pralidoxime and Acute-Disease

Topics: Acute Disease; Cholinesterase Inhibitors; Cholinesterase Reactivators; Humans; Insecticides; Organophosphate Poisoning; Pralidoxime Compounds; Randomized Controlled Trials as Topic; Treatment Outcome

Organophosphates may cause serious life-threatening conditions, such as an initial acute cholinergic crisis and intermediate syndrome. Each of these conditions has a potential for respiratory failure requiring ventilatory support. For this reason, it is very important to recognize them early, especially to institute appropriate management. The diagnosis of organophosphate poisoning is based essentially on a clinical assessment, followed by laboratory examinations. Sometimes the diagnosis may be difficult, as in case 1, identified initially as brainstem stroke. However, if neurological syndromes associated with organophosphate poisoning are well known, they can easily be distinguished from other conditions that resemble them. Two cases displayed the symptoms and signs of intermediate syndrome; however, one case (no. 2) did not have severe poisoning on admission but needed artificial ventilation. Each case recovered completely from organophosphate poisoning as a result of early diagnosis and appropriate therapy. Therefore, we would like to describe the clinical and laboratory features of these syndromes, observed in three interesting cases, and to emphasize the importance of early and accurate diagnosis for the appropriate management of acute organophosphate poisoning.

Topics: Acetylcholinesterase; Acute Disease; Adult; Aged; Antidotes; Atropine; Emergency Medicine; Female; Humans; Insecticides; Male; Organophosphorus Compounds; Poisoning; Pralidoxime Compounds; Treatment Outcome

Acute organophosphorus (OP) pesticide poisoning is widespread in the developing world. Standard treatment involves the administration of intravenous atropine and an oxime to counter acetylcholinesterase inhibition at the synapse, but the usefulness of oximes is uncertain.. To assess the evidence on the use of oximes in OP poisoning.. Systematic review.. We searched Medline, Embase, and Cochrane databases (last check 01/02/02) for 'organophosphate' or 'oxime' together with 'poisoning' or 'overdose'. We cross-referenced from other articles, and contacted experts to identify unpublished studies. A Web search engine [www.google.com] was also used, with the keywords 'organophosphate', 'oxime', and 'trial' (last check 01/02/02).. We found two randomized controlled trials (RCTs) involving 182 patients treated with pralidoxime. The RCTs found no benefit with pralidoxime, and have been used to argue that pralidoxime should not be used in OP poisoning.. The RCT authors must be congratulated for attempting important studies in a difficult environment. However, their studies did not take into account recently clarified issues regarding outcome, and their methodology is unclear. A generalized statement that pralidoxime should not be used in OP poisoning is not supported by the published results. Oximes may well be irrelevant in the overwhelming self-poisoning typical of the tropics, but a large RCT comparing the current WHO-recommended pralidoxime regimen (>30 mg/kg bolus followed by >8 mg/kg/h infusion) with placebo is needed for a definitive answer. Such a study should be designed to identify any patient subgroups that might benefit from oximes.

Topics: Acute Disease; Atropine; Drug Overdose; Humans; Insecticides; Organophosphorus Compounds; Oximes; Pralidoxime Compounds; Randomized Controlled Trials as Topic; Research Design

The mortality rate caused by organophosphate (OP) poisoning is still high, even the standard treatment such as atropine and oxime improves a lot. To search for alternative therapies, this study was aimed to investigate the effects of packed red blood cell (RBC) transfusion in acute OP poisoning, and compare the therapeutic effects of RBCs at different storage times.Patients diagnosed with OP poisoning were included in this prospective study. Fresh RBCs (packed RBCs stored less than 10 days) and longer-storage RBCs (stored more than 10 days but less than 35 days) were randomly transfused or not into OP poisoning patients. Cholinesterase (ChE) levels in blood, atropine usage and durations, pralidoxime durations were measured.We found that both fresh and longer-storage RBCs (200-400 mL) significantly increased blood ChE levels 6 hours after transfusion, shortened the duration for ChE recovery and length of hospital stay, and reduced the usage of atropine and pralidoxime. In addition, fresh RBCs demonstrated stronger therapeutic effects than longer-storage RBCs.Packed RBCs might be an alternative approach in patients with OP poisoning, especially during early stages.

Topics: Acute Disease; Atropine; Cholinesterase Reactivators; Cholinesterases; Erythrocyte Transfusion; Female; Gastric Lavage; Humans; Male; Organophosphate Poisoning; Pralidoxime Compounds; Prospective Studies; Time Factors

To determine a new pralidoxime (PAM) treatment guideline based on the severity of acute organophosphate intoxication patients, APACHE II score, and dynamic changes in serum butyrylcholinesterase (BuChE) activity.. This is a randomization trial. All patients received supportive care measurements and atropinization. Each enrolled patient was treated with 2 gm PAM intravenously as the loading dose. The control group was treated according to the WHO's recommended PAM regimen, and the experimental group was treated according to their APACHE II scores and dynamic changes in BuChE activity. If a patient's APACHE II score was ≧26 or there was no elevation in BuChE activity at the 12th hour when compared to the 6th, doses of 1 g/h PAM (i.e., doubled WHO's recommended PAM regimen) were given. The levels of the serum BuChE and red blood cells acetylcholinesterase and the serum PAM levels were also measured.. Forty-six organophosphate poisoning patients were enrolled in this study. There were 24 patients in the control group and 22 patients in the experimental group. The hazard ratio of death in the control group to that of the experimental group was 111.51 (95% CI: 1.17-1.613.45; p = 0.04). The RBC acetylcholinesterase level was elevated in the experimental group but was not in the control group. The experimental group did not exhibit a higher PAM blood level than did the control group.. The use of PAM can be guided by patient severity. Thus, may help to improve the outcomes of organophosphate poisoning patients.

Topics: Acetylcholinesterase; Acute Disease; Adult; Aged; Erythrocytes; Female; Humans; Male; Middle Aged; Organophosphate Poisoning; Pralidoxime Compounds; Treatment Outcome

In developing countries, including Sri Lanka, a high proportion of acute poisoning and other medical emergencies are initially treated in rural peripheral hospitals. Patients are then usually transferred to referral hospitals for further treatment. Guidelines are often used to promote better patient care in these emergencies. We conducted a cluster randomized controlled trial (ISRCTN73983810) which aimed to assess the effect of a brief educational outreach ('academic detailing') intervention to promote the utilization of treatment guidelines for acute poisoning.. This cluster RCT was conducted in the North Central Province of Sri Lanka. All peripheral hospitals in the province were randomized to either intervention or control. All hospitals received a copy of the guidelines. The intervention hospitals received a brief out-reach academic detailing workshop which explained poisoning treatment guidelines and guideline promotional items designed to be used in daily care. Data were collected on all patients admitted due to poisoning for 12 months post-intervention in all study hospitals. Information collected included type of poison exposure, initial investigations, treatments and hospital outcome. Patients transferred from peripheral hospitals to referral hospitals had their clinical outcomes recorded. There were 23 intervention and 23 control hospitals. There were no significant differences in the patient characteristics, such as age, gender and the poisons ingested. The intervention hospitals showed a significant improvement in administration of activated charcoal [OR 2.95 (95% CI 1.28-6.80)]. There was no difference between hospitals in use of other decontamination methods.. This study shows that an educational intervention consisting of brief out-reach academic detailing was effective in changing treatment behavior in rural Sri Lankan hospitals. The intervention was only effective for treatments with direct clinician involvement, such as administering activated charcoal. It was not successful for treatments usually administered by non-professional staff such as forced emesis for poisoning.. Controlled-Trials.com ISRCTN73983810 ISRCTN73983810.

Topics: Acute Disease; Antidotes; Charcoal; Cluster Analysis; Education, Continuing; Hospitalization; Hospitals, Rural; Humans; Outcome Assessment, Health Care; Personnel, Hospital; Poisoning; Practice Guidelines as Topic; Pralidoxime Compounds; Sri Lanka

Acute organophosphorus (OP) poisoning is relatively common and a major cause of death from poisoning in developing countries. Magnesium has been shown to be of benefit in animal models.. We conducted a phase II study of bolus doses of (MgSO4) in 50 patients with acute organophosphate poisoning. Patients eligible for inclusion had ingested OP and had cholinergic symptoms consistent with moderate or severe poisoning. All patients received standard care of atropinization titrated to control muscarinic symptoms and pralidoxime. The trial was run in 4 sequential groups of patients. Participants in each group received a different total dose of MgSO4 (20%) administered as intermittent bolus doses infused over 10-15 min or placebo. There was one control patient for every 4 patients who received MgSO4. Group A (16 patients) received a total of 4 gm MgSO4 as a single bolus, group B (8 patients) received 8 gm (in two 4 gm doses q4H), group C (8 patients) received 12 gm (in three 4 gm doses q4H) group D (8 patients) received 16 gm (in four 4 gm doses q4H) and control (10 patients) received placebo). Patients were closely monitored for any adverse reaction like significant clinical neuromuscular disturbance and respiratory depression.. No adverse reactions to magnesium were observed. The 24 hour urinary magnesium concentration were statistically different between 16 gm (234.74 ± 74.18 mg/dl) and control (118.06 ± 30.76 mg/dl) (p = 0.019), while it was much lower than the 80% of the intravenous magnesium load. Six patients died in control group compared to 3 in 4 gm, 2 in 8 gm and 1 in 12 gm group. There was no mortality in 16 gm group.. Magnesium was well tolerated in this study. Larger studies are required to examine for efficacy.

Topics: Acute Disease; Adolescent; Adult; Atropine; Bangladesh; Cholinesterase Reactivators; Dose-Response Relationship, Drug; Female; Hospitals, University; Humans; Infusions, Intravenous; Magnesium; Magnesium Sulfate; Male; Middle Aged; Muscarinic Antagonists; Organophosphate Poisoning; Pralidoxime Compounds; Severity of Illness Index; Young Adult

The neuromuscular transmission failure in acute organophosphate (OP) poisoning occurs because of the irreversible inactivation of the enzyme acetylcholinesterase located in the neuromuscular junction, and is distinguished neuroelectrophysiologically by single electrical stimulus-induced repetitive responses and either a decremental or a decrement-increment response upon high-rate repetitive nerve stimulation (RNS). Understandably, the administration of pharmacological agents with actions at different sites in the neuromuscular junction would alter the neuroelectrophysiological findings in acute OP poisoning.. The effect of several pharmacological agents including pralidoxime (10 patients), magnesium sulphate (4 patients) and pancuronium (7 patients) on the neuroelectrophysiological abnormalities was studied in 21 patients with acute OP poisoning.. Pralidoxime administration produced neurophysiological amelioration in 11 out of 15 occasions. In those cases where it produced a beneficial effect, pralidoxime administration was continued and its neuroelectrophysiological effects were studied daily. The efficacy of pralidoxime administration was demonstrated by neuroelectrophysiological testing for a maximum of 6 days after poisoning. Three types of neuroelectrophysiological responses to pralidoxime were noted: (i) lack of neuroelectrophysiological improvement (two patients); (ii) initial improvement with subsequent lack of improvement (two patients); and (iii) initial improvement with subsequent normalisation of neuromuscular transmission (5 patients). Normalisation of the electrodiagnostic tests and the failure of pralidoxime to ameliorate the neuromuscular transmission abnormalities were neuroelectrophysiological indications for the discontinuation of pralidoxime treatment. The administration of magnesium sulphate (MgSO4.7H2O, 4 g intravenous) resulted in a decrease in the CMAP amplitude, loss of the repetitive response and conversion of the decrement-increment response at high-rate RNS to an incremental response. Repetitive responses and the decremental response at high-rate RNS also disappeared after the administration of pancuronium (0.5 mg intravenous) to 6 patients. However, in one case where pancuronium administration was preceded by pralidoxime, there occurred a dramatic worsening of the neuromuscular transmission defect.. While the administration of all 3 agents-- pralidoxime, magnesium sulphate and pancuronium-- resulted in the reversion of the neuroelectrophysiological defects, only pralidoxime is contended to be therapeutically useful. The therapeutic benefit due to its administration is limited by a short duration of action, and hence it is recommended that it should be administered for a longer period of time under neuroelectrophysiolgical guidance.

Topics: Acute Disease; Antidotes; Electroencephalography; Humans; Insecticides; Magnesium Sulfate; Monitoring, Physiologic; Neuromuscular Diseases; Neuromuscular Junction; Nicotinic Antagonists; Organophosphorus Compounds; Pancuronium; Pralidoxime Compounds; Synaptic Transmission; Treatment Outcome

Organophosphate poisoning (OPP) accounts for 200,000 deaths annually in developing countries. Serum cholinesterase (SChE) is of diagnostic value in patients with OPP and is checked repeatedly during the course of treatment. This study aimed to investigate the recovery pattern in patients with OPP using linear mixed models.. Using a retrospective cohort study design, we included 212 adult OPP patients who had visited the emergency department (ED) in a tertiary medical center between 2000 and 2010. One hundred and thirty-one patients were available for analysis, as 81 patients did not meet the criteria and were excluded. Information regarding basic personal characteristics, initial vital signs and severity scores, laboratory data, type and amount of organophosphate ingested, treatment, and serial SChE values was collected. A random coefficient model with a random intercept and a random slope of time were added to address the dynamic relationships of SChE with time and other associated factors.. The initial SChE activity and recovery rates varied among patients with OPP. The type of organophosphate, the first SChE activity, and the initial APACHE II score were significantly related to the SChE recovery trend. Chlorpyrifos and methamidophos had significantly slower and faster SChE recovery rates, respectively, than other organophosphates. Sex, dose of Pralidoxim (2-PAM), and delay in obtaining medical assistance did not significantly affect SChE recovery.. This study demonstrated the pattern and associated correlates of SChE activity recovery in patients with acute OPP. Chlorpyrifos appeared to have a slower SChE activity recovery rate than other organophosphates.

Topics: Acute Disease; Antidotes; Chlorpyrifos; Cholinesterases; Critical Illness; Female; Humans; Insecticides; Male; Middle Aged; Organophosphate Poisoning; Organothiophosphorus Compounds; Pralidoxime Compounds; Retrospective Studies; Severity of Illness Index; Suicide, Attempted; Tertiary Care Centers; Time Factors

Topics: Acute Disease; Adult; Antidotes; Antiparkinson Agents; Benserazide; Cholinesterase Inhibitors; Humans; Insecticides; Levodopa; Male; Organophosphate Poisoning; Parkinson Disease; Pralidoxime Compounds; Trihexyphenidyl

Anticholinesterase poisoning is an important health problem in our country, and a complete understanding of its underlying mechanisms is essential for the emergency physician. Thus, we aimed to investigate the cardiac biochemical parameters and mortality in dichlorvos-induced poisoning in rats. Rats were randomly divided into 5 groups as control (corn oil), dichlorvos, atropine, pralidoxime, and atropine+pralidoxime groups. Immunohistochemical analyses of apoptosis and inducible nitric oxide synthase showed no change in cardiac tissue for all of the groups. Serum cholinesterase levels were suppressed with dichlorvos, and these reductions were inhibited with atropine and/or pralidoxime pretreatment. Serum levels of creatine kinase, creatine kinase-MB, cardiac troponin I, myoglobin, and N-terminal probrain natriuretic peptide were not affected with poisoning. Malondialdehyde and glutathione levels were not statistically significant between the groups. Although serum nitric oxide levels in the dichlorvos group were lower than those in the control group, cardiac nitric oxide levels in the atropine+pralidoxime group were markedly higher than those in the dichlorvos group. Atropine, pralidoxime, and atropine+pralidoxime pretreatments markedly reduced the mortality. In conclusion, our results implied that measured cardiac markers especially N-terminal probrain natriuretic peptide may not contribute to the early (first 6 hours) diagnosis of cardiotoxicity in dichlorvos-induced poisoning in rats. These results also showed that acute dichlorvos administration did not cause significant cardiac damage, and oxidative stress does not play a marked role in dichlorvos-induced poisoning. Besides, cardiac nitric oxide may produce protective effect on myocardium with atropine+pralidoxime therapy in rats.

Topics: Acute Disease; Analysis of Variance; Animals; Antidotes; Atropine; Biomarkers; Cholinesterase Inhibitors; Dichlorvos; Heart; Immunohistochemistry; In Situ Nick-End Labeling; Male; Nitric Oxide; Organophosphate Poisoning; Pralidoxime Compounds; Random Allocation; Rats; Rats, Wistar; Survival Rate

A prospective study was undertaken to find the incidence of hyperamylasemia and acute pancreatitis in patients with anticholinesterase poisoning. This was done by serial estimation of total serum amylase and pancreatic imaging by ultrasonography and confirmed, if necessary, by computerized tomography. Anticholinesterase poisoning was caused by either ingestion or accidental exposure to organophosphates or carbamates; it was diagnosed when patients presented with features of cholinergic crisis, depressed serum butyrylcholinesterase activity of >50% and showed improvement following administration of atropine alone or atropine and 2-PAM. All the patients admitted with anticholinesterase poisoning between July 2001 and June 2005 were prospectively studied for elevated serum amylase. The serum amylase levels were estimated daily up to 10 days in survivors and in nonsurvivors till they survived. Ultrasonography of the abdomen was carried out in all to find swelling of the pancreas. Computerized tomography was undertaken in those who had a swollen pancreas or whose serum amylase levels were elevated significantly (> or =800 S.U). Of the 86 patients enrolled, 79 were taken up for analysis as data were incomplete in 7. Of the 79 patients, serum amylase was found to be elevated that is, >200 S.U. in 37 patients (46.95%). In three patients it was 800 S.U. One of them showed swollen pancreas on ultrasonography, which was confirmed by computerized tomography. This patient had ingested propoxyfur. In the other two patients, evidence of acute pancreatitis was not observed (on autopsy in one who died and on imaging in the other who survived). They had ingested chlorpyrifos. There was no significant correlation between the nature of the compounds (organophosphate or carbamates), inhibition of serum BUChE at admission, duration and severity of cholinergic syndrome and increase and time course of increase in serum amylase. Except for fenthion, significant persistent increase in serum amylase was not observed with individual compounds. The other associated abnormalities were polymorphonuclear leukocytosis (TLC >11,000/cumm) in all 37 patients who had elevated amylase, hyperglycemia (6/37) and, elevated transaminases (6/37). Mild elevation of serum amylase is common in patients with anticholinesterase poisoning. However, acute pancreatitis is rare.

Topics: Acute Disease; Adolescent; Adult; Amylases; Atropine; Butyrylcholinesterase; Carbamates; Cholinesterase Inhibitors; Cholinesterase Reactivators; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Humans; Hyperamylasemia; Male; Middle Aged; Occupational Exposure; Organophosphate Poisoning; Organophosphates; Pancreatitis; Pralidoxime Compounds; Prospective Studies; Radiography; Respiration, Artificial; Suicide, Attempted; Transaminases; Ultrasonography

To observe the treatments on the patients with acute methamidophos dichlorvos (DDV) and omethoate poisoning and provide the reliable basis for the rational treatments on these three organophosphorus pesticides poisoning.. 101 patients with AOPP in 7 hospitals were divided into three groups: Group A, 59 patients with acute methamidophos poisoning, Group B, 32 patients with acute DDV/dipterex (DEP) poisoning, Group C, 10 patients with acute omethoate/dimethoate poisoning. The levels of erythrocyte AChE and the therapeutic efficacies of pralidoxime chloride (PAM-Cl) were compared among the three groups.. The AChE activities of all the three groups were inhibited on level of (9.12 +/- 7.99) U/g Hb (group A), 7.32 +/- 4.62 U/g Hb (group B) and (12.01 +/- 9.53) U/g Hb (group C), among which no significant difference was found (P > 0.05). All the patients recovered from acute cholinergic excitation or crisis after the treatment of PAM-Cl. The erythrocyte AChE activities were obviously reactivated in group A three hours later after admission to hospital, each on level of (11.37 +/- 8.67) U/g Hb, (12.51 +/- 6.98) U/g Hb, (15.90 +/- 7.31) U/g Hb, (18.33 +/- 4.78) U/g Hb and (18.91 +/- 7.00) U/g Hb at the 12th, 24th, 48th, 72nd hour and discharge (P < 0.05), and the upgrade tendency was continuous. AChE activities in group B were also reactivated after treatment, each on level of (8.91 +/- 5.89) U/g Hb, (1.31 +/- 6.61) U/g Hb, (13.00 +/- 7.55) U/g Hb, (14.22 +/- 7.80) U/g Hb, (12.78 +/- 7.07) U/g Hb and (16.87 +/- 7.06) U/g Hb at the 3rd, 12th, 24th, 48th, 72nd hour and discharge, but the upgrade tendency turned slowly after 12 hours, the inhibited AChE activities were not reactivated in group C from the beginning to the end.. After the treatment of PAM-Cl, the AChE activities of the patients with acute methamidophos poisoning could be continuously reactivated, the AChE activities of the patients with acute DDV/DEP poisoning could also be reactivated in 12 hours, and then keep stable, but the AChE activities of the patients with acute omethoate/dimethoate poisoning could not be reactivated. However, PAM-Cl has therapeutic efficacy against acute toxicity of all the three organophosphorus pesticides. Oximes should be vigorously used in the treatment of AOPP, including acute omethoate/dimethoate poisoning.

Topics: Acetylcholinesterase; Acute Disease; Adult; Cholinesterase Reactivators; Dichlorvos; Dimethoate; Female; Humans; Male; Middle Aged; Organophosphate Poisoning; Organothiophosphorus Compounds; Pralidoxime Compounds; Retrospective Studies

To study the therapeutic efficacy and mechanism of oxime drug, pralidoxime chloride (PAM-Cl), on acute dichlorvos (DDV) poisoning.. The toxic signs and survival rate were recorded and ChE activity in blood was determined in treatment group with PAM-Cl and non-treatment group after DDV was given to rats and mice by gastrogavage; the therapeutic efficacy and reactivation of DDV-inhibited ChE by PAM-Cl were observed on the patients with acute DDV poisoning.. (1) The alleviated and delayed toxic signs as well as higher survival rate were found in PAM-Cl treatment group compared with non-treatment group. (2) After the rats were exposed to DDV, the ChE activities of whole blood in different time within 24 h were statistically significantly higher in PAM-Cl treatment group than in non-treatment group (P < 0.05). (3) After PAM-Cl treatment, muscular fasciculation and other nicotinic signs in poisoned patients were disappeared and the inhibited blood ChE activities were gradually reactivated to normal level.. PAM-Cl has therapeutic efficacy against acute toxicity of DDV through its reactivation of inhibited ChE.

Topics: Acute Disease; Adolescent; Adult; Animals; Antidotes; Cholinesterases; Dichlorvos; Female; Humans; Insecticides; Male; Mice; Mice, Inbred Strains; Middle Aged; Poisoning; Pralidoxime Compounds; Rats; Rats, Sprague-Dawley; Treatment Outcome

We investigated the ultrastructural effects of the organophosphate compound methamidophos and treatment with atropine and pralidoxime (2-PAM) on rat kidneys. Male Wistar albino rats were assigned to four groups. Group 1 received 30 mg/kg methamidophos, the LD50 for this compound in rats, via oral gavage. Group 2 received only physiologic saline. Group 3 rats received 30 mg/kg methamidophos and were treated with 2-PAM and atropine via intraperitoneal injection when cholinergic symptoms were noted. Group 4 served as a control, and received physiologic saline in equivalent volumes and routes to Group 3. Kidney tissues were prepared for electron microscopic studies. No ultrastructural changes were detected in Group 1 after acute poisoning with methamidophos and in Group 3 treated with antidotes after poisoning. Acute organophosphate poisoning and antidotal treatment in this model are not associated with histopathological changes in the rat kidney but the models with different organophosphate compounds, by administrating the different dosages, may be more illuminative in explaining the effects of these chemicals in kidney.

Topics: Acute Disease; Animals; Antidotes; Disease Models, Animal; Kidney; Kidney Diseases; Kidney Function Tests; Male; Organothiophosphorus Compounds; Pralidoxime Compounds; Random Allocation; Rats; Rats, Wistar; Reference Values

We investigated the ultrastructural effects of methamidophos and the positive effects of 2-pralidoxime (2-PAM) on the liver. Male Wistar-albino rats were assigned to 4 groups and all were treated per os: Group 1 (n=10) received 30 mg/kg methamidophos; Group 2 (n=7) (serving as controls for Group 1) received physiologic NaCl; Group 3 (n=10) received 30 mg/kg methamidophos and was treated with 2-PAM and atropine when cholinergic symptoms were noted; and Group 4 (n=7) (serving as controls for Group 3) was treated with physiologic NaCl. Plasma cholinesterase was measured using radioimmunoassay. Liver tissues were prepared for electron microscopic studies. Methamidophos treatment of Group 1 led to serious changes in hepatocytes and organelles. These changes were not detected in Group 3. In Group 1, the chromatin content of some hepatocyte nuclei and cytoplasmic density increased; these cells also became vacuolar in appearance as a result of lysis in the mitochondrial matrices. In some cells, the lipid content constituted the majority of the cytoplasm. Furthermore, these cells were surrounded by glycogen accumulation. In some areas of the perisinusoidal zone, collagen fibers had increased to form bands. None of these changes were noted in Group 3. These findings suggest that acute organophosphate poisoning causes serious histopathological effects in rat liver, but that these changes are reversible with appropriate treatment strategies.

Topics: Acute Disease; Animals; Animals, Laboratory; Antidotes; Insecticides; Liver; Organothiophosphorus Compounds; Pralidoxime Compounds; Rats; Rats, Wistar

Two children were admitted for poisoning by organophosphate pesticides applied as hair rinses against lice. These chemical agents inhibit the acetylcholinesterase enzyme at various sites. The resultant accumulation of the transmitter acetylcholine causes abnormal signs and symptoms. The diagnosis is based on a reduction in the blood cholinesterase activity. The specific treatment comprises the administration of atropine and pralidoxime.. Accidental poisoning by organophosphate insecticides may occur, due to the misuse of such substances as shampoo against lice. An accurate information for users is necessary.

Topics: Abdominal Pain; Acute Disease; Animals; Antidotes; Child; Child, Preschool; Cholinesterase Reactivators; Confusion; Decontamination; Diarrhea; Emergency Treatment; Female; Hair Preparations; Humans; Insecticides; Lice Infestations; Male; Organophosphorus Compounds; Pediculus; Portugal; Pralidoxime Compounds; Scalp Dermatoses; Time Factors; Vomiting

To study the effects of improving the neuromuscular transmission (NMT), "non-AChE-reactivating effects", by oximes in treating acute isocarbophos poisoning.. The effect of pralidoxime chloride(PAM-Cl) on the neuromuscular transmission(NMT) in rats exposed to isocarbophos was studied by using the stimulation single fiber electromyography (SSFEMG) to determine the single fiber action potential.. After the rats exposed to isocarbophos were treated by PAM-Cl, the mean consecutive difference(MCD) value [(25.99 +/- 5.84) microsecond] of single fiber action potential was significantly lower than that before PAM-Cl treatment [(33.21 +/- 4.09) microsecond, (P < 0.01)], but no AChE reactivation in blood and gastrocnemius was observed.. PAM-Cl has "non-AChE-reactivating effects", it could markedly improve isocarbophos-induced NMT block of gastrocnemius.

Topics: Acute Disease; Animals; Antidotes; Cholinesterase Inhibitors; Insecticides; Malathion; Neuromuscular Junction; Pralidoxime Compounds; Rats; Synaptic Transmission

An acute poisoning in a 44-y-old female who ingested 50 ml of ethyl parathion concentrate (25 g) is described. She was treated by gastric lavage, administration of pralidoxime and atropine, and mechanical ventilation. As signs of intoxication disappeared at day 3, treatment was discontinued. The patient had a relapse of acute cholinergic crisis at day 4, and the same treatment was applied again. The acute poisoning phase was followed by an intermediate syndrome and delayed distal polyneuropathy. The clinical course of this severe ethyl parathion poisoning was favorable after 40 d.

Topics: Acute Disease; Adult; Atropine; Cholinesterase Reactivators; Drug Overdose; Drug Therapy, Combination; Female; Gastric Lavage; Humans; Insecticides; Muscles; Parathion; Peripheral Nervous System Diseases; Pralidoxime Compounds; Recurrence; Respiration, Artificial; Suicide, Attempted; Syndrome; Treatment Outcome

Various organophosphorus compounds with low acute toxicity levels are widely used as insecticides. Human acute poisoning by organophosphates has often occurred accidentally. We determined the activity and isoenzyme patterns of serum cholinesterase (ChE) obtained from 13 human patients who attempted suicide with various organophosphates, i.e. Fenitrothion, Malathion, Isoxathion, Pyridaphenthion and Trichlorfon, and studied on the changes in the activity and isoenzyme patterns of serum ChE after ingestion. The following results were obtained. 1) Twenty ChE isoenzyme bands from normal human serum were detected by electrophoretic separation on polyacrylamide gradient gel. The main bands in the ChE isoenzyme pattern in normal serum were bands 4 and 5 which had the highest activity of acetylcholinesterase (AChE) with a molecular weight of 600,000-800,000, and bands 7, 12, 14, 17 and 18. 2) Inhibition of serum ChE activity was more severe as the amount ingested increased in patients who took Fenitrothion and Malathion. Reactivation of serum ChE activity was very slow in patients treated with PAM (2-pyridine aldoxime methiodide) in the late stage of ingestion or whose symptoms reappeared. 3) There were no differences in the patterns of serum ChE isoenzyme by organophosphorus compound. Band 7 disappeared in the serum ChE isoenzyme of almost every patient, and bands 12, 18, 14 and 17 of the serum ChE isoenzyme disappeared successively with the decline of serum ChE activity. Only band 5 of the isoenzyme remained in cases who had serum ChE activity lower than 5% of normal. 4) All 13 patients were treated with PAM and atropine immediately after being admitted to hospitals. We could not clearly determine the efficacy of PAM on reactivation of serum ChE activity and isoenzyme, because it was impossible in human poisoning to compare PAM efficacy with no treatment and with pre- and post-PAM treatment. 5) The activity and isoenzyme patterns of serum ChE recovered rapidly after combined hemoperfusion and hemodialysis treatment (HP-HD treatment) of the patients poisoned with Malathion. But HP-HD treatment had no effect on poisoning by Fenitrothion and Isoxathion. These findings demonstrated the changes in the activity and isoenzyme pattern of serum ChE in patients poisoned with several organophosphates after PAM and HP-HD treatment.

Topics: Acute Disease; Adult; Aged; Animals; Cholinesterases; Female; Hemoperfusion; Humans; Isoenzymes; Male; Middle Aged; Organophosphate Poisoning; Poisoning; Pralidoxime Compounds; Rats; Renal Dialysis

Respiratory failure (RF) developed in 43 (40.2 percent) of 107 patients with acute organophosphate or carbamate poisoning; 22 (51.2 percent) died. The 64 patients who did not develop RF survived. All cases of RF developed within 96 hours after poisoning: within 24 hours in 35 patients (acute onset) and between 24 and 96 hours in eight patients (subacute onset). Severity of poisoning was the primary determinating factor for RF. Cardiovascular collapse and pneumonia were also associated with RF. In 19 patients with cardiovascular collapse, 17 had acute onset of RF and two had subacute onset. In 28 patients with pneumonia, 17 developed acute onset of RF and eight developed subacute onset. No organophosphorus compound caused RF more frequently than another. The duration of ventilator support for subacute RF was significantly longer than for acute RF (287 +/- 186 vs 115 +/- 103 hours, p = 0.02). The use of pralidoxime did not reduce the incidence of RF. We found that severity of poisoning, cardiovascular collapse, and pneumonia were the predisposing factors to RF. The golden time for treatment of acute organophosphate or carbamate poisoning was the initial 96 hours. No RF occurred after this time. Aggressive treatment and prevention of the above three factors will reduce the incidence of RF, or in other words, reduce the mortality.

Topics: Acute Disease; Adolescent; Adult; Aged; Aged, 80 and over; Antidotes; Atropine; Carbamates; Child; Child, Preschool; Female; Humans; Infant; Insecticides; Male; Middle Aged; Organophosphorus Compounds; Pneumonia; Pralidoxime Compounds; Respiration, Artificial; Respiratory Insufficiency

Organophosphate insecticides are widely used agents which are quickly absorbed through the skin and mucous membranes. The effects of acute exposure to these agents can be severe and intensive therapy may be required. Specific drugs are available to reverse the muscarinic, nicotinic and central effects of these poisons. When given early they are very effective and early diagnosis and treatment may therefore be life-saving. A case of acute poisoning with an organophosphate anticholinesterase insecticide is reported. The signs and symptoms of acute poisoning are described and a rational approach to specific treatment is discussed.

Topics: Acute Disease; Adult; Atropine; Cholinesterase Reactivators; Critical Care; Humans; Insecticides; Male; Organophosphate Poisoning; Organothiophosphates; Organothiophosphorus Compounds; Pralidoxime Compounds

Topics: Acute Disease; Adolescent; Adult; Antidotes; Child; Child, Preschool; Cholinesterases; Female; Humans; Insecticides; Intensive Care Units; Malaysia; Male; Middle Aged; Organophosphorus Compounds; Pralidoxime Compounds; Respiratory Distress Syndrome; Respiratory Insufficiency