Decompressive craniectomy following snakebite envenomation: An uncommon manifestation of a common emergency

INTRODUCTION

Snakebite envenomation is a major, yet neglected tropical disease, leaving over 80,000 people dead annually, especially in the South and Southeast Asia.^[1] Roughly half of these deaths occur in India, disproportionately affecting the rural population.^[1] The World Health Organization has recognized it as a critical public health priority, as a category of neglected tropical disease.^[1]

Venomous snakes are broadly divided into Elapidae, including cobras, kraits, and mambas, the Viperidae, including the Russell’s viper and pit vipers, and the sea snakes belonging to the Hydrophiinae family.^[2] While the neurotoxic and hemotoxic syndromes of viperine and elapid bites are well characterized, thrombotic complications have received less attention compared to the extensively described hemorrhagic manifestations.^[2] The elapid venom primarily affects the neuromuscular transmission, while the viper venom causes perturbation of coagulation and impairs vascular integrity by means of its complex venom.^[2] While viper bites leading to intracranial bleeds have been recognized, the occurrence of ischemic stroke has been rarely reported with bites from Daboia russelii and Bothrops species.^[3]

Very rarely have there been cases recorded of a thrombotic event so severe that it warrants surgical decompression, which although lifesaving, can be dangerous in the setting of disseminated intravascular coagulation (DIC) and precarious coagulation. We aim to highlight the pathophysiological mechanisms, challenges in management, and a review of Indian literature.

CASE REPORT

A 47-year-old previously healthy gentleman sustained a snake bite on his left middle finger while working in his agricultural field at around 10.30 AM on the October 3^rd, 2025. The snake was not captured, but was described as slender and darkly striped. The patient then walked back home, asymptomatic, but shared the details with his wife.

Within a couple of hours, the patient developed vomiting, drooping of both eyelids, and bleeding from the nose and mouth associated with drowsiness, which rapidly progressed to loss of consciousness. He was shifted to the local government hospital, where he was intubated and mechanically ventilated in view of poor sensorium and shallow breathing. He was administered neostigmine and atropine on suspicion of neurotoxicity due to the snake bite. He was transfused 4 units of fresh frozen plasma (FFP) and one packed red blood cell. Forty vials of polyvalent anti-snake venom (ASV) were administered. However, despite these measures, the patient’s bleeding persisted and was brought to our hospital for further management. Details of initial laboratory findings from the initial hospital were not available.

On arrival, the patient had a Glasgow coma scale of E1 Vt M4, bilateral sluggishly reacting pupils, paucity of movement on the right side, blood pressure of 110/70 mmHg, and heart rate of 104/min. The patient was afebrile, but had bleeding from the nasal and oral cavities. Local examination revealed a puncture mark over the swollen left middle finger. Initial laboratory assessment showed hemoglobin of 12.6 g%, platelets (Plt) of 1.2 lakhs/mL. International normalized ratio was 1.5, and the initial thromboelastogram (TEG) showed a flat line, suggestive of no clotting. The TEG is shown in Figure 1A. Apart from elevated creatine phosphokinase and lactate dehydrogenase (LDH), the other blood parameters were unremarkable.

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Figure 1:

(A) Initial thromboelastogram and (B) Preoperative computed tomography scan showing left middle cerebral artery territory infarcts with hemorrhagic transformation

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A non-contrast computed tomography scan of the brain showed frontal, temporal and parietal hypodensities with patchy hemorrhages with diffuse edema involving the left hemisphere with a midline shift of 8 mm and an uncal herniation. The scan is shown in Figure 1B. These features were suggestive of raised intracranial pressure (ICP) warranting measures to rapidly ameliorate the life-threatening situation.

The patient was administered four additional vials of polyvalent ASV, hypertonic saline, and anti-epileptic medications. In view of the need for emergent surgery, 10 units of cryoprecipitate and 4 units of FFP were administered, which optimized the TEG. The patient was taken up for left frontotemporoparietal decompressive craniectomy under general anesthesia. Diffuse ooze was noted from the skin incision onward; meticulous hemostasis was achieved in each step.

The brain was found to be tense and non-pulsatile with thready-looking veins. Cisternostomy was done to let cerebrospinal fluid (CSF) out, but minimal CSF could be released. Lax duraplasty was done, and closure was done in layers after achieving absolute hemostasis. Postoperatively, the patient was managed with anti-epileptic medication, sedation, and medical measures to control ICP. Repeat scan showed reduction of midline shift and new hypodensity on the right fronto-parietal region. Venogram revealed no occlusive disease. Figure 2A shows the intra operative picture and 2B shows the post operative CT scan. Sedation was stopped, and the patient was able to move his left lower limb purposefully. The patient was tracheostomized on postoperative day (POD) 3. Patient remained hemodynamically stable and coagulation parameters optimized. The patient was weaned from mechanical ventilation by POD#5 and was shifted to the ward for further rehabilitative care. The patient developed multiple spikes of fever; tracheal culture grew Acinetobacter baumannii, with patches in the right lung, which was managed with antibiotics. Sutures were removed on POD#14, wound was healthy. He continues to have severe neurological deficits and is on multidisciplinary rehabilitative care. The lab values are presented in Table 1.

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Figure 2:

(A) Intraoperative findings- Tense, non-pulsatile brain and (B) Post operative scan-showing resolving intracranial pressure and new hypodensities in the opposite side.

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DISCUSSION

A devastating consequence of envenomation remains cerebrovascular effects. Neurotoxic venom disrupts the neuromuscular junction, and hemotoxic venoms are complex enzymatic cocktails that affect various steps in the coagulation cascade.^[1] The primary mediators of venom-induced consumptive coagulopathy are Phospholipase A₂, metalloproteinases, serine proteases, and prothrombin activators such as ecarin and carinactivase.^[3] They cause cleavage of prothrombin and factor X, generating excessive thrombin and forming fibrin clots that are unstable and rapidly lyse, leading to consumption of fibrinogen and platelets.^[3]

The widespread activation of the coagulation cascade produces microthrombi in the microcirculation, leading to DIC.^[1] The venom-induced endothelial damage, cytokine release, and platelet activation continue the cycle of coagulation and fibrinolysis. Depletion of the coagulation factors manifests as bleeding. Our patient had the bleeding manifestations, marked by oral and nasal bleeds and a flat TEG, and the thrombotic manifestation in the form of an infarct noted.

The potential mechanism of the stroke could be phospholipase A₂-induced endothelial apoptosis and vasculitis leading to thrombosis. Other proposed mechanisms include a thrombotic microangiopathy akin to hemolytic–uremic syndrome, explaining the coexistence of elevated LDH. However, there are multiple pathways through which a snake bite can lead to an ischemic stroke, such as direct procoagulant action, endothelial inflammation, and vasculitis.^[4]

Studies have suggested that Daboia russelii, Bothrops atrox, and Cerastes cerastes are the commonest snakes causing cerebrovascular complications.^[1,2] Menon et al. in 2017 reported a viper bite patient who developed a delayed intracerebral bleed, localized to the frontal lobe, after 2 days of admission. He underwent craniectomy and made a gradual recovery.^[5] Senthilkumaran et al., in 2023, reported 3 patients who developed ischemic stroke after snake bites who recovered with conservative care without long-term sequelae.^[6] Sirur et al. in 2022 reported a patient who developed a left-sided middle cerebral artery territory infarct who succumbed to the disease.^[7] Naveen et al. reported a patient who succumbed to a viper bite.^[8] Dutta et al. in their description of a 62-year-old who presented with neurological symptoms without a history of a snake bite, but was treated with ASV due to suspicion of a bite mark, noted that multiple species such as Bothrops, Daboia, Notechis, and Pseudonaja can cause stroke in patients.^[9]

Bilateral involvement often portends a poor prognosis: a review of 80 patients with snake bite leading to cerebrovascular involvement.^[1] In the study, Daboia russlei accounted for 37.31% of the cases.^[1] The most important aspect of treatment remains the ASV administration and symptomatic care. Risks in administration of ASV include allergic reactions, bronchospasm, hypotension, and even life-threatening anaphylaxis. Guidelines recommend ASV in the setting of a suspected snake bite with systemic envenomation (hemostatic abnormalities, neurotoxic signs, cardiovascular abnormalities, acute kidney injury, and supporting laboratory evidence of systemic envenoming).^[10] Supportive treatment, such as management of shock, assisted ventilation, and renal dialysis to mitigate the acute phase of injury, plays an important role.^[10]

CONCLUSION

While snakebites are not uncommon, cerebrovascular complications are relatively rare manifestations and may be fatal. In the setting of raised ICP and concomitant DIC, the optimization of the coagulation parameters to perform a safe surgery is of paramount importance. This case reminds us that snakebites are not merely a toxicological emergency, but can manifest as a neurosurgical emergency. In such settings, early recognition of neurological signs, aggressive correction of coagulopathy, decisive neurosurgical intervention, and subsequent care including rehabilitation are of importance. This entails interdisciplinary coordination between emergency physicians, intensivists, physicians, and neurosurgeons indispensable.