Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

INITIAL

suspected poisoning

1st line – resuscitation + supportive care

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INITIAL
|
suspected poisoning
1st line – 

resuscitation + supportive care

Cardiorespiratory resuscitation, intravenous fluids, airway maintenance, and ventilation should be used early on. The American Heart Association recommends early endotracheal intubation for life-threatening organophosphate poisoning.[14]​ All patients should have an intravenous line inserted.

Frequent vital signs are needed, as a rapid deterioration may be seen, even in patients with initially minor symptoms.

Plus – decontamination

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INITIAL
|
suspected poisoning
Plus – 

decontamination

Treatment recommended for ALL patients in selected patient group

Contaminated clothes should be removed, the skin washed, and stomach contents aspirated if the airway is protected.[14]

Universal precautions for staff should be followed: simple gloving and gowning, and increasing ventilation of the area. Appropriate healthcare professional personal protective equipment depends on the circumstances of the organophosphate exposure and potency of the involved organophosphate.[14]

Treatment of patients contaminated with nerve agents presents a more significant hazard for staff; however, such risks are not relevant to the much less volatile and less toxic pesticides.

Decontamination should never take priority over supportive care and resuscitation.

Plus – atropine

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INITIAL
|
suspected poisoning
Plus – 

atropine

Treatment recommended for ALL patients in selected patient group

Atropine is given to control secretions, particularly those interfering with respiration. It may also counteract bradycardia, hypotension, and hypothermia, and reduce central nervous system effects.[12][14]​​[25]

Treatment is largely titrated against secretions, with doubling bolus doses given every 5 minutes until the chest is clear.[15] The heart rate should be over 80 bpm, and the skin should feel dry when a patient is adequately dosed with atropine. Pupils will also be dilated, but this may be delayed.

Tachycardia should not preclude further use of atropine if secretions are not controlled; over-treatment is preferable to under-treatment.

Once secretions are initially controlled, the patient can be managed with an intravenous infusion. Atropine requirements are extremely variable; daily doses range between 10 mg and 1000 mg or more. Consult a specialist for guidance on infusion doses.

Primary options

atropine: 1-2 mg intravenously initially, followed by double doses (e.g., 4 mg, 8 mg, 16 mg, etc.) every 5 minutes until secretions are controlled

ACUTE

occupational or accidental poisoning

1st line – resuscitation + supportive care

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ACUTE
|
occupational or accidental poisoning
1st line – 

resuscitation + supportive care

Cardiorespiratory resuscitation, intravenous fluids, airway maintenance, and ventilation should be used early on. The American Heart Association recommends early endotracheal intubation for life-threatening organophosphate poisoning.[14]​ All patients should have an intravenous line inserted.

Frequent vital signs are needed, as a rapid deterioration may be seen, even in patients with initially minor symptoms.

Gastric aspiration or lavage may be performed if the airway is protected. However, organophosphates are rapidly absorbed, and there is no evidence to support the effectiveness of gastric aspiration or lavage.[16] Evidence suggests that activated charcoal is ineffective in reducing clinical effects.[17]

Plus – decontamination

Back
ACUTE
|
occupational or accidental poisoning
Plus – 

decontamination

Treatment recommended for ALL patients in selected patient group

Contaminated clothes should be removed, the skin washed, and stomach contents aspirated if the airway is protected.[14]

Universal precautions for staff should be followed: simple gloving and gowning, and increasing ventilation of the area. Appropriate healthcare professional personal protective equipment depends on the circumstances of the organophosphate exposure and potency of the involved organophosphate.[14]

Decontamination should never take priority over supportive care.

Plus – atropine

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ACUTE
|
occupational or accidental poisoning
Plus – 

atropine

Treatment recommended for ALL patients in selected patient group

Symptoms are usually mild to moderate in these patients.

Atropine is given to control secretions, particularly those interfering with respiration. It may also counteract bradycardia, hypotension, and hypothermia and reduce central nervous system effects.[12][14]​​[25]

Treatment is largely titrated against secretions, with doubling bolus doses given every 5 minutes until the chest is clear.[15] The heart rate should be over 80 bpm and the skin should feel dry when a patient is adequately dosed with atropine. Pupils will also be dilated, but this may be delayed.

Tachycardia should not preclude further use of atropine if secretions are not controlled; over-treatment is preferable to under-treatment.

Once secretions are initially controlled, the patient can be managed with an intravenous infusion. Atropine requirements are extremely variable; daily doses range between 10 mg and 1000 mg or more. Consult a specialist for guidance on infusion doses.

Primary options

atropine: 1-2 mg intravenously initially, followed by double doses (e.g., 4 mg, 8 mg, 16 mg, etc.) every 5 minutes until secretions are controlled

deliberate ingestion or terrorism/warfare with nerve agent

1st line – resuscitation + supportive care

Back
ACUTE
|
deliberate ingestion or terrorism/warfare with nerve agent
1st line – 

resuscitation + supportive care

Cardiorespiratory resuscitation, intravenous fluids, airway maintenance, and ventilation should be used early on.[14]​ The American Heart Association recommends early endotracheal intubation for life-threatening organophosphate poisoning.[14]​ All patients should have an intravenous line inserted.

Symptoms are usually severe in these patients.

Gastric aspiration or lavage may be performed if the airway is protected. However, organophosphates are rapidly absorbed, and there is no evidence to support the effectiveness of gastric aspiration or lavage.[16] Evidence suggests that activated charcoal is ineffective in reducing clinical effects.[17]

Several manifestations of severe organophosphate poisoning are frequently refractory to standard treatment. In particular, severe hypotension is an ominous sign; high doses of atropine and vasopressors may be tried, but success is likely to be limited. Central nervous system features and paralysis often do not respond well to antidotes, and prolonged intensive supportive care may be required.

Plus – decontamination

Back
ACUTE
|
deliberate ingestion or terrorism/warfare with nerve agent
Plus – 

decontamination

Treatment recommended for ALL patients in selected patient group

Contaminated clothes should be removed, the skin washed, and stomach contents aspirated if the airway is protected.[14]

Universal precautions for staff should be followed: simple gloving and gowning, and increasing ventilation of the area. Appropriate healthcare professional personal protective equipment depends on the circumstances of the organophosphate exposure and potency of the involved organophosphate.[14]

Treatment of patients contaminated with nerve agents presents a more significant hazard for staff.

Decontamination should never take priority over supportive care and resuscitation.

Plus – atropine

Back
ACUTE
|
deliberate ingestion or terrorism/warfare with nerve agent
Plus – 

atropine

Treatment recommended for ALL patients in selected patient group

Atropine is given to control secretions, particularly those interfering with respiration. It may also counteract bradycardia, hypotension, and hypothermia, and reduce central nervous system effects.[12][25]

Treatment is largely titrated against secretions, with doubling bolus doses given every 5 minutes until the chest is clear.[15] The heart rate should be over 80 bpm and the skin should feel dry when a patient is adequately dosed with atropine. Pupils will also be dilated, but this may be delayed.

Tachycardia should not preclude further use of atropine if secretions are not controlled; over-treatment is preferable to under-treatment.

After secretions are initially controlled, the patient can be managed with an intravenous infusion. Atropine requirements are extremely variable. Daily doses of atropine range between 10 mg and 1000 mg or more. Consult a specialist for guidance on infusion doses.

A combination proprietary product containing atropine and pralidoxime in an autoinjector pen is available.

Doses should be titrated according to patient response.

Primary options

atropine: 2 mg intravenously initially, followed by double doses (e.g., 4 mg, 8 mg, 16 mg, etc.) every 5 minutes until secretions are controlled

Consider – benzodiazepines

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ACUTE
|
deliberate ingestion or terrorism/warfare with nerve agent
Consider – 

benzodiazepines

Treatment recommended for SOME patients in selected patient group

Given to control seizures or agitation.[14]​ Also useful to maintain sedation in intubated patients.

Few risks in intensive-care situations, but there is a possibility of excess sedation if the patient is not sufficiently monitored.

Primary options

diazepam: 5-10 mg intravenously every 10-15 minutes initially up to a maximum of 30 mg, then 5-10 mg every 2-4 hours when required

OR

lorazepam: 2-4 mg intravenously every 10-15 minutes initially up to a maximum of 8 mg

Consider – pralidoxime

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ACUTE
|
deliberate ingestion or terrorism/warfare with nerve agent
Consider – 

pralidoxime

Treatment recommended for SOME patients in selected patient group

Pralidoxime (an oxime) can be given to reactivate inhibited acetylcholinesterase. However, it only reactivates "non-aged" acetylcholinesterase-organophosphate complexes.[14]​ "Aging" is the process whereby phosphorylated acetylcholinesterase loses an alkyl side chain nonenzymatically, leaving a hydroxyl group in its place, with the result that regeneration is no longer possible.

Pralidoxime is, therefore, of limited or no effectiveness against organophosphates that form rapidly aging acetylcholinesterase complexes.

Pralidoxime is often given in severe poisoning cases. Evidence is conflicting and generally negative.[18][19][20][21] One study suggested that routine use of high doses of prolidoxime may cause more harm than benefit in many cases, despite reactivating red blood cell (RBC)-acetylcholinesterase.[22] Adverse effects may be serious and are more common if high bolus doses of pralidoxime are given rapidly. Further clinical trials are required to determine if certain dosing strategies may be useful in particular groups of patients.

If given outside of trials, prolidoxime doses should be titrated according to patient response as measured by nerve conduction studies or RBC-acetylcholinesterase assays.[23]

Plasma cholinesterase may also be reactivated by pralidoxime but the response is variable, smaller, and not sustained. Therefore, it should not be used to monitor response to oximes.[24]

A combination proprietary product containing atropine and pralidoxime in an auto-injector pen is available.

Primary options

pralidoxime (2-PAM): 1000-2000 mg intravenously initially, followed by 400-600 mg/hour continuous infusion

ONGOING

intermediate syndrome

1st line – supportive care

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ONGOING
|
intermediate syndrome
1st line – 

supportive care

About 1 to 5 days postpoisoning, often when other signs are resolving, increasing proximal muscle weakness and cranial nerve palsies can occur. In severe cases of intermediate syndrome, respiratory failure may occur.

organophosphate-induced delayed neuropathy

1st line – supportive care and rehabilitation

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ONGOING
|
organophosphate-induced delayed neuropathy
1st line – 

supportive care and rehabilitation

Delayed neuropathy may occur 1 to 5 weeks after ingestion. It may overlap with an intermediate syndrome. This is predominantly a motor neuropathy, but there may also be upper motor neuron problems and cognitive defects. There is no known treatment, but it may resolve slowly over months to years.

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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