Abstract

Scorpion envenomation is a life-threatening toxicological emergency and considered as a major public health problem, especially in endemic regions (India, Africa, Latin America); it is generally characterized by low resources and tropical or subtropical weather. Scorpion envenomation is especially fatal in the first hours, usually due to respiratory and/or cardiovascular collapse. The neurologic manifestations, triggered by multiple neurotoxic mechanisms, are varied and complex and mostly reported in children. The aim of this review is to clarify the epidemiologic characteristics and clinical manifestations as well as diagnosis and management of neurologic complications following scorpion envenomation. The management of patients with severe clinical forms is based on early recognition of the sting, antivenom serum administration, and cardiorespiratory and systemic support.

Highlights

  • BackgroundScorpion envenomation is a life-threatening and endemic toxicological emergency

  • The aim of this review is to present the epidemiological characteristics and clinical manifestations as well as diagnosis and management of neurological complications following scorpion envenomation

  • Scorpion envenomation may affect all individuals, but it is more prevalent in young people; 60% to 80% of them are older than 15 years but it is more severe in children principally due to minor corporal surface [1,2,3,4]

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Summary

Introduction

Scorpion envenomation is a life-threatening and endemic toxicological emergency. It is prevalent in certain tropical and subtropical regions of the world with low-to-moderate resources, such as Africa, India, and Latin America [1,2]. Scorpion envenomation can produce a variety of clinical presentations, including cardiovascular (myocarditis, cardiogenic and/or distributive shock), respiratory (acute respiratory distress syndrome [ARDS]), hematological (disseminated intravascular coagulation [DIC]), renal (acute kidney injury), and neurological (seizures, autonomic dysfunction, and ischemic or hemorrhagic stroke) [4,5,6]. Mechanisms that may lead to neurological manifestations include embolic stroke secondary to myocarditis and arrhythmia, acute increase in blood pressure following autonomic storm, cerebral vessel vasospasm due to excessive catecholamine, and toxin-mediated endothelial injury and vasculitis [14,15,16,17,18,19,20,21]. The mortality rate of cerebrovascular compromise following scorpion envenomation is reported at 28%; most of these patients suffer from other venom-mediated toxicities, including shock, coagulopathy, rhabdomyolysis, and acute renal failure, simultaneously [5,6]. Other possible but nondemonstrated explanations are that in children, the inflammatory response and catecholamines release phenomena are more intense

Autonomic alterations
Peripheral nervous system compromise
Conclusions
Disclosures
Cupo P
Findings
26. Cañas CA
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