Organophosphate Insecticide Poisoning Research Articles

Intensive care management of organophosphate insecticide (sniper) poisoning: a Preventable death—a case series

Background Organophosphate poisoning is the commonest accidental and suicidal poisoning in developing countries like Nigeria. Respiratory distress, unconsciousness, and acute cholinergic crisis are reasons for critical care. Objective We determined the clinical presentation and outcome following sniper poisoning in critically ill patients. Methods This was a retrospective case series of 13 patients managed for sniper poisoning in a six-bed private intensive care unit in Lagos, Nigeria, from June 2016 to June 2022. The diagnosis of sniper poisoning was made based on a positive history of ingestion of sniper before presentation, and clinical signs of cholinergic hyperactivity. Results A total of 13 patients were reviewed, 3 females and 10 males with median age and APACHE II score of 23.5 years (IQR, 5.75, 27.75) and 26 (IQR, 24, 27.5), respectively. Deliberate ingestion of sniper occurred in 10 patients. Respiratory insufficiency/unconsciousness, and bradycardia/hypoxia occurred in 11 and 10 patients, respectively. The median duration of ICU admission was 6.5 days, (IQR: 4, 8). Intravenous atropine and glycopyrrolate were administered in 10 and 2 patients, respectively. The median dose of atropine on days 1, 2, and 3 were 38.9 mg, 27.6 mg and 18.5 mg, respectively. Mechanical ventilation was initiated in 10 patients, 8 of whom were discharged home. Out of 13 patients, 10 survived, while 3 died. Conclusion This case series showed that sniper poisoning is a life-threatening condition that requires immediate diagnosis and treatment. Early referral for critical care, initiation of atropine, and supportive mechanical ventilation can save lives.

Study of Organophosphorus Poisoning at a Tertiary Care Teaching Hospital

Introduction: Organophosphate (OP) insecticides inhibit both cholinesterase and pseudo-cholinesterase activities. The inhibition of acetylcholinesterase causes accumulation of acetylcholine at synapses, and overstimulation of neurotransmission occurs as a result of this accumulation. The mortality rate of OP poisoning is high. Early diagnosis and appropriate treatment is often life saving. Treatment of OP poisoning consists of intravenous atropine and oximes. The clinical course of OP poisoning may be quite severe and may need intensive care management. Methods: A retrospective study was performed on the patients with OP poisoning. Fifty patients were included. Diagnosis was performed from the history taken either from the patient or from the patient's relatives about the agent involved in the exposure. Diagnosis could was confirmed with serum and red blood cell anticholinesterase levels. Intravenous atropine and pralidoxime was administered as soon as possible. Other measures for the treatment were gastric lavage and administration of activated charcoal via nasogastric tube, and cleansing the patient's body with soap and water. The patients were intubated and mechanically ventilated if the patients had respiratory failure, a depressed level of consciousness, which causes an inability to protect the airway, and hemodynamic instability. Mechanical ventilation was performed as synchronized intermittent mandatory ventilation + pressure support mode, either as volume or pressure control. Positive end expiratory pressure was titrated to keep SaO2 above 94% with 40% FIO2. Weaning was performed using either T-tube trials or pressure support weaning. The chi-square test was used for statistical analysis. Data are presented as mean ± standard deviation. Results: There were 26 female and 24 male patients. Thirty-five were suicide attempts and 15 were accidental exposure. The gastrointestinal route was the main route in 44 patients. The most frequent signs were meiosis, change in mental status, hypersalivation and fasciculations. Ten patients (20.0%) required mechanical ventilation. Complications were observed in 35 patients. These complications were respiratory failure (14 patients), aspiration pneumonia (10 patients), urinary system infection (6 patients), convulsion (4 patients) and septic shock (1 patient). The duration of the intensive care stay was 5.2 ± 3.0 days. Discussion: Ingestion of OP compounds for suicidal purposes is a major problem, especially in developing countries. Thirty-five of our patients used the OP insecticide for suicide. The average respiratory rate of these patients increased from 22 to 38 breaths/min, which is an important sign of respiratory distress. The nurse to patient ratio was increased after these events. Early recognition of respiratory failure resulting in intubation and mechanical ventilation is a life-saving intervention for patients with OP poisoning. Respiratory failure is the most troublesome complication, which was observed in 35 patients. Patients with OP poisoning may have respiratory failure for many reasons, including aspiration of the gastric content, excessive secretions, pneumonia and septicemia complicating acute respiratory distress syndrome. Conclusions: OP insecticide poisoning is a serious condition that needs rapid diagnosis and treatment. Since respiratory failure is the major reason for mortality, careful monitoring, appropriate management and early recognition of this complication may decrease the mortality rate among these patients.

O-EV002. Auditory event-related potential changes over 6 months following acute organophosphate insecticide poisoning: A follow-up study

Introduction . Ingestion of organophosphate insecticides (OPIs) is a common method of self-harm and a major clinical problem is Asia. Apart from acute cholinergic effects, OPIs are also claimed to be associated with long-term neurobehavioural deficits. However, neurophysiological evidence for such long-term deficits is scarce in humans. We aimed to assess long-term changes in the pre-attentive (N1) and attentive (P3b) components of auditory event-related potentials (ERPs) following acute OPI self-poisoning. Methods . We recruited 203 patients (147 men) hospitalised following OPI ingestion (OP Group; all had significant red cell cholinesterase inhibition) and 50 patients (23 men) hospitalised with paracetamol overdose (Control Group) as a means of self harm. We recorded their EEG in an auditory oddball task and derived the averaged ERPs. The subjects underwent three testing sessions: on discharge from hospital (around 14 days post-ingestion), 6 weeks and 6 months post-ingestion. We compared the reaction time and ERP indices of the two groups at each time point, adjusting for sex, age, education and psychiatric comorbidities in multiple regression models. Results . After adjusting for covariates, OP Group had significantly slower reaction time than the Control Group on discharge (mean difference [SE] = 65[20] ms, p = 0.001) and at 6 weeks (mean difference [SE] = 45[20] ms, p = 0.024), but not at 6 months. Parietal (PZ) P3b amplitudes were significantly smaller in the OP group on discharge (mean difference [SE] = 2.23[0.84] V, p = 0.009) and at 6 months (mean difference [SE] = 3.34[1.43] V, p = 0.021). P3b latencies or frontal (FZ) N1 component did not show significant intergroup differences. Conclusion . Acute exposure to clinically significant doses of OPIs seem to cause impairment in behavioural and neurophysiological indices of stimulus discrimination, that outlast the cholinergic phase of intoxication. The behavioural impairment seems to disappear over months, but the underlying neurophysiological deficits of attentive processing seem to last even after 6 months post-exposure.

Atropine Induced Psychosis in Organophosphate Insecticide Poisoning and it's Management: A case series

Atropine is an established antidote in organophosphorus poisoning. It is an anticholinergic that inhibits the muscarinic actions of acetylcholine at postganglionic parasympathetic neuroeffector sites including secretory glands, smooth muscle, and CNS sites. In the literature, the cases of atropine intoxication are not uncommon. We report a case series of five cases of atropine induced psychotic disorder in patients, who manifested with delirium, hallucinations, nervousness, drowsiness, weakness, irrelevant talk, flushing along with tachycardia, and non-reactive dilated pupils suggesting possible anti-cholinergic abuse. The patients reported at the Department of Medicine-Unit II, Sheikh Zayed Medical College/Hospital, Rahim Yar Khan, from January to June 2019. The patients were managed symptomatically by titrating down the atropine's dose, administration of benzodiazepine, and antipsychotics.

Atropine Induced Delirium in Organophosphate (OP) Insecticide Poisoning: A Case Report

: Delirium is a condition associated with disturbances in mental abilities attributing to the reduced awareness of one’s environment. The onset of delirium is usually rapid, which may last for hours or even few days. Organophosphate poisoning (OP poisoning) is one of the leading causes associated with suicidal attempts and major admissions in the intensive care unit. Few literatures have been reported regarding the use of atropine and the concurrent risk of adverse reactions. Manifestations of atropine overdose and misuse includes dryness of the mouth, tachycardia and in addition, psychotic symptoms such as restlessness and excitement, hallucinations, delirium etc. A 14 year-old female patient who manifested with delirium and associated symptoms after atropine administration during the management of OP poisoning. Atropine administrations should be monitored based on the acetyl cholinesterase enzyme estimation and the dose may be titrated to prevent the worsening of the present conditions. Monitoring of the signs and symptoms is the key element to prevent the adverse effects.Key words: Atropine, Organophosphate, Poison, Delirium, Adverse drug reaction, Acetyl cholinesterase estimation.

Hypoalbuminemia as a Predictor of 30-day Mortality in Patients with Acute Organophosphate Insecticide Poisoning

Purpose: The association of hypoalbuminemia with 30-day in-hospital mortality in patients with organophosphate insecticide poisoning (OPI) was studied. Methods: This retrospective cohort study was conducted between January 2006 and November 2013 in the emergency department (ED) after OPI poisoning. A Kaplan-Meier 30-day survival curve and the log-rank test were used to analyze patients stratified according to serum albumin levels on ED admission (hypoalbuminemia or normo-albuminemia). Independent risk factors including hypoalbuminemia for 30-day mortality were determined by multivariate Cox regression analysis. Results: A total of 135 patients were included. Eighty-eight (65%) patients were male and the mean age was $57.3{pm}17.0$ years. Serum albumin, mean arterial pressure, and Glasgow coma scale score were significantly higher in the survival group than the non-survival group. APACHE II score was significantly lower in the non-survival group than the survival group. The mortality of the hypoalbuminemia group (serum albumin <3.5 g/dl) was 68.8%, while that of the normo-albuminemia group (serum albumin ${geq}3.5g/dl$) was 15.1%. The area under the ROC curve of the serum albumin level was 0.786 (95% CI, 0.690-0.881) and the APACHE II score was 0.840 (95% CI, 0.770-0.910). Conclusion: Hypoalbuminemia is associated with 30-day mortality in patients with OPI poisoning.

Base deficit is a predictor of mortality in organophosphate insecticide poisoning.

Organophosphate insecticide (OPI) self-poisoning is a major medical problem in many countries. Several studies have demonstrated that the base deficit (BD) is a prognostic tool that is correlated with the severity of injury and predicted mortality, particularly in trauma patients. Here, we aimed to investigate the prognostic significance of BD in OPI poisoning. This retrospective observational study was conducted between January 1, 2006, and January 31, 2015, at a single emergency department (ED). The BD values were divided into quartiles according to the number of patients: 3 mEq/L or less, 3-5.9 mEq/L, 6-9.9 mEq/L, and 10 mEq/L or greater. Survival at 30 days from ED admission was estimated using the Kaplan-Meier survival analysis. Among 154 patients, 31 died, yielding a mortality of 20.1%. The highest BD quartile (≥ 10 mEq/L) and the 6-9.9 mEq/L group were associated with an increased risk of 30-day mortality. Patients with a BD of 10 mEq/L or greater had a 5.85-fold higher risk of 30-day mortality and patients with a BD of 6-9.9 mEq/L had a 5.40-fold higher risk of 30-day mortality compared to patients with a BD of 3 mEq/L or less. The area under the curves of the BD and the Acute Physiology and Chronic Health Evaluation II score for mortality were 0.748 (95% confidence interval (CI), 0.660-0.835) and 0.852 (95% CI, 0.789-0.915), respectively. This study showed that the BD is a predictor of 30-day mortality in patients with OPI poisoning.

Evaluation of Organophosphorus Poisoning: Case Series

Organophosphate insecticide compounds inhibit both acetyl cholinesterase and pseudocholinesterase activities. Acute organophosphate insecticide poisoning can manifest three different phases of toxic effects namely, acute cholinergic crisis, intermediate syndrome (IMS), and delayed polyneuropathy. Diagnosis is based on history of exposure and clinical manifestations. Management is beneficial with supportive measures along with specific antidotes. In this case reports, two patients with organophosphate insecticide poisoning are described. Both patients tried to commit suicide by ingesting an unknown amount of organophosphorus poison and both of them have developed intermediate syndrome. But one patient collapsed due to cardiac arrest and other patient was discharged with no complaints. Treatment for both patients mainly included atropine and parlidoxime.

A retrospective review of intensive care management of organophosphate insecticide poisoning: Single center experience.

Organophosphate (OP) compounds are used as insecticides. Given the widespread availability and use of these chemicals, OP poisoning is quite common following either accidental or intentional exposures. Immediate intensive care management can save lives in these patients. We aimed to investigate intensive care management provided to OP poisoning patients in a tertiary care hospital in Turkey. This was a retrospective chart review of 62 patients, admitted to the Intensive Care Unit (ICU) with OP poisoning between 2000 and 2012. Of the 62 patients studied, 40 (65%) were male, 45 (73%) were suicide attempts, 59 (95%) ingested the OP compounds, and three patients (5%) (two patients with suicide and 1 with accidental exposure) died in the ICU. There were statistically significant differences between survivors and nonsurvivors for Glasgow Coma Scale (GCS) on admission (P = 0.034), Acute Physiology and Chronic Health Evaluation II (APACHE II) score (P = 0.003), Sequential Organ Failure Assessment (SOFA) score (P = 0.024), time to initiation of treatment (P = 0.034) and serum lactate dehydrogenase (LDH) levels (P = 0.007). Organophosphate poisoning is a life-threatening condition that requires immediate diagnosis and management. GCS, APACHE II score, SOFA score, and time to admission to the emergency department and LDH levels can provide prognostic information and predict outcomes.

Red cell distribution width as a predictor of mortality in organophosphate insecticide poisoning

ObjectiveSuicide by organophosphate insecticide (OPI) poisoning is a major clinical concern (predominantly in developing countries), and 200000 deaths occur annually worldwide. Red cell distribution width (RDW) has been used to predict outcome in several clinical conditions. Here, we aimed to investigate the relationship between the RDW and 30-day mortality during OPI poisoning. MethodsThis retrospective analysis was performed between January 2008 and July 2013 in patients admitted to the emergency department after OPI poisoning. A Kaplan-Meier 30-day survival curve was analyzed in patients stratified according to the optimal cut-off point of RDW defined using a receiver operating characteristic (ROC) curve. Multivariate Cox proportional hazards analyses were conducted to determine the independent prognostic factors for 30-day mortality. ResultsAmong 102 patients, 21 died, yielding a mortality of 20.6%. Elevated RDW was significantly associated with early mortality in patients with OPI poisoning. Levels of RDW that exceeded 13.5% (hazard ratio, 2.64; 95% confidence interval [CI], 1.05-6.60) were associated with increased mortality in the multivariate analysis. The area under the ROC curve of RDW was 0.675 (95% CI, 0.522-0.829). ConclusionsThis study showed that RDW is an independent predictor of 30-day mortality in patients with OPI poisoning.

Acute reversible Parkinsonism following accidental exposure to organophosphate insecticide

Organophosphate insecticide (OPI) poisoning is one of the most common poisonings seen in rural south India. OPIs act by inhibiting acetylcholine esterase enzyme activity and thereby increasing acetylcholine at synapses. The usual neurological complications of OPI compounds are acute cholinergic crisis, intermediate syndrome, and delayed sensorimotor polyneuropathy. Extrapyramidal symptoms, though very rare, can also occur following OPI exposure. Parkinsonism is a movement disorder that develops as a consequence of reduced function of the dopaminergic neurons within the basal ganglia. The etiology of parkinsonism is multifactorial, with both genetic and environmental determinants. The development of typical parkinsonism following brief inhalational OPI exposure is very rare and there are only a few reports in the literature. We report a 50-year-old male who presented with cholinergic crisis following acute accidental inhalational exposure to chlorpyriphos, an OPI compound; he developed features of parkinsonism on day 6 of hospital admission, but recovered completely without treatment in 7 days.

Antidote for organophosphate insecticide poisoning: atropine and pralidoxime

Acute organophosphate (OP) poisoning produces cholinergic symptoms resulting from the inhibition of cholinesterase, and the overstimulation of muscarinic and nicotinic receptors in the synapses. The dominant clinical features of acute cholinergic toxicity include bradycardia, miosis, lacrimation, salivation, bronchorrhea, and bronchospasm. All symptomatic patients should receive therapy with oxygen, atropine, and pralidoxime. Atropine works as a physiologic antidote by competitively occupying muscarinic receptor sites, reducing the effects of excessive acetylcholine. Atropine should be immediately administered, and the dose can be titrated according to the severity of OP poisoning. A large dose may be necessary to overcome the excessive cholinergic state in case of severe poisoning. Pralidoxime is a biochemical antidote that reactivates acetylcholinesterase by removing OP from it. It is effective in treating both muscarinic and nicotinic symptoms. After some period of time, the acetylcholinesterase-OP compound undergoes a conformational change, known as aging, which renders the enzyme irreversibly resistant to reactivation by a pralidoxime. There has been a great deal of controversy over the effectiveness of pralidoxime in acute OP poisoning. However, it may be beneficial to administer pralidoxime for a sufficient period in case of severe poisoning with a large quantity of OP, which is common in Korea.

Erythrocyte Cholinesterase Enzyme Activity and Hemoglobin Values in Cacao Farmers of Southwestern Nigeria as Related to Insecticide Exposure

ABSTRACT The blood of 76 cacao farmers from Southwestern Nigeria was monitored for erythrocyte cholinesterase enzyme activity (AChE) and hemoglobin values before and after insecticide application. Eight farmers had 30% to 50% baseline AChE activity, which suggests chronic organophosphate insecticide poisoning. AChE activity inhibition suggestive of occupational exposure (20% to 30%) was manifested by 28% of the farmers, whereas 30% to 50% inhibition suggestive of hazard was manifested by 11%. Significantly depressed post–insecticide application hemoglobin values were similarly recorded among the farmers. AChE activity inhibition, depression in hemoglobin values, and the years of involvement of the farmers in insecticide application on cacao, were positively correlated. Occupational exposure hazard due to organophosphate insecticides is therefore real among cacao farmers in Southwestern Nigeria. Regular biomonitoring of their blood for AChE activity and hemoglobin level is necessary.

Organophosphate Insecticide Poisoning and Parkinsonism

Extrapyramidal parkinsonism in a 14 year-old boy developed 5 days after the accidental ingestion of a raw eggplant sprayed with the organophosphate dimethoate (Rogor), in a report from Meyer Children Hospital, Rappaport School of Medicine, Haifa, Israel.

Extrapyramidal Parkinsonism Complicating Acute Organophosphate Insecticide Poisoning

The aim of this study is to report our experience with a child who developed extrapyramidal perturbations complicating acute organophosphate insecticides poisoning and to review the literature reporting on basal ganglia impairment associated with this poisoning. Our patient had developed overt parkinsonism presenting with a resting tremor, expressionless face, and lack of blinking along with marked cogwheel rigidity and a stooped, slow gait. He was alert, coherent, and cooperative, yet agitated. The parkinsonian perturbations developed 5 days after an accidental ingestion of a raw eggplant sprayed with the organophosphate dimethoate (Rogor) when he had already recovered from the acute cholinergic crisis, the first stage of organophosphate poisoning. Such a presentation was initially perceived by his caregivers as severe reactive depression or even psychosis. Once a parkinsonian syndrome was diagnosed, he was begun on amantadine and completely recovered within 1 week with no relapse of symptoms. Basal ganglia impairment should be considered in any patient who develops extrapyramidal symptoms such as marked rigidity and bradykinesia or choreoathetosis while recovering from the acute cholinergic phase of organophosphate insecticide poisoning. Thus, administration of a drug such as amantadine, which probably enhances neurotransmission, may hasten the rate of recovery and prevent long-term neurologic and emotional sequelae.

Accidental Organophosphate Insecticide Poisoning: a Fatal Child case with Hazards to Emergency Department Staff

A 2-year-old boy was accidentally poisoned by one spoonful of organophosphate insecticide and presented in cardiac arrest. Spontaneous circulation was restored after initial resuscitation and antidote therapy (atropine and pralidoxime) but the boy finally succumbed with multiple complications. We reviewed the literature on the clinical features and management of acute organophosphate poisoning, and the appropriate protective equipment for preventing secondary poisoning of healthcare workers.

Potential therapeutic agents in the management of organophosphorus poisoning.

This letter is a response to the report by Sungur and Guven [1] on intensive care management of organophosphate insecticide poisoning, which was recently published in Critical Care. Insect damage costs the world loses approximately 6 billion pounds sterling every year. Use of pesticides has increased food production in parallel with population growth in many parts of the world. Many insect-borne diseases have been eliminated or controlled by the use of insecticides. Organophosphorus compounds are widely used as insecticides and as agents of chemical warfare. According to the World Health Organization [2], 1 million serious accidental and 2 million suicidal poisonings with insecticides occur worldwide every year, and of these approximately 200,000 die, mostly in developing countries. Atropine and oximes are traditionally used in the management of such poisonings but they have failed to reduce the attendant mortality and morbidity. Some agents have been found to reduce the toxicity of organophosphorus compounds in animal experiments, and they have potential as therapeutic agents in the management of organophosphorus poisoning. These agents are magnesium, clonidine and fluoride. Kiss and Fazekas [3] reported control of premature ventricular contractions with intravenous magnesium. Magnesium was considered to counteract the direct toxic inhibitory action of organophosphorus compounds on sodium–potassium ATPase. It also inhibits acetylcholine release [4]. Singh and coworkers [5] found that intravenous magnesium reversed the neuro-electrophysiological effect of organophosphorus poisoning. Pretreatment of mice with clonidine (0.1–1 mg/kg) resulted in protection against toxic manifestations of soman – an organophosphorus compound [6]. Increased survival rates, reduction in centrally mediated symptoms such as tremor and straub tail, and reduction in excessive salivation were noted. The protective effects of clonidine are probably due to blockade of acetylcholine release and postmuscarinic receptors, together with transient inhibition of acetylcholinesterase. Thus, clonidine may prove useful in the management of organophosphorus poisoning. Pretreatment of mice with atropine and sodium fluoride resulted in greater antidotal effect than atropine alone against the toxic actions of soman and sarin [7,8]. It was hypothesized that the antidotal effect of fluoride is due to its antidesensitizing action at the nicotinic receptors in the neuromuscular junction and sympathetic ganglia [9]. Increased cholinesterase levels were observed in workers handling fluorine compounds in a plastics factory [10]. The role of fluoride in management of poisoning with organophosphorus must be studied further. Although the role of the above compounds in the management of organophosphorus poisoning must be studied further, I feel that it is worth using them (particularly magnesium and clonidine) in intensive care management of such patients to control excessive acetylcholine activity. The potential health problems associated with the organophosphorus compounds calls for collaborative research between medically advanced countries and those developing countries where most of the poisoning occurs.

Intensive care management of organophosphate insecticide poisoning.

Organophosphate (OP) insecticides inhibit both cholinesterase and pseudo-cholinesterase activities. The inhibition of acetylcholinesterase causes accumulation of acetylcholine at synapses, and overstimulation of neurotransmission occurs as a result of this accumulation. The mortality rate of OP poisoning is high. Early diagnosis and appropriate treatment is often life saving. Treatment of OP poisoning consists of intravenous atropine and oximes. The clinical course of OP poisoning may be quite severe and may need intensive care management. We report our experience with the intensive care management of serious OP insecticide poisonings. A retrospective study was performed on the patients with OP poisoning followed at our medical intensive care unit. Forty-seven patients were included. Diagnosis was performed from the history taken either from the patient or from the patient's relatives about the agent involved in the exposure. Diagnosis could not be confirmed with serum and red blood cell anticholinesterase levels because these are not performed at our institution. Intravenous atropine and pralidoxime was administered as soon as possible. Pralidoxime could not be given to 16 patients: 2 patients did not receive pralidoxime because they were late admissions and 14 did not receive pralidoxime because the Ministry of Health office was out of stock. Other measures for the treatment were gastric lavage and administration of activated charcoal via nasogastric tube, and cleansing the patient's body with soap and water. The patients were intubated and mechanically ventilated if the patients had respiratory failure, a depressed level of consciousness, which causes an inability to protect the airway, and hemodynamic instability. Mechanical ventilation was performed as synchronized intermittent mandatory ventilation + pressure support mode, either as volume or pressure control. Positive end expiratory pressure was titrated to keep SaO2 above 94% with 40% FIO2. Weaning was performed using either T-tube trials or pressure support weaning. The chi-square test was used for statistical analysis. Data are presented as mean +/- standard deviation. There were 25 female and 22 male patients. Thirty-two (68%) were suicide attempts and 15 (32%) were accidental exposure. The gastrointestinal route was the main route in 44 (93.6%) patients. The mortality rates for the patients who did and did not receive pralidoxime were 32 and 18.7%, respectively, and were not statistically different. The most frequent signs were meiosis, change in mental status, hypersalivation and fasciculations. Ten patients (21.2%) required mechanical ventilation. The mortality rate for the patients who required mechanical ventilation was 50%, but the rate was 21.6% for the patients who were not mechanically ventilated. Intermediate syndrome was observed in 9 (19.1%) patients. Complications were observed in 35 (74.4%) patients. These complications were respiratory failure (14 patients), aspiration pneumonia (10 patients), urinary system infection (6 patients), convulsion (4 patients) and septic shock (1 patient). The duration of the intensive care stay was 5.2 +/- 3.0 days. Ingestion of OP compounds for suicidal purposes is a major problem, especially in developing countries. Thirty-two (68%) of our patients used the OP insecticide for suicide. Two patients did not receive pralidoxime because of delayed admission and they were successfully treated with atropine alone. Three of the patients who did not receive pralidoxime because of unavailability died. The mortality rate was no different between the patients treated with pralidoxime or those without pralidoxime. De Silva and coworkers have also reported that the mortality rate was not different between each group. Three patients with intermediate syndrome died due to delay for endotracheal intubation. The average respiratory rate of these patients increased from 22 to 38 breaths/min, which is an important sign of respiratory distress. The nurse to patient ratio was increased after these events. Early recognition of respiratory failure resulting in intubation and mechanical ventilation is a life-saving intervention for patients with OP poisoning. Respiratory failure is the most troublesome complication, which was observed in 35 (74.4%) patients. Patients with OP poisoning may have respiratory failure for many reasons, including aspiration of the gastric content, excessive secretions, pneumonia and septicemia complicating acute respiratory distress syndrome. OP insecticide poisoning is a serious condition that needs rapid diagnosis and treatment. Since respiratory failure is the major reason for mortality, careful monitoring, appropriate management and early recognition of this complication may decrease the mortality rate among these patients.

The phosphoryl oxime-destroying activity of human plasma.

The potential of obidoxime and other pyridinium-4-aldoximes to reactivate dimethyl- and diethylphosphorylated cholinesterases is markedly restricted by the inevitable formation of rather stable phosphoryl oximes (POXs) with high anticholinesterase activity. This effect is hardly seen with very dilute enzyme preparations, but becomes significant at physiological enzyme concentrations. Human plasma with the butyrylcholinesterase irreversibly blocked by soman was able to stimulate obidoxime-induced reactivation of concentrated erythrocyte acetylcholinesterase (Ery-AChE) to the same extent as was observed with a dilute preparation, suggesting phosphoryl oxime-destroying capacity. The inactivating factor, which was tentatively termed POX-hydrolase, had (1) a molecular weight of >100 kDa; (2) required Ca2+ , which could not be substituted by Zn2+ or Mg2+; and (3) lost its catalytic activity reversibly in the presence of ethylenediamine-tetraacetic acid (EDTA). The enzyme activity varied widely (20-fold) among different subjects and did not follow the activity pattern of human serum paraoxonase (PON1). Rabbit plasma with its particularly high paraoxonase content showed only weak POX-hydrolase activity. These data suggest POX-hydrolase to be a different entity. POX-hydrolase was most active with the putative phosphoryl-obidoxime from paraoxon-ethyl, less with the product from paraoxon-methyl and least with that from diisopropylfluorophosphate. The analogue TMB-4 reacted similarly to obidoxime. The putative phosphonyl oximes arising by the reaction of obidoxime with nerve agents were apparently not cleaved. The variation in POX-hydrolase activity may additionally contribute to the variable response to oxime therapy in patients with organophosphate insecticide poisoning.

Methods for serum cholinesterase assay and classification of genetic variants

Two cholinesterases are found in man: the one in red cells, nerve endings, lung, spleen, and grey matter of the brain is commonly called acetylcholinesterase (ACHE, acetylcholine acetylhydrolase, EC 3.1.1.7), the other in serum, liver, pancreas, heart, and white matter, is called serum cholinesterase (CHE, acylcholine acylhydrolase, EC 3.1.1.8). Only the serum enzyme is currently clinically relevant, and used as a test of hepato-cellular function, to confirm acute organophosphate insecticide poisoning, and to detect increased sensitivity to the muscle relaxant succinylcholine (suxamethonium).