Malabar pit viper envenomation to the face: A case report

Case report

A 55-year old male, with no known comorbidity, while cutting trees, sustained a snakebite to the left cheek at 12 noon in Thirthahalli, Shimoga, in the Western Ghat region of Karnataka. He presented with persistent mild bleeding at the bite site. The snake was identified as a Malabar pit viper based on our patient's positive identification from a collage of commonly encountered snakes in the region, its clinical syndrome and habitat.

He had visited a Primary Health Centre three hours after being bitten. The 20-min Whole Blood Clotting Test was normal at 4:00pm, but became abnormal when repeated at 8:00 pm and 11:30 pm. He had been administered Trypsin-Chymotrypsin ascan anti-inflammatory agent, Pantoprazole, Cefotaxime and one vial of Anti snake venom (ASV).

Upon arrival at our tertiary care centre at 2:00am revealed swelling and erythema on the left side of the face, head, and neck. But with full orientation. He had a tachycardia (120 b/min), was normotensive (150/90 mmHg), and not hypoxaemic (oxygen saturation 98%), mildly tachypnoeic (22 b/min) with no neurological deficit.

Laboratory investigations revealed a coagulopathy, with an initial (the 14^th hour) prothrombin time (PT) of 48.6 s, International normalised ratio (INR) 4.71, activated partial thromboplastin time (APTT) 30.4 s, and fibrinogen 2.5 g/L. Repeat testing at the 19^th hour showed PT 30.0 s, INR 2.84, and APTT 28.6 s, followed by further improvement at the 25^th hour with PT 20.9 s, INR 1.94, and APTT 27.4 s. Elevated creatinine levels (1.63 mg/dL) suggested acute kidney injury. C-Reactive Protein of 48.06 mg/L and an elevated Creatine Phosphokinase of 12.5 ukat/L were suggestive of systemic inflammation and possible muscle injury. Improved creatine levels (135 μmol/L) were seen by the 10^th day.

Twenty vials of ASV were administered as two separate infusions of 10 vials each in 400 mL of 5% dextrose, at approximately the 15^th and 20^th hour after the bite, in view of progressive coagulopathy and the risk of systemic bleeding. Subsequent coagulation profiles demonstrated a steady decline in PT/INR values, consistent with recovery from venom-induced consumptive coagulopathy (VICC) (Fig. 1).

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Figure 1.

A) Fang marks. B) Victim's face showing fang marks on the left cheek with oedema extending to the neck.

Although the fibrinogen level temporarily fell below 2 g/L, reflecting significant clotting factor consumption, it subsequently recovered. No additional bleeding was noted.

A prophylactic antibiotic regime was continued for one week.

Discussion

Malabar Pit Viper envenomation is increasingly recognized as a clinically significant cause of morbidity. ¹ Proteomic studies reveal a complex venom profile, including metalloproteases, serine proteases, phospholipase A2, and L-amino acid oxidases, ¹ which causes local tissue injury and VICC.

Indian polyvalent ASV designed for the “Big Four” shows poor binding and neutralization against Malabar Pit Viper venom. ¹ Although protocols for ASV use in Malabar Pit Viper envenomation are lacking, case reports suggest benefit and temporary improvement in coagulation parameters, hence ASV was administered.^2,3 A larger cohort of cases needs to be analysed to compare the change in INR with and without ASV.

In many low- and middle-income countries, snakebite management is complicated by limited resources, limited diagnostics, poor pre-hospital care and limited antivenom efficacy. ⁴ Species identification is important, and syndromic diagnosis based on clinical presentation, habitat, and bite circumstances remains crucial for appropriate care. ⁵

While conservation is not a focus of acute care, clinicians must understand any snake's habits and ecology. The Malabar Pit Viper is increasingly reported in bite incidents, possibly due to greater awareness or rising human – habitat interactions. Awareness of these aspects helps clinicians suspect envenomation, understand its burden, plan preventive strategies, and optimize treatment.

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