Approach

The main goal of treatment is to reduce the high mortality rate and severity of serious complications by using atropine and/or pralidoxime plus supportive care and decontamination of the patient. Management of these patients should involve early expert help and critical care input. The American Heart Association recommends early endotracheal intubation for life-threatening organophosphate poisoning.[22]

Symptoms are usually mild to moderate in patients who have had an accidental dermal or respiratory exposure, and severe in those who have deliberately ingested organophosphate or have been exposed to nerve agents.

If deliberate self-poisoning has taken place, a consultant mental health assessment should also be requested at the earliest opportunity.[19]​ See Suicide risk mitigation.

Resuscitation and supportive care

All patients with suspected significant exposure to an organophosphorus compound should be treated presumptively, as treatment needs to be started before test results are returned. The initial approach for patients with suspected and confirmed organophosphate poisoning is focused on cardiorespiratory resuscitation and supportive care, including intravenous fluids, airway maintenance, and ventilation as required.[5][22]​ Patients require frequent monitoring of vital signs, as a rapid deterioration may be seen, even in patients with initially minor symptoms.

Decontamination

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]

Appropriate personal protective equipment is recommended when caring for patients with organophosphate poisoning, which will depend 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.

Atropine

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]​ Rapidly escalating doses of atropine are given until secretions are controlled and the chest is clear.[5][22][26]​ After secretions are initially controlled, the patient can be managed with an intravenous infusion. Atropine requirements are extremely variable.​

Benzodiazepines

Benzodiazepines may be required in some patients to control seizures or to sedate ventilated patients.[5][22][25]

Pralidoxime

The antidote pralidoxime (also known as 2-PAM) can be given to reactivate inhibited acetylcholinesterase.[22]​ However, it only reactivates 'non-aged' acetylcholinesterase-organophosphate complexes. '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, but 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 of pralidoxime 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 dose 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 the response to oximes.[33]

Refractory hypotension and paralysis

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. No treatments have been shown to prevent delayed neuropathy, but this is an uncommon complication.

Intermediate syndrome

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. Treatment is supportive with close monitoring and assisted ventilation, if required. Ventilation for up to 2 to 3 weeks is often needed. Recurrence of respiratory failure the day following extubation requiring re-intubation is also common.[34]

Organophosphate-induced delayed neuropathy

Delayed neuropathy may occur 1 to 5 weeks after ingestion. It may overlap with 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.

Use of this content is subject to our disclaimer