SNAKE BITE

Snake bite is a common accident in rural India, though majority of them are by non-poisonous snakes. Poisonous snakebites (envenomation) are often fatal, unless treated promptly and adequately.

Incidence of snakebite depends on human-snake inter­action, being more common in older children, males and rural, tribal or coastal regions. Although underreported, snake envenomation is responsible for ~5000 deaths annually in India, commonest being in Maharashtra, West Bengal and Tamil Nadu.

Types: According to herpetologists, ~300+ species of snakes exist in India, of which only 20% are poisonous, usually belonging to four species: (a) elapidae, e.g. cobra, kraits, coral snakes, etc., (b) viperidae, e.g. saw-scaled viper, Russel-viper, etc., (c) crotalidae, e.g. pit vipers and

(d) Hydrophidae, e.g. sea-snakes. Vipers, cobra and kraits are commonest offending snakes in India, responsible for ~50%, 25% and 15% poisonous bites, with following important features:

Viper has a flat, triangular head with long and mobile front fangs, vertical pupils and usually diamond-shaped black/brown spots over body. These snakes injects ~ 15-60 mg of venom/bite (lethal dose 8-15 mg), which is mainly hematotoxic, leading to hemolysis, bleeding and DIC.

Cobra is characterized by oblong head with fixed front fangs, cephalic hood with 'spectacle' mark and long- tapering tail. They generally inject ~60 mg of venom/bite (lethal dose 12 mg), which is predominantly neurotoxic or cardiotoxic.

Kraits are smaller but most poisonous snakes with flat head, fixed front fangs and steel-blue body with white cross bars or yellow body with black cross bands. They injects ~15 mg of venom/bite (lethal dose 6 mg), which is predominantly neurotoxic or cardiotoxic.

Sea-snake bites are common in coastal regions, characterized by severe rhabdomyolysis, myoglobinuria and renal failure.

Pathophysiology: Although species-specific, Snake venom is a mixture of many enzymes, which damage tissue barriers and toxins, e.g. neurotoxins, hemotoxins, cardiotoxins and myotoxins.

Venom from elapidae and hydraphidae snakes is primarily neurotoxic, with a curare-like effect, i.e. block­ade of transmission across the neuromuscular junctions, leading to paralysis and respiratory failure.

Viper-venom is predominantly cytotoxic or hemotoxic, leading to massive tissue necrosis, vascular leaks and coagulopathies followed by shock, ARDS and renal failure.

TABLE 27.23: Determinants of severity in snake bite

• Age (more severe in children)

• Species of offending snake

• Site of bite (more severe face and trunk bites)

• Amount of venom injected:

- Number and depth of fang marks

- Bites over uncovered areas (e.g. bare-foot)

• Spread of venom

- #8593; due to running* after the bite

- E due to immediate torniquet application

• Quality of first-aid

^increases local vascularity

Clinical manifestations of a poisonous snake bite usually begin within 15-30 minutes, though may be delayed as much as 24-48 hours, depending on various factors (Table 27.23) and include:

• Asymptomatic bites by non-poisonous snakes, 'dry bites' or bites over covered areas, e.g. shoes.

• Local manifestations, e.g. burning pain, swelling, bullae formation or gangrene.

• Systemic manifestations depending on the species of snake and include:

- Neurological: Drowsiness, ptosis, dysarthria, dysphagia, bulbar palsy and progressive flaccid paralysis, terminating into coma.

- Hemorrhagic: Purpura, hematuria, hemoptysis, hematemesis, intracranial bleeding or DIC.

- Cardiovascular: Hypotension, shock or arrhythmia.

- Muscular: Myalgia, myoglobinuria gt; renal failure.

Untreated cases with systemic manifestations often die within 24-48 hours, while dramatic recovery is common after anti-snake venom (ASV) therapy. However, many ASV responders develop recurrence of symptoms after 24-48 hours due to ongoing venom absorption from the local site or clearance of ASV (half-life 1-4 hours).

Diagnosis mainly aims to differentiate between poi­sonous and non-poisonous bites, depending on the - (a) examination of killed snake, if possible, (b) fang marks, and (c) clinical presentation. Presence of 2-4 clear and deep fang marks (1-8 mm depth), without other teeth impressions indicates poisonous bites.

In addition, relevant laboratory investigations are necessary to monitor and prognosticate the course of illness, including—(a) blood profile for hemolysis, thrombocytopenia and clotting defects, (b) metabolic profile for hypokalemia, hypoxemia and acidosis,

(c) urine examination for hematuria, hemoglobinuria or myoglobinuria, and (d) ECG for arrhythmia.

Management: All snake bites should be considered as potentially poisonous and need basic first-aid as well as earliest hospitalization for observation till minimum 24 hours. Important steps in management include: a. Immediate first-aid with—(a) reassurance and immobilization as any muscular activity tends to

increase the spread of venom, (b) application of a wide tourniquet, proximal to the bite to block lymphatic and venous spread, (c) local incision of 1.0 ? 0.5 cm size within 15 min of bite, (d) irrigation of local wound with saline and (e) referral to nearest hospital.

b. General supportive measures on hospitalization include: (a) ABC of resuscitation, (b) fluid and electrolyte therapy (preferably with colloids, e.g. plasma/blood, as crystalloid solutions may be lost to extravascular space due to increased capillary permeability), (c) tetanus toxoid, (d) prophylactic antibiotics, and (e) supportive therapy. Steroids are not indicated and sedation should be avoided during early stages.

IV Neostigmine is useful in selected cases of neurotoxin-induced paralysis, while heparin therapy may be needed in those with DIC-like manifestations. Recent studies have reported beneficial effects of IVIG therapy in cases with coagulopathy, but not in those with neurotoxic manifestations.

c. Anti-snake venom (ASV) is indicated only in—(a) bite by a identified poisonous snake, (b) serious systemic manifestations or laboratory abnormalities, (c) extensive and rapidly progressive local reaction.

Presently, a polyvalent ASV of equine origin is avail­able in India as freeze-dried powder, which needs to be dissolved in 10 ml of saline/vial, before use. While exact dose is not established, 50-150 ml of reconstituted ASV (5-15 vials) must be infused slowly @ lt; 2 ml/ min. Sensitivity testing is not necessary and delays the therapy. However, resuscitation measures to manage anaphylaxis must be ready. Clinical response in neurotoxic cases is often dramatic with near-normal recovery within 15-30 minutes, though repeat doses are necessary in many cases. Normalization of clotting time is taken as end­point of ASV therapy in hemotoxic cases, though clinical recovery may take many days.

Prognosis: Overall mortality with snake envenomation is ~10-20%, depending on the severity of manifestations and quality of first aid/hospital care. In recovered cases, local and mild systemic abnormalities may persist for many weeks.

27.5.6