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

ACUTE

acute organophosphate poisoning

1st line – resuscitation + supportive care

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ACUTE
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acute organophosphate poisoning
1st line – 

resuscitation + supportive care

Cardiorespiratory resuscitation, intravenous fluids, airway maintenance, and ventilation should be used early on as required.[22]​ The American Heart Association recommends early endotracheal intubation for life-threatening organophosphate poisoning.[22]​ All patients should have an intravenous line inserted.

Patients require frequent monitoring of vital signs, as a rapid deterioration may be seen, even in patients with initially minor symptoms. Symptoms are usually severe in patients who have deliberately ingested organophosphate or have been exposed to nerve agents.

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

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ACUTE
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acute organophosphate poisoning
Plus – 

decontamination

Treatment recommended for ALL patients in selected patient group

After the patient is stabilised, the next step is decontamination.[5][22]​ This involves washing the patient, having first removed their contaminated clothes.

If the airway is protected, aspiration of stomach contents may be done; however, organophosphates are rapidly absorbed, and there is no evidence to support the effectiveness of gastric aspiration or lavage.[23]​ Evidence suggests that activated charcoal is ineffective in reducing clinical effects.[24]

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.[22]

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

Decontamination should never take priority over supportive care and resuscitation.

Consider – atropine

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ACUTE
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acute organophosphate poisoning
Consider – 

atropine

Additional treatment recommended for SOME patients in selected patient group

Atropine is indicated in patients who have clinical symptoms of organophosphate poisoning. Rapid administration of atropine to patients with organophosphate poisoning who present with rhinorrhoea and bronchorrhoea may be life saving so early recognition and administration is important.[13]​ In practice, patients who are known to have been exposed to organophosphate may also be considered for atropine to control secretions before symptoms become severe. Patients who have had a minor exposure to organophosphate may not need treatment with atropine, but most patients with suspected or confirmed organophosphate poisoning will require atropine.

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.[5][22]​​[25]

Treatment is largely titrated against secretions, with doubling bolus doses given every 5 minutes until the chest is clear.[26] 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.

A combination proprietary product containing atropine and pralidoxime in an auto-injector pen is available. However, in some countries this product has restricted distribution.

Primary options

atropine: 1-3 mg intravenously as a single dose initially, may double dose every 3-5 minutes when required according to response; 2-4 mg (mild to moderate symptoms) or 6 mg (severe symptoms) intramuscularly as a single dose initially, followed by 2 mg every 5-10 minutes when required according to response

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Consider – benzodiazepine

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ACUTE
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acute organophosphate poisoning
Consider – 

benzodiazepine

Additional treatment recommended for SOME patients in selected patient group

Given to control seizures or agitation.[22]​ 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
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acute organophosphate poisoning
Consider – 

pralidoxime

Additional treatment recommended for SOME patients in selected patient group

The antidote pralidoxime (also known as 2-PAM) can be given to reactivate inhibited acetylcholinesterase. However, it only reactivates 'non-aged' acetylcholinesterase-organophosphate complexes.[22]​ 'Ageing' is the process whereby phosphorylated acetylcholinesterase loses an alkyl side chain non-enzymatically, 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.[27][28][29][30] One study suggested that routine use of high doses of pralidoxime may cause more harm than benefit in many cases, despite reactivating red blood cell (RBC)-acetylcholinesterase.[31] 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, pralidoxime doses should be titrated according to patient response as measured by nerve conduction studies or RBC-acetylcholinesterase assays.[32]

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.[33]

Atropine should be given before pralidoxime.

A combination proprietary product containing atropine and pralidoxime in an auto-injector pen is available.​ However, in some countries this product has restricted distribution.

Primary options

pralidoxime: intravenous (intermittent): 1-2 g intravenously as a single dose initially, may repeat in 1 hour, then every 10-12 hours if muscle weakness persists or every 3-8 hours if poisoning is due to ingestion; intravenous (infusion): 30 mg/kg (maximum 2 g/dose) intravenously as a single dose, followed by 8 mg/kg/hour intravenous infusion, maximum 500 mg/hour; intramuscular (mild symptoms): 0.6 g intramuscularly as a single dose initially, may repeat every 15 minutes for 2 doses, maximum 1.8 g/total dose; intramuscular (severe symptoms): 0.6 g intramuscularly as a single dose initially, then repeat 2 doses in rapid succession, maximum 1.8 g/total dose, may repeat the 3-dose regimen (1.8 g/total dose) 1 hour after last dose if symptoms persist

ONGOING

intermediate syndrome

1st line – supportive care

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ONGOING
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intermediate syndrome
1st line – 

supportive care

About 1 to 5 days post-poisoning, 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
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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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