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.

IDENTIFICATION BY CLINICAL EFFECTS

The appearance of a bite site cannot be used to reliably identify the snake.

The constellation of symptoms and signs may be used to a limited degree in identification. For example, within the common genera, paralysis associated with procoagulopathy may be caused by a Tiger Snake, Taipan, Brown Snake, Rough-scaled Snake, Hoplocephalus spp. or Red-bellied Black Snake, but if rhabdomyolysis also occurs, a bite by a Brown Snake is improbable. Paralysis associated with anticoagulation may be caused by a Black Snake (other than a Red-bellied Black Snake), Copperhead or Death Adder, but if rhabdomyolysis occurs, a bite by a Death Adder is improbable. Paralysis with neither coagulopathy nor rhabdomyolysis may be caused by a Death Adder bite.

This information is of limited practical importance. It is essential to administer antivenom at the first opportunity when indicated, rather than wait until the full syndrome becomes apparent to enable an ‘educated clinical guess’ in selection of the appropriate antivenom.

MANAGEMENT OF SNAKE ENVENOMATION

The essentials of management are:

• resuscitation: mechanical ventilation and restoration of blood pressure with intravenous fluids, inotropic and vasoactive agents as needed

• application of a pressure-immobilisation first-aid bandage

• administration of antivenom

• performance of investigations

From a practical point of view, one of three clinical situations arises after snake bite. A plan of management for each of these is summarised in Figure 76.1.

• Victim presents with a critical illness

• Victim envenomated but not critically ill

• Victim bitten but does not appear envenomated

Figure 76.1 Management of snake bite.

When the envenomated victim is not critically ill, more time is available to identify the snake by investigations and to administer specific monovalent antivenom. A pressure-immobilisation bandage should be applied if not already in place, and not removed until antivenom has been administered.

When the victim has been bitten, but not apparently envenomated, admission to hospital is advisable with observation and examination hourly for at least 12 hours in the case of a child but less time for an adult. The syndrome of envenomation may be very slow in onset over numerous hours with an initial period free of symptoms. A test of coagulation should always be performed. If a coagulopathy is present, specific monovalent antivenom should be administered after identification of the species or as indicated by a VDK test. If only a mild coagulopathy is present it may be acceptable to withhold antivenom in the anticipation of spontaneous resolution but coagulation should be checked at intervals and the victim maintained under surveillance until coagulation is normal.

THE PRESSURE-IMMOBILISATION TECHNIQUE OF FIRST AID

Since at least 95% of snake bites occur on the arms or legs,¹ Sutherland’s first-aid pressure-immobilisation technique⁵ is applicable to the majority of cases. With this technique, a crêpe (or crêpe-like) bandage is applied from the fingers or toes up the limb as far as possible, encompassing the bite site. It should be as firm as required for a sprained ankle. Additional immobilisation is applied to the entire limb by a rigid splint, with the aim of immobilising the joints either side of the bite site.

Venom is usually deposited subcutaneously. The systemic spread of venom is largely dependent on its absorption by way of the lymphatics ⁶ or the small blood vessels. Application of a pressure less than arterial to the bitten area when combined with immobilisation of the limb effectively delays the movement of venom to the central circulation.⁵ Although it is a first-aid technique designed for use in the field, it should be part of initial management in hospital since it halts further absorption of venom. There is some experimental¹ and anecdotal⁷ evidence with Death Adder bites that the technique inactivates some venom at the bite site but prolonged application has not been subjected to a controlled study.

Removal of the pressure-immobilisation bandage

Removal may precipitate a sudden elevation in blood concentration of venom and collapse of the victim. On the other hand, first aid has not been proven to inactivate venom in humans. Its removal therefore should be dictated by the circumstance. When an asymptomatic snake-bite victim reaches hospital with the recommended first-aid measures in place, these should not be disturbed until antivenom, appropriate staff and equipment have been assembled. If the victim is symptomatic and antivenom is indicated, the first-aid measures should not be removed until after antivenom has been administered, and reapplied if the victim’s condition deteriorates. A swab of the bite site may be obtained by removing the splint temporarily and then cutting a window in the bandage. Thereafter the bandage should be made good and the splint reapplied.

ANTIVENOM

CSL Ltd (Parkville, Australia) produces highly purified equine monovalent antivenoms against the venoms of the main terrestrial snakes, including Tiger Snake, Brown Snake, Black Snake, Death Adder and Taipan. A polyvalent antivenom – a mixture of aliquots of all these – is also available. A sea-snake antivenom is also produced from horses immunised with Beaked Sea-Snake (Enhydrina schistosa) and Tiger Snake venom.

Antivenom should be administered according to the identity of the snake or, if unknown or doubtful, according to the result of a VDK test (Table 76.3). If neither of these criteria can be fulfilled, and if the situation warrants immediate antivenom therapy, the geographical location may be used a guide, since the distribution of many species is known (Table 76.4). Polyvalent antivenom should not be used when a monovalent antivenom could be used appropriately. For bites by uncommon snakes, when antivenom is indicated, polyvalent antivenom, or a monovalent antivenom as indicated by a VDK test, should be chosen.

Dose

One vial of specific antivenom neutralises in vitro the average yield on ‘milking’ – a process whereby venom is harvested by inducing the snake to bite through a latex membrane. If the amount of venom injected at a bite is greater than the average yield on milking, one vial of antivenom will not be adequate therapy. In severe cases of envenomation, a number of vials of antivenom will need to be administered. Absorption of venom from a bite site(s) is a continuing process.

The initial doses of antivenom are given in Tables 76.3 and 76.4. The need for subsequent doses should be guided by the clinical response. After bites by species with coagulopathic effects the victim’s coagulation status is a useful guide.

The dose of antivenom required varies because the amount of venom injected cannot be determined, and snakes may bite multiple times. Victims may present late after envenomation when toxins have already become bound to target tissues and cannot be easily neutralised. Some victims in this circumstance have required mechanical ventilation for many weeks despite large amounts of appropriate antivenom. A child requires more antivenom than an adult envenomated by the same amount of venom, and a victim in poor general health will likewise require more. Finally, antivenoms are manufactured against specific species and may have less neutralising ability against different species of the same genus or against unrelated species, even when the antivenom chosen is nonetheless appropriate.

Administration

The decision to administer antivenom must be based on clinical criteria of envenomation, not restricted to the result of a VDK test. A positive VDK test establishes the diagnosis of envenomation and the choice of antivenom, but does not imply that antivenom should or should not be given.

However, if the victim is significantly envenomated, antivenom must be administered since there is no other effective treatment. Antivenom may be withheld if envenomation is so mild that spontaneous recovery may occur or the consequences of antivenom administration are likely to outweigh the benefit to be gained, e.g. in a herpetologist known to have allergy to antivenom.

Snake antivenoms must be given by the intravenous route, or in dire circumstances if a vein cannot be cannulated, by the intraosseous route in a child. The large volume of fluid and slow absorption render the intramuscular route useless in emergencies.

A test dose of antivenom to determine allergy should not be done. It is unreliable and a waste of precious time.

Premedication

Antivenom should be preceded by premedication with subcutaneous adrenaline (epinephrine), approximately 0.25 mg for an adult and 0.005–0.01 mg/kg for a child, at least 5–10 minutes before commencement of infusion. In the moribund or critically ill victim, when it is essential to administer antivenom quickly, the epinephrine may be given intramuscularly or even intravenously in smaller doses. However, in general, epinephrine is not recommended by either of those routes because of the risk of intracerebral haemorrhage due to the combination of possible hypertension and coagulopathy. Although intracerebral haemorrhage has been recorded in the past in association with premedication, all such cases were accompanied by intravenous epinephrine, none with subcutaneous epinephrine. On the other hand, the incidence of adverse reactions (8–13%) to antivenom is sufficient to warrant premedication with epinephrine, which is the only medication proven effective in reducing the incidence of antivenom-induced reactions and their severity.⁸

It is not prudent to forgo premedication and elect to treat anaphylaxis if it occurs. Iatrogenic anaphylaxis has a high mortality despite vigorous and expert resuscitation.⁹ If an adverse reaction to the first vial of antivenom has not occurred, subsequent vials do not need to be preceded by epinephrine. The reaction rate to polyvalent antivenom is higher than to monovalent antivenoms and should not be used when a monovalent antivenom or combinations will suffice.

The antihistamine, promethazine, is ineffective in this setting ¹⁰ and may cause obtundation and hypotension, both of which may exacerbate and confound a state of envenomation. It is not recommended. Other drugs such as steroids and aminophylline are also not useful in preventing anaphylaxis because their actions, apart from being unproven, are too slow in onset, but steroids are useful for preventing serum sickness.

Infusion

The antivenom may be injected slowly into a running intravenous line or diluted in Hartmann’s or other crystalloid solution in approximately 1 in 10 volumes in a burette and administered over 15–30 minutes if the situation is not critical. This measure reduces the risk of an anaphylactoid reaction resulting from its binding with complement. For small children, if multiple vials are required, the dilution may be less to prevent excessive fluid administration. In emergencies the antivenom may be infused quickly in high concentration.

Adverse reactions

Antivenom infusion should always be administered in a location equipped and staffed by personnel capable of managing anaphylaxis. Management of anaphylaxis is discussed in detail in Chapter 58. Intramuscular epinephrine is the key treatment in a dose of approximately 0.25–1.00 mg for adults and 10 μg/kg for children. Antivenom therapy should be discontinued temporarily and restarted when the victim’s condition is stable.

Lesser degrees of immediate adverse reaction restricted to headache, chest discomfort, fine rash, arthralgia, myalgia, nausea, abdominal pain, vomiting, and pyrexia may be managed by temporary cessation of infusion and administration of steroids and antihistamine before recommencement.

A delayed hypersensitivity reaction, serum sickness, should be anticipated and patients warned of the symptoms and signs which usually appear several days to 2 weeks after antivenom administration. Severity may range from a faint rash and pyrexia to serious multisystem disease including lymphadenitis, polyarthralgia, urticaria, nephritis, neuropathy and vasculitis. The incidence of serum sickness appears to be greater with the use of multiple doses of monovalent antivenom and with polyvalent antivenom. Prophylactic treatment is a course of steroids, e.g. prednisolone 1 mg/kg per day for 5 days.

INVESTIGATIONS AND MONITORING

Tests should be performed regularly, interpreted quickly and treated promptly to counter venom effects and its complications. Serial coagulation tests and tests of renal function are especially important. Absorption of venom from the bite site is a continuing process and management must anticipate unabsorbed venom. Apart from regular monitoring of vital signs and oxygenation, the following are specifically needed.

SEA-SNAKE BITE

Some sea-snake venoms cause widespread damage to skeletal muscle with consequent myoglobinuria, neuromuscular paralysis or direct renal damage. Many have not been researched. The principles of treatment are essentially the same as for envenomation by terrestrial snakes. The venoms of significant species are neutralised with CSL Ltd Beaked Sea-Snake (Enhydrina schistosa) antivenom. If that preparation is not available, Tiger Snake or polyvalent antivenom should be used. Sea-snake bites are uncommon in Australia and no deaths have been recorded.

UNCOMMON AND EXOTIC SNAKE BITE

Zoo personnel, herpetologists and amateur collectors who catch, maintain or breed species of uncommon Australian snakes or who import or breed exotic (overseas) snakes are at risk, as are personnel in the Australian Quarantine and Inspection Service (AQIS). There are no specific antivenoms to the venoms of uncommon Australian snakes, but neutralisation is provided by polyvalent antivenom or by monovalent antivenom, as indicated by the VDK. Exotic snake antivenoms are maintained by Venom Supplies Ltd, Tanunda, South Australia (Tel: 08 8563 0001), Royal Melbourne Hospital (Tel: 03 9342 7000), Royal Adelaide Hospital (Tel: 08 8223 4000), Australian Reptile Park (Tel: 02 4340 1022) and by Taronga Zoo (Mosman, Tel: 02 9969 2777). The locations of antivenoms in Australia for treatment of bites by specific exotic snakes are maintained by AVRU at http://www.avru.org/reference/reference_avhold.html.

LONG-TERM EFFECTS OF SNAKE BITE

After appropriate treatment, recovery is expected but it may be slow, taking many weeks or months, particularly from a critical illness or after delayed presentation with neurotoxicity and rhabdomyolysis. Isolated neurological or ophthalmic signs may persist. Long-term loss of taste or smell occurs occasionally.

SPIDERS

Although several thousand species of spiders exist in Australia, only Funnel-web Spiders (genera Atrax and Hadronyche) and the Red-back Spider (Latrodectus hasselti) have caused death or significant systemic illness. All spiders have venom and a few, particularly the White-tailed Spider (Lampona cylindrata) and the Common Black House Spider (Badumna insignis), have caused severe local injury, although this occurs rarely.^1,^12,¹³ Causes for ulcerated skin lesions other than spider bites should be sought.

FUNNEL-WEB SPIDERS

Many species of the Funnel-web genera Atrax and Hadronyche inhabit Queensland, New South Wales, Victoria, Tasmania and South Australia but only spiders from New South Wales and southern Queensland have caused significant illness and death. These are large dark-coloured aggressive spiders. A systematic review involving 138 cases identified 77 cases of severe envenomation with 13 deaths, but none occurred after introduction of antivenom in 1981 and the vast majority (97%) responded to antivenom therapy.¹⁴ All deaths were attributed to the Sydney Funnel-web Spider (A. robustus)¹ which inhabits an area within an approximate 160 km radius of Sydney and is inclined to roam after rainfall, enter houses and seek shelter among clothes or bedding, giving a painful bite when disturbed.

Severe envenomation is also caused by the southern tree (H. cerberea), northern tree (H. formidabilis), Port Macquarie (H. sp. 14), Toowoomba or Darling Downs (H. infensa) and Blue Mountains (H. versuta) species. In contrast to other spiders, male Funnel-web Spiders have more potent venom than female spiders.

Bites do not always result in envenomation, but envenomation may be rapidly fatal. The early features of the envenomation syndrome include nausea, vomiting, profuse sweating, salivation and abdominal pain. Life-threatening features are usually heralded by the appearance of muscle fasciculation at the bite site, which quickly involves distant muscle groups. Hypertension, tachyarrhythmias, vasoconstriction, hypersalivation and bronchorrhoea occur. The victim may lapse into coma, develop central hypoventilation and have difficulty maintaining an airway free of secretions. Finally, respiratory failure, pulmonary oedema and severe hypotension culminate in death. The syndrome may develop within several hours but it may be more rapid. Several children have died within 90 minutes of envenomation, and one died within 15 minutes. An active component in the venom is a polypeptide which stimulates the release of acetylcholine at neuromuscular junctions and within the autonomic nervous system, and the release of catecholamines.

Treatment consists of the application of a pressure-immobilisation bandage, intravenous administration of antivenom and support of vital functions, which may include airway support, mechanical ventilation and intensive cardiovascular support.

RED-BACK SPIDER

This spider is distributed throughout Australia and is found outdoors in household gardens in suburban and rural areas. Related species and similar effects of envenomation (‘Latrodectism’) occur in many parts of the world. Red-back Spider bite is the most common cause for antivenom administration in Australia at 300–400 per annum. The adult female is identified easily. Its body is about 1 cm in size and has a distinct red or orange dorsal stripe over its abdomen. When disturbed, it gives a pin prick-like bite. The bite site becomes inflamed and, during the following minutes to several hours, severe pain, exacerbated by movement, commences locally and may extend up the limb or radiate elsewhere. The pain may be accompanied by profuse sweating, headache, nausea, vomiting, abdominal pain, fever, hypertension, paraesthesias and rashes. In a small percentage of cases when treatment is delayed, progressive muscle paralysis may occur over many hours, requiring mechanical ventilation. Untreated, muscle weakness, spasm and arthralgia may persist for months after the bite. Death has not occurred since the introduction of an antivenom in 1956.

If the effects of a bite are trivial and confined to the bite site, antivenom may be withheld; otherwise, antivenom should be given intramuscularly. The antivenom may be given intravenously in cases of refractory pain but the risk of anaphylaxis may be higher than by the intramuscular route which is very low (< 0.5%). A premedication with promethazine is recommended and epinephrine should be at hand. In contrast to a bite from a snake or Funnel-web Spider, a bite from a Red-back Spider is not immediately life threatening. There is no proven effective first aid, but application of a cold pack or iced water may help relieve pain. Bites by Steatoda spp. (cupboard spiders) may cause a similar syndrome and can be treated effectively with Red-back Spider antivenom.¹⁵

BOX JELLYFISH

This creature, Chironex fleckeri, is probably the most venomous in the world. It has caused at least 63 deaths in the waters off northern Australia.¹⁶ It has a cuboid bell up to 30 cm in diameter. Numerous tentacles arise from the corners of the bell and trail several metres. It is semitransparent and difficult to see by anyone wading or swimming in shallow water. The tentacles are lined with millions of nematocysts which, on contact with skin, dischargea threaded barb which pierces subcutaneous tissue, including small blood vessels. Contact with the tentacles causes severe pain and envenomation, from which death may occur within minutes. Death is probably due to both neurotoxic effects causing apnoea and direct cardiotoxicity, although the precise mode of action of the venom is unknown. In mechanically ventilated animals, fatal hypotension occurs rapidly on envenomation.¹⁷ The skin which sustains the injury may heal with disfiguring scars.

First aid, which must be administered on the beach, consists of dousing the skin with acetic acid (vinegar) which inactivates undischarged nematocysts. Adherent tentacles can then be removed. Cardiopulmonary resuscitation may be required on the beach. An ovine antivenom is available but prevention is of paramount importance. Water must not be entered when this jellyfish is known to be close inshore. Wet suits, clothing and ‘stinger suits’ offer protection.

IRUKANDJI

Stings by the Irukandji, Carukia barnesi, and possibly by other jellyfish may cause a syndrome known as the Irukandji syndrome. The Irukandji is a small cubozoan jellyfish with a squarish bell a little more than 1 cm in diameter. Single tentacles trail from its corners. When submerged it is virtually impossible to see.

Its sting is mild and marked only by a small area of erythema. However, severe general illness may follow with abdominal cramps, hypertension, back pain, nausea and vomiting, limb cramps, chest tightness and marked distress.¹⁸ Occasionally, cardiogenic pulmonary oedema has necessitated mechanical ventilation and inotropic therapy, while hypertension has caused two deaths by stroke. The mechanism is uncertain, but experimental studies in animals have shown that Irukandji extracts cause a hyperadrenergic syndrome secondary to massive release of catecholamines¹⁹ which may explain at least in part the cause of heart failure. Pain relief is the most important feature of management in mild to moderate cases. In a series of 10 victims with ‘Irukandji syndrome’, intravenous magnesium salts provided pain relief and a reduction in blood pressure.²⁰ Antihypertensive therapy with phentolamine or a ‘titratable’ nitrate may be required in the initial phase of management.