Dichlorvos Poisoning: A Mystery Case of Distributive Shock Unraveling with Atropine

DISCUSSION

Though cardiovascular complications due to the above-mentioned common killer in Indian population are not uncommon, in this case we have come across a patient whose only presenting symptom was a distributive shock after dichlorvos ingestion. He was treated with liberal intravenous crystalloids and required inotropes and ventilatory support for 4-days. In dichlorvos poisoning, hypotension can be explained by cardiotoxicity or arrhythmias. However, cardiac investigations did not show any abnormality. CVP monitoring showed consistently low values despite fluid therapy after a negative history of any fluid loss. Also, we failed to elicit other common signs and symptoms of OP poisoning.

A well-known toxidrome in OP poisoning consists of salivation, lacrimation, urination, defecation, gastric cramps, and emesis symptoms. The manifestations are based on the type of receptor that is being dramatically stimulated by acetylcholine. The nicotinic receptors of neuronal subtype Nn or N2 on activation lead to tachycardia and hypertension whereas the receptor subtype Nm or N1 leads to weakness, fasciculations, and cramps. The muscarinic receptor subtype M1–M5 stimulation leads to anxiety, restlessness, ataxia, convulsions, insomnia, dysarthria, tremors, coma, respiratory depression, and circulatory collapse. Also, the M2 receptor activation leads to bradycardia and hypotension.⁴ Animal study for the vascular effects of OP compounds noted peripheral vasodilatation due to the effect of acetylcholine on muscarinic receptors on the vascular endothelium and these compounds may also block nicotinic transmission at the sympathetic and parasympathetic ganglia further leading to inhibition of the baroreceptor reflexes. Chronic OP exposure may cause oxidative damage to the vascular endothelium as noticed on the histopathological examination in the animal models.⁶ The similar effects in acute OP exposure are questionable. However, in our present case, we see it.

Organophosphate-induced delayed polyneuropathy (OPIDN) appears to follow the phosphorylation and subsequent aging of an enzyme in axons called neuropathy target esterase.⁷ OPIDN usually sets in after 7–21 days of exposure. The spectrum of symptoms is paresthesias and calf pain. The weakness of subacute onset and slow progression over 2 weeks involving the distal leg muscles causing foot drop is the initial presentation followed by small muscles of the hands which later involve even the truncal muscles while the cranial nerves and the autonomic nervous system are not involved. Deep tendon jerks are absent. Clinical involvement of the corticospinal tracts and the dorsal columns becomes apparent when the peripheral neuropathy improves showing brisk ankle and knee jerks. The prognosis of patients with mild neuropathy is good though those with severe neuropathy are usually left with persistent deficits like claw hand, foot drop, persistent atrophy, spasticity, and ataxia. Delayed OP neurotoxicity, especially with triorthocresyl phosphate, has been reported following the outbreaks in Mumbai where 58 patients were affected. After that, four outbreaks have been reported from Bengal And in 2015–2016, eight cases were reported from Western India; however, the substances of OP were not characterized.⁸

Based on the experience of managing two patients with atropine in OP-associated vasodilatory shock, Buckley et al. summarize atropine therapy is preferable as compared to inotropic therapy as OP compounds have variable responses on the blood vessels.⁹ It causes vasodilation as well as vasoconstriction of a few organs. Administering inotropic agents causes more harm by deranging the organ functions. This undesired effect is not expected with atropine administration, even in larger doses. The same thing happened in our case where the requirement of inotropes decreased and stopped before the atropine.

Another case report of three patients who had distributive shock following dimethoate ingestion, all of them presented with cholinergic features that responded to atropine administration but continued to have a shock that required high-dose inotropic support. All three expired unfortunately but a special note was made of the first two patients who had peripheral vasodilatation as noticed by the distended veins in their extremities. The second patient's blood pressure responded to the addition of dobutamine to a dopamine infusion, but the initial presentation of the patient was poor and he developed cardiac arrest during intubation.¹⁰

The clinical course of patients in terms of the duration of intensive care unit stay, mechanical ventilation, and inotropic support is not predictable. Various factors including pseudocholinesterase (PChE), GCS score, acute physiology and chronic health evaluation II score, and creatine phosphokinase are used by various clinicians to assess the severity of OP poisoning. A study by Pradeep Kumar et al. showed PChE levels <1000 IU/L were associated with a more morbid course in acute OP poisoning with a need for prolonged mechanical ventilation and vasopressor support as well as a longer hospital stay.¹¹

In a cohort study by Jayasinghe et al. to see autonomic function anomalies in acute OP poisoning, a statistically significant autonomic dysfunction was seen in the first assessment of patients compared to the controls in the change of diastolic blood pressure three minutes after standing, heart rate on deep breathing (HR-DB), sympathetic skin response–amplitude, latency, postvoid urine volume, and size of the pupils.¹² At 6 weeks, recovery of autonomic dysfunction was observed except in HR-DB similar to our case. However, sensory–motor neuropathy appeared as a delayed phenomenon. The reason for the same is unclear, maybe due to the initial presentation of a distributive shock.

This syndromic presentation of dichlorvos poisoning is dramatic, can mimic many other medical conditions, and will be a challenge for physicians from a diagnostic point of view as well as in the management. A lot more evidence needs to be sought for in the management of this type of syndromic case.