Snakes are elongated; legless, carnivorous ectothermic reptiles covered with scales of suborder Serpentes. Out of the total 256 snake species found in India, about 52 species are venomous while most are non-venomous [1]. The major families of venomous snakes in India are Elapidae, Viperidae and Hydrophiidae. Viperidae are represented by true vipers and pit vipers. The Elapidae family includes Cobras, King Cobras, Kraits and Coral Snakes. The spectacled Cobra (Naja naja) is one of the commonest snakes in India. Kraits are nocturnal snakes, which enter human dwelling at night in search of prey and many victims are bitten in their sleep [2]. 

Snake Bite (Incidence and Demography)

Snake bite is generally considered a rural problem and is often linked with environmental and occupational conditions. Snake bites show classical seasonal variations, most cases being reported in summers and rainy season. Nearly 75% cases occur outdoors and 75-90% in rural areas [3]. Most of the bites are caused by non-venomous snakes (90.5%) [2].

Most frequent site of bite is lower limb (2/3rd) of which 50% occur in feet al.,one. The percentage of dry bites ranges from 10-80% for various venomous snakes [3]. The peak age for bites is children  adolescents and young adults. The most vulnerable to snake bites are boys aged more than 5 years [4].

Snake Bites and Envenomation

The risk of envenoming after venomous snake bites varies with species but is on an average only about 50%. Bites in which the fangs pierce the skin but no envenoming results are known as “dry bites”. Venomous snakebite can cause rapid and irreversible complications like shock, systemic bleeding, respiratory muscle paralysis, acute renal failure and necrosis of tissue at the site of the bite.

Snake Venom Composition

The toxic component of snake venom can be classified into four broad categories: enzymes, polypeptides, glycoproteins, and compounds of low molecular weight [1]. They can also be classified as    protein (90–95%) and nonprotein (5–10%) compounds.

Table 1: Chemical Composition of Snake Venom

Table 2: Factors Contributing to Fatal Outcome

The clinical signs and symptoms in snake bites are the result of identification of antigenic protein and the non-protein component of snake venom by the immune system and arousal of inflammatory response in the victim's body. An enzyme, Phospholipase A2 inhibits electron transfer at cytochrome C level and renders mitochondrial-bound enzymes soluble, thus damaging blood cells causing hemorrhages. Another enzyme, Hyaluronidase, helps in spread of venom through tissues while proteolytic enzymes are responsible for local edema, blistering, and necrosis. Among the non enzyme polypeptides, neurotoxins first cause release of acetylcholine at the nerve endings at the myoneural junction and then damage the endings, preventing further release of the transmitter leading to a flaccid paralysis of the victim.

Factors Affecting Envenomation

Envenomation due to snakes is multifactorial and depends on a number of factors like age, site of bite, activity while bite, season, snake type etc. The children generally receive larger envenomation doses relative to their body size [5].

Clinical Characteristics

Clinic-toxicologically, snake envenomation is categorized as hemotoxic, neurotoxic and myotoxic.⁶ According to Wheeless’ Textbook of Orthopaedics, snake envenomation is divided into four grades.

• Grade 0:  No envenomation, fang marks present and minimal pain.

• Grade I:  Minimal envenomation, fang marks present, pain, 1 to 5 inches of edema and erythema in 1st 5 hours; no systemic symptoms.

• Grade II: moderate envenomation, fang marks present, pain, 6-12 inches of edema in first 12 hours; systemic symptoms may be present along with rapid progression of signs from grade I and may have bleeding from bite site.

• Grade III: severe envenomation, fang marks present, pain, edema greater than 12 inches in first 12 hours; systemic symptoms, including coagulation defects; signs of grade I and II envenomation appear in rapid progression.

• Grade IV: very severe envenomation, local reaction develops rapidly. Edema may involve an ipsilateral trunk. Possess high potential for compartment syndrome.

Severe local symptoms are defined as swelling rapidly crossing a joint or involving half of the bitten limb, in the absence of a tourniquet.

Snake Bite Management

The prevalence of this type of snake varies in different geographical parts of the country. Therefore, the clinical manifestations and management practices also vary accordingly. An early and adequate medical management of snake bite is needed to avoid prolonged hospitalization and mortality. Therefore, the Health and Family Welfare Department, Government of India has prepared a National Snakebite Management Protocol [1,6] to provide the best scientific approach to deal with this problem [7].

Anti Snake Venom (Asv)

Antivenom is an immunoglobulin [usually pepsin-refined F(ab’)2 fragment of whole IgG] purified from the plasma of a horse, mule or donkey (equine) or sheep (ovine) that has been immunized with the venoms of one or more species of snake. At IGMC, Lyophilized form of ASV i.e. Snake Venom Antiserum IP (Polyvalent, enzyme refined, equine antivenom immunoglobulin fragments) manufactured by VINS Bioproducts Limited, at Telangana, India is used. Antivenom administration is the only specific treatment for snakebite envenoming, but existing Anti snake venom covers only the “Big 4” species i.e., only medically significant species. Hence presence of antivenom only against these big 4 and diversity of venomous species in Himachal sometimes questions the effectiveness of ASV in our state.

Treatment Protocol

The current guidelines for first aid according to WHO include the following: 

• Reassure the victim (70% of all snakebites are by non-venomous snakes and 50% of bites by venomous species are dry bites) [1]

• Pressure immobilization method (PIM): Immobilize the affected limb (by bandage or clothes to hold splint, but tight arterial compression is not recommended)

• Promptly transfer of victim to hospital

General Care

Patient evaluation should begin with the assessment of the airway, breathing, circulatory status, and consciousness. Oxygen should be administered to every envenomed patient and a large-bore intravenous catheter should be inserted. A bolus of normal saline or Ringer's lactate should be given to all patients with suspected envenomation.

Specific Care

The patient is administered specific treatment only after a precise history has been taken and thorough physical examination has been done. Antivenom should ideally be administered within 4 h of the bite, but is also effective within 24 h. Freeze-dried (lyophilized) antivenoms are reconstituted, usually with 10 ml of sterile water for injection per ampoule [6] Two methods of administration are recommended:

• Intravenous “push” injection: Reconstituted freeze-dried antivenom or neat liquid antivenom is given by slow intravenous injection (not more than 2 ml/minute)

• Intravenous infusion: Reconstituted freeze-dried or neat liquid antivenom is diluted in approximately 5-10 ml of isotonic fluid per kg body weight (i.e. 250-500 ml of isotonic saline or 5% dextrose in the case of an adult patient) and is infused at a constant rate over a period of about one hour

Response to antivenom infusion is assessed by normalization of blood pressure. While bleeding stops in 15-30 minutes, coagulation disturbances may take up to 6 h to normalize. Neurotoxicity begins to improve within the first 30 min, but patients may require 24–48 h for full recovery [8].

Asv Reaction

Approximately 20% patients treated with ASV develop either early or late reaction. If anaphylaxis occurs, antivenom administration must be temporarily stopped and adrenaline (1 in 1000) is given intramuscularly in an initial dose of 0.01 mg/kg body weight. The dose can be repeated every 5–10 min if necessary. After adrenaline, an anti-H1 antihistamine such as chlorpheniramine maleate (0.2 mg/kg) should be given intravenously. It may be followed by intravenous hydrocortisone (2 mg/kg). Late (serum sickness–type) reactions are usually treated by a 5-day course of oral antihistamine (e.g., chlorpheniramine 0.25 mg/kg/day in divided doses in children) [9].

1. Warrell D.A. “Snake bite: a neglected problem in twenty-first century India.” 2011.

2. Bhardwaj A., Sokhey J. “Snake bites in the hills of north India.” National Medical Journal of India, vol. 11, 1998, pp. 264–265.

3. Saikia U., Sharma D.K., Sharma R.M. “Checklist of the reptilian fauna of Himachal Pradesh, India.” Reptile Rap, vol. 8, 2007, pp. 6–9.

4. Joseph J.K. et al. “First authenticated cases of life-threatening envenoming by the hump-nosed pit viper (Hypnale hypnale) in India.” Transactions of the Royal Society of Tropical Medicine and Hygiene, vol. 101, no. 1, 2007, pp. 85–90.

5. Singh S. et al. “Changing pattern of childhood poisoning (1970–1989): experience of a large north Indian hospital.” Indian Pediatrics, vol. 32, 1995, pp. 331–331.

6. Directorate General of Health and Family Welfare. “National snakebite management protocol, India.” Ministry of Health and Family Welfare, India, 2008. Available at: www.mohfw.nic.in.

7. Fernando P., Dias S. “A case report: Indian kraits bite poisoning.” Ceylon Medical Journal, vol. 27, 1982, pp. 39–41.

8. Theakston R.D., Warrell D.A., Griffiths E. “Report of a WHO workshop on the standardization and control of antivenoms.” Toxicon, vol. 41, 2003, pp. 541–557.

9. Syed M.A. et al. “Emergency treatment of a snake bite: pearls from literature.” Journal of Emergencies, Trauma, and Shock, vol. 1, no. 2, 2008, pp. 97–105.