organophosphate poisoning

ORGANOPHOSPHATEPOISONING

NOOR HAFIZAH BINTI HASSAN2007287236

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REFERENCES1. Early management after self-poisoning with an organophosphorus

or carbamate pesticides-a treatment protocol for junior doctors. Michael Eddleston, Andrew Dawson, Lakshman Karalliedde, Wasantha Dissanayake, Ariyasena Hittarage, Shifa Azher and Nick A Buckley. Critical Care 2004, 8:R391-R397

• Common Mechanism of Toxicity: A Case Study of Organophosphorus Pesticides. Mileson, B. E., Chambers, J. E., Chen, W. L.,Dettbarn, W., Enrich, M., Eldefrawi, A. T., Gaylor, D. W.,Hamernik, K., Hodgson, E., Karczmar, A. G., Padilla, S., Pope,C. N., Richardson, R. J., Saunders, D. R., Sheets, L. P., Sultatos,L. G., and Wallace, K. B. (1998). Toxicol. Sci. 41, 8-20.

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INTRODUCTION

• Organophosphate widely used in agricultural sector as PESTICIDES.

• Nerve agents sarin, tabun, soman, VX, VE• Mortality a/w self-poisoning with pesticides:– 50-70 % in developing world– 0.3 % in developed world

• Malaysia 2nd after paraquat poisoning (Sirajuddin, 2002).

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Distribution of Poisoning Cases by Types of Poison from 2001-2005

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PHYSIOLOGY REVISITED

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COVALENT BOND

AGING

MECHANISM OF ACTION OF ORGANOPHOSPATE POISONING

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MECHANISM OF ACTION OF ORGANOPHOSPATE POISONING

Irreversibly bind to serine-OH group at the active site of acetylcholinesterase (AChE) establish covalent bond

(phosphorylation)↓

AGING: loss of alkyl group + strengthening of covalent bond↓

Phosphorylated AChE is very stable↓

Inhibition of enzyme activity accumulation of ACh in the synapse and NMJ

↓Overstimulation of cholinergic receptors

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CLINICAL PRESENTATION

MUSCARINIC: SLUDGES-SalivationL-LacrimationU-UrinationD-DiarrhoeaG-GI upsetE-Emesis

NICOTINIC: MATCHM-Muscle weakness

and fasciculationA-Adrenal medulla

activity ↑T-TachycardiaC-Cramping of skeletal

muscleH-Hypertension

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PRINCIPLE OF MANAGEMENT• History taking: What, When, How much, Why• 1° survey: protect yourself + decontaminate• Initial assessment: A B C D E• Recognition of organophosphate poisoning– MIOSIS– DIAPHORESIS– ↓/POOR AIR ENTRY– BRADYCARDIA– HYPOTENSION

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• Antidote: Atropine & Pralidoxime

• IV fluid• Confirmation of exposure to cholinergic compounds

– Measure butyryl cholinesterase or red cell AChE activity

LOADING DOSE: IV 0.5-2 mg over 5-10 min until atropinization achieved

MAINTENANCE DOSE:(8 mg mix in 100 mL normal saline) at a rate of 0.02-0.08 mg/kg/hr

• effective within 24 hours of exposure

• 1-2 g IV in 100 mL normal saline within 30min.

• repeat if muscle weakness did not relieve in 1 hour

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CASE:- 14 y/o Indian girl - Brought to resus HSB on 8th Feb 2009 at 1050 by

family after mom noted a strange smell - Took insecticides from the back of her house at

around 0900- Minimal amount (< 1/3 of the bottle content)- No suicidal note- Claimed that she was stressed friends keep

commenting on the PIMPLES on her face.

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ASSESSMENT- On arrival: alert and

conscious- Vital signs:

- Heart rate: 132 beats/min

- Blood pressure: 143/90 mmHg

- O2 saturation: 89% on room air

- Pulse rate: 21 breaths/min

- Temperature: 37°C

- Vomiting- Throat & abdominal

discomfort- No chest pain / SOB- Pupils 2mm constricted- Sweaty peripheries- Lungs: transmitted

sound- PA: soft, non tender

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MANAGEMENT• 2 large bore IV needle• High flow mask 15L/min• IVD Normal Saline• Clean-sponging & change clothes• Close monitoring of vital signs• Gastric lavage & Ryle’s tube inserted• Activated charcoal 50mg• IV Atropine 0.25 mg every 2min until atropinization achieved• IV ranitidine • Suicidal precaution • Blood ix: FBC; RP; LFT; amylase; PCM, salicylate,

benzodiazepine level; CXR, urine paraquat

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Thank you

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