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Internal Medicine

Organophosphate (OP) poisoning

Poisoning due to organophosphates (OPs).

  • Mortality > 15%

Aetiology

Organophosphorus pesticides are used widely for agriculture, vector control, and domestic purposes.

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Figure 3 Chemical classes of organophosphorus pesticides Structures of organophosphorus pesticides from diethyl (A, B, C), dimethyl (D), and S-alkyl (E,F) classes. Most organophosphorus pesticides are thioates, with a double-bonded sulphur atom linked to the phosphate (A, C, F) that needs to be converted to the active oxon (eg, A to B). A few organophosphorus pesticides are oxons (eg, D, E) and do not need activation; they are able to inhibit acetylcholinesterase directly as soon as they are absorbed. | Eddleston, M., Buckley, N. A., Eyer, P., & Dawson, A. H. (2008). Management of acute organophosphorus pesticide poisoning. Lancet (London, England), 371(9612), 597–607. https://doi.org/10.1016/S0140-6736(07)61202-1

Pathophysiology

Irreversible acetylcholinesterase inhibition:

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Interactions of organophosphorus compounds in vivo; relative rates of each reaction vary between organophosphorus compounds | Eyer P. The role of oximes in the management of organophosphorus pesticide poisoning. Toxicol Rev 2003;22:165-90.

Clinical features

 

Acute organophosphorus poisoning may induce multisystem toxicity leading to severe toxicity and death.

Acute cholinergic crisis:

Caused by the accumulation of acetylcholine at cholinergic synapses. 

  • Muscarinic receptors:
    • D = Defecation/diaphoresis
    • U = Urination
    • M = Miosis
    • B = Bronchospasm/bronchorrhea
    • E = Emesis
    • L = Lacrimation
    • S = Salivation
  • Nicotinic receptors:
    • Monday = Mydriasis
    • Tuesday = Tachycardia
    • Wednesday = Weakness
    • Thursday = Hypertension
    • Friday = Fasciculations
  • Central nervous system (CNS):
    • Altered level of consciousness, respiratory failure, and seizures

Organophosphorus induced delayed polyneuropathy:

Unrelated to acetylcholinesterase inhibition and occurs because of inhibition of other enzymes, in particular neurotoxic target esterase characterised by demyelination of long nerves, when neurological dysfunction occurs 1-3 weeks after acute exposure, particularly motor dysfunction but also sensory dysfunction, which may be chronic or recurrent.

 


Management

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Decision tree for management of patients presenting with history of acute organophosphorus poisoning: Patients may have variable degrees of miosis, salivation, diaphoresis, urinary frequency, or lacrimation, which may assist in diagnosis of organophosphorus poisoning. Because these manifestations are not considered to influence outcome they are not included in this decision tree. †Assessment of respiratory status includes respiratory rate and depth, presence of adventitious sounds such as rales and rhonchi, presence of bronchorrhoea, and objective measurements of pulse oximetry, arterial blood gases, and forced vital capacity or forced expiratory volume in one second. ‡Muscle weakness: difficulty in mobilisation or reduced forced vital capacity on spirometry before development of paralysis and respiratory failure. §Caution with patients with a history of exposure to fenthion (or highly fat soluble organophosphorus compounds). Patients with fenthion poisonings are usually characterised by minimal or absent cholinergic symptoms for 24-48 hours, after which they develop increasing muscle weakness and respiratory failure | Roberts, D. M., & Aaron, C. K. (2007). Management of acute organophosphorus pesticide poisoning. BMJ (Clinical research ed.), 334(7594), 629–634. https://doi.org/10.1136/bmj.39134.566979.BE

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