Basal ganglia hemorrhage secondary to scorpion sting: a fatal presentation

Avirup Majumdar,Virendra Atam,Shahnawaz Ali Ansari,Satish Kumar,Akriti Bhardwaj

doi:10.1186/s41983-020-00198-9

Avirup Majumdar, Virendra Atam + Show 3 more

Open Access

https://doi.org/10.1186/s41983-020-00198-9

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Abstract

IntroductionCerebrovascular manifestations are uncommon presentations of scorpion sting in the Indian subcontinent. Encephalopathy, cerebral edema, subarachnoid hemorrhage, non-hemorrhagic strokes, and cortical necrosis are a few CNS complications described in the medical literature due to scorpion envenomation.Case descriptionWe report a rare case of scorpion envenomation in a 40-year old, non-hypertensive farmer, who presented in an unconscious state. Non-contrast CT head revealed intracerebral hemorrhages in left temporoparietal lobe extending into left basal ganglia with intraventricular extension.Discussion and evaluationToxin-induced autonomic storm is mostly responsible for the acute hypertensive crisis in affected individuals leading to stroke (commonly cerebral infarct) as a CNS complication.ConclusionBasal ganglia bleed following scorpion sting is an extremely rare scenario which is usually fatal as was in our case. Early suspicion and prompt institution of treatment (prazosin) is crucial in the management of intracranial bleed secondary to scorpion sting.

Highlights

Cerebrovascular manifestations are uncommon presentations of scorpion sting in the Indian subcontinent
Scorpion sting is a medical emergency; it is more common in rural parts of India
We demonstrate a rare but fatal case of scorpion envenomation resulting in basal ganglia hemorrhage

Summary

Introduction

Scorpion sting is a medical emergency; it is more common in rural parts of India. Farmers and laborers who are exposed to outdoor activities are often the worst victims. Among many constituents of scorpion venom, alpha toxins produce significant human toxicity by binding to sodium channels in cell membranes, and inhibiting inactivation of action potentials [3] causing prolonged depolarization and excessive release of acetylcholine, epinephrine, and norepinephrine from autonomic ganglia. This excessive release of neurotransmitters results in autonomic storms. The patient returned from work with headache, vomiting, and pain at the site of the sting He developed weakness of the right side of the body and lost his consciousness within 4 h. Complete hemogram (hemoglobin 120 g/L; total leucocyte count, 14 × 109/L; platelets, 160 × 109/L), liver

Discussion and evaluation

Conclusion

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