The Impact of Pesticides - Academy Publish

This recommendation was supported by Peng et al. (2004) who conducted arandomized controlled clinical trial involving 108 patients aimed to assess theefficacy of hemoperfusion with charcoal in treatment of acute severe dichlorvospoisoning. The authors concluded that the rapid fall in blood dichlorvos level andthe dramatic clinical response suggest that hemoperfusion with charcoal is effectivein the treatment of acute severe dichlorvos poisoning. However, two clinical trialsdesigned to evaluate the effectiveness of activated charcoal in OP poisoned patientsfailed to confirm these results. A randomised controlled trial of single and multipledoses of activated charcoal in Sri Lanka failed to find a significant benefit of eitherregimen over placebo in more than 1000 patients poisoned with pesticides(Eddleston et al., 2005a). In addition, Eddleston et al. (2008) conducted an openlabel,parallel group, randomised, controlled trial in three Sri Lankan hospitalsaimed to assess whether routine treatment with multiple-dose activated charcoaloffers benefit compared with no charcoal. Among 2338 patients who ingestedpesticides (1310 cases of poisoning with OP and carbamate pesticides) there wereno differences in mortality between patients treated with or no charcoal. The authorsconcluded that they cannot recommend the routine use of multiple dose activatedcharcoal in poisonings with OP and carbamate pesticides and suggest that furtherstudies of early charcoal administration might be useful.Specific TreatmentAtropinePatients acutely poisoned with OP compounds should be treated with atropine,diazepam and an oxime. Atropine acts by blocking the effects of excessconcentrations of acetylcholine at muscarinic cholinergic synapses following OPinhibition of AChE. Atropine is the initial drug of choice in acute OP poisoning.Atropine sulphate in combination with an oxime has been used in traditional therapyfor OP intoxications including insecticides. Atropine can relieve the followingsymptoms of OP poisoning: sweating, salivation, rhinorrhoea, lacrimation, nausea,vomiting and diarrhea, and can help control of bradycardia and circulatorydepressions, dilating the bronchi and abolishing bronchorrhoea. Atropine does notbind to nicotinic receptors and cannot relieve nicotinic effects in OP poisoning(World Health Organization, 1986).According to IPCS (1998) an initial trial dose of atropine, 1 to 2 mg (0.05 mg/kg)intravenously, should be given slowly over three minutes, and then repeated everyfive to ten minutes if there is no observable adverse effect. In symptomatic children,intravenous dose of 0.015 to 0.05 mg/kg atropine should be administered every 15minutes as needed. Atropine may then be repeated or increased in increments at 15to 30 minute intervals until bronchosecretion is cleared and the patient is atropinized(dilated pupils, dry skin, skin flushing) which should be maintained during furthertreatment. Repeated evaluations of the secretions through regular auscultation of thelungs is the only adequate measure of atropinization in the severely poisonedpatient. The dose may be increased as required. Patients poisoned with OP appear tobe resistant to toxic effects of atropine and may require relatively large doses ofatropine administered during prolonged periods. In severe OP poisoning total doseof atropine given during 5 weeks of treatment can be as high as 30000 mg (IPCS,2002).AcademyPublish.org - The Impact of Pesticides47