Ischemic Stroke Following Calloselasma rhodostoma Snakebite: A Rare Case Report

Background

Snakebites are prevalent and often fatal, particularly in rural parts of tropical developing countries.¹ In Indonesia, the species responsible for most bites from Viperidae families, are Calloselasma rhodostoma, primarily found in Java and Madura Island, while Daboia siamensis in East Java, Komodo, Flores, and Lomblen.² Local poisoning is the most prevalent symptom of a viper bite, followed by neurotoxicity, coagulopathy, and hemostatic disorders. Snakebite cases resulting in cerebrovascular disorders are most frequently hemorrhagic but rarely ischemic.³

There were only a few snakebite cases in Indonesia, all based on hospital reports.⁴ Incidence of strokes after snakebite is a scarce case. There are only a few cases in Asia, particularly in India.^5,6 In Indonesia, no single case was reported in any journal. Despite rare cases of snake attacks, the lack of published cases of ischemic stroke following snakebite is of great interest.

Case Presentation

A 72-year-old Mongoloid male was admitted to the emergency department at Bethesda Hospital, Yogyakarta, Indonesia with a history of snakebite in the right lower leg one day before hospital admission. The snake was identified as a Malayan Pit Viper (Calloselasma rhodostoma). He appeared with a swollen right leg and fang marks on his right leg (Figure 1). Two vials of local antivenom serum (ASV) in 500 mL of sodium chloride were administered within five hours as the initial treatment.

Figure 1 A swollen right leg with fang marks (fang marks were circled in red).

On admission, the patient was conscious with 15 GCS (Glasgow Coma Scale). The patient’s temperature was 36.5°C, the pulse rate was 90 beats per minute, the respiration rate was 30 breaths per minute, and the blood pressure was 162/109 mmHg. The neurological examination showed left-side weakness and headache. The patient was suffering from severe pain with a burning sensation at the snakebite mark and was treated with intravenous ketorolac 10 mg and ceftriaxone one gram twice a day. The patient and patient’s family had no history of hypertension, diabetes mellitus, or heart disease.

The blood laboratory results were presented with; leucocytosis, thrombocytopenia, low haemoglobin, high urea concentration, and normal creatinine serum. The patient was transfused with one bag of a packed red cell (PRC) due to low haemoglobin and thrombocyte. The values of prothrombin time (PT) and activated partial thromboplastin time (aPTT) were prolonged. His computerized tomogram (CT) scan showed an ischemic infarct in the pericallosal of the right lateral periventricular anterior horn (Figure 2). An electrocardiogram (ECG) revealed sinus rhythm with no left ventricle enlargement. The patient’s condition improved and became more stable two days after being bitten by a snake. Although haemoglobin and thrombocyte levels had increased, they remained low. As such, further monitoring was required. After the ninth day of treatment, the patient was discharged and instructed to monitor his condition regularly.

Figure 2 CT scan showed an ischemic infarct in the pericallosal of the right lateral periventricular anterior horn.

Discussion

To our knowledge, this study was the first to report a case of ischemic stroke after snakebite in Indonesia. The pathological consequences of envenoming can vary and be complex due to the variety of poisonous components found in snake venom; variables such as bite location and amount of venom released can also vary.⁷ After being bitten by a Viperidae, patients may experience a burning or throbbing feeling in the bite area, and local swelling occurs rapidly around the bite mark, perhaps affecting the entire limbs and adjacent trunk.⁸ The clinical significance of recognizing the type of snake that bites can assist health care professionals in providing and administering proper treatments, such as antivenom serum.⁹ Because antivenom serum is only effective against a limited number of venomous snakes and has the potential for lethal adverse effects such as fatal allergic reactions, it should not be used to treat bites from non-venomous snakes, especially considering the scarcity and high cost of venom in many countries.¹⁰

Leukocytosis was detected in the laboratory, indicating that the body responded to the toxin’s effects with stress and inflammation.¹¹ Additionally, snakebites were related with anemia, thrombocytopenia, hypofibrinogenemia, leukocytosis, coagulopathy, proteinuria, and azotemia.¹² In a study in India, most patients of all genders developed hypertension following a snakebite, despite the venom’s ability to reduce blood pressure, impede muscle control, and destroy red cells.¹³ The mechanism of hypertension following a snakebite remained unknown; it is thought that catecholamine in snake venom is released from adrenergic nerve terminals, resulting in hypertension-like symptoms.¹⁴ The previous statement is also supported by the fact that our patient has no history of hypertension, diabetes mellitus, or heart disease. During the acute stage, the effects of snake venom can cause fatal harm to the body, resulting in death if not treated properly. However, with antivenom serum and proper medical treatment, these symptoms can resolve on their own.¹ However, what sometimes escapes health workers’ attention are long-term symptoms that can lead to fatal complications.¹⁵

The Viperidae venom may cause systemic bleeding because of hemorrhagins in its venom, which damages vascular endothelium¹ and increased vascular permeability.⁶ Hemorrhagins also develop a microthrombi formation leading to low-grade disseminated intravascular coagulopathy resulting in ischemia and infarction¹⁶ due to occlusion of small and large blood vessels.¹⁷ One of the most abundant components of Viperidae venom is Snake Venom-C-Type Lectin-Related Protein (SV-CLRPs), which inhibits the interaction of clotting factors and various receptors on platelets, immune, and endothelial cells.¹⁸ The pro-coagulant properties of serine proteinases and snake venom metalloproteinases (SVMPs) result in defibrinogenation and incoagulability. In some cases, the pro-coagulant components of snake venoms or damage to the endothelium lining result in regional thrombosis with subsequent local or remote ischemia events, all of which contribute to the complicated pathophysiology of cardiovascular changes associated with snakebite poisoning.¹⁹ Endothelial and vascular damage are plausible reasons for cerebral infarction.¹⁷ Due to the absence of additional risk factors, we believe that our patient’s cerebral infarction was caused by toxin-induced vascular spasm and endothelial damage.

Conclusion

Although ischemic stroke following a snakebite is uncommon, it must be considered and monitored.