Organophosphate Poisoning Guideline
Organophosphate Poisoning Guideline
Organophosphate Poisoning Guideline
Guideline
Policy Statement
Protective equipment necessary for the management of Organophosphate Poisoning will be available for staff and visitor protection. Staff involved in patient care will wear the prescribed personal protective equipment at all times: charcoal mask, impermeable gown, rubber gloves. The patient will be cared for in a single room with negative pressure airflow with the doors to remain closed. Neuromuscular blocking agent: succinylcholine, and morphine are contraindicated in the management of the patient. The environment and spills within the environment are to be cleaned using dilute hypochlorite solution (household bleach).
Background
Poisoning:
Organophosphates are toxic chemicals that may be ingested, inhaled or absorbed. Dermal or occupational exposure differs in severity from oral ingestion. Oral ingestion is associated with a 100-1,000 fold greater concentration of poisoning. Metabolism is via hydrolysis in the liver. Some organophosphates are readily stored in body fat and released slowly and intermittently, complicating management. Excretion of organophosphates from the patient is via skin, body fluids and exhaled air. Organophosphates cause irreversible inhibition of the enzyme acetylcholinesterase. Carbamates (including physostigmine, neostigmine and edrophonium (Tensilon) are reversible inhibitors of the enzyme acetylcholinesterase. Inhibition of acetylcholinesterase allows the neurotransmitter acetylcholine (ACh) to remain active in the synapse - resulting in sustained depolarisation of the post-synaptic neuron. Effects are seen in the: Central Nervous System: Sensory and behavioural disturbances, incoordination, depressed motor function, coma and possible seizure activity. Muscarinic sites in the peripheral nervous system: Sustained stimulation of the parasympathetic nervous system where nerve junctions with smooth muscle and gland cells are stimulated causing: Contraction of intestinal and bronchial smooth muscle - diarrhoea, vomiting, bronchospasm, bronchorrhoea. Decreased pupil size - miosis, absent pupillary reflex. Increased secretions from all secretory glands - lacrimation, salivation. Decreased sinus node activity, bradycardia, AV conduction defects, occasional ventricular arrhythmias. Nicotinic sites in the sympathetic and parasympathetic ganglia and nicotinic sites at the neuromuscular junction these sites are stimulated and then depressed: Excess ACh may be excitatory (causing muscle twitching) but at higher levels it may also weaken and paralyse the cell by depolarising the motor endplate. Sympathetic stimulation may result in tachycardia and hypertension, then hypotension. Respiratory depression and pulmonary oedema are the usual causes of death without prompt intervention.
Excretion:
Mode of Action/Response
Author: M. Edgtton-Winn
Guideline
ICU management
Airway: protection, prevention of aspiration, clearance of secretions and adequate ventilation. If unable to protect airway - intubate and ventilate; do not use neuromuscular blocking (NMB) agent succinylcholine, as it may result in prolonged paralysis of hours to days. If using non-depolarising NMBs, there may be delayed onset with higher dosage required to obtain effect. Breathing: Improve tissue oxygenation prior to administration of atropine - minimises risk of ventricular fibrillation. If ventilated - establish a "gas scavenger" set-up: an external reservoir of exhaled gas that is 'suctioned' away; see Protocol in the ICU Clinical Resource Manual. Circulation: Blood pressure support with cautious use of noradrenaline. Blood pressure may be high or low. Deficits: seizures may occur - treat with atropine followed by benzodiazepines, may require further treatment with barbiturates.
Author: M. Edgtton-Winn
Guideline
Drug Therapy:
Atropine competitively blocks the effects of acetylcholine. 1-2mg IV in moderate poisoning; 2-5mg IV in severe poisoning or as an infusion at 1020mg/hour. Continue stat doses every 10 - 30 minutes until muscarinic signs (sweating, salivation, bronchorrhoea) subside. Infusion: 60mg atropine in a 50mL syringe: 50 x 1.2mg ampoules. Titrate from 100 micrograms/hour (0.1mL/hour) to 10-20mg (8.5 to 17mL/kour) Nebulised atropine may improve respiratory distress and oxygenation by decreasing bronchial secretions, however; where ingestion results in hydrocarbon aspiration, an ARDS picture occurs (refractory pulmonary oedema and poor oxygenation). Tachycardia is not a contraindication to therapy (it may be secondary to hypoxia or sympathetic stimulation). Pupillary dilatation is not a sign of adequate therapy. Atropine is ineffective against nicotinic effects - (thus respiratory depression, muscle weakness remain in the presence of atropine). Pralidoxime; regenerates acetylcholinesterase and acts synergistically with atropine. Before administering, ensure blood specimen (heparinised tube) is taken for acetylcholinesterase analysis. Rapid administration may result in tachycardia, laryngeal spasm, muscle rigidity and transient neuromuscular blockade. Pralidoxime is used in moderate/severe poisoning where respiratory function or seizures/coma occur. Do not use in carbamate poisoning (as in neostigmine, physostigmine, Tensilon) Delayed presentation of a symptomatic patient is not a contraindication to the use of pralidoxime. Initial dose of 2 grams IV over 30 minutes. In mild to moderate poisoning, administer 1 gram IV every 8 hours. In severe poisoning the infusion rate is at 500mg/hour: 1gram in 40mL (total of 50mL) at 25mg/hour (20mL/hour). Infusion is ceased based upon clinical testing and mixed plasma cholinesterase test. Pralidoxime is metabolised by the liver and excreted by the kidneys. Frusemide is considered for persistent pulmonary oedema after full atropinization. Activated charcoal is administered in the emergency department as the first dose; nil further administrations are required in the Intensive Care Unit.
Observe for deterioration post reduction of drug therapies, auscultate lung bases for crackles. If crackles heard or there is a return of miosis, bradycardia or sweating, re-establish atropinization. Continuous monitoring is required for 72 hours or longer as organophosphate may be intermittently released from fat stores.
Contraindications: do not prescribe/administer morphine, succinylcholine, theophylline, phenothiazines, reserpine. Pain relief:
Administer paracetamol and non-opioid analgesia for relief of muscle pain. Ensure discharge planning/rehabilitation process has commenced upon admission. Involve patient in simple activities such as reading, listening to radio/CDs, watching TV during isolation and periods of reduced contact with staff, relatives, carers.
Author: M. Edgtton-Winn
Guideline
Safety precautions for staff and visitors during the acute stage of management
Charcoal mask and impermeable gown are to be worn in the isolation room. When caring for the patient, rubber gloves are to be worn (as per chemotherapeutic precautions). When the patient is exhibiting signs and symptoms of moderate/severe poisoning the above precautions are to be maintained. In severe poisoning, industrial goggles for eye protection/comfort should be worn. When the patient is admitted to the ICU without adequate decontamination or in cases of severe poisoning: Consider hourly rotation of staff on patient admission. Consider rotation of staff as per discomfort - headache, nausea, distress from noxious odour of the organophosphate metabolism.
Staff rotation
Bed linen
Author: M. Edgtton-Winn
Guideline
References
Reigart, J.R. and Roberts, J.R. (1999). Recognition and Management of Pesticide Poisonings in National th Pesticide Telecommunications Network. (5 Ed.). http://ace.orst.edu/info/nptn/rmpp.htm Jackson, J.E. and Aaron, C.K. (1996). Cholinergic Agents. In Rippe, J.M., Irwin, R.S., Fink, M.P. and Cerra, F.B. (Third Ed., Volume II). Intensive Care Medicine. Boston: Little, Brown and Company. 1546 - 1553. Morgan, D.P. (1989). Organophosphate Insecticides. In Recognition and Management of Pesticide Poisonings. (4th Ed.). Environmental Protection Agency: Iowa and University of Florida. Cholinesterase - (1998). Pesticide Fact Sheet and Tutorial at http://pmep.cce.cornell.edu/facts-slidesself/facts/gen-posaf-chol.html Lesson of the Week: A foodbourne outbreak of organophosphate poisoning. (2001). British Medical Journal 317:268-269 at http://www.hedleytech.com/980725_britishmedicaljournal.htm Slapper, D. (2001). Toxicity, Organophosphate and Carbamate from Emergency Medicine/Toxicology. 1st February, 2001: www.emedicine.com/emerg/topic346.htmHu, H. and Speizer, F.E. (1994). Environmental and occupational hazards. In Isselbacher, K.J., Braunwald, E., Wilson, J.D., Martin, J.B., Fauci, A.S. and Kasper, D.L. Harrison's Principles of Internal Medicine. (13th Ed.). New York: McGraw-Hill Inc. Paraquat. (1999). Hazardous Substance Fact Sheet. New Jersey Department of Health and Senior Services September 1999. Nosocomial poisoning associated with emergency department treatment of organophosphate toxicity - Georgia, 2000. MMWR - January 5th, 2001. Pp: 1156-1159. Bruzel, A. (1998). New Acetylcholinesterase Inhibitors. From About http://chemistry.about.com/science/c.../aa040698a.htm?iam=dpile&terms=%2Bcarbamat Chemistry:
Policy Author(s): M. Edgtton-Winn, ICU - CNC, L. Williams, ICU - NUM. Reviewed by: Director of ICU, CNC ICU.
Author: M. Edgtton-Winn