Extensive spontaneous cerebral haemorrhage after Russell’s viper bite

Abstract

A 30-year-old man presented with altered sensorium following Russell’s viper bite, which was found to be secondary to intracranial hemorrhage secondary to venom-induced consumptive coagulopathy. He was managed conservatively with blood component transfusion and antivenom injection, and successfully discharged.

Background

Snake envenomation is a potentially lethal health problem widely seen in tropical countries, and is recognised as a neglected tropical disease by WHO, accounting for about 125 000 deaths per year.¹ Most snakebites are inflicted by non-poisonous snakes and only 15% of snakes are considered poisonous. The family Viperidae is the largest family of poisonous snakes followed by Elapidae and the subfamily Crotalidae. Cerebrovascular complications following snakebite is rare, but both haemorrhagic and thrombotic complications have been reported in the literature.^{2 3} Viperine bites are the most common bites found in India and majority are due to Russell’s viper, and manifest as coagulopathy or systemic haemorrhage.⁴

Case presentation

A 30-year-old chronic alcoholic non-diabetic non-hypertensive man presented with altered sensorium following a history of Russell’s viper (Daboia russelii) bite. There was no history of abnormal haemorrhage, oliguria, head trauma, vomiting, seizures or headache.

On examination, he had a Glasgow Coma Scale of 9 (E2V3M4), and bilateral upgoing plantar reflexes. There was no other abnormality on systemic examination, or signs of raised intracranial pressure.

Investigations

There was no detectable abnormality in haemogram, except for mild thrombocytopenia (platelet count 110×10⁹/L). Renal and liver function tests were normal. He had mild hyponatremia (Na 131 mEq/L), with normal blood glucose. Twenty minutes whole blood clotting time was prolonged, he had elevated prothrombin time (INR 1.56), activated thromboplastin time, fibrinogen degradation product (FDP) (12.69 µg/mL (normal <10)) and d-dimer (2694 ng/mL (normal <500)).

Non-contrast computed tomography (NCCT) of head revealed multiple intraparenchymal haemorrhages in bilateral frontal, parietal and temporal regions, with no evidence of bony injury (figure 1).

Figure 1.

Non-contrast CT of head (axial section) showing multiple intraparenchymal haemorrhages in bilateral frontal, parietal and temporal regions, with no evidence of bony injury.

Differential diagnosis

The possibility of viper-bite-induced coagulopathy resulting in intracranial haemorrhage was kept as the primary diagnosis. Alcohol-induced liver dysfunction was ruled out in view of otherwise normal liver function test and no evidence of portal hypertension.

Treatment

In view of deranged coagulation parameters with intracranial haemorrhage, he was started on polyvalent antivenom therapy immediately on arrival, and was managed conservatively with fresh frozen plasma and platelet concentrate transfusion. Local wound asepsis was maintained, and he was discharged well on day 5 of hospital stay, and he was able to ambulate with support.

Outcome and follow-up

Repeat NCCT brain at 30-day follow-up shows regression of previous haemorrhages and normalisation of coagulation parameters including FDP (1.4 µg/mL) and d-dimer (0.74 ng/mL) values. There was no residual neurological deficit.

Discussion

The pathophysiology of snake envenomation-related coagulopathy is not fully understood. Various components in venom have separate roles in the spread of the toxin and its resultant systemic effect.⁵ Venom-induced consumptive coagulopathy (VICC) is the most common coagulation abnormality resulting from viperine venom, which has different concentrations of enzymes including proteases, phospholipase A2, hyaluronidase and arginine ester hydrolase.⁶ The hyaluronidase facilitates venom spread by disrupting mucopolysaccharides in the tissue, while phospholipase A2 causes haemolysis secondary to the lysis of red cell membranes, as well as causing myonecrosis.

Thrombogenic enzymes promote the formation of weak fibrin clots, resulting in the activation of plasmin, which leads to consumption of coagulation factors and haemorrhage.⁷ Prothrombin activators such as ecarin and carina activase cause reductions in factors V, VII and fibrinogen levels.⁶

Al-Sadawi et al reviewed 83 cases with acute cerebrovascular accident following snake envenomation, out of which one-fifth had intracranial haemorrhage, out of which Russel’s viperine bite was associated with higher mortality.⁸ Ehelepola et al reported a 52-year-old man who expired due to intracranial haemorrhage attributed to VICC.⁹

Our patient had deranged coagulation parameters and increased levels of FDP, suggesting VICC as the cause for intracerebral haemorrhage. Changes in laboratory parameters do not always correlate with actual risk of haemorrhage. Similarly, after initial correction, clinical relapse with the return of deranged coagulation parameters are well recognised, which is supposedly the result of delayed leaching of venom from deeper areas in the bite site or the disruption of the antigen–antibody complexes, with recirculation of unbound venom constituents.⁹

Learning points.

• Spontaneous intracranial bleed is an uncommon manifestation of hematotoxic snake bite and can often be misleading for the clinician.

• Venom-induced consumptive coagulopathy has been reported in viperine bites, but has rarely been associated with intracranial haemorrhage.

• Early identification of aetiology and correction of haemorrhaging diathesis is the mainstay of treatment, along with antivenom administration.