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Funnel Web Spiders
The funnel web spiders are found only along the eastern seaboard of Australia. The 3 species in the genus Atrax range from the Hunter River in New South Wales to Victoria's Snowy River.
A. robustus (the Sydney funnel web spider) is said to be limited to a radius of 160 km from Sydney (Sutherland, 1983).
The 39 Hadronyche species are widely distributed over 5 states from north Queensland to Tasmania.
Funnel-web spiders (FWS) (Hexathelidae: Atrax and Hadronyche spp.) are the most dangerous Australian spiders. FWS bites are uncommon and severe envenoming rare. There are about 5 - 10 severe envenomings annually. Severe envenoming has only been reported in six species of FWS confined to NSW and southern Queensland, including:
- Sydney FWS (Atrax robustus)
- Southern Tree FWS (Hadronyche cerberea)
- Northern Tree FWS (H. formidabilis)
- Blue Mountains FWS (H. versuta)
- Toowoomba or Darling Downs FWS (H. infensa)
- Port Macquarie FWS (H. sp 14)
Local effects of FWS bites include puncture marks or grazes and local bleeding. Local pain is often severe and may last for 1 to 4 hours. Severe envenoming develops in only a proportion of cases and is characterised by:
- Massive autonomic stimulation/excitation (both sympathetic and parasympathetic) with generalised diaphoresis, hypersalivation, lacrimation, piloerection, hypertension, bradycardia or tachycardia, and miosis or mydriasis;
- Neuromuscular excitation: paraesthesia (local, distal and oral), fasciculations (local or generalised, commonly tongue fasciculations) and muscle spasms;
- Non-specific systemic effects: nausea, vomiting, abdominal pain and headache.
- Non-cardiogenic pulmonary oedema and less commonly myocardial injury
- Central nervous effects: agitation/anxiety, drowsiness and coma (CNS depression appears to be more common in children)
There are 13 recorded deaths due to funnel web spider bite. All of these have been attributed to the male A. robustus and all preceded the widespread availability of antivenom.
Death may occur rapidly, particularly in small children where a death within 15 minutes has been recorded (Sutherland, 1983).
Prior to the development and trialling of funnel web spider antivenom in 1980, victims of funnel web envenomation often became critically ill. No deaths have been reported since its introduction. Similar clinical toxicity has been well documented for spiders of the Hadronyche species. The application of pressure-immobilisation first aid may alter outcome by both retarding venom movement and facilitating peripheral inactivation.
MECHANISM OF TOXIC EFFECTS
Robustoxin is the lethal component of A. robustus venom. It is a presynaptic neurotoxin that induces spontaneous firing of autonomic and motor neurons resulting in an “autonomic storm” (Gage and Spence, 1977; Harris et al., 1981). There is a surge of endogenous acetylcholine, noradrenaline and adrenaline (Duncan et al., 1980). The only Hadronyche venom to be sequenced (versutoxin) seems to be a closely related protein (Brown, 1889). The male A. robustus is said to have a venom potency 4-19 times greater than that of the female due to a higher concentration of robustoxin (Sutherland, 1983; White et al., 1995b; Sheumack et al.,1984).
Lethality indices for individual spiders cover a huge range for both genders and all species due to variations in size, health and feeding habits of the spiders. The season and locale also affect venom potency. (Sheumack et al., 1984; Sutherland, 1983).
It should be emphasised that the majority of bites do not result in systemic envenomation. It appears that only 1 in 5 to 1in 10 bites will produce toxicity, however all should be treated as potentially life-threatening (Hartman and Sutherland,1984; White et al., 1995b). The extent and severity of the envenomation appears dependent upon the volume and potency of the venom injected, the size, health and age of the patient, and the speed of first aid application (Sutherland, 1990).
Funnel web spider toxicity: a biphasic envenomation syndrome
Phase one may occur within minutes of the bite. This consists of pain at the bite site, perioral tingling, piloerection and fasciculations (most prominent in the face, tongue and intercostals). Fasciculations may progress to more overt muscle spasm; masseter and laryngeal involvement may constitute a threat to the airway (Sutherland, 1983).
Other features include tachycardia, hypertension, cardiac arrhythmias, nausea, vomiting, abdominal pain, gastric dilatation, diaphoresis, pupillary asymmetry, lachrymation, salivation, and frank pulmonary oedema (Duncan et al., 1980; White et al., 1995b).
Death in phase one is often attributable to severe, probably neurogenic, pulmonary oedema. Most patients remain alert and anxious but confusion, impaired consciousness and coma have been reported, perhaps due to complications of envenomation (e.g.. hypoxia) rather than a direct venom action.
The second phase sees a resolution of the overt cholinergic and adrenergic crisis; secretions dry up, fasciculations, spasms and hypertension resolve. This apparent improvement may be followed, in untreated patients, by the gradual onset of refractory hypotension, apnoea and cardiac arrest (Sutherland, 1983; Duncan et al., 1980).
Doubt still exists over the potency of venom from many Hadronyche species due to limited clinical experience. Although there are no confirmed Hadronyche fatalities, at least 6 species have induced a life-threatening illness identical to that of A. robustus envenomation ( Miller et al, 2000).
The application of pressure-immobilisation first aid is vital. Not only is venom movement retarded; it has been shown that A. robustus venom, injected subcutaneously in monkeys, is slowly inactivated in the periphery with the use of a compression bandage (Sutherland et al., 1980b).
A precipitous envenomation may evolve after removal of pressure-immobilisation first-aid or a tourniquet (not recommended). It is thus vital to ensure that skilled staff, resuscitation facilities and, most importantly, adequate supplies of antivenom are available should the patient deteriorate.
Prior to the development and trialling of funnel web spider antivenom in 1980, victims of funnel web envenomation often became critically ill. No deaths have been reported since its introduction. The antivenom is supplied as a powder which is reconstituted with water in the ampoule and injected intravenously as a bolus.
- 2 ampoules if systemic signs of envenomation
- 4 ampoules if the patient is extremely unwell (pulmonary oedema or reduced level of consciousness)
- Single ampoule doses are repeated 15 minutely until clinical improvement is seen (White, 1995a)
The manufacturer no longer recommends premedication. The amount of foreign protein is minimal (Sutherland, 1983; Fisher etal., 1981) and no cases of anaphylaxis have been reported (Sutherland, 1990). Nonetheless, drugs and equipment necessary to deal with anaphylaxis should be immediately at hand. Only one case of serum sickness secondary to funnel web spider antivenom has been reported (Miller et al., 1999) and routine steroid prophylaxis is not recommended.
Clinical experience to date has shown the antivenom to be effective against a broad spectrum of Hadronyche venoms ( Dieckmann et al, 1989 ; Harrington et al, 1999; Knight and Sutton, 1992; Sutherland, 1983; Hartman and Sutherland, 1984; Sutherland, 1992) although antivenom requirements may be larger than in A. robustus envenomation (Miller et al, 2000).
Due to limited antivenom availability (especially in the more remote Hadronyche prone communities) health care workers must be prepared to apply pressure-immobilisation first aid, provide advanced life-support, and organise access to a generous supply of antivenom. This can be logistically challenging as a serious envenomation can readily exhaust local supplies (Miller et al, 2000).
Patients with copious airway secretions, pulmonary oedema or coma unresponsive to antivenom may require intubation and mechanical ventilation. Pulmonary oedema alone may respond to mask-CPAP in co-operative and alert patients. Early pulmonary oedema responds rapidly to antivenom. Late development of pulmonary oedema can occur. An anecdotal lack of response to antivenom suggests the late oedema may be the result of an early pulmonary vascular injury rather than ongoing venom absorption.
Atropine has been used to dry secretions prior to antivenom availability. Its value in conjunction with antivenom is uncertain and it probably should be avoided so as not to mask or mimic features of ongoing envenomation.
The need for tetanus prophylaxis is based on the patient's immunisation history.
Any patient possibly bitten by a funnel web spider should be observed in the emergency department for at least 6 hours from the time of the bite or removal of first aid measures. Those patients with symptoms and signs of envenomation need antivenom and admission to intensive care or the emergency department for 24 hours of close observation due to the risk of late pulmonary oedema.
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