MANAGEMENT OF SNAKEBITE

The management of snake envenomation is controversial. It can be divided into first aid and pre-hospital care, specific antivenom therapy and the supportive therapy.

First aid and prehospital care

Reassurance and immobilisation of the affected limb with prompt transfer to a hospital are of prime importance. The application of a "constriction band" to delay the absorption and venom spread has been advocated during transit to hospital for bites to the limb. A firm, but not tight, ligature may be applied just above the bite. The tension is correct if one finger can pass between the limb and the bandage. This will impede lymphatic drainage, but not arterial or deep venous flow. It should preferably not be released until the administration of anti-snake venom. If the limb becomes edematous the band should be advanced proximally. However, the band should not be left in place for too long due to the risk of venous thrombo-embolism and distal ischaemia. An increase in local envenomation has also been reported subsequent to release of the band. Venous or arterial tourniquets are contraindicated.

The site of bite should be wiped & covered with a handkerchief or dressing. Incision and mechanical suction of the bite (intended to open the puncture wound so that suction can be more effective) may be beneficial when performed by a health care worker within a few minutes of the bite in a victim who is more than 30 to 60 minutes from hospital. The incision should be parallel to the axis of the extremity and should be only approximately 6 mm long and 3mm deep and cross cuts or multiple cuts should be avoided.

Mechanical suction ("extractor" device found in Sawyer first aid kit) is preferable to mouth suction in order to avoid wound contamination with oral flora and to prevent possible envenomation of the rescuer through breaks in their oral mucosa. Suction should be maintained for about 30-60 minutes for maximal benefit, but due care should be taken as laceration of nerves, tendons & vessels has been reported following suction by untrained rescuers.

Application of cooling measures such as ice packs or cryotherapy, at the site of bite were initially advocated but have not been observed to be effective and this practice is not now recommended.

Anti tetanus toxoid should always be given following snakebite. There is controversy about use of drugs as part of first-aid care. It has been suggested that NSAIDS (Aspirin) may be beneficial to relieve local pain but it may precipitate bleeding especially if the venom is vasculotoxic. Paracetamol and / or codeine may be useful, however there are no clear-cut recommendations for the use of sedatives.

If the snake has been killed, it should be taken to hospital, otherwise it should be left alone, since attempts to find or kill it may result in further bites. The snake, even if judged to be dead, should be handled very carefully, since decapitated heads can bite for up to one hour!

Patient assessment

Evaluation should begin with the assessment of the airway, breathing and circulatory status. Oxygen should be administered to every envenomated patient and a large bore intravenous line with normal saline or Ringer's lactate established in the unbitten limb. Cardiac monitoring and pulse oximetry, if available, is indicated. Attempts should be made to determine whether a venomous snake has actually bitten the patient, and the severity of envenomation should be assessed. (Table 3)

During the initial evaluation, several locations on the bitten extremity (at the bite site and at least two sites more proximal) should be marked and the circumferences should be measured every 15 minutes until swelling is no longer progressing and every 1-4 hours thereafter. The extremity should be placed in a well- padded splint for at least 24 hours.

Laboratory Investigations

Although lab tests are of little value in the diagnosis of snake envenomation, nevertheless they are useful for monitoring the patient and deciding about specific interventions and prognosis. They should include a full blood count, electrolytes, glucose, creatinine, serum amylase, creatinine phosphokinase (CPK), prothombin time (PT), partial thromboplastin time (PTT), fibrinogen and fibrin degradation products (FDP's). Commonly hyperkalaemia and hypoxaemia with respiratory acidosis may be seen, particularly with neuroparalysis. Urine examination can reveal haematuria, proteinuria, haemoglobinuria or myoglobinuria. Arterial blood gases and urine examination should be repeated at frequent intervals during the acute phase to assess progressive systemic toxicity.

Blood changes include anaemia, lecuocytosis (raised white cell count) and thrombocytopenia (low platelet count). The peripheral blood film may show evidence of haemolysis especially in viperine bites. Clotting time and prothrombin time may be prolonged and a low fibrinogen may be present. Blood should be typed and crossmatched on the first blood drawn from the patient, as both direct venom and anti-venom effects can interfere with later cross matching. Some specialised centers can identify species of snake involved.

Non specific ECG changes such as bradycardia and atrioventricular block with ST,T segment changes may be seen.

Recently EEG changes have also been reported in many patients of snake envenomation. They may manifest within hours of bite without any clinical features suggestive of encephalopathy.

Anti venom therapy

Anti snake venoms (ASV) are prepared by immunising horses with venom from poisonous snakes and extracting serum & purifying it. The WHO has designated the Liverpool School of Tropical Medicine as the international collaborating center for anti-venom production and testing. Anti-venoms may be species specific (monovalent) or effective against several species (polyvalent) (Table 4).

The correct use of antivenom is the most important component of the hospital care and not every bite, even with a poisonous snake, merits its use. Administration of anti-venom should be selective and based on severity of clinical symptoms. The main concern about the empirical use of antivenom is the risk of allergic reactions, its relative scarcity in some centers and the cost factor. Moreover in a study of Elapid envenomation, all victims with neuromuscular paralysis survived without receiving any anti- venom. Shamesh et al did a preliminary evaluation of the possibility of reducing the dose of anti-venom or totally avoiding it in some viper species. They concluded that about half of the bitten patients in their study did not show systemic symptoms and therefore did not require antivenom treatment. They further observed that anti-venom treatment based on systemic symptoms was effective and the dose required was also less than the fixed amount advocated for each patient, thereby reducing the incidence of serum sickness.

Administration of Antivenom

Antivenom should be given within 4-6 hours of the bite and the dosage required varies with the degree of envenomation. Serum sensitivity should be tested by injecting 0.2 ml of antivenom subcutaneously. If a severe reaction occur within 15 minutes, anti-venom is contra-indicated. Adrenaline should be readily available in a syringe for moderate reactions that may occur despite negative tests for sensitivity. Initial dose should depend upon an estimate of amount of envenomation. (Table 5) However no upper limit has been described and up to 45 vials have been successfully used in a patient! In children and small adults (body weight <40 kgs) up to 50% higher dose of ASV should be administered to neutralise the relatively higher venom concentration.

ASV is administered intravenously either in an undiluted form at a rate of not more than 1ml per minute or diluted in 500ml of IV fluid & administered as rapidly as tolerated over 1-2 hours.

Additional infusions containing 5-10 vials (50-100ml) should be repeated until progression of swelling in the bitten part ceases and systemic signs & symptoms disappear. However it is not advisable to infiltrate ASV at the local site. Delayed reactions may occur following anti-venom therapy and their frequency of occurrence is proportional to the amount of anti-venom administered. Therefore all patients receiving ASV should be observed for several days.

Role of Anticholinesterase Agents

Since Elapidae snakes result in primarily neurotoxic features as a result of selective d-tubocurarine like blockade, the post synaptic toxin of the venom leads to pathophysiological changes resembling those of myasthenia gravis; This prompted some of the workers to use anticholinesterase agents such as neostigmine in addition to a conventional antivenom therapeutic regimen with dramatic results. However the use of anticholinesterase drugs alone without ASV has also been recommended. Neostigmine can be given as 50-100 (g/kg 4 hourly or as a continuous infusion. Edrophonium can also be used in dose of 10mg in adult or 0.25mg/ kg in children over 2 minutes & if the response is positive then one can switch over to long acting preparations like neostigmine. However prospective studies are required to fully establish the efficacy of neostigmine with or without ASV. Glycopyrrolate 0.2 mg preceding neostigmine can be given, as unlike atropine it does not cross blood brain barrier

Supportive therapy

The patient should be moved to an appropriate are of the hospital - ICU will be required for severe envenomation. Fasciotomy should be undertaken in patients with compartment syndrome and debridement should be performed for necrotic tissue. Coagulopathies should be corrected with fresh frozen plasma and platelets. Blood transfusion should be given to replace blood loss from haemolysis & bleeding. Ventilatory support and haemodialysis may be necessary for pulmonary and renal complications due to severe envenomation. Corticosteroids are of no proven value and in fact may interfere with the action of ASV. However, corticosteroids may be used for hypersensitivity reactions to ASV. Prophylactic antibiotics are of no proven value. If infection occurs broad-spectrum cover such as ciprofloxacin and clindamycin should be used.

Intravenous immunoglobin therapy has also been used for envenomation and it may improve coagulopathy but has no effect on neurotoxicity. Certain reports on the evaluation of intravenous immunoglobin suggest that it may reduce the need for repeat antivenom therapy for envenomations associated with coagulopathy.

A compound (2-hydroxy 4-methoxy benzoic acid) isolated and purified from anatamul (Hemidesmus indicus R.Br.), an Indian herb, has also been observed to have potent anti inflammatory, antipyretic and antioxidant properties, especially against Russel's viper venom.

Analgesia should be given - opioids may be required.

Other envenomations

Scorpion venom poisoning.

There are more than 1,400 species of scorpions in the world but the number of medically important species is limited. The venom of the Bark scorpion (C. exilicauda) contains at least five distinct neurotoxins that stimulate depolarization of the neuro muscular junction & autonomic nervous system via release of acetylcholine, norepineprine & epinephrine. It may also have cardiotoxic effects.  

Most stings are minor though serious envenomations can occur in children. The sting is followed by the onset of intense local pain with hyperesthesia (increased skin sensitivity to touch) but local swelling and ecchymosis are absent. Systemic symptoms, when present, reflect sympathetic, parasympathetic and neuromuscular excitation. Tachypnoea, respiratory distress, wheezing, stridor, muscle fasciculations and spasm follow initial restlessness and anxiety. There may be convulsions, paralysis and involuntary voiding of stools/urine, priapism (persistent penile erection) and anxiety. Other systemic features may include hypertension, supraventricular tachycardia and hyperpyrexia.

The majority of stings can be treated with mild analgesics & cold compresses. In the event of severe envenomatiom, the patient should be resuscitated and appropriate symptomatic treatment should be instituted. A goat-derived anti-venom is available in Arizona. Most adults can be safely treated at home, but children should always be admitted and any child less than a year old or having neurological findings should be admitted to ICU.

Further reading

1. Hawgood BJ, Hugh AR. Investigation and treatment of snakebite. Toxicon 1998;36:431-46.
2. Theakston RDG, An Objective Approach to Antivenom Therapy and Assessment of First Aid Measures in Snakebite. Annals of Tropical Medicine and Parasitology. 1997;91:857-65.
3. Iyaniwura TT: Snake venom constituents: biochemistry and toxicology (parts I & II). Vet Hum Toxical 1991;33:468-80.
4. Reid HA, Theakston RDG. The management of snake bite. Bulletin of World Health Organisation. 1986;61:885-95.
5. Zamudio KR, Hardy DJ, Martins M, Greene HW. Fang tip spread, puncture distance and suction for snakebite, Toxicon. 2000;38:723-28.
6. Sailor JG, Sagernan SD, Geller RJ, Eldridge JC, Fleming LL Venomous snake bite: current concepts of treatment. Orthopaedics 1994,17:707-14.
7. Reid HA. Diseases due to infection and Infestation. In: Sir Ronald Bodley Scott (ed.). Price's Textbook of Practice of Medicine. 12th edition: Oxford Medical Publications, London. 1978; 242-6.
8. Norris RL. Envenomations. In: Rippe JM, Irwin RS, Alpert JS, Fink MP. (eds.) Intensive Care Medicine. 2nd edition. Little, Brown and Company, London. 1985;1266-78.
9. Shemesh IY, Kristal C, Langerman L, Bourvin A. Preliminary evaluation of vipera palaestinae snakebite treatment in accordance to the severity of the clinical syndrome. Toxicon 1998; 36: 867- 73.