MANAGEMENT OF SNAKE ENVENOMATION

Dr. Shashi Kiran and Dr T.A. Senthilnathan, Department of Anaesthesia and Critical Care, Postgraduate Institute of Medical Sciences, Rohtak -124001. INDIA.

Address for correspondence: Dr. Shashi Kiran, 42/ 9J, Medical Enclave, Rohtak-124001. INDIA
e-mail: gupta3@vsnl.com

Introduction

Out of more than 3000 species of snake identifiable world wide, only one tenth of them are dangerous to human beings. There are three major families of venomous snakes:

• Elapidae (Land snakes like cobra, krait and coral snakes) - Snakes of this family have short & fixed fangs, which contain venom channels. Their tricolor bands (black red &yellow/ white) encircle the body and they lack laureal shields (shield on the lateral aspect of head separating those shields bordering eyes from those bordering the nostril).
• Viperidae (Russell's viper, bamboo snakes) - These are further classified into pit vipers(crotalinae) and viperine vipers(Viperinae).Their fangs are long & movable. Their pupils are vertically elliptical. The ventral plates caudal to anus are in a single row. These snakes have a heat sensing pit as a small depression on the side of head for location of prey.
• Hydrophiladae (Sea snakes) - These snakes have a flattened tail.

Epidemiology

Although a major public health problem in many countries; the epidemiology of snakebite is still fragmentary, mainly due to lack of statistical data. This is compounded by the fact that the majority of victims come from rural areas, out of reach of the available medical facilities. It is estimated that snakebites may exceed 5 million per year, out of which approximately 100,000 develop severe sequelae. The incidence also shows a distinct seasonal pattern with a higher frequency in summers and during rains when the reptiles come out of their shelters. Epidemics of snake bite following floods owing to human & snake populations getting concentrated together have been noted in Pakistan, India & Bangladesh.

Snakebite is observed in all age groups, the majority (90%) affecting 11-50 year olds with males affected twice more often than females. Most bites occur between midnight and early morning and a large number of bites occur in fields, as most individuals are unable to spot the snake due to tall grass & crops. Fortunately every bite does not result in complete envenomation and more than half the victims escape without serious poisoning. However, if sufficient venom is injected during the bite to cause serious poisoning, the mortality can be high.

PATHOPHYSIOLOGY

Snake venom is a very complex chemical poison, containing approximately 5-15 enzymes and 3-12 non-enzyme proteins & peptides besides carbohydrates and metals, which exerts toxic & lethal effects on skin, hematological, nervous, respiratory and cardiovascular systems (Table 2). Different species have differing proportions of above mixtures. The picture may be further complicated by the release of endogenous mediators such as histamine, bradykinin & adenosine. Therefore snake venoms cannot be classified purely as 'neurotoxic' or 'cardiotoxic', although they may have some predominantly specific action. The effects however may conveniently, though arbitrarily, be classified into vasculotoxic for vipers, neurotoxic for elapids & myotoxic for sea snakes.

Viper venom. This is primarily vasculotoxic. It causes rapidly developing swelling of the bitten part. Local necrosis is mainly ischaemic as thrombosis blocks the local blood vessels and causes dry gangrene. Systemic absorption is via lymphatics. Some vipers such as Vipera berus (European Viper) cause vomiting, abdominal pain, explosive diarrhoea and shock within a few minutes of bite, which resolves spontaneously within half an hour. Persistence of the shock may however be fatal. Several viper venoms result in intracranial haemorrhage due to direct endothelial damage by 'haemorrhagin' (a venom component), which however does not affect the coagulation. In contrast other viper venoms (Crotalus, Bothrops) affect coagulation and a very small amount of venom can cause complete fibrinogen consumption. It can also differentiate various species of vipers, which can help in instituting appropriate antivenom therapy.

Elapid venom. Local necrosis causes a picture like 'wet gangrene' with a characteristic putrid smell due to direct cytolytic action of venom. Systemic absorption occurs through venous channels. These result in primarily 'neurotoxic features' causing selective neuromuscular blockade of the muscles of eyes, tongue, throat and chest leading to respiratory failure in severe poisoning.

Sea snake venom. The effects are both myotoxic and neurotoxic resulting in clinical and pathological changes typical of segmental myopathic lesions in the skeletal muscles. Muscle pains may be last for several months unless treated.

CLINICAL FEATURES OF SNAKEBITE

The clinical presentation of a snakebite victim varies with the size and species of snake, the number and location of bites, and the quantity of venom injected. As many 30% of Pit viper bites and 50% of elapid bites may result in no envenomation, sometimes referred to as "dry bites". The venom channel is recessed above the tip of the fang and the venom injected may be reduced by poor penetration or glancing blows, causing venom to be lost over skin & clothing surface. The volume of the venom available to a particular snake may also be reduced by previous bites. The age and health of the victim are also important determinants in the clinical presentation. However, whether the snake is poisonous or non-poisonous and regardless of the venom injected, the commonest symptom following snakebite is 'fright' which may lead to a vasovagal episode (faint).

Usually the minority of victims who receive a venom dose large enough to cause systemic poisoning will already have signs of this by the time they seek medical help, and differentiation of viperine from elapid systemic poisoning is usually obvious from simple clinical evaluation. A persistent bloody ooze from the fang marks may suggest the presence of snake venom anticoagulant. In difficult cases the presence of pain out of proportion to the size of the wound suggests snake envenomation whereas mild pain is more normally caused nonvenomous snakes, anthropod bites (centipedes, spiders), bacterial fascilitis or myonecrosis.

Local manifestations

After envenomation local swelling starts within few minutes.

Fang marks may be difficult to see. Local pain with radiation and tenderness and a small reddish wheal are first to develop, followed by oedema, swelling and the appearance of bullae, all of which can progress quite rapidly and extensively. In most viper bites paraesthesia commences around the wound, and tingling and numbness over tongue, mouth & scalp can occur. The local bite may become necrosed & gangrenous. Russell's viper has been reported to cause Raynaud's phenomenon & gangrene in the limb other than the one bitten. Secondary infection including tetanus & gas gangrene can also result. Since the venoms are largely absorbed by the lymphatics, lymphangitis may appear early. Petichae or purpura may also be present due to the anticoagulant effect of some venom. These characteristic changes are useful clinically - for example if after a known Crotalid bite the victim demonstrates no local changes over next several hours of observation, he can be released from the hospital as significant envenomation is unlikely.

In contrast Elapid snakebites are associated with minimal local changes.

Systemic manifestations

Cobra and vipers produce symptoms within a few minutes to several hours after the bite. Sea snake bites almost always produce myotoxic features with 2 hours so that the bite can be reliably excluded if no symptoms are evident within this period. Although snakes are classified into predominantly neurotoxic, hemorrahagic and myotoxic types on the basis of their venoms, each species can result in any kind of manifestations.

• Viper bites - 75% cause envenomation, 35% mild, 15% severe. Pit viper venom can involve virtually every organ system. Nausea and vomiting are common and if present early suggest severe envenomation. Weakness, sweating, fever, chills, dizziness and syncope may occur. Some patients complain of a minty, rubbery or metallic taste in their mouths with increased salivation. Tingling or numbness in the tongue, scalp, face and digits are indications of moderate to severe envenomation as are fasciculations of the face, neck, back or the bitten extremity. Systemic anticoagulation can lead to gingival bleeding, epistaxis, hemoptysis, haematuria, haemetemesis and rectal bleeding or malena. Intra-abdominal or intracranial haemorrhages may occur. Visual disturbances may result from retinal haemorrhages. There may be tachycardia or bradycardia, often accompanied by hypotension. Delayed shock may occur due to excessive blood loss and hemolysis. Severe envenomation can result in pulmonary oedema as a result of destruction of the intimal lining of pulmonary blood vessels and pooling of pulmonary blood. The venom and associated hypotension along with haemoglobin, myoglobin and fibrin deposition in renal tubules can contribute to nephrotoxicity.
• Elapid bites. The venom of elapid bites is primarily neurotoxic. Neurotoxic features are a result of selective dtubocurarine like neuromuscular blockade, which results in flaccid paralysis of muscles. Ptosis is the earliest manifestation of cranial nerve dysfunction followed closely by double vision. Paralysis usually then progresses to involve muscles of swallowing, but not strictly in that order.
  Generally muscles innervated by cranial nerves are involved earlier. However pupils are reactive to light until terminal stages.
  The muscles of the chest are involved relatively late with the diaphragm being most resistant. Respiratory paralysis is therefore often a terminal event. Even prior to respiratory failure, airway obstruction due to vomit or secretions can result in sudden death.
  Reflex activity is generally not affected and deep tendon jerks are preserved until late. Symptoms that suggest severe envenomation include repeated vomiting, blurred vision, paraesthesiae around mouth and hyperacusis (increased sensitivity to sound), headache, dizziness, vertigo and signs of autonomic hyperactivity. Tachycardia, hypotension and ECG changes may occur. Tetanic contraction of heart following a large dose of cobra venom has also been documented.
• Sea snakes. Muscle pain is the most common presentation. Muscle necrosis may result in myoglobinuria and severe sea snake poisoning causes myoglobinuria and respiratory failure within a few hours. Coagulaopathy is not a feature of coral snake bites.  

In severe systemic poisoning following either elapid or viper bites, the electrocardiogram may show T-wave inversion and ST segment deviation. In sea snake bites, an ECG is especially valuable in detecting hyperkalemia, which can result from damage to muscles. Tall, peaked T-waves in chest leads may appear within a few hours of bite and give early warning of impending death or acute renal failure.

Unusual presentations of snake envenomation

• A species Naja nigricollis (spitting cobra) can eject venom from a distance of 6-12 feet. The venom is aimed at victim's eyes resulting in conjuctivitis and corneal ulceration. It may result into anterior uveitis and hypopion. A dull headache may persist beyond 72 hours.
• Occasionally a recently killed snake or snakes with several heads can eject venom into those handling them.
• Rarely recurrence of snake envenomation manifestations may occur hours or even days after initial good response to the antivenom. This may be due to ongoing absorption of the venom.

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