Envenomation

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Chapter 76 Envenomation

Envenomation by species of snakes, spiders, ticks, bees, ants, wasps, jellyfish, octopuses or cone shell snails may threaten life, while envenomation by other creatures may cause serious illness.¹ Although this chapter focuses on Australia, the principles of management are widely applicable elsewhere except for stings by scorpions which are not a significant health problem in Australia. Immediate advice on management may be obtained from the Australian Venom Research Unit (AVRU) advisory service on their 24-hour telephone number within Australia on 1300 760 451, from overseas on 61 3 8344 7753 or from their website at http://www.avru.org.

SNAKES

EPIDEMIOLOGY

Australia is habitat to a large number of venomous terrestrial and marine snakes (Families Elapidae and Hydrophiidae). The genera responsible for the majority of serious illness are Brown Snakes (Pseudonaja), Tiger Snakes (Notechis), Taipans (Oxyuranus), Black Snakes (Pseudechis) and Death Adders (Acanthophis).

The mean death rate in Australia from 1981 to 1999 was 2.6 per year ¹ (∼0.014/100 000), usually occurring because of massive envenomation, snake bite in remote locations, rapid collapse, or due to delayed or inadequate antivenom therapy. However, as many as 2000 people are bitten each year and of these at least 300 require antivenom treatment. This morbidity and mortality is far less than that observed in surrounding countries. Death and critical illness is due to (1) progressive paralysis leading to respiratory failure, (2) bleeding, or (3) renal failure occurring as a complication of rhabdomyolysis, disseminated intravascular coagulation (DIC), haemorrhage, haemolysis or to their combinations. Rapid collapse within minutes after a snake bite is due to anaphylaxis to venom or possibly due to the myocardial effects of DIC causing hypotension.

Snake bite is often ‘accidental’ when a snake is trodden upon or suddenly disturbed. However, many bites occur when humans deliberately interfere with snakes or handle them. The herpetologist or snake collector is at special risk. Not only do they invariably sustain bites in the course of their work ² or hobby, but they are also at risk of developing allergic reactions to venoms and to the antivenoms used in their treatment. Contact with exotic snakes has additional problems.

SNAKE VENOMS

Venoms are complex mixtures of toxins, usually proteins, which kill the snake’s prey and aid its digestion. Many are phospholipases. The main toxins cause paralysis, coagulopathy, rhabdomyolysis and haemolysis (Table 76.1). Coagulopathy may be due to a procoagulant effect by prothrombin activators (Factor Xa-like enzymes), with consumption of clotting factors, or due to a direct anticoagulant effect.

Table 76.1 Main components of Australian snake venoms

Neurotoxins

Presynaptic and postsynaptic neuromuscular blockers present in all dangerous venomous snakes. May cause paralysis

Postsynaptic blockers readily reversed by antivenom

Presynaptic blockers are more difficult to reverse, particularly if treatment is delayed

Some presynaptic blockers are also rhabdomyolysins

Prothrombin activators

Present in many important species

Cause disseminated intravascular coagulation with consumption of clotting factors including fibrinogen

Intrinsic fibrin(ogen)lysis generates fibrin(ogen) degradation products

Significant risk of haemorrhage

Anticoagulants

Present in a relatively small number of dangerous species

Prevent blood clotting without consumption of clotting factors

Rhabdomyolysins

Some presynaptic neurotoxins also cause lysis of skeletal and cardiac muscle

Apart from loss muscle of mass, may cause myoglobinuria and renal failure

Haemolysins

Present in a few species

Rarely a serious clinical effect

SNAKE BITE AND ENVENOMATION

Although a bite may be observed, envenomation is less common because no venom or a variable amount of venom is injected. Bites are relatively painless and may be unnoticed. This is in marked contrast to many overseas crotalid and viperid snakes, where massive local reaction and necrosis are often a major feature as a result of proteolytic enzymes. Paired fang marks are usually evident but sometimes only scratches or single puncture wounds are found. In general, Australian snake venoms do not cause extensive damage to local tissues and are usually confined to mild swelling and bruising, and continued slight bleeding from the bite site.

SYMPTOMS AND SIGNS OF ENVENOMATION

Not all possible symptoms and signs occur in a particular case: in some cases, one symptom or sign may dominate the clinical picture, and in other cases they may wax and wane (Table 76.2). These phenomena are explained by variations in toxin content of venoms of the same species in different geographical areas, and by variable absorption of different toxins.

Table 76.2 Progressive onset of major systemic symptoms and signs of untreated envenomation (in massive envenomation or in a child, a critical illness may develop in minutes rather than hours)

< 1 hour after bite

Headache

Nausea, vomiting, abdominal pain

Transient hypotension associated with confusion or loss of consciousness

Coagulopathy (laboratory testing)

Regional lymphadenitis

1–3 hours after bite

Paresis/paralysis of cranial nerves, e.g. ptosis, double vision, external ophthalmoplegia, dysphonia, dysphagia, myopathic facies

Haemorrhage from mucosal surfaces and needle punctures

Tachycardia, hypotension

Tachypnoea, shallow tidal volume

> 3 hours after bite

Paresis/paralysis of truncal and limb muscles

Paresis/paralysis of respiratory muscles (respiratory failure)

Peripheral circulatory failure (shock), hypoxaemia, cyanosis

Rhabdomyolysis

Dark urine (due to myoglobinuria or haemoglobin)

Renal failure

The cause of transient hypotension soon after envenomation is obscure but it may be related to intravascular coagulation.^3,⁴ Prothrombin activators gain access to the circulation within a number of minutes after subcutaneous injection. There is often tachycardia and relatively minor ECG abnormalities. Other causes of hypotension such as direct cardiac toxicity remain unproven. Hypotension may be secondary to myocardial hypoxaemia.

Tender or even painful regional lymph nodes are moderately common but are not per se an indication for antivenom therapy, since lymphadenitis also occurs with bites by mildly venomous snakes which do not cause serious systemic illness.

Occasionally intracranial haemorrhage occurs. In the case of untreated or massive envenomation, rhabdomyolysis may occur. This usually involves all skeletal musculature and sometimes cardiac muscle. The resultant myoglobinuria may cause renal failure. Direct nephrotoxicity has been suspected in a few cases of Brown Snake bites, but is as yet unproven.

A high intake of alcohol by adults before snake bite is common, and may make management quite difficult initially. Pre-existing treatment (e.g. warfarin therapy) or disease (e.g. gastrointestinal tract ulceration) may complicate management of coagulopathy.

SNAKE BITE IN CHILDREN

Snake bite in young children presents additional problems. It is difficult to diagnose when a bite has not been observed. The symptoms of early envenomation may pass unsuspected and the signs, particularly cranial nerve effects, are difficult to elicit. Bite marks may be difficult to distinguish from the effects of everyday minor trauma. Lastly, the onset of the syndrome of envenomation is likely to be more rapid than in adults and the severity of envenomation more acute because of the relatively higher ratio of venom to body mass. Presentation may be cardiorespiratory failure.

IDENTIFICATION OF THE SNAKE

Identification of the snake guides selection of the appropriate antivenom, and provides an insight into the expected syndrome. Administration of the wrong antivenom may endanger the victim’s life because there may be very little neutralisation of venom. A venom detection kit can be used to identify the snake venom. If the snake cannot be identified, a specific antivenom, or a combination of monovalent antivenoms or polyvalent antivenom should be administered on a geographical basis (see Tables 76.3 and 76.4).

Table 76.3 Antivenom and initial dosages when snake identified

Snake	Antivenom	Dose (units)
Common Brown Snake	Brown Snake	4000
Chappell Island Tiger Snake	Tiger Snake	12 000
Copperheads	Tiger Snake	3000–6000
Death Adders	Death Adder	6000
Dugite	Brown Snake	4000
Gwardar	Brown Snake	4000
Mulga (King Brown) Snake	Black Snake	18 000
Papuan Black Snake	Black Snake	18 000
Red-bellied Black Snake	Tiger Snake or Black Snake*	3000
		18 000
Rough-scaled (Clarence River) Snake	Tiger Snake	3000
Sea-Snakes	Sea-Snake or	1000
	Tiger Snake	3000
Small-scaled (Fierce) Snake	Taipan	12 000
Taipans	Taipan	12 000
Tasmanian Tiger Snake	Tiger Snake	6000
Tiger Snake	Tiger Snake	3000

* Smaller protein mass Tiger Snake antivenom preferable. Antivenom units per vial: Brown Snake 1000; Tiger Snake 3000; Black Snake 18 000; Taipan 12 000; Death Adder 6000; polyvalent 40 000. Note: (1) If the victim on presentation is critically ill, 2–3 times these amounts should be given initially; (2) additional antivenom may be required in the course of management since absorption of venom may be delayed.

Table 76.4 Antivenom and initial dosages when identity of snake uncertain

State	Antivenom	Dose (units)
Tasmania	Tiger Snake	6000
Victoria	Tiger Snake and	3000
	Brown Snake	4000
New South Wales and ACT; Queensland; South Australia; Western Australia; Northern Territory	Polyvalent	40 000
Papua New Guinea	Polyvalent	40 000

Note: (1) If the victim on presentation is critically ill, 2–3 times these amounts should be given initially; (2) additional antivenom may be required in the course of management since absorption of venom may be delayed.

IDENTIFICATION BY VENOM DETECTION KIT TEST

The venom detection kit (VDK) is an in vitro test for detection and identification of snake venom at the bite site, in urine, blood or other tissue in cases of snake bite in Australia and Papua New Guinea. It is an enzyme immunoassay using rabbit antibodies and chromogen and peroxide solutions. A positive result will indicate the type of antivenom to be administered. It detects venom from a range of snake genera including Tiger, Brown, Black, Death Adder and Taipan. Individual species of snake cannot be identified by the test and several genera may yield a positive result in a specified well. The incidences of false-positive and false-negative tests of the kit remain unknown, but are generally regarded as low. The test is very sensitive, able to detect venom in concentrations as low as 10 ng/ml, and can yield a visual qualitative result in test wells in approximately 25 minutes. On occasion, a positive test may be present but the patient is asymptomatic. A decision to administer antivenom should be made on clinical grounds. A very high concentration of venom in a sample may overwhelm the test and yield a spuriously negative result (Hook effect). If that possibility exists, a diluted sample should be re-tested.

IDENTIFICATION BY PHYSICAL CHARACTERISTICS

This can be misleading. Non-herpetologists should consult an identification guide ¹ with reference to scale patterns to identify a specimen correctly if antivenom therapy is to be based on morphological characteristics alone.