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PubMed2005

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 microg/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.

Acute Disease↗

PubMed1997

Brain involvement in organophosphate poisoning.

Organophosphate poisonings cause substantial morbidity and mortality worldwide; however, the neurological effects have not been clearly established. We have studied cerebral perfusion to investigate neurotoxic effects. Clinical effects, plasma cholinesterase activity, and brain single photon emission computerization tomography (SPECT) data were investigated in 16 patients with organophosphate poisonings. The subjects were from an adult intensive care unit in a university hospital. Cholinesterase activity in plasma was determined upon admission and then every day in the morning. Brain SPECT studies were performed during the first week, at the end of therapy, and 3 months after discharge. Patients were classified into 3 groups using a modified Namba classification: latent poisoning (Group A); mild and moderate poisoning (Group B); or severe poisoning (Group C). None of the 6 patients in Group A showed any symptoms; 3 patients in Group B had muscarinic and nicotinic effects; 5 patients in Group C had muscarinic, nicotinic, and central nervous system symptoms. The average plasma cholinesterase for Groups A, B, and C were 54.16 +/- 9.10, 42.2 +/- 12.02, and 13 +/- 4.84 U/ml, respectively (normal range of plasma cholinesterase is 40-80 U/ml). Only 1 patient from Group A required treatment with oxime; 2 patients from Group B and all patients in Group C were given oxime, atropine sulfate, and mechanical ventilation. In the brain SPECT studies, the patients in Group A showed fewer perfusion defect areas than did Group B and C patients. All cases showed perfusion defects especially in the parietal lobe. In addition, perfusion improvement took more time for Group C than for the other groups. The intensive care unit stays of Group C were statistically longer than for Groups A and B. We concluded that brain SPECT is a highly sensitive diagnostic method, together with clinical symptoms and plasma cholinesterase activity, for monitoring the clinical prognosis of organophosphate poisonings.

Adult↗

PubMedDate not supplied

The comparison of therapeutic effects of atropine and pralidoxime on cardiac signs in rats with experimental organophosphate poisoning.

Organophosphate poisoning causes disturbances in cardiac conduction and potentially fatal severe cardiac rhythm abnormalities. This study investigated the cardiac effects of atropine and pralidoxime in the treatment of organophosphate poisoning in rats. Three groups of 10 adult male Wistar rats were anesthetized with an intraperitoneal injection of ketamine 100 mg/kg and xylazine 10 mg/kg and connected to a computerized electrocardiographic monitor. Each rat was then injected intraperitoneally with the pesticide dichlorvos 70 mg/kg. Sixty seconds after the injection, 10 rats were injected with saline, 10 with pralidoxime mesylate 20 mg/kg, and 10 with atropine 10 mg/kg. During the computerized electrocardiographic monitoring, each rat's heart rate and QT(c) intervals were recorded and analyzed as the injections were administered. The heart rates in all 3 groups did not differ before the dichlorvos was administered, nor at 60 seconds afterward, but in the atropine group, the time elapsed before the first decline in heart rate was significantly longer than that in the control group (P<.05). In addition, the interval before death was significantly longer in the atropine group than in either the control group or the pralidoxime group (P<.05 for both). The QT(c) was almost identical in each of the groups. Atropine has beneficial effects on the heart rate, prolongs the time before the heart rate declines, and delays death but has no effect on the QT(c) interval. Further research about the toxic effects of organophosphate compounds on myocardial cells is warranted.

Animals↗

PubMed2006

Severe acute pancreatitis caused by organophosphate poisoning.

Organophosphate intoxication may be caused pancreatitis, but the role of diagnostic imaging for pancreatitis in these patients has not been well defined. We recently encountered a patient with organophosphate poisoning showing hyperamylasemia who was proven to have severe acute pancreatitis by CT findings. The patient was a 69-year-old woman who presented to a local hospital with disturbance of consciousness. She was initially treated for cerebral infarction, but an extremely low level of ChE was noted on Day 3. The patient was then referred to our institution. Examination of the abdomen revealed weak intestinal peristalsis, blood chemistry showed an increased level of serum amylase, and the urinary organophosphate test was positive. Based on the findings obtained by abdominal CT scanning, severe acute pancreatitis was diagnosed. Clouding of her consciousness resolved on day 21, but a pancreatic pseudocyst was detected on day 41.

Acute Disease↗

PubMed2005

Diagnostic aspects of organophosphate poisoning.

Organophosphate (OP)-type chemical warfare agents (nerve agents) present a constant threat to the population. Sensitive and specific methods for the detection and verification of exposure to nerve agents are required for diagnosis, therapeutic monitoring, health surveillance and forensic purposes. Determination of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activity in blood remains a mainstay for the fast initial screening but lacks sensitivity and specificity. Quantitative analysis of nerve agents and their degradation products in plasma and urine by mass spectrometric methods may prove exposure but is limited to hours or days after the incident due to the short residence time of the analytes. Investigation of protein adducts extends the time interval between exposure and sampling and may be suitable to detect low-level exposure. Definitive prove of exposure requires a spectrum of different methods, expensive and sophisticated equipment and will be limited to specialized laboratories.

Acetylcholinesterase↗

PubMed1990

Organophosphate poisoning.

Organophosphate compounds insecticides are the most commonly associated with serious human toxicity. We reviewed the adult cases of organophosphate poisoning seen at HURRA from January 1986 to January 1990. We had 14 cases, all male patients. The most common mode of exposure was by ingestion in a suicidal attempt, (8/14 cases). The most common symptom observed was nausea (6/14 patients), and the most common sign was increased bronchial secretions (8/14 patients). Laboratory abnormalities were similar to those previously reported in the literature: leukocytosis (10/14 cases), hyperglycemia (5/14 cases) and hypokalemia (4/14 cases). Patients were treated following accepted guidelines. None of our patients developed seizures nor ventricular arrhythmias. One of our patients developed respiratory failure and required mechanical ventilation. Two patients developed pneumonic processes, requiring intravenous antibiotic therapy. The hospital stay of these two patients was prolonged (7 and 10 days respectively). For the other 12 patients, the hospital stay ranged from 2 to 4 days. We had no mortality in our series. We were able to obtain follow-up interview by telephone with 10 of the 14 patients and we did not find any history of symptoms of delayed clinical toxicity.

Adult↗

PubMed2004

Organophosphate poisoning.

Organophosphates are commonly used as pesticides around the world. Exposures to organophosphates cause a significant number of poisonings and deaths each year. Organophosphates bind and inhibit cholinesterase enzymes. Acute toxicity manifests as a cholinergic crisis with excessive glandular secretions, altered mental status, and weakness. Several delayed syndromes have also been associated with organophosphate exposure, including a myasthenic-like syndrome, peripheral neuropathies, neuropsychiatric abnormalities, and extrapyramidal disorders. Clinical features and management of organophosphate poisoning is reviewed with emphasis on those affecting the central and peripheral nervous system.

Humans↗

PubMed1987

Organophosphate poisoning.

Organophosphate insecticides have become increasingly popular for agricultural, industrial, and home use and represent a significant potential health risk. We have reviewed the history, pathophysiology, clinical presentation, laboratory findings, differential diagnosis, therapy, and complications of toxic exposure to organophosphates. Promp recognition and aggressive treatment of acute intoxication are essential in order to minimize the morbidity and mortality from these potentially lethal compounds.

Diagnosis, Differential↗

PubMedDate not supplied

Rapid and sensitive quantitative analysis of alkyl phosphates in urine after organophosphate poisoning.

Organophosphate compounds are widely used as pesticides. After ingestion by humans, organophosphates decompose into alkyl phosphates. Decomposition continues postmortem. We developed a rapid (< 3 h), quantitative, and sensitive analysis of the human organosphosphate metabolites O,O-dimethylphosphate (DMP), O,O-diethylphosphate (DEP), O,O-dimethylthiophosphate (DMTP), O,O-diethylthiophosphate (DETP), O,O-dimethyldithiophosphate (DMDTP), and O,O-diethyldithiophosphate (DEDTP). Urine is dried under azeotropic conditions with isopropanol and nitrogen. All metabolites are converted into their corresponding benzyl esters reacting with benzyl bromide and diazotoluene. The protocol prevents the isomerization of DMTP and DETP occurring when diazo compounds are used exclusively. The benzyl ester derivatives are purified on solid-phase extraction silica columns. The quantitative analysis is performed by gas chromatography-mass spectrometry. All metabolites can be identified by the parent molecular ions. Urine samples from eight cases of fatal suicidal poisoning dialkyl phosphates were quantitated. The limits of detection ranged from 3 to 6 ng/mL. Hence, this protocol is sufficiently sensitive to detect and quantitate organophosphate metabolites beyond cases of fatal poisoning, in the clinical setting, and even following average environmental exposure.

Forensic Medicine↗

PubMed2002

Prolonged apnea following succinylcholine administration in undiagnosed acute organophosphate poisoning.

Organophosphates (OP) are irreversibly bound to cholinesterase, causing deactivation of acetylcholinesterase. As a result of inhibition of plasma cholinesterase, increased sensitivity to drugs hydrolyzed by this enzyme can occur, e.g. succinylcholine and mivacurium. A case of more prolonged succinylcholine-induced paralysis in a child with undiagnosed acute OP insecticide poisoning is presented. A 7-h period of apnea and paralysis after administration of succinylcholine was attributed to the decreased rate of succinylcholine metabolism resulting from inhibition of pseudocholinesterase by the insecticide. In seven previously reported cases of prolonged succinycholine apnea after OP poisoning, exposure to insecticide was in chronic or subacute form without any obvious symptoms, and the duration of apnea did not extend up to 4 h, whereas in our case with acute, severe poisoning, succinylcholine led to more prolonged muscle paralysis. In the anesthetic management of patients with acute OP poisoning, succinylcholine should be avoided.

Acute Disease↗

PubMedDate not supplied

The effects of N-acetylcysteine on oxidative stress in organophosphate poisoning model.

Organophosphate compounds act by irreversible inhibition of cholinesterase. In addition to their muscarinic, nicotinic, and central nervous system effects, some organophosphate insecticides cause oxidative stress by increasing lipid peroxidation in erythrocytes and by increasing levels of the enzymes superoxide dismutase and catalase. In this study, the effects of an antioxidant, N-acetylcysteine (NAC), in organophosphate poisoning were investigated. After obtaining Animal Ethics Committee approval, 16 male Wistar rats were divided into 2 groups. Following anesthesia, rats were tracheostomized and mechanically ventilated. Invasive hemodynamic monitoring was begun and all rats were injected with 70 mg/kg of dichlorvos (DDVP) intraperitoneally. The rats in group 1 received placebo intravenous 0.9% NaCl and the rats in group 2 received 150 mg/kg intravenous NAC. Blood samples were obtained before injection of DDVP and 60 minutes after injection to determine levels of malondialdehyde, superoxide dismutase, and catalase. Hemodynamic data and biochemistry test results were compared by analysis of variance and Wilcoxon test. P<.05 was regarded as statistically significant. Superoxide dismutase and malondialdehyde levels were significantly increased in group 1 while no difference was observed in group 2. It was concluded that organophosphate compounds might cause oxidative stress by interfering with antioxidant defense mechanisms in erythrocytes and that NAC might prevent increased lipid peroxidation. In addition to classic treatments, drugs with antioxidant effects might therefore be promising in the treatment of organophosphate poisoning.

Acetylcysteine↗

PubMed2006

Pancreatic pseudocyst after acute organophosphate poisoning.

Acute organophosphate poisoning (OP) shows several severe clinical symptoms due to its strong blocking effect on cholinesterase. Acute pancreatitis is one of the complications associated with acute OP, but this association still may not be widely recognized. We report here the case of a 73-year-old man who had repeated abdominal pain during and after the treatment of acute OP. Hyperamylasemia and a 7-cm pseudocyst in the pancreatic tail were noted on investigations. We diagnosed pancreatic pseudocyst that likely was secondary to an episode of acute pancreatitis following acute OP. He was initially treated with a long-term intravenous hyperalimentation, protease inhibitors and octerotide, but eventually required surgical intervention, a cystgastrostomy. Acute pancreatitis and hyperamylasemia are known to be possible complications of acute OP. It is necessary to examine and assess pancreatic damage in patients with acute OP.

Acute Disease↗

PubMed2006

Prognostic value of human erythrocyte acetyl cholinesterase in acute organophosphate poisoning.

Acute organophosphate poisoning (OPP) such as dichlorvos may be monitored by the measurement of the erythrocyte acetyl cholinesterase (EAChE) and the serum cholinesterase (SChE) activities. The aim of this study was to look at correlation between the severity of the OPP judged by certain parameters such as coma, hemodynamic disturbances, respiratory failure, and the decrease of cholinesterases enzymes including EAChE and SChE at admission. Cholinesterase activity was determined upon admission and then on days 3 and 15 in the morning. Clinical effects, EAChE, and SChE activities data were investigated in 42 patients with OPP aged of 29.6 +/- 11.8 years with acute cholinergic crisis in all cases. They were comatose in 29% of cases, presenting both hypotension or shock and hypoxemia in 17% of cases. Fifteen of them (36%) required mechanical ventilation. The mean EAChE activity at admission was 24.3 +/- 11.6 micromol/mL per hour at 37 degrees C; it was 1260 +/- 2204 IU/L for SChE. There were no correlations between the EAChE and the SChE activities. The EAChE was decreased only in comatose patients and those presenting hypotension, hypoxemia, and bradycardia with a cutoff of 23.5 micromol/mL per hour at 37 degrees C. Death was observed in 2 patients with a deep decrease of the EAChE at 5 micromol/mL per hour at 37 degrees C in 1 case and 9 micromol/mL per hour at 37 degrees C in another. The kinetics of improvement of the EAChE activity below the cutoff showed the absence of statistical improvement of the EAChE activity on day 3 (16.6 +/- 9 vs 19.5 +/- 5.7 micromol/mL per hour at 37 degrees C); this improvement was remarkable on day 15 (16.6 +/- 9 vs 27.5 +/- 6.5micromol/mL per hour at 37 degrees C, P = .0004). In summary, the marked decrease of EAChE activity appears in this study as prognostic factor in acute OPP, and coma, respiratory failure, hemodynamic disturbances, and death are associated with a decrease of the EAChE of less than 23.5 micromol/mL per hour at 37 degrees C.

Acetylcholinesterase↗

PubMedDate not supplied

Enzymes hydrolyzing organophosphates as potential catalytic scavengers against organophosphate poisoning.

Enzymes hydrolyzing organophosphates could be used as catalytic scavengers for treatment of organophosphate poisoning and for decontamination. Two organophosphorus hydrolases (OPH) were selected: the Flavobacterium sp/Pseudomonas diminuta phosphotriesterase (PTE) and human paraoxonase (HuPON). Genes encoding these enzymes were cloned and functional recombinant enzymes expressed. PTE was expressed in E. coli. Natural HuPON was purified from human plasma; recombinant HuPON was expressed in human embryonic kidney 293 T cells. Although HuPON displays interesting catalytic properties, a site-directed mutagenesis program was undertaken to improve its catalytic efficiency. PTE has high efficiency in hydrolysis of organophosphates, including nerve agents. PTE injected in rat has a half-life of 100 min. However, to overcome pharmacokinetic problems of injected OPH and/or immunological incompatibility, the model enzyme (recombinant PTE) was immobilized onto a hollow-fiber reactor. This reactor designed for extracorporeal blood circulation is under experimentation for post-exposure detoxification.

Animals↗

PubMed2002

Review of the value of huperzine as pretreatment of organophosphate poisoning.

Today, organophosphate (OP) nerve agents are still considered as potential threats in both military or terrorism situations. OP agents are potent irreversible inhibitors of central and peripheral acetylcholinesterases. Pretreatment of OP poisoning relies on the subchronic administration of the reversible acetylcholinesterase (AChE) inhibitor pyridostigmine (PYR). Since PYR does not penetrate into the brain, it does not afford protection against seizures and subsequent neuropathology induced by an OP agent such as soman. Comparatively, huperzine (HUP) is a reversible AChE inhibitor that crosses the blood-brain barrier. HUP is presently approved for human use or is in course of clinical trials for the treatment of Alzheimer's disease or myasthenia gravis. HUP is also used as supplementary drug in the USA for correction of memory impairment. Besides, HUP has also been successfully tested for pretreatment of OP poisoning. This review summarizes the therapeutical value of HUP in this field. Moreover, the modes of action of HUP underlying its efficacy against OP agents are described. Efficacy appears mainly related to both the selectivity of HUP for red cell AChE which preserves scavenger capacity of plasma butyrylcholinesterases for OP agents and to the protection conferred by HUP on cerebral AChE. Finally, recent data, showing that HUP seems to be devoid of deleterious effects in healthy subjects, are also presented. Globally, this review reinforces the therapeutical value of HUP for the optimal pretreatment of OP poisoning.

Alkaloids↗

PubMed2003

Oral treatment of organophosphate poisoning in mice.

OBJECTIVE: Organophosphates are used as pesticides, herbicides, and chemical warfare agents. Treatment of organophosphate poisoning is with intravenous atropine and pralidoxime in addition to supportive care. This study determined the efficacy of oral agents in preventing death from organophosphate poisoning. METHODS: The organophosphate paraoxon (8 mg/kg) was used in a murine model with lethality at four and 24 hours as an end point. For oral treatment, 15 male Balbc mice were given either atropine sulfate (4 mg/kg), or a combination of atropine sulfate (4 mg/kg) with pralidoxime (100 mg/kg), by oral gavage. A control group of 22 mice received water by oral gavage. Chi-square analysis was used to compare results in the different groups. RESULTS: Of the control group, six of 22 survived to four hours after paraoxon exposure. Of the exposed animals treated with oral atropine, eight of 15 survived to four hours. Of the exposed animals treated with a combination of atropine and pralidoxime, 13 of 15 survived to four hours. All animals surviving to four hours survived to 24 hours. The increased survival of animals in the atropine group relative to the control group was not significant (p = 0.09). Survival was significant in the group treated with atropine and pralidoxime relative to atropine alone (p = 0.02) and to the control group (p = 0.0002). All treated mice surviving at four hours were alive at 24 hours. CONCLUSIONS: Both oral atropine and a combination of oral atropine and pralidoxime improved survival, and combination therapy achieved statistical significance. Generalization of this result to other organophosphate pesticides, other doses of paraoxon, and other species cannot be made without further investigations.

Animals↗

PubMed1979

Arrhythmias in organophosphate poisonings.

168 cases of organophosphate poisonings are reviewed with special respect to frequent arrhythmias. In 134 cases toxic repolarisation with QT prolongation, ST- and T- anomalies were present. 56 patients had arrhythmias and the prevalence of ventricular arrhythmias was impressive. In five patients a transient picture of myocardial infarction was seen. The great incidence of ECG alterations and arrhythmias necessitate the permanent monitoring of patients with organophosphate poisoning in an intensive care unit.

Adolescent↗

PubMed2001

Organophosphate poisoning and management, an update.

Organophosphate poisoning is characterised for the most part, by acute incidents. Management is by way of first aid (in mild poisoning) and use of atropine with or without the oximes, (in moderate to severe poisoning). Of late, it has become apparent that subchronic and chronic organophosphate poisoning are a common manifestation. This review paper summarises this triphasic nature of organophosphate poisoning. Possible future diagnostic and management techniques are also discussed.

Acute Disease↗