Organophosphate Pesticide Poisoning Bishan Rajapakse MBChB Otago Emergency Medicine Advanced Trainee Registrar, MPhil Student (ANU), South Asian Clinical Toxicology. – A free PowerPoint PPT presentation (displayed as a Flash slide show) on PowerShow.com - id: 450343-ZjM4Y. The PowerPoint PPT presentation: 'Organophosphate Toxicity Lessons from Anuradhapura' is the property of its rightful owner. Do you have PowerPoint slides to share? If so, share your PPT presentation slides online with PowerShow.com.
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Organophosphate Poisoning
In this article
The organophosphate (OP) pesticides inhibit acetylcholinesterase. Hence, acetylcholine accumulates at nerve synapses and neuromuscular junctions, stimulating muscarinic and nicotinic receptors and the central nervous system. They are used as pesticides but can also be used as 'nerve gas'. This is prohibited under the Geneva Convention but could be used by terrorists or rogue regimes. There is some suggestion that the use of OP pesticides may have caused some neurotoxicity and be responsible for 'Gulf War syndrome'. Certainly, insecticides were freely used, as were many other chemicals. The syndrome is inconsistent in those affected but is neither simply a post-traumatic stress disorder nor the result of acute OP poisoning and is likely to represent low-level chronic toxicity.[1, 2, 3, 4] This is supported by a case control study which reported that chronic exposure to OP pesticides can lead both to depressive and anxiety disorders and also to cognitive defects (unrelated to psychiatric disorders).[4] This is a significant problem which may also affect children and further research in this field is necessary.[5]
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Epidemiology
There are no accurate figures kept about the incidence of OP poisoning.
The vast majority of cases are accidental from the use of pesticides. There is a much higher incidence in rural areas of the third world.
Hospital admissions for intentional OP poisoning are twice as numerous as for accidental poisoning. Intentional self-harm tends to involve much higher doses than accidental exposure.
Fortunately, terrorist or warfare use of OP is rare but the potential exists to expose a great many people at once. Sarin is an OP poison and there are two recorded episodes of deliberate release - both in Japan.[6] One was in Matsumoto in 1994 and the other was in the Tokyo subway in 1995. Theses two incidents caused 18 deaths. A single drop on the skin can be rapidly fatal.
According to the World Health Organization (WHO), there are about 1 million people a year admitted to hospital with accidental poisoning and 2 million with suicidal intent. It is estimated that there could be as many as 25 million agricultural workers in the developing world suffering an episode of poisoning each year.[7]The WHO figures appear to be an underestimate and a recent call was made for more reliable data to be collected.[8]
Causes for suspicion
If symptoms follow spraying then those who conducted the spraying should know exactly what was being released.
If people start to get symptoms of poisoning and there is no obvious source then deliberate self-ingestion must be considered.[9]
If there has been an accident and damage to a container then the container should have the appropriate hazard symbol on the side, giving an indication of the contents, plus a telephone number to call for further information.
The affected person may smell of garlic, due to the OP, or of petrol due to the solvent.
Physical properties
OPs tend to be colourless-to-brown liquids at room temperature. Some have a fruity smell but others are odourless.
They are volatile to varying degrees and can therefore be sprayed or distributed as an aerosol and inhaled.
The vapours are denser than air and may accumulate in low-lying areas and enclosed spaces.
After the deliberate releases of sarin in Japan in 1994, there were secondary effects in healthcare workers who treated patients who had not been decontaminated. In emergency medicine departments, personal protective equipment (PPE) should be available for use in such cases.
Presentation
The presentation of OP poisoning depends upon whether the poisoning is mild, moderate or severe. The symptoms are basically those of excessive acetylcholine activity.
Collapse, respiratory depression or respiratory arrest.
Coma.
Death.
Differential diagnosis
The essential features of this type of acute poisoning are those of excessive cholinergic activity. There are a number of other possibilities to consider when deliberate poisoning is suspected: Could this be cyanide? Very rapid onset of symptoms in seconds or minutes with gasping, air hunger and acidosis. There are confusion, convulsions, collapse and coma. There is decreased respiratory rate, respiratory arrest or sudden death. Cyanosis is unusual but there may be cherry pink skin (only seen post-mortem in carbon monoxide poisoning). Pupils are dilated or normal with no fasciculation and secretions are normal.
Could this be a nerve agent or organophosphate? Rapid onset of cholinergic symptoms, including small or pinpoint pupils, painful dim vision, increased respiratory rate, breathing difficulty and bronchospasm. There are excess secretions, saliva and sweat. There is muscle twitching, convulsions, coma, arrest.
Carbamates have a similar effect to OPs but they are less of a problem as they are more easily reversed.[10]
Could this be lewisite? Rapid onset of burns or blistering within minutes of exposure.
Could this be mustard gas? Burns or blistering usually beginning 2-12 hours after exposure.
Could this be phosgene? No history of exposure to chlorine. Rapid-onset eye and/or skin irritation with rapid or delayed respiratory symptoms. Could this be chlorine, other irritant gas, or a riot control agent? Exposure to pungent greenish yellow gas (chlorine) or other irritant. Rapid-onset eye and/or skin irritation and choking/coughing/wheezing.
Is chemical exposure still a possibility? Unexplained sudden death in a healthy adult. Unexplained reduction in level of consciousness. Patient reports unusual sight, smell or taste. A number of patients with the same symptoms. Symptoms in a family or group with common exposure. Known incident or exposure or cause unknown.
Investigations
A&E departments have been supplied with toxicological analytic sampling kits and these kits should be used, where possible, for toxicological sampling.
Decontaminate the patient before obtaining any samples.
Collect samples as early as possible, preferably before treatment; however, do not delay life-saving treatment to obtain them.
Do NOT clean the venepuncture site with alcohol or proprietary skin wipes or swabs, as these contain solvents that can interfere with some assays. Use sterile water or, if the skin is visibly clean, dry cotton wool.
Label all specimens as high-risk.
If there is difficulty in obtaining specimens, the following are given as order of priority:
10 ml blood in plastic lithium heparin tube; 5 ml for children.
5 ml blood in glass lithium heparin tube; may be omitted for children.
4 ml blood in EDTA tube, adults and children.
30 ml urine with no preservative, adults and children.
Plasma cholinesterase level may be used to screen for exposure. RBC cholinesterase level correlates better with severity and prognosis or a mixed cholinesterase ratio is best for determining if sufficient pralidoxime is being given.
Management[11]
General principles
When aiding those who have or may have been exposed to dangerous chemicals, it is important to consider not just the welfare of the patient but your own safety. It is one of the axioms of disaster management that those who are there to rescue should not add to the problem by becoming victims.
Ensure either that you are wearing chemical PPE and/or that the patient has been decontaminated.
Decontaminate the patient in the NHS decontamination unit or decontamination area if this has not already been done. Do not attempt to do it in the A&E department or GP surgery.
If there has been ingestion of an OP or carbamates within the previous two hours, activated charcoal may be used.
Stabilise the airway with oxygen by mask, intubate and ventilate if needed, control any haemorrhage and set up intravenous (IV) access if needed.
Assess the cause, give antidotes if appropriate, reassess, and in the UK alert the local Health Protection Team (HPT), and seek expert advice if needed from HPT, Toxbase[12] or the Public Health England (PHE) poisons helpline.[13]
Hydrocarbon solvents used with OPs often persist after decontamination and can lead to fear that OP is still present. These solvents can lead to symptoms too, including headache and nausea.
Lipophilic compounds can cause delayed or persistent toxicity as they slowly move out of the tissues.
Remember that accurate, contemporaneous notes are essential.
Specific aspects
If you suspect exposure to a nerve agent or OP, ensure that either they have been decontaminated or that you are wearing PPE.
Maintain an airway, give oxygen, use suction on secretions.
Remove the patient's clothing if not already done (place in a double bag, sealed, labelled and stored securely). Shower, wash down or rinse-wipe-rinse with liquid soap and water, or dilute detergent. Remove any contact lenses if present and irrigate the eyes with lukewarm water or normal saline solution.
Check triage tags for details of prehospital treatment.
For severe or moderate symptoms, establish IV access, arrange assessment by an anaesthetist and, as soon as possible, give atropine:[14]
An adult requires atropine, between 0.6 mg and 4 mg IV and a child needs 20 micrograms per kg IV. Give every 10-20 minutes until secretions dry up and the heart rate rises to 80 to 90 beats per minute. This may need as much as 20 mg to achieve this. Do NOT rely on reversal of pinpoint pupils as a guide to adequate atropine administration. Normalisation of cardiovascular parameters and absence of oropharyngeal secretions are better clinical markers of adequate atropine administration.
Pralidoxime is given at 2 g or 30 mg/kg IV for an adult, over 4 minutes. Then continue with the same every 4-6 hours or infuse IV at 8 to 10 mg/kg/hour. The rate of fixing of the bond between cholinesterase and the OP varies between compounds and so the window of opportunity for pralidoxime varies but is usually between 12 and 36 hours. Pralidoxime may be continued for 7 days or until atropine is not required for 24 hours. However, recent studies have suggested that pralidoxime with atropine therapy does not offer any appreciable benefit over atropine in the management of OP poisoning although further trials are needed to explore different dosing regimens of pralidoxime in order to further determine its efficacy in OP poisoning.[15, 16]
Diazepam is given at 5-10 mg IV for an adult or 1-5 mg IV for a child. Repeat as required.[17]
Intubate and ventilate if there is apnoea or severe respiratory distress but avoid succinylcholine.
Check arterial blood gases, U&E, and glucose. Monitor the ECG and treat any arrhythmias.
Contact the PHE Poisons Information Service for advice if there is no response, or slow response, to antidotes.
Paralysis may mask seizures. Consider electroencephalogram (EEG) monitoring.
For mild symptoms only with eye signs but no bronchospasm, bronchorrhoea or fits, observe for 2 hours after exposure, consider atropine or 0.5% tropicamide eye drops for painful or blurred vision and, if there is no progression of symptoms, complete a chemical exposure record form and discharge the patient with an information sheet.
Progression of symptoms suggests continued exposure, inadequate decontamination or inadequate treatment.
Late effects
Between 1 and 4 days after exposure to OPs, acute respiratory failure can occur with flaccid paralysis. It is refractory to pralidoxime and ventilation is required. An intermediate syndrome can occur as proximal weakness presents after resolution of the initial crisis. This is different from a potentially permanent peripheral neuropathy.
Expert advice
Expert advice may be sought from PHE which has helplines for Chemicals 0844 8920555 and Poisons 0844 892 0111.
Prognosis
Later effects of acute exposure include EEG changes, poor concentration and memory and post-traumatic stress disorder.[18]
The respiratory system is often the first to be affected, as the agent is usually inhaled; however, there do not appear to be long-term respiratory problems.[19]
Chronic, usually industrial exposure, gives a lower exposure but for a longer time.
The long-term neuropsychological effects in orchard sprayers in England have been examined and it is difficult to obtain a clear result.[20] A survey of agricultural workers in the USA found a more clear relationship with cumulative dose of OPs.[21] A survey from Spain was also quite clear about a cumulative dose effect.[22]Studies have also suggested that sheep farmers are at increased risk of neurological abnormalities.[4, 23]
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Roberts DM, Aaron CK; Clinical Review: Management of acute organophosphorus pesticide poisoning. BMJ 2007 334:629-634 (24 March).
Hyams KC, Brown M, White DS; Resolving disputes about toxicological risks during military conflict : the US Gulf War experience. Toxicol Rev. 200524(3):167-80.
Ismail K, Lewis G; Multi-symptom illnesses, unexplained illness and Gulf War Syndrome. Philos Trans R Soc Lond B Biol Sci. 2006 Apr 29361(1468):543-51.
Coggon D; Work with pesticides and organophosphate sheep dips. Occup Med (Lond). 2002 Dec52(8):467-70.
Mackenzie Ross SJ, Brewin CR, Curran HV, et al; Neuropsychological and psychiatric functioning in sheep farmers exposed to low Neurotoxicol Teratol. 2010 Jul-Aug32(4):452-9. Epub 2010 Mar 20.
Rastogi SK, Tripathi S, Ravishanker D; A study of neurologic symptoms on exposure to organophosphate pesticides in the Indian J Occup Environ Med. 2010 Aug14(2):54-7.
Vale A; What lessons can we learn from the Japanese sarin attacks? Przegl Lek. 200562(6):528-32.
Alavanja MC; Introduction: pesticides use and exposure extensive worldwide. Rev Environ Health. 2009 Oct-Dec24(4):303-9.
Litchfield MH; Estimates of acute pesticide poisoning in agricultural workers in less developed countries. Toxicol Rev. 200524(4):271-8.
Leibson T, Lifshitz M; Organophosphate and carbamate poisoning: review of the current literature and summary of clinical and laboratory experience in southern Israel. Isr Med Assoc J. 2008 Nov10(11):767-70.
Eddleston M, Buckley NA, Eyer P, et al; Management of acute organophosphorus pesticide poisoning. Lancet. 2008 Feb 16371(9612):597-607.
Emergency contacts: public health; Public Health England, August 2013
Eddleston M, Buckley NA, Checketts H, et al; Speed of initial atropinisation in significant organophosphorus pesticide poisoning--a systematic comparison of recommended regimens. J Toxicol Clin Toxicol. 200442(6):865-75.
Banerjee I, Tripathi SK, Roy AS; Efficacy of pralidoxime in organophosphorus poisoning: revisiting the controversy in Indian setting. J Postgrad Med. 2014 Jan-Mar60(1):27-30. doi: 10.4103/0022-3859.128803.
Syed S, Gurcoo SA, Farooqui AK, et al; Is the World Health Organization-recommended dose of pralidoxime effective in the treatment of organophosphorus poisoning? A randomized, double-blinded and placebo-controlled trial. Saudi J Anaesth. 2015 Jan9(1):49-54. doi: 10.4103/1658-354X.146306.
Dickson EW, Bird SB, Gaspari RJ, et al; Diazepam inhibits organophosphate-induced central respiratory depression. Acad Emerg Med. 2003 Dec10(12):1303-6.
Ohtani T, Iwanami A, Kasai K, et al; Post-traumatic stress disorder symptoms in victims of Tokyo subway attack: a 5-year follow-up study. Psychiatry Clin Neurosci. 2004 Dec58(6):624-9.
Niven AS, Roop SA; Inhalational exposure to nerve agents. Respir Care Clin N Am. 2004 Mar10(1):59-74.
Stephens R, Sreenivasan B; Neuropsychological effects of long-term low-level organophosphate exposure in orchard sprayers in England. Arch Environ Health. 2004 Nov59(11):566-74.
Kamel F, Engel LS, Gladen BC, et al; Neurologic symptoms in licensed private pesticide applicators in the agricultural health study. Environ Health Perspect. 2005 Jul113(7):877-82.
Roldan-Tapia L, Parron T, Sanchez-Santed F; Neuropsychological effects of long-term exposure to organophosphate pesticides. Neurotoxicol Teratol. 2005 Mar-Apr27(2):259-66. Epub 2005 Jan 8.
Tahmaz N, Soutar A, Cherrie JW; Chronic fatigue and organophosphate pesticides in sheep farming: a retrospective study amongst people reporting to a UK pharmacovigilance scheme. Ann Occup Hyg. 2003 Jun47(4):261-7.
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Abstract
Organophosphate (OP) poisoning is common in India. Only few case reports of parenteral OP poisoning have been described. We report a case of self-injected methyl parathion poisoning, presenting after four days with seizure, altered sensorium, and respiratory distress which posed a diagnostic and therapeutic dilemma. Despite nonavailability of history of OP poisoning, he was treated based on suspicion and showed a good clinical response to treatment trial with atropine and pralidoxime, and had a successful recovery. Atypical presentations may be encountered following parenteral administration of OP poison, and even a slight suspicion of this warrants proper investigations and treatment for a favorable outcome. Persistently low plasma cholinesterase level is a useful marker for making the diagnosis.
Organophosphate (OP) poisoning is common in developing countries and especially so in India. Poisoning occurs mostly by voluntary ingestion, inhalation, or by absorption through the skin. Toxicity can also occur rarely by self injection through intramuscular or intravenous route. OP poisoning by parenteral route has been described by very few authors.[1–] If the history of parenteral administration of the compound is not available, diagnosis becomes difficult. OP poisoning by parenteral route may manifest acutely with cholinergic crisis and respiratory distress, intermediate syndrome, or with delayed toxicity. We describe a case of self injected methyl parathion, presenting with seizure and abscess in the arm, pulmonary edema, and flaccid quadriparesis, which was successfully treated on clinical judgment.
CASE REPORT
A male student, aged 20 years, was admitted in neuro ICU with an episode of seizure and altered sensorium. He had no premorbid illness. He had travelled to Mumbai four days before admission. Relatives denied consumption of any poison and medications. At the time of hospitalization, he was restless and was in postictal state. Vital signs revealed pulse rate of 62/minute, blood pressure of 120/80 mmHg, respiratory rate of 14 per minute, afebrile, and had plenty of oral secretions. Neurological examination revealed GCS of 6/15 with reduced movements of all four limbs. Pupils were pin point bilaterally with absent Doll’s eye movement. Plantar reflex was extensor bilaterally. Deep tendon reflexes were sluggish. There were no fasciculation and no smell of OP compound. He had cellulitis of left arm. Examination of chest showed bilateral crepitations. Examination of other systems was normal. Investigations at admission showed normal renal functions, liver functions, and normal serum levels of sodium, potassium, calcium, and magnesium. Blood picture showed leukocytosis. Chest X-ray showed bilateral haziness suggesting acute respiratory distress syndrome. Ultrasonography of left arm showed pus collection in the intramuscular plane. Debridement was done and 250 ml of pus was drained. At this point of time, differential diagnosis of metabolic encephalopathy, toxic encephalopathy due to sepsis, possible brain stem diseases, and OP poisoning/drug over dosage were considered. Computed tomography and magnetic resonance imaging scan of the brain, lumbar puncture and CSF analysis were done and they were normal. His EKG, cardiac enzymes, and echocardiography were normal and blood, urine, and pus cultures were sterile. Screening for benzodiazepine, antiepileptic drugs were negative. Serum cholinesterase level was 1234 units (reference range- 5000 – 9000 units). On day 2, he developed respiratory distress with carbon dioxide retention, ABG revealed PaCO2 of 54 mmHg, and he required ventilator support. At this point of time, we had reasonably excluded metabolic and structural causes for his problem; hence, possibility of OP poisoning was considered on the basis of respiratory failure, pulmonary secretions, supported by low plasma cholinesterase level. Ryle’s tube aspiration was done at the time of hospitalization and gastric aspirate was minimal. Empirically, he was treated with atropine and pralidoxime along with broad spectrum antibiotics. Atropine was given 5 mg bolus, followed by infusion at the rate of 2 mg/h, and the dose was titrated as per his clinical response and signs of atropinisation. Response to atropine treatment was good and over five days gradual improvement in sensorium was noticed. Pralidoxime was given at a dose of 1 gm infusion, three times per day for initial two days. He was treated with phenytoin sodium for seizures. Initial antibiotics were piperacillin-tazobactam and metronidazole but during the course of illness, there were worsening of chest shadows and antibiotics were changed to meropenem and linezolid. Cultures of endotracheal tube secretions were sterile. His chest X-ray and oxygenation improved. In the initial three to four days, fluctuation in the sensorium was noticed but continued to have neuroparalysis, neck muscle weakness, and his respiratory efforts were poor. His restlessness was controlled with diazepam. He continued to require ventilator support for breathing. We kept talking to relatives regarding possible consumption of OP poison, but they had no clue about any such event. Plasma cholinesterase level was repeated and value had gone down to 934 units. His restlessness was better, became more alert and neuroparalysis started recovering slowly. The entire problem got sorted out on sixth day, when he communicated to us in writing that he had injected metacid (methyl parathion) to his left arm while travelling in train. He required ventilator support for 12 days and recovered completely. He revealed that he had injected poison with suicidal intention and all the legal protocols were done as per the hospital rules. Following recovery, he was evaluated by psychiatrists and revealed that injection of poison was an impulsive act due to poor social and financial support from family.
DISCUSSION
India is a predominantly agrarian country with large rural population. OP pesticides are used commonly for suicidal purpose. Although ingestion with suicidal intent is a common mode, occupational exposure while spraying in fields is an important modality of poisoning. The clinical presentations and outcome of OP poisoning depend not only on the pesticide but also on the dose, the route of administration, and the time between poisoning and start of treatment. The clinical features of OP poising are as follows: (i) acute cholinergic crisis, which manifests within 24 to 72 hours due to accumulation of acetylcholine at muscarinic and nicotinic sites and accumulation in CNS leading to headache, giddiness, seizure, and altered sensorium; (ii) intermediate syndrome, which manifests after 24 to 96 hours due to prolonged activity of acetyl choline at nicotinic receptors resulting in weakness of ocular, neck, limb, and respiratory muscles. The diagnosis of OP poisoning is made from history of ingestion or mucocutaneous exposure, clinical features, and plasma cholinesterase levels. The depressed plasma cholinesterase levels confirm the diagnosis of OP poisoning and the levels continue to be depressed for 4 to 7 weeks. The estimation of red blood cell cholinesterase is more specific. In cases of ingestion of OP compound, gastric lavage is done and sample is collected for analysis and for medico legal purposes. Atropine acts as physiological antidote as it antagonizes muscarinic receptor-mediated actions. Atropine is given as the initial loading dose of 2 to 5 mg and repeated every 5 to 10 minutes until signs of atropinisation appear. After this, it is given as infusion at the rate of 0.02 to 0.08 mg/kg/min and the dose is titrated as per the clinical response.[7,] Role and dose of oximes are controversial. Pralidoxime is generally used in dose of 1 gm every 6 to 8 hours; recent studies have shown better outcome with high-dose infusion, 18 to 24 gm/day.[] OP-induced seizure is treated with diazepam. Legal issues are of concern while managing these kinds of cases. While dealing with the cases of suspected poisoning, stomach wash, excreta, and other articles like empty bottle capsules or liquids should be collected and preserved. We registered this case in medico legal registry and notification was sent to the police.[10]
The toxicity of OP poison depends on rapidity with which it gets absorbed to systemic circulation. If the OP compound is administered through parenteral route, absorption and systemic manifestations vary in accordance with plane of administration. Few authors have reported the development of acute cholinergic crisis within 30 minutes of IV administration.[1,2,] With self injection, symptoms will appear after some delay and if the quantity administered is less, there may be only local abscess. The case we described presented after four days of injection. He had developed abscess in the arm, which may be related to usage of contaminated material. Pus culture was sterile. Possibility of sepsis was considered; however, it was difficult to explain his flaccid quadriperesis, pulmonary edema only on the basis of sepsis, and he showed good response to treatment with atropine. Local site abscess formation is also reported by Nishioka.[] Local inflammatory findings are to be expected in cases of subcutaneous or intramuscular injection of insecticides. Such injuries are also a potential portal of entry to various organisms. Local debridement is required for drainage of abscess and may have role in clearance of pesticide, if done early.
In all the so far published cases of parenteral OP poisoning, history of injection of the compound was available. The case we described posed a significant dilemma in the diagnosis, as history of injection of the compound was not available at the beginning of treatment. The patient could not provide history because he was in altered sensorium. OP poisoning presenting with seizure is rare and development of seizure following parenteral administration has not been reported yet.
Literature search revealed few cases of parenteral OP poisoning. Badhe and Sudhakar[1] described IV monocrotophos poisoning resulting in intermediate syndrome requiring ventilator support. Raina et al.[2] described two cases of dichlorvos poisoning treated with atropine and pralidoxime. Nishioka reported two cases, of which one died because of respiratory failure and the other had only local reaction without systemic toxicity. Guven et al.[] reported an IV methamidophos poisoning which developed features of acute cholinergic crisis within 30 minutes. Zoppellari et al.[] reported a case of injected isofenphos by intramuscular route and developed cholinergic crisis 5 hours after injection, and the signs and symptoms lasted for 3 weeks. The compound which he had injected is commercially marked as metacid-methyl parathion. These are esters of phosphoric acid and methyl parathion is an aryl phosphate. Metacid is the most commonly used and most toxic OP compound in south Asian countries. Fatal dose of this compound is 80 mg by intramuscular route and 175 mg by oral administration.
CONCLUSION
OP compound toxicity by parenteral route is a diagnostic challenge. Onset of symptoms may be delayed and presentations may be atypical. Even though the symptoms are mild initially, observation for longer period is required. As there are no decontaminating measures, even a small quantity of injection may be fatal. The treating physicians should be vigilant, and appropriate treatment has to be administered in the event of suspicion of OP poison.
Footnotes
Source of Support: Nil
Conflict of Interest: None declared.
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