Internal Diseases and Therapy · MU Sofia

127. Acute exogenous poisoning with organophosphorus compounds

Covers organophosphorus compounds, mainly found in pesticides and sometimes used as nerve agents, and how they inhibit acetylcholinesterase to cause excess acetylcholine. It lists muscarinic, nicotinic and central nervous system symptoms, then the delayed neuropathy that can follow. It also explains diagnosis by serum cholinesterase and ECG changes, and treatment with atropine, pralidoxime, benzodiazepines and activated charcoal, with a diagram of the cholinergic synapse.

Inside: 1 section · 1 labelled picture · 14 flashcards · 2 min

Topic 128 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 1 section, about 273 words (2 min of reading), with 14 flashcards.

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  1. Acute exogenous poisoning with organophosphorus compounds

Acute exogenous poisoning with organophosphorus compounds

Organic phosphorus compounds (OPC) are most commonly found in pesticides. They can be phosphoric acid esters or thiophosphoric acid esters and are common in the world. They have also been used as chemical warfare nerve agents and in terrorist attacks.

The main mechanism of toxicity is through inhibition of acetylcholinesterase in neuronal synapses leading to excess acetylcholine and overstimulation in the peripheral nervous system.

Image: “Cholinergic synapse” by Smedlib , based on original work by Pancrat, CC BY-SA 4.0, via Wikimedia Commons.

Acute symptoms of OPC toxicity are:

  • Muscarinic symptoms - bronchospasm, bronchorrhea, bradycardia, diarrhea, urination, miosis, emesis and salivation
  • Nicotinic symptoms - paralysis, fasciculations
  • CNS toxicity (rarer) - seizures, altered mental status, apnea
  • Treat fast!!!

There are also chronic symptoms of OPC toxicity, these are the so called organophosphorus induced delayed neuropathy (OPIDN), characterised by bilateral paralysis of the distal muscles (mostly lower extremities), 7-10 days after ingestion.

Diagnosis of OPC toxicity is through the measurement of serum cholinesterase activity, which decreases. Additional tests are FBCs, U&Es, and ECG (expect prolonged QT interval, elevation of ST, sinus tachy, sinus brady and in rare cases complete heart block may all occur).

Treatment is ABC, oral activated charcoal is a reasonable intervention after GI poisoning if ingestion was within the last hour. Atropine, pralidoxime (2-PAM), and benzodiazepines, are the mainstays of pharmaceutical treatment, beginning with the adequate use of atropine. Large doses of atropine are often needed, start at 2-5mg IV dose and then work up! This helps to prevent reflex bradycardia and control heart rate. In severe cases, doses far above 16mg may be required (no maximum: titrate until bronchial secretions are dry).

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