Snakebite and its management

Arul Kumar

First-year MEM.CCT, Emergency Medicine, Kauvery Hospital, Cantonment, Trichy

Background

Snakebite affects between 1.8 to 2.7 million people worldwide each year, and it is estimated to cause between 80,000 and 138,000 deaths. A mixture of toxins (venom) is injected into the body following a bite by a venomous snake.Envenoming can be a highly dynamic clinical event. Symptoms can progressively worsen to a life-threatening emergency. Snakebites can have long-term physical sequelae such as amputation, paralysis and disability, and psychological health consequences.

The three major families of venomous snakes are the Elapidae, the Viperidae, and the Hydrophidae (WHO 2010).

Elapidae (cobra, king cobra, krait, and coral snake): These snakes have heads that are about the same width as their necks. The head is covered with large scales but lacks laureal shields. Their pupils are round and they are oviparous. These snakes have grooved fangs that are short, fixed, and covered by mucous membranes. Several species of cobra can spit their venom for one metre or more towards the eyes of perceived enemies.

Viperidae (vipers): The head of a viper is triangular, wider than the neck, and has laureal shields. They have vertically elliptical pupils and are ovi-viviparous. Their fangs are long, movable, and canalized like hypodermic needles. They are further subdivided into pit viper and pitless viper subfamilies. The Crotalinae (pit vipers) have a special sense organ, the pit organ, to detect their warm-blooded prey. This is situated between the nostril and the eye. Viperidae are relatively short, thick-bodied snakes with many small rough scales on the top (dorsum) of the head and characteristic patterns of coloured markings on the dorsal surface of the body.

Hydrophidae (sea snake): Sea snakes are found in the vicinity of the seacoast. They have a small head and a flattened tail that helps them swim. Though venomous, they seldom bite.

Fig. 1A. Russell viper, B. Cobra, C. Saw scaled viper, D. Common krait

In this article, we discussed about the management of snake bite.

Case Presentation

A 52-year-old female with no co-morbidities came to Kauvery Speciality Hospital at 7.30 pm with an alleged H/O snake bite on her left lower limb, sustained at her farm the previous night, with h/o bleeding and pain around the bite mark. Patient recalled the snake to have a glossy look with a scaly pattern and short tail, most likely to be a viper. Initially patient went to GH where 20 min WBCT was not clotted and 10 vials of ASV were administered. In view of bleeding 4 units of FFP were transfused after neutralising the venom with ASV. The patient came here for further management.

On arrival in ER, GCS-E3V5M6, BP-160/80, HR-78/min, SPO2-88% on RA, 98% with 4 L O2. On examination no pallor, icterus, cyanosis, clubbing, or lymphadenopathy. On systemic examination, her cardiovascular system, respiratory system and abdominal system were normal. She was conscious, and oriented, having 5/5 power in all group of muscles and bilateral plantars were flexors.

Patient had left leg and foot swelling up to 10 cm below the knee and warmth and blisters developed progressively. In ER 20 min WBCT was clotted. Patient had anemia with a Hb of 6.3 and 1 Unit of PRBC was transfused. Antibiotics-meropenam and clindamycin- were started, CVC secured and Nor-ad infusion was started at 2 mcg/kg/min with BP of 80/60 mmhg and shifted to ICU.

In ICU, initial blood labs showed hypokalemia with K+ of 2.7 and raised RFT with Creatinine-3.33. Urine output was adequate. Norad was slowly tapered and stopped.

Plastic surgery was involved for left leg necrotising fasciitis and the patient was taken up for fasciotomy and wound debridement. Post Op, patient labs improved. The patients wound worsened and tissue culture showed growth of pan-sensitive pseudomonas and MDR Klebsiella. Appropriate antibiotics were added, the wound continued to worsen and the patient was taken up for below-knee amputation.

Post-surgery analgesics were added. The patients wound was healthy and shifted to ward. With further clinical improvement patient was discharged.

Discussion

Snake bite and necrotising fasciitis

In our case, the clinical presentation was highly suggestive of cytotoxic venom damage. This contains various mixtures of myotoxic phospholipase (PPL) and metalloproteinases (MTP). PPL-based toxins act by causing damage to phospholipid cell membranes of muscle leading to myonecrosis, while MTP toxins hydrolyse the basement membrane of the capillary endothelia by breaking down type IV collagen and damage the endothelial cell-to-cell adhesion. The result is compromised microvascular structural integrity, increased permeability, extravasation and development of oedema. MTP toxins additionally degrade the dermal epidermal interface causing skin damage and blister formation as observed in our case. Cytotoxic venoms also cause damage to other local soft tissues including lymphatics, blood vessels and nerves. The net result is the accumulation of necrotic tissue that triggers an intense local inflammatory response. The introduction of bacteria to the wound either from the snakebite or from applied traditional herbs can rapidly lead to the development of infections such as necrotizing fasciitis.

Guidelines for management

Initial management

(1). Check history for type of snakebite and look for obvious evidence of a bite (fang puncture marks, bleeding, swelling of the bitten part etc.). However, in krait bite, no local marks may be seen.

(2). Reassure the patient that around 70% of all snakebites are from non-venomous species.

(3).Immobilize the limb in the same way as a fractured limb. Use bandages or cloth to hold the splints (wooden stick), but do NOT block the blood supply or apply pressure. Ideally, the patient should lie in the recovery position (prone, on the left side) with his/her airway protected to minimize the risk of aspiration of vomitus.

(4). Traditional remedies have NO PROVEN benefit in treating poisonous snakebites.

(5). Remove shoes, rings, watches, jewellery and tight clothing from the bitten area as they can act as a tourniquet when swelling occurs.

(6). Leave the blisters undisturbed.

Rapid primary clinical assessment and resuscitation

CABDE approach

Circulation (arterial pulse)

Airway

Breathing (respiratory movements)

Disability of the nervous system (level of consciousness)

Exposure and environmental control (protect from cold etc.)

Ptosis in neuroparalytic snake bite

Anti Snake Venom (ASV)

If signs and symptoms of envenomation are present with or without evidence of laboratory tests, administer the full dose. There are no absolute contraindications to ASV.

Do not routinely administer ASV to any patient claiming to have been bitten by a snake as ASV exposes such patients to the risks of ASV reactions unnecessarily; However, at the same time do not delay or withhold ASV on the grounds of anaphylactic reaction to a deserving case.

Do NOT give incomplete doses. Purely local swelling, even if accompanied by a bite mark from an apparently venomous snake, is not a ground for administering

ASV. Swelling, a number of hours old is also not a ground for giving ASV. However, the rapid development of swelling indicates bite with envenoming requiring ASV.

ASV Dosage

The total required dose will be between 10 vials to 25 vials as each vial neutralises 6 mg of Russellâ€™s Viper venom. Not all victims will require 10 vials as some may be injected with less than 63 mg. Not all victims will require 25 vials. However, starting with 10 vials ensures that there is sufficient neutralising power to neutralise the average amount of venom injected and during the next 12 h to neutralise any remaining free-flowing venom.

If the biting snake is identified to be a Saw Scaled Viper, 5 vials may be given as a starting dose. Otherwise, in all cases, starting dose remains 10 vials.

There is every chance to detect remaining free-flowing Viper venom by 20WBCT at 6 h from completion of the first dose of 10 vials of ASV, additional 2nd dose can be given after 6 h from the 1st dose.

For neuroparalytic snakebite ASV 10 vials stat as an infusion over 30 min followed by 2nd dose of 10 vials after 1 h if no improvement within 1st hour.

For vasculotoxic snakebite – Two regimens low dose infusion therapy and high dose intermittent bolus therapy can be used. Low-dose infusion therapy is as effective as high-dose intermittent bolus therapy and also saves scarce ASV doses

Low Dose infusion therapy: 10 vials for Russel’s viper or 6 vials for Saw scaled viper as stat as infusion over 30 min followed by 2 vials every 6 h as infusion in 100 ml of normal saline till clotting time normalizes or for 3 days whichever is earlier.

High dose intermittent bolus therapy: 10 vials of polyvalent ASV stat over 30 min as an infusion, followed by 6 vials 6 hourly as bolus therapy till clotting time normalizes and/or local swelling subsides.

No ASV for Sea snakebite or pit viper bite as available ASV does not contain antibodies against them.

Monitoring of Patients on ASV therapy

All patients should be watched carefully every 5 min for the first 30 min, then at 15 min for 2 h for manifestation of a reaction. At the earliest sign of an adverse reaction suspend temporarily. Maintain a strict intake output chart and note colour of urine to detect acute kidney injury early.

Role of neostigmine in paralytic snake bite

Cobra toxins bind to post synaptic Ach receptors

Neostigmine (Anticholinesterase), prolongs the life of Ach -which can reverse respiratory failure and neurotoxic symptoms (postsynaptic as in cobra as the toxins bind to Ach receptors).

Neostigmine test; 1.5 2.0 mg IM preceded by 0.6 mg atropine IV

Observe for 1 h

If the victim responds continue 0.5 mg Neostigmine IM Â½ hourly with 0.6 mg Atropine IV over 8 h.

If no improvement in symptoms after 1 h stop Neostigmine

Surgery and Snakebite

Surgical interventions are a contributory factor in resolving snakebite but must be used with caution. Some interventions are necessary and should be deployed when required such as life-saving procedures and removal of necrotic tissue. Others such as fasciotomy should be used sparingly and under very defined conditions.

Skin grafting and amputation of a necrotic digit may be required in some cases of Snakebite. These cases should be referred to the Surgeons after completion of Anti venom treatment. Surgical interventions in these cases are in the general principles of surgery, not much related with Anti venom therapy.

Conclusion

Patients who are clinically stable or asymptomatic with persistently negative 20WBCT after 24 h may be discharged. Educate patients and their families on snakebite prevention and first aid, preferably using printed leaflets with clear visually represented information and minimal reliance on text. Inform patients who have received antivenom to report late adverse reactions. Arrange a follow-up after two weeks to review late reactions and sequelae.

Dr. Arul Kumar

MEM Resident

Snakebite and its management