital. Thirty-two patients with acute organophosphorous poisoning, admitted in one medical unit over 17 months, were included in the study. They were clinically assessed for severity of poisoning and paralysis during the first 10 days of their hospitalisation. Temporal profiles of butyrylcholinesterase (BuChE) and oxidative stress parameters, for 4, 7 and 10 days of hospitalisation, were established in 25 of these patients. Type I and II paralysis were associated with severe poisoning. The majority of patients with type II paralysis had prior evidence of type I paralysis. The pattern of muscles that were paralysed in type I paralysis occurring alone and in type I paralysis proceeding to type II paralysis were similar. BuChE was significantly inhibited in all patients. Oxidative stress occurred in acute organophosphate poisoned patients and was greater in severe poisoning. The results suggest that type I paralysis may progress to type II paralysis in severely poisoned patients. They demonstrate early occurrence of oxidative stress in severe acute organophosphate poisoning. However, the development of type II paralysis is not associated with the level of oxidative stress. They suggest that mechanisms other than acetylcholine induced oxidative stress may be involved in the progression of type I to type II paralysis.

Central nervous system effects of acute organophosphate poisoning in a two-year follow-up

Patients hospitalized for acute organophosphate poisoning in León, Nicaragua, were followed for effects on the central nervous system (CNS) over a 2-year period. Immediate verbal memory (Rey verbal learning), visuomotor performance (digit symbol), and neuropsychiatric symptoms (Q-16) were assessed for 53 poisoned persons at the time of hospital discharge, 7 weeks postpoisoning, and 2 years postpoisoning, and, at the same time intervals, for 28 persons who had never been poisoned. The poisonings were classified as moderate occupational (31), severe occupational (15), and severe through the oral route (7), representing low, medium, and high exposure, respectively. Longitudinal confounder-adjusted between-category comparisons and longitudinal analyses of variance and covariance were used to assess the effects of the exposure. Immediate verbal learning showed deficits in the high-exposure group, in particular at the time of discharge, but the estimate of the difference when compared with the values of the unexposed was imprecise. Visuomotor performance showed a deficit at 7 weeks in the medium-exposure group, but it had improved after 2 years relative to that of the unexposed, for whom improvement had occurred at 7 weeks and persisted during the 2 years of follow-up, possibly a test-retest effect. Neuropsychiatric symptoms were in excess 2 years after the hospital discharge in the low- and medium-exposure groups and all the groups combined. All the results were imprecise for the small high-exposure group. Visuomotor performance and possibly short-term verbal memory seem to be affected early after severe acute organophosphate poisoning and recover, either truly or by some compensatory mechanism. Neuropsychiatric symptoms seem to increase after a longer latency period.

A case of acute poisoning due to organophosphate insecticide

A case of acute severe organophosphate poisoning by deliberate self administration is reported. The patient required intensive therapy for 30 days. Unusual features of the case were the avoidance of atropine, because of the high risk of ventricular fibrillation, and the ineffectiveness of pralidoxime.

Antidotal therapy of severe acute organophosphate poisoning: A multihospital study

Out of 859 consecutive cases treated for exposure to organophosphate (PO) insecticides, 53 were included in the study. Criteria for inclusion were severe OP poisoning necessitating artificial ventilation, intensive care monitoring and treatment according to a standard protocol. The protocol was based on relatively high doses of obidoxime, relatively low doses of atropine and overriding with a pacemaker in cases of ventricular arrhythmias and prolonged Q-T interval. Seven patients died during hospitalization. Thirty-two patients (60%) had major central nervous system (CNS) involvement. Five (9.4%) presented severe psychiatric sequelae. Twenty-two patients (41.5%) presented cardiac arrhythmias. Five (9.4%) had liver dysfunction. High frequency of cardiac arrhythmias was observed in patients who received high cumulative doses of atropine and obidoxime; impairment of liver functions was significantly higher in patients who received high cumulative doses of obidoxime. We conclude that each drug should be titrated separately: atropine dosage should be adjusted to the severity of tracheobronchial secretions and bronchospasm, while full doses of obidoxime are justified for the period before “aging” sets in.