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.[14]

Suspected poisoning

All patients with suspected significant exposure should be treated presumptively, as treatment needs to be started before test results are returned. The initial approach is focused on cardiorespiratory resuscitation and supportive care.[12] This involves very early use of rapidly escalating doses of atropine until secretions are controlled and the chest is clear, as well as intravenous fluids, airway maintenance, and ventilation.[12][14][15]​ After the patient is stabilised, the next step is decontamination.[12][14]​ This involves washing the patient, having first removed their contaminated clothes, and aspiration of stomach contents if the airway is protected. 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.[14]

Occupational or accidental poisoning

Symptoms are usually mild to moderate in these patients, who may report dermal or respiratory exposure to a particular agent. Supportive care and decontamination procedures are recommended. 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] Atropine is recommended to control secretions.[12][14]​​

Deliberate ingestion or terrorism/warfare with nerve agent

Symptoms are usually severe in these patients, who may be confused or semi-conscious. Supportive care and decontamination procedures are recommended.[14]​ 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] Atropine is used to control secretions.

Pralidoxime (an oxime) can also be given to reactivate inhibited acetylcholinesterase.[14]​ 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.[18][19][20][21] 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.[22] 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.[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 the response to oximes.[24]

Benzodiazepines may be required in some patients to control seizures or to sedate ventilated patients.[12][14]​​[25]

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.[26]

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.

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