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Guideline

Organophosphate Poisoning: Emergency Department
Management of Organophosphate Poisoning



Document No: SSW_GL2007_003

Functional Sub-Group: Clinical Governance
Corporate Governance

Summary: This guideline is for use only in the case of known
organophosphate exposure.

Approved by: Director Clinical Governance / Clinical Quality Council

Publication (Issue) Date: November 2007

Next Review Date: November 2009

Replaces Existing Guideline: Yes (distributed as correspondence)

Previous Review Dates: November 2006


Note: Sydney South West Area Health Service (SSWAHS) was established on 1 J anuary 2005 with
the amalgamation of the former Central Sydney Area Health Service (CSAHS) and the former
South Western Sydney Area Health Service (SWSAHS).
In the interim period between 1 J anuary 2005 and the release of single Area-wide SSWAHS
guidelines (dated after 1 J anuary 2005), the former CSAHS and SWSAHS guidelines were
applicable as follows:-
SSWAHS Eastern Zone : CSAHS
SSWAHS Western Zone: SWSAHS
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Date Issued: November 2007



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ORGANOPHOSPHATE POISONING: EMERGENCY DEPARTMENT
MANAGEMENT OF ORGANOPHOSPHATE POISONING


CONTENTS

1. Background............3

2. Outcome..3

3. Guideline Statement...3

4. Triage Process3

4.1 Decontamination Advice
4.2 General Notes Regarding Nosocomial Risk for Staff Involved in Treatment

5. Clinical Information to guide the treatment of the Poisoned Patient..5

5.1 Poisoning
5.2 Excretion
5.3 Mode of Action / Response
5.4 Systems Affected
5.5 Symptoms and Signs of Cholinergic Excess

6. Grading of Severity of Poisoning.6

7. Emergency Department Initial Management..7

8. Laboratory Tests.7

9. Drug
Therapy.7

10. Monitoring and Observation..8

11. Transfer from ED8

12. Holding and Disposal of Poison and Clothing / Leather Items8

13. References...9
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ORGANOPHOSPHATE POISONING: EMERGENCY DEPARTMENT MANAGEMENT OF
ORGANOPHOSPHATE POISONING


1. Background

This guideline should be used only in the case of known organophosphate (OP)
exposure and does not apply to the situation of exposure to an unknown toxic
substance.


2. Outcome

The safety of all staff, patients and visitors to the Health Service is maintained during
the acute treatment of a patient with suspected or known organophosphate exposure.

The person presenting to the Emergency Department will receive timely, efficient and
effective health care.

3. Guideline Statement


All care provided within the Sydney South West Area Health Service
(SSWAHS) will be in accordance with infection control guidelines, manual
handling guidelines and minimisation and management of aggression
guidelines.
Resuscitation and further treatment should ideally take place in a well-
ventilated area with regular rotation of staff.
Only staff treating the patient should be within the immediate proximity of the
patient.
All staff with direct patient contact should observe standard precautions
normal gloves, gowns, eye protection and normal mask (where required).
Staff must have protective equipment on prior to commencing treatment
including mask, gloves, gowns and eye protection
Patients with skin exposure should undergo external decontamination as
soon as practicable: clothes removed and bagged, and the person washed
with soap and water. This process should take place immediately but not to
the detriment of timely resuscitation and medical assessment.
Patients with internal exposure (inhalation / ingestion) should be triaged and
moved immediately to the resuscitation area for initial assessment and
management.
Staff who are in direct contact with patients bodily secretions should
immediately and thoroughly wash the affected area with soap and water.
Other patients particularly those who have respiratory problems should be
removed from the area


4. Triage Process

Treatment is to be instituted immediately based upon the clinical picture of
organophosphate poisoning.

In the case of dermal / inhalation exposure:
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If stable at presentation, the patient should be sent to a supervised shower
for decontamination.
If unstable, triage immediately to resuscitation area for treatment and
decontamination after stabilisation.

Samples of the product brought with the patient should be placed in an
appropriately sized and sealed bag and clearly labelled with the patient's
identification label and be clearly marked as POISON.

Senior clinical advice should be sought early by the use of local clinical expertise
(where available). An alternate source of clinical expertise and advice is the
Poisons Information Centre on 13 11 26: an on-call clinical toxicologist is
available 24hours, 7 days a week.


4.1 Decontamination Advice

If the person has skin contamination, then the persons clothes should be
removed and placed in a contaminated waste bag and the person washed with
soap and water.

Skin - contamination of skin, clothing, hair, eyes.

Flush the chemical from the eyes with copious amounts of sterile
0.9% sodium chloride solution.
Remove clothing and wash patient / shampoo hair, using copious
amounts of soap and water.
Ensure skin folds and underneath of fingernails are cleansed.
Contaminated leather articles should be removed (including watch
bands) and placed with the patient's clothing in an appropriately sized
and sealed bag and clearly labelled with the patient's identification
label and be clearly marked as Contaminated Personal Belongings.

Soap containing chlorhexidine and alcohol helps remove lipophilic
compounds.

For ingestion, there may be minor contamination from spillage or vomitus
that may require local decontamination.

4.2 General Notes Regarding Nosocomial Risk for Staff Involved in Treatment

There are no case reports of actual poisoning occurring when staff care for
a patient with OP poisoning.
However, the hydrocarbon solvent (not the organophosphate compound)
associated with OPs may cause self limiting symptoms for staff caring for
the OP poisoned patient. The hydrocarbon is commonly associated with a
noxious odour.
Staff should be rotated out of the clinical area if they become symptomatic
from this exposure.




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5. Clinical Information to Guide the Treatment of the Poisoned Patient:

5.1 Poisoning

Organophosphates are toxic chemicals that may be ingested, inhaled or
absorbed.

5.2 Excretion

Metabolism is via hydrolysis in the liver.
Some organophosphates are readily stored in body fat and are released
slowly and intermittently, resulting in delayed symptoms.

5.3 Mode of Action / Response

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.

5.4 Systems Affected

1. Central Nervous System: Sensory and behavioural disturbances,
incoordination, depressed motor function, coma and possible seizure
activity.

2. 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.

3. 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, hypertension, then
hypotension.

Respiratory depression and pulmonary oedema are the usual causes of death
without prompt intervention.
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5.5 Symptoms and signs of cholinergic excess:

Secretions: tears, saliva, sputum, gastric acid and perspiration.
Respiratory symptoms: wheeze, cough, shortness of breath, large mucous
production (bronchorrhea), decreased respiratory muscle function.
Neurological symptoms: seizure, coma, delirium, respiratory centre
depression, fasciculation, ataxia, long-term neuropsychiatric sequelae,
depression, and peripheral neuropathy.
GIT: diarrhoea, vomiting, pancreatitis (spasm of the sphincter of Oddi,
check serum amylase).
CVS: increased and unbalanced autonomic outflow (especially vagal),
tachy and brady arrhythmias, Torsades de Pointes VT, hypo/hypertension.
Onset of symptoms is usually within 12 hours of exposure (exception:
highly fat-soluble OP esters).


6. Grading of Severity of Poisoning

Mild Moderate Severe

Walks and talks.
Headache, dizzy.
Nausea and
vomiting.
Abdominal pain.
Sweating,
salivation.
Rhinorrhoea.



Serum
acetylcholinesterase
enzyme (ACHe) is
20-50% of normal.

Cannot walk.
Soft voice.
Muscle twitching.
(fasciculation)
Weakness.
Anxiety,
restlessness.
Small pupils
(miosis).


Serum
acetylcholinesterase
enzyme (ACHe) is
10-20% of normal.
Unconscious, no
pupillary reflex.
Muscle twitching,
flaccid paralysis.
Increased bronchial
secretions.
Dyspnoea,
crackles/wheeze.
Possible
convulsions.
Respiratory failure.

Serum
acetylcholinesterase
enzyme (ACHe) is <10%
of normal.



7. Emergency Department Initial Management

Airway: goal of therapy - airway protection, prevention of aspiration, clearance of
secretions and adequate ventilation.
If unable to protect airway - intubate and ventilate.
If using non-depolarising NMBs, there may be delayed onset with higher
dosage required to obtain the desired effect.

Breathing: risk of weakness / paralysis of respiratory muscles combined with
secretions leading to respiratory failure. Improve tissue oxygenation with
supplemental oxygen and administration of atropine eliminating hypoxia
minimises the risk of ventricular fibrillation.
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Circulation: blood pressure may be high or low.
Provide blood pressure support as required with the cautious use of
noradrenaline if hypotensive.

Deficits: seizures may occur check glucometer, continue to treat with atropine
followed by benzodiazepines, the patient may require further treatment with
barbiturates. You should seek toxicological advice on this situation.


8. Laboratory Tests:

NB: Specific antidote treatment should be instituted based on the clinical picture and
not on test results:

Alert the laboratory to the fact you will be requesting these tests to assist
in rapid processing.
Measure serum pseudocholinesterase (heparinised tube) to confirm exposure
(only needs to be done once).
RBC cholinesterase and mixed cholinesterase levels will be done serially to look
for evidence of persistence of the OGP agent and need for ongoing antidote
treatment.
Measure ABGs, FBC, BSL, LFTs, Lipase and EUC (renal function): Metabolic
disturbances include possible: hypo/hyperglycaemia, abnormalities of liver
function and pancreatitis.
ECG, CXR and formal spirometry (once secretions have dried up).


9. 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 10-20mg/hour.
When commencing treatment, double the dose every 3 5 minutes until
muscarinic features (sweating, salivation, bronchorrhoea) subside.
If initially unable to gain intravenous access, commence atropinisation with
intramuscular atropine at the dose of 2mg. Increase doses as above.
Then commence an 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) /hour
based on initial requirements.
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 and
muscle weakness remain in the presence of atropine).
If crackles are heard on auscultation or there is a return of miosis, bradycardia or
sweating, re-establish atropinisation.

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.
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Pralidoxime is used in moderate / severe poisoning where impaired 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 2grams IV over 30 minutes.
In mild to moderate poisoning, administer 1gram 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).
Pralidoxime is metabolised by the liver and excreted by the kidneys.

Drug Contraindications: Do not prescribe / administer morphine, theophylline,
phenothiazines, reserpine.

Pain Relief: Administer paracetamol and non-opioid analgesia for relief of muscle
pain.


10. Monitoring and Observation:

Observations should include continuous ECG, NIBP and SpO
2
monitoring.
The patient may require intra-arterial BP and CVP monitoring if more severely
affected.
Observe for deterioration post reduction of drug therapies, auscultate lung bases
for crackles.
Continuous monitoring is required for 72 hours or longer.


11. Transfer from ED

The patient should be admitted under the care of a Toxicologist or Physician (as
per usual local arrangements).
Ensure admission is to the Intensive Care.
There is no need for isolation of the patient.
The odour due to hydrocarbons can be managed by regular staff rotations.
Where intentional harm relating to OP poisoning is considered, ensure
psychiatric referral for later assessment is made.
The ED bay is to be cleaned with dilute hypochlorite (bleach) solution.


12. Holding and Disposal of Poison and Clothing/Leather Items

Patients bringing into the ED a container with the OP that has occasioned the
poisoning are to have the item placed in an appropriately sized and sealed bag
and clearly labelled with the patient's identification label and be clearly marked as
Poison.
This bag is retained within the ED until such time as it is no longer required for
forensic examination, as per the ED consultant (and police investigators - where
indicated).
The patient's clothing and all leather items (watch band, necklaces, shoes etc)
are to be placed in an appropriately sized and sealed bag and clearly labelled
with the patient's identification label and be clearly marked as Contaminated
Personal Belongings.
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These belongings are retained within the ED until such time as they are no
longer required for forensic examination, as per the ED consultant (and police
investigators - where indicated).
Once Forensic Examination has been satisfied (and there is no need for the
clothing / leather to be given over to Police Investigation) or is not required, the
clothing and leather is to be disposed of in general waste.
Family / Carers are to be informed of the necessity for the disposal of clothing
and leather items, and their disposal and conversation with the family
representative / carer is to be documented in the health care record.
The name of the person to whom you have explained the need for disposal of
clothing and leather items is to be documented in the health care record.


13. References

Consensus statement: Risk of nosocomial organophosphate poisoning in emergency
departments. M.Little. L Murray, EMA: (2004) 16, 456458.
Liverpool ICU Policy and Procedure manual.

Guideline Author(s): Dr J ohn Sammut, on behalf of OP Working Party for SSWAHS
Guideline Reviewers: ED Directors, ED CNCs, ED Nurse Practitioners, Area/Zone
Toxicologist.
Guideline Publication Date: J anuary 2007. Date for Review: J anuary 2009.