Discussion
On an annual basis, in excess of a million reports of scorpion stings are made across the globe, with a 20 per 100,000 population figure for prevalence. While roughly 5% of reported cases are severe, only about 0.3% of severe cases result in mortality. 1
The Asian forest scorpion( Heterometrus species) is the most common scorpion found in Nepal, is responsible for non-fatal envenomations, and usually leads to local skin manifestations. The eastern Indian scorpion, or Hottentotta tamulus , is a species of scorpion belonging to the Buthidae family is also found in the tropics of Nepal. It is nocturnal and is reported to be deadly.8
Patients presenting with scorpion envenomation have been split into three grades: Patients in grade (I) merely have local pain; those in grade (II) have systemic symptoms; and those in grade (III) have significant neurological impairment (coma and/or convulsions) or cardiorespiratory symptoms, primarily cardiogenic shock and pulmonary edema. 1,2,3
Depending on the species of arachnid and the toxin’s plasma levels, the clinical symptoms can vary considerably. The release of endothelin, neuropeptide Y, and nitric oxide is prompted by the toxin. It triggers the complement and coagulation systems, which leads to an upward spiral of neurological harm (seizures, cerebral edema), inflammation, and microthrombosis. 1,4,5,6
Because venom is hydrophilic, it has low blood-brain barrier permeation. In young kids, the central nervous system may be heavily involved in the envenomation process since the blood-brain barrier remains fragile. The central nervous system outcomes (grade III) resulting from scorpion stings can vary widely and manifest as diminished consciousness, convulsions, subarachnoid hemorrhage, intracerebral hemorrhage, and ischemic infarcts. 3,6
Neurological complications from scorpion stings are well reported in South America, Venezuela, India, and Turkey. Eight percent of patients in a case series drawn from southern India had neurological involvement; of these, four percent had hemorrhagic stroke and four percent had ischemic stroke. 2,5
Cerebral infarcts typically appear more than 48 to 72 hours after the initial scorpion envenomation. 2,3 Contrary to this, our patient exhibited signs and symptoms of cerebral ischemia in less than 24 hours, which made this case more atypical for reporting.
Scorpion stings are a problem in emerging economies, where medical costs are always a concern. The cornerstone of treatment in these areas is typically prazosin and supportive care. 1
Antivenin is theoretically the specific management. Purified anti-venom F(ab)2 is currently in widespread usage. Venom is released into the circulation during the initial cholinergic phase. Antivenom works best during this time and can neutralize free venom in about 5 hours. This stops the ensuing sympathetic storm. However, due to unavailability of antivenin in Nepal, we managed the cause with combination of prazosin, anticoagulants, and antiplatelet agents.1,3
The main takeaway from this case report is that, despite being extremely common, scorpion stings can seldom surface as an ischemic stroke. Various explanations were put forth to delineate the pathophysiology behind the occurrence of cerebral infarction in scorpion envenomation. They can be summarized as briefly due sympathetic storm, myocarditis (left ventricular systolic dysfunction due to myocarditis, causing stagnation of blood and subsequent thromboembolism), venom vasculitis, and defibrination syndrome. 6,7