1.   NAME

     1.1  Scientific Name

          Atrax robustus
          Atrax spp. (2 undescribed species)
          Hadronyche adelaidensis
          Hadronyche cerberea
          Hadronyche eyrei
          Hadronyche flindersi
          Hadronyche formidabilis
          Hadronyche infensa
          Hadronyche meridiana
          Hadronyche modesta
          Hadronyche pulvinator
          Hadronyche valida
          Hadronyche venenata
          Hadronyche versuta
          Hadronyche spp. (at least 20 undescribed species)

          (Gray 1988)

     1.2  Family

          Hexathelidae (Note:  previously placed in Dipluridae)

          Sub-family:  Atracinae

     1.3  Common Names

          Funnel web spiders (whole group)

          Atrax robustus            Sydney funnel web spider
          Hadronyche formidabilis   Northern tree funnel web spider
          Hadronyche cerberea       Southern tree funnel web spider
          Hadronyche versuta        Blue mountains funnel web spider

    2.   SUMMARY

     2.1  Main risks and target organs

          While the majority of funnel web spider bites, even by the proven 
          lethal Atrax robustus, are minor and without systemic 
          envenomation, when severe effects do occur they may prove 
          difficult to treat and end fatally.  Antivenom has had a 
          significant effect in reducing the likelihood of fatal outcome.  
          Only Atrax robustus is a proven cause of fatalities.  It is now 
          established that Hadronyche formidabilis, H. infensa, H. versuta, 
          H cerberea, Hadronyche spp.7 can cause dangerous bites in man.  
          For most other Hadronyche spp there is no present evidence that 
          they are dangerous to man, though this may merely reflect the 
          infrequency of bites.  Male Atrax robustus are generally more 
          dangerous than females.  This may not be true for all species.



          Main risks are:  cardiovascular disturbance; pulmonary oedema; 
          acid-base disturbances; intracranial hypertension (proven in 
          monkeys, not in man).

          Target organs: envenomation causes a complex multi-system disease 
          involving the cardiovascular system, lungs, central nervous 
          system and peripheral nervous system including the autonomic and 
          neuromuscular systems. 

     2.2  Summary of clinical effects

          Local:  Bite causes severe local pain, in part due to mechanical 
          injury from large powerful fangs.  Some local erythema may 
          develop.  Local necrosis not recorded.

          Systemic:  Minority of cases.  Symptoms and signs may develop 
          within 10 minutes of the bite (if no first aid used; and more 
          rapidly in children than adults).  The major features indicative 
          of systemic envenomation are:

          Muscle fasciculation in the limbs involved or remote from the 
          bite, usually first seen in tongue or lips when systemic spread 
          of venom has occurred.

          Marked salivation or lachrymation.

          Piloerection.

          Tachycardia.

          Hypertension in a previously normotensive patient (late in the 
          syndrome the patient may become hypotensive). 

          Dyspnoea.

          Disorientation, confusion or a depressed level of consciousness.

          Note also pulmonary oedema and raised intracranial pressure.

     2.3  Diagnosis

          -    Electrolytes, acid base, renal function.
          -    Arterial blood gases.
          -    Complete blood picture and platelet count.
          -    Serum/plasma creatine kinase.
          -    Urinary catecholamines.

     2.4  First-aid measures and management principles

          The pressure-immobilisation method is the only recommended first-
          aid and has been proven effective in studies with monkeys, and in 
          clinical experience.

          Maintain life with cardiopulmonary resuscitation measures as 
          indicated.


          Reassure and rest the patient.


          Remove spider if still attached, ensuring no further bites occur.

          Immediately apply a firm broad constrictive bandage (such as 
          crepe) over the bite site at the same pressure as for a sprained 
          ankle.  Extend the bandage to cover as much of the bitten limb as 
          possible, at the same pressure (ie, the bandage should NOT act as 
          a tourniquet). 

          Ensure immobilisation of the limb by using a splint.

          Transport patient to hospital.

          Do NOT give food or fluid by mouth.

          Do NOT cut, suck or apply chemicals or patent medicine "cures" to 
          wound. 

          Do NOT use a tourniquet.

          Treatment principles

          -    Maintenance of vital functions.

          -    Neutralisation of venom by prompt IV administration of 
               specific Funnel-web Spider Antivenom (CSL, Melbourne). 

          -    General measures may include:

          -    Oxygen
     
          -    Atropine

          -    Intermittent positive pressure ventilation (also positive 
               end expiratory pressure, and high tidal volume may be 
               necessary to correct respiratory acidosis). 

          -    Nurse patient on side due to the risk of vomiting and excess 
               salivation with pooling. 

          -    Avoid fluid overload (danger of pulmonary oedema due to 
               envenomation); however, hypovolaemia may also develop 
               requiring cautious administration of albumin and volume 
               expanders. 

          -    Serum sickness has not been reported following therapy with 
               funnel-web spider antivenom.  In the event of occurrence, 
               steroid therapy may be worth consideration. 

          -    Local antisepsis of wound site, and tetanus prophylaxis.

          -    Sympathetic blockade for hypertension and severe tachycardia 
               has been suggested.  While alpha blockade has been used, it 
               requires massive doses, and beta blockade might well prove 

               lethal in this situation, therefore neither is advocated for 
               funnel-web spider envenomation. 



     2.5  Venom apparatus, poisonous parts or organs

          Funnel-web spiders have paired venom production and delivery 
          organs, with one large fang on each end of the two chelicerae, 
          the fangs being paraxial, approximately 6 mm long in adult male 
          spiders of Atrax robustus.  The venom glands are approximately 5 
          mm long and are connected by 4 mm long ducts to the base of the 
          fangs.  Expulsion of venom is under at least partial voluntary 
          control. Detailed information on other Atrax spp. and Hadronyche 
          spp. not available. 

     2.6  Main toxins

          Funnel-web spider venom has only been studied in detail for Atrax 
          robustus, and to a lesser extent in Hadronyche formidabilis,  
          Hadronyche infensa, and Hadronyche versuta. 

          For Atrax robustus:

          Yield (male spiders)  -  average 140 mg (dry weight).

          Principal toxin  -  Robustoxin; protein, 4854 D, 42 amino acids.  
          Interferes with neuronal transmission throughout much of nervous 
          system.  Responsible for clinical syndrome of funnel-web 
          envenomation, and lethality of venom. 

          Other components  -  numerous, but do not appear to have 
          significant role in lethal activity of venom. 

    3.   CHARACTERISTICS

     3.1  Description of the animal

          3.1.1 Special identification features

               Funnel-web spiders are arthropods (phylum Arthropoda), of 
               the class Arachnida, order Araneae (spiders), and sub-order 
               Mygalomorphae (trapdoor and funnel web spiders ). They 
               include 35 species in 2 genera, Atrax and Hadronyche, placed 
               within the subfamily Atracinae, family Hexathelidae ( Gray 
               1988 ).

               In addition to the general features of spiders, including, 4 
               pairs of walking limbs plus 1 pair of palps (modified as 
               mating organs in males) plus 1 pair of chelicerae, attached 
               to a rigid forebody (cephalothorax), soft, unsegmented, 
               petiolate abdomen and abdominal silk spinning organs (silk 
               glands and spinnerets), and features of Mygalomorph spiders 
               including 2 pairs of book-lungs visible on the ventral 
               abdomen, chelicerae with paraxial fangs, attached 
               horizontally to the cephalothorax rather than vertically; 

               funnel-web spiders also have the following distinguishing 
               characteristics (figures 3.1.1 to 3.1.11):  (Gray 1987,
               1988)

               They are large to very large spiders, body length 15 - 45 mm 
               (excluding the jaws or chelicerae ), dark brown to black in 
               colour overall, the abdomen often dark plum coloured. The 
               carapace covering the front part of the body is almost 
               hairless and so appears smooth and glossy. The body lacks 
               any obvious patterning.

               Spinnerets obvious, four in number, the apical segments of 
               the large posterior spinnerets always longer than wide 
               (figures 3.1.9 and 3.1.10).

               Eyes closely spaced.

               The labium, a small ventral plate found on the ventral 
               cephalothorax in the midline, immediately in front of the 
               sternum, and between the two maxillae, is studded with many 
               short peg-like spines (cuspules) (figure 3.1.11). 

               The fang grooves, into which the fangs fold at rest, have a 
               row of strong teeth along both margins (marginal teeth), and 
               a variable number of smaller teeth within the groove itself 
               (figures 3.1.7 and 3.1.8).

               Carapace foveal groove concave forwards.

               The tarsal segments of the legs are spined and lack thick 
               scopulae or claw tufts.  (Figures 3.1.1 - 3.1.4.) 

               The second leg of male spiders may have a spur (spined 
               apophysis) of variable shape, on the ventral tibia (figures 
               3.1.1 - 3.1.3).  However, males of many Hadronyche species
               lack obvious apophyses (Figure 3.1.4). 

               Distinguishing features for each genus are:


               Atrax:  Carapace weakly raised and obviously longer than 
               wide (figure 3.1.6).  Central fang groove teeth confined to 
               basal half of groove (figure 3.1.8).  Male second leg 
               (figure 3.1.6) with a large, conical tibial apophysis 
               (figure 3.1.1).  Posterior lateral spinnerets with a long 
               cylindrical apical segment (figure 3.1.9). 



               Hadronyche:  Carapace moderately to strongly raised (figure 
               3.1.5), often almost as wide as long.  Central teeth 
               typically occupy full length of fang groove (figure 3.1.7) 
               in one or several rows, but occasionally restricted to basal 
               region.  Male second leg with a variably developed rounded 
               tibial apophysis (figures 3.1.2 and 3.1.3) or apophysis
               absent (figures 3.1.4). Apical segment of posterior lateral 

               spinnerets of variable length but often rather short (figure 
               3.1.10). 

          3.1.2 Habitat

               They are mostly terrestrial spiders, which build typical 
               silk-lined tubular burrow retreats, with a collapsed 
               "tunnel" or open "funnel" entrance from which irregular silk 
               triplines radiate out over the ground. These distinctive 
               surface triplines, whose function is to alert the spider to 
               the movement of prey animals in the vicinity, provide a 
               reliable means of identifying the retreats of funnel web 
               spiders. Exceptions, which lack triplines but may have 
               trapdoors, are those Hadronyche from SA, viz Hadronyche 
               adelaidensis, Hadronyche eyrei and Hadronyche flindersi.

               The silk entrance tube may be split into 2 openings, in a Y 
               or T form.  In the case of Hadronyche formidabilis the 
               burrow may be in the hollow of a tree trunk or limb, many 
               metres above ground level.


               Significant numbers of these spiders may aggregate their 
               burrows within a small area, forming colonies.  The spiders 
               usually forage at the burrow entrance, seizing prey that 
               walks over the triplines.  Adult male spiders leave the 
               burrow permanently to seek a mate.  Such wandering male 
               spiders may enter houses, sometimes even find their way into 
               clothing, and thus account for many bites.

               Most funnel-web spiders are ground or log dwellers but at 
               least two are tree dwellers (Hadronyche formidabilis and 
               Hadronyche cerberea the Northern and Southern tree funnel 
               web spiders respectively).  They are moist-adapted animals 
               largely restricted to temperate to sub-tropical regions of 
               south east Australia in both sclerophyll and closed (rain-
               forest) forest habitats.  At the western edges of 
               distribution some species occupy dryer woodland habitats 
               where they dig deep burrows in sheltered microhabitats 
               (shaded ground in leaf litter, under rocks or logs etc). 
               Typically funnel web spiders prefer sheltered microhabitats 
               and in many urban areas these are plentiful, eg garden 
               rockeries, dense shrubberies, wooden sleeper or stone paths 
               and retaining walls and any long-term ground detritus such 
               as old building materials.  In areas such as the damp garden 
               suburbs of Sydney, urbanisation may actually have increased 
               funnel web abundance. 

          3.1.3 Distribution

               Restricted to south-eastern Australia (figure 3.1.12).

               Atrax is confined to south-eastern coastal Australia and 
               adjacent highlands (figure 3.1.12, 3.1.13).  Atrax robustus, 
               the Sydney funnel-web spider, has a distribution centring on 
               Sydney, extending north to the Hunter River and south to the 

               Shoalhaven River, and narrowing westwards as far as Lithgow. 

               Hadronyche has a considerably wider distribution as shown in 
               figures 3.1.12, 3.1.14 - 3.1.18.  Many species distributions
               can be related to local topography (figure 3.1.19).  
               Overall, the distribution of Hadronyche is correlated with 
               the coastal trend of the eastern highlands from Tasmania to 
               south east Queensland, where the western trend of the main 
               range into dryer inland regions approximates the northern 
               limits of the genus (Gray 1987). 

     3.2  Poisonous/venomous parts

          See section 2.5.

          Paired flask-shaped venom glands in the chelicerae connect via 4 
          mm venom ducts to openings at the base of the paired paraxial 
          fangs, approximately 6 mm long in Atrax robustus. At rest the 
          fangs are folded into the fang grooves on the ventral surface of 
          the chelicerae, but for attack the front of the body is elevated 
          above the prey and the fangs open downwards on widely separated 
          chelicerae preparatory to the downward thrust of attack.  (Gray 
          and Sutherland 1978; Sutherland 1983) 

          The venom exits the fang near its tip, and is apparently under 
          some degree of voluntary control, as venom initially exuded on 
          the fang tip when the spider is threatened can then be withdrawn 
          back into the fang.  Venom yield has been reported for Atrax 
          robustus as 0.28 mg for females and 0.175 mg for males, on 
          milking, and 0.25 mg (F) and 0.81 mg (M) on dissection of 
          spiders.  An average figure was 140 mg dry weight.  Yields are 
          apparently higher in summer than winter months.  (Wiener 1957, 
          Sutherland 1983)

     3.3  The toxins

          3.3.1 Names

               Robustoxin (Atraxotoxin), Versutoxin

          3.3.2 Description

               While the venoms of most species of Hadronyche and the two 
               unnamed Atrax have not been studied, those known to cause 
               significant clinical effects in man, particularly Atrax 
               robustus, have been examined in detail. Consensus of these 
               studies is that lethal activity (for man) is contained in 
               just one component of these multicomponent venoms. In Atrax 
               robustus male venom toxicity is consistently several times 
               (4 - 6) higher than female venom.

               Robustoxin (from male Atrax robustus venom)

               (Note:  A component with similar or identical properties to 
               robustoxin has been described by other authors, and named 
               atraxotoxin (and possibly atraxin).  As the most complete 

               studies are for robustoxin, this name is adopted as the 
               "type" even though, historically, atraxotoxin has 
               precedent.) (Gregson & Spence 1981, Myelcharane et al 1983, 
               1984, 1985, Sutherland 1972a, 1972b, 1973b, 1983) 

               Robustoxin is a unique presynaptic neurotoxin, lethal in 
               man, other primates, and newborn mice, but non-lethal in 
               many other laboratory animals (or lethal only at very high 
               doses). 



               It is a protein, MW 4854 (calculated from amino acid 
               sequence), with 42 amino acid residues, with a high 
               proportion of basic residues, 8 cysteine residues with 4 
               disulphide bridges and has a pI >9 and an LD50 (SC newborn 
               mice) of 0.16 mg/kg.  Robustoxin alone causes a typical 
               syndrome of envenomation in primates and man of whole male 
               Atrax robustus venom. (Sheumack et al 1983, 1984, 1985) 

               Versutoxin (from male and female Hadronyche versuta venom.)

               Structurally very close to robustoxin, a protein neurotoxin, 
               MW 4852, 42 residues, highly basic, pI >9, 4 disulphide 
               bridges.  8 residues different to robustoxin, and considered 
               conservative changes.  LD50 (SC newborn mice) 0.22 mg/kg.  
               Versutoxin alone causes almost typical syndrome of 
               envenomation in primates and man of whole male Atrax 
               robustus venom, the difference being the sustained 
               hypotension typical of robustoxin, which is not seen with 
               either versutoxin or whole Hadronyche versuta venom. Strong 
               antigenic cross-reaction between robustoxin and versutoxin. 
               (Sheumack et al, 1984) 

               Venoms of important related species

               Hadronyche formidabilis - Venom reported as approximately 
               equal in toxicity (both male and female) as male Atrax 
               robustus venom, has caused similar cases of envenomation in 
               man (no definite fatalities), and therefore probably 
               contains a robustoxin-like component.   (Sutherland 1983) 

               Hadronyche infensa - Venom reported as approximately equal 
               or greater in toxicity (females and males) as male Atrax 
               robustus venom, and therefore may contain a robustoxin-like 
               component.  (Sutherland 1983) 

          3.3.3 Other physico-chemical characteristics

               Several other components or properties of male Atrax 
               robustus venom have been reported.  These include: GABA; 
               Spermine Complex; Lactic acid; Trimethylsilyl or 
               pentafluoropropionate derivatives; Citric acid; Glycerol; 
               Urea; Glucose; Glycine; Spermidine; Tyramine; Octopamine. 

     3.4  Other chemical contents

          No data

    4.   CIRCUMSTANCES OF POISONING

     4.1  Uses

          Medical - Extraction of venom for production of antivenom and for 
          research.

          Commercial - Some spiders killed and set in plastic for 
          educational purposes or, less usefully, as "tourist trophies".


          Agricultural - Components of the venom may prove useful as new 
          insecticides, this being the subject of current research. 

     4.2  High risk circumstances

          In areas where dangerous species occur, especially Atrax 
          robustus, but also Hadronyche infensa, Hadronyche formidabilis, 
          Hadronyche versuta, Hadronyche cerberea, Hadronyche sp.7.

          -    Walking barefoot, especially at night, outside places of 
               abode.

          -    Dressing in items of apparel left on or near the floor where 
               wandering male spiders might easily enter, including 
               footwear.

          -    Working in areas likely to have high concentrations of 
               spiders, eg gardens and other disturbed sheltered urban 
               habitats in some parts of the Sydney region.

          -    Activities associated with camping.

          -    Activities associated with handling spiders such as in 
               laboratories milking venom, or field researchers.  NOTE:  No 
               bites in such circumstances are recorded. 

          High risk times:

          During the funnel web mating period male wandering activity and 
          abundance is highest.   The summer - autumn period (December - 
          June) is the time of greatest activity for males of many species. 
          While most bites occur during this period funnel web spiders can 
          be encountered throughout the year. In addition pesticide 
          spraying to kill spiders stimulates wandering activity and 
          excitability in much of the target funnel web population and is 
          not recommended. Increased activity after heavy rainfall also 
          occurs because of burrow flooding. 

     4.3  High risk geographical areas

          Particularly the Sydney-Newcastle-Illawarra region.  See 
          distribution information for Atrax robustus, Hadronyche infensa, 

          Hadronyche formidabilis and Hadronyche versuta, section 3.1.3 and
          figures 3.1.12 - 3.1.20.

    5.   ROUTES OF ENTRY

     5.1  Oral

          Not applicable.

     5.2  Inhalation

          Not applicable.


     5.3  Dermal

          Not recorded.

     5.4  Eye

          Not recorded.

     5.5  Parenteral

          The only recorded route of envenomation in man is by a bite from 
          a spider, in most serious and all fatal cases a male Atrax 
          robustus.  One or two fangs may enter.  In most cases this is 
          likely to result in subcutaneous inoculation of venom.


          In experimental conditions intravenous inoculation is often used, 
          and intramuscular and intraperitoneal injection are theoretically 
          applicable.

          Stings do not occur (no sting apparatus).

     5.6  Other

          Not recorded.


    6.   KINETICS

     6.1  Absorption by route of exposure

          The recorded method of envenomation of humans by funnel-web 
          spiders is purely by bite with inoculations of venom into the 
          skin, presumably subcutaneously in most cases. 

     6.2  Distribution by route of exposure

          The venom, when injected experimentally in monkeys, rapidly 
          causes systemic problems, these being immediate (IV) and delayed 
          about 2 minutes (SC), suggesting that the venom may be rapidly 
          transported from the bite site systemically.  The role of 
          lymphatics in venom transport is uncertain, but in view of the 

          rapid envenomation often seen, lymphatic transport of most venom 
          seems unlikely.  However, the compression-immobilisation 
          technique of first aid is effective.  (Sutherland et al 1980)

          Having reached the systemic circulation the main toxin (to man) 
          in the venom is rapidly distributed to target organs, principally 
          nerve cells, and particularly synaptic junctions where the toxin 
          is apparently bound presynaptically (autonomic and motor 
          neurons). 



     6.3  Biological half-life by route of exposure

          There is no published information on the half-life of the venom 
          or its components.  Human fatalities have occurred from 15 
          minutes to 6 days after bites.  Cases with survival following 
          systemic envenomation have an average hospital stay of 14 days 
          (if no antivenom treatment). (Sutherland 1983) 

     6.4  Metabolism

          No information.

     6.5  Elimination by route of exposure

          No information.


    7.   TOXINOLOGY

     7.1  Mode of action

          Studies on the mode of action of both whole venom and Robustoxin 
          are hampered by low availability of venom and relative resistance 
          to venom in many common laboratory animals, contrasting with the 
          exquisite sensitivity to venom toxins in primates, including man 
          (50 - 100 times more sensitive in some preparations). (Sutherland 
          1983)

          The clinical effects of funnel-web spider envenomation in man 
          (and monkeys) appear directly attributable to one venom 
          component, Robustoxin.  This appears to act as a presynaptic 
          neurotoxin.  On the autonomic system the venom causes both 
          inhibition of neurally mediated release of transmitters (eg 
          noradrenaline, acetylcholine) and an increase in spontaneous 
          transmitter release.  A similar action on the skeletal muscle 
          neuromuscular junction has been postulated. (Sutherland 1983; 
          Sutherland & Duncan 1980, Sutherland et al 1980, Tibballs et al 
          1987)

          Given the current paucity of relevant in vitro studies of the 
          mode of action of the venom, the detailed in vivo studies in 
          primates (Macaca fascicularis) are most relevant.  In summary, 
          the effects recorded after experimental envenomation (IV or SC) 
          with whole venom from male Atrax robustus were:


          Cardiovascular - initial fall in blood pressure (BP), then rise 
          to hypertensive level, lasting several hours, followed by return 
          to normal or progressive hypotension (lethal).  Tachycardia, 
          ventricular ectopic beats, bigeminy and transient second degree 
          atrio-ventricular blocks were seen, though not in all monkeys.

          Pulmonary oedema - seen in 3 of 9 monkeys.

          Acid-base disturbances - all developed acute metabolic acidosis 
          about 1 hour post envenomation, resolving spontaneously by 4 
          hours.  Most developed a respiratory acidosis. 

          Intracranial hypertension - seen in all monkeys.

          Temperature - all developed hyperthermia.

          Catecholamine excretion - marked increase in urinary 
          catecholamines, peaking at about 2 hours after envenomation. 

          Fluid shifts - all showed haemoconcentration.

          Creatine kinase - all showed massive rises in CK.

          Pharmacological denervation - both pre and post-envenomation 
          administration of atropine + phenoxybenzamine + propranolol 
          abolished the major features of envenomation and allowed survival 
          of "massive" doses of venom. 

     7.2  Toxicity

          7.2.1 Human data

               7.2.1.1    Adults

                     The lethal dose is not known, but a single bite from 
                     an adult male A. robustus is potentially lethal and 
                     the average venom yield is 176 mg.  The recommended 
                     initial dose of antivenom is sufficient to neutralise 
                     in vitro about 8 times this amount of venom. 

               7.2.1.2    Children

                     Children, especially those under 12 years of age, are 
                     more susceptible to severe or lethal envenomation, 
                     presumably due to a lower body mass and higher per kg 
                     doses of venom. 

          7.2.2 Animal data

               Most experimental animals, being relatively resistant to the 
               venom, are inadequate models of human toxicity.  For 
               experimental purposes two groups of animals appear useful, 
               having susceptibility to the venom of male A. robustus, 
               sufficient for comparative clinical studies (monkeys) or for 
               toxicity assay (new born mice).  (Sutherland 1983, Wiener 

               1956, 1957)

               -     Monkeys (Macaca fascicularis)
                     lethal dose 0.2 mg/kg
               -     New born mice (up to 2 days old, 2 g weight)
                     lethal dose 1.5 mg/kg

          7.2.3 In vitro data

               Not relevant.


     7.3  Carcinogenicity

          No data.

     7.4  Teratogenicity

          No data.

     7.5  Mutagenicity

          No data.

     7.6  Interactions

          While not demonstrated in clinical cases, theoretically 
          adrenaline might have adverse effects in an envenomated patient 
          (and is therefore not recommended as pre-medication for antivenom 
          therapy), because catecholamine levels may already be elevated as 
          a result of envenomation.  (Sutherland 1983) 

          Both experimentally and clinically, atropine and diazepam may 
          ameliorate the toxic effects of venom. 

          Experimentally the effects of venom (on isolated nerve-muscle 
          preparations) were suppressed by gallamine, suxamethonium, 
          lignocaine and tetrodotoxin; were enhanced by physostigmine; and 
          were unaffected by neostigmine, choline or acetylcholine.

    8.   TOXICOLOGICAL/TOXINOLOGICAL AND OTHER BIOMEDICAL INVESTIGATIONS:

     8.1  Material sampling plan

          8.1.1 Sampling and specimen collection

               8.1.1.1    Toxicological analyses

                     Not available.

               8.1.1.2    Biochemical analyses

                     For standard tests (eg. serum/plasma electrolytes, CK, 
                     creatinine, urea) collect venous blood in a container 
                     with appropriate anticoagulant as issued by the 
                     laboratory (usually heparin).

               8.1.1.3    Arterial blood gas analysis

                     Collect arterial blood by sterile arterial puncture 
                     into a container as issued by the laboratory. 


               8.1.1.4    Haematological analyses

                     For whole blood clotting time as a "bedside" test 
                     collect 5 - 10 ml of venous blood without 
                     anticoagulant (either in the collection syringe or 
                     from a central line or other venous access line that 
                     may have anticoagulant ) and place in a glass test 
                     tube. Carefully observe the time till a clot appears. 

                     For standard tests (eg. coagulation studies, complete 
                     blood picture) collect venous blood in appropriate 
                     containers with anticoagulant as issued by the 
                     laboratory ensuring that the right amount of blood is 
                     used (for coagulation studies citrate will usually be 
                     the anticoagulant, while EDTA will be used for 
                     complete blood pictures). 

               8.1.1.5    Others (unspecified) analyses

                     No data.

          8.1.2 Storage of laboratory samples and specimens


          8.1.2.2 Biomedical analyses

               For samples for standard tests refer to laboratory. In 
               general keep at 4°C, particularly for samples for 
               coagulation studies. 

          8.1.3 Transport of laboratory samples and specimens

          8.1.3.2 Biomedical analyses

               Use an insulated container.

     

     8.3  Biomedical investigations and their interpretation

          8.3.1 Biochemical analyses

               8.3.1.1    Blood, plasma or serum

                     Electrolytes: Look for imbalance, particularly 
                     evidence of dehydration, hyponatraemia (inappropriate 
                     ADH syndrome?), hyperkalaemia (renal damage, 
                     rhabdomyolysis?). 


                     Urea, creatinine: Look for evidence of renal function 
                     impairment. 

                     CK: If high may indicate rhabdomyolysis (due to 
                     secondary muscle damage), usually greater than 1000 
                     U/l. 

               8.3.1.2    Urine

                     Output: Low output may indicate renal damage or poor 
                     fluid input. 

                     Electrolytes if indicated (eg. inappropriate ADH 
                     syndrome) 


               8.3.1.3    Other biological specimens
     
                     No data.

          8.3.2 Arterial blood gas analyses

               Performed in the setting of impaired respiratory function, 
               usually secondary to pulmonary oedema; look for evidence of 
               poor oxygenation and its sequelae. 

          8.3.3 Haematological analyses

               Whole blood clotting time: If greater than 10 mins suspect 
               presence of secondary coagulopathy (rare). 
          
               Coagulation studies: (if indicated clinically) If possible 
               these should be performed as well as or instead of whole 
               blood clotting time as they will give a more comprehensive 
               picture of any coagulopathy. 

          8.3.5 Interpretation of biomedical investigations

               The interpretation of the above tests should be made in the 
               context of total patient assessment including clinical 
               evidence of pathology such as respiratory failure, pulmonary 
               oedema, shock, coagulopathy and renal damage. 

     8.4  Other biomedical (diagnostic) investigations and their 
          interpretation: 

          May be indicated in response to secondary effects of 
          envenomation. If there is renal failure there may be a 
          hyperkalaemia, hence an ECG may be appropriate. 

          Overall interpretation of the results of the above tests will 
          depend on the clinical setting. Results should never be 
          interpreted in isolation from an overall clinical assessment. 


    9.   CLINICAL EFFECTS

     9.1  Acute poisoning/envenomation by:

          9.1.1 Ingestion

               Not known.

          9.1.2 Inhalation

               Not known.


          9.1.3 Skin Exposure

               Not known.

          9.1.4 Eye contact

               Not known.

          9.1.5 Parenteral exposure

               All known cases of human envenomation are due to bites. 
               (Sutherland 1983) 

               General: In the majority of cases of funnel-web spider bite, 
               systemic envenomation does not occur, and any symptoms are 
               confined to the local effects of the bite.  The outcome 
               cannot be predicted at the outset however, and all bites 
               should be assumed to be potentially lethal. 

               Local:  One or two large fangs enter the victim with some 
               force.  The bite is very painful for about 30 minutes or 
               more, with local erythema, and occasionally local 
               piloerection, sweating, and muscle fasciculation.  Local 
               necrosis does not occur. 

               Systemic:  Onset of systemic envenomation may occur from 10 
               minutes up to an hour or more after the bite (with further 
               delay if appropriate first aid used). 

               Earliest systemic symptoms are usually tingling around the 
               mouth which often occurs within 15 mins of the bite,  tongue 
               spasms, followed by nausea and vomiting, abdominal pain, 
               profuse sweating, brisk salivation, lachrymation, and severe 
               dyspnoea. 


               The level of consciousness may rapidly deteriorate, with 
               confusion or coma. Hypertension is usually noted at this 
               time.  Severe pulmonary oedema may develop quite early, and 
               is a potential cause of fatality, particularly in children.  
               The pulmonary oedema is mixed in origin, similar to 
               neurogenic pulmonary oedema, with catecholamine release, 
               high filling pressures, and membrane leak. 


               While classic neurotoxic paralysis does not occur, local and 
               generalised muscle fasciculation is commonly seen, including 
               spasms of muscle groups such as jaw musculature.  In severe 
               cases coma has been reported, and some authors believe it 
               may be due to raised intracranial pressure (not relieved by 
               adequate control of oxygenation or BP), although this has 
               not been proven in man.  However clinical experience 
               suggests coma is not common, and is probably a dubious sign 
               of envenomation, most envenomed patients being anxious and 
               alert until anaesthetized. On current experience, patients 
               treated with antivenom do not develop coma. 

               After several hours the above symptomatology may subside, 
               with decreased secretions, although generalised muscle 
               activity and coma may continue.  There may be a gradual 
               resolution or an insidious and intractable hypotension may 
               develop, sometimes preceded by a brief period of semi-
               normality.  The hypotension may end in death due to 
               irreversible cardiac arrest, a possible mode of death in 
               fatal cases in adults, sometimes many hours after the bite. 

               The venom does not cause primary coagulopathy or renal 
               failure, though these may occur as complications. 

               Funnel-web spider envenomation is a complex multisystem 
               disease.  The findings in monkeys are relevant to human 
               envenomation and should be consulted in conjunction with 
               this section (see 7.1).

     9.2  Chronic poisoning

          9.2.1 Ingestion

               Not known.

          9.2.2 Inhalation

               Not known.

          9.2.3 Skin contact

               Not known.

          9.2.4 Eye contact

               Not known.

          9.2.5 Parenteral exposure

               Not known.

          9.2.6 Other

               No data.

     9.3  Course, prognosis, cause of death

          The likelihood of systemic envenomation is not presently 
          predictable from the appearance of the bite site or local 
          symptoms.

          The only recorded fatalities have followed bites by male Atrax 
          robustus.  Severe envenomation not ending fatally has occurred 
          following bites by Hadronyche formidabilis (male specimens, but 
          females also considered dangerous), and H. infensa (one possible 
          fatal case), and more recently,  H. versuta, H. cerberea, and 
          Hadronyche sp.7.  H. versuta in any case should be considered as 
          potentially dangerous since its venom contains a Robustoxin-like 
          substance, Versutoxin. Bites from virtually all other funnel-web 
          spiders are unknown.  A single bite from H. adelaidensis did not 
          result in envenomation. (Beazley 1930, Cleland 1932, Diexman et 
          al 1989, Fisher 1989, Fisher & Bowey 1989, Fisher et al 1980, 
          Fisher et al 1981, Hartman & Sutherland 1984, Ingram & Musgrave 
          1933, Irwin 1952, Kaire 1961, 1963, Knight & Sutton 1982, Irwin 
          1952, Kaire 1961, 1963, Knight & Sutton 1982, Musgrave 1927, 
          1949a, 1949b, Sutherland 1972c, Torda et al 1980, Watkins 1939, 
          White 1987, 1989, Wiener 1959).

          Sutherland has noted that children usually die early in the 
          asphyxial stage (important role of pulmonary oedema), often 
          within 1 - 2 hours of the bite (shortest time 15 minutes, longest 
          3 days); adults die later, often due to intractable hypotension 
          or secondary complications, mean 11 hours (excludes one case 
          dying at 6 days with complications including a coagulopathy, 
          renal failure and brain damage).  This picture is clearly 
          modified by the growing experience with patients treated by 
          specific antivenom therapy, which has proved very effective in 
          modifying symptomatology, and preventing a fatal outcome.  

     9.4  Systematic description of clinical effects

          (Based on both studies in monkeys and/or human cases of 
          envenomation prior to the development of specific antivenom).  
          (See refs. sect. 9.3) 

          9.4.1 Cardiovascular

               Initial fall in BP and development of tachycardia, followed 
               by hypertension lasting several hours, and cardiac 
               arrhythmias. This is followed by apparent resolution which 
               in severe cases indicates the onset of intractable 
               hypotension, and ultimately cardiac arrest in fatal cases.  
               Peripheral circulatory failure with peripheral cyanosis has 
               been recorded.  (Mostly based on monkey studies.) 


          9.4.2 Respiratory

               Early development of severe pulmonary oedema (see 9.1.5.3).  
               While some clinicians have described this as similar to the 
               adult respiratory distress syndrome, with increased 
               pulmonary capillary membrane permeability, it appears more 

               similar to neurogenic pulmonary oedema, which is mixed in 
               origin with catecholamine release, high filling pressures, 
               and membrane leak. 

          9.4.3 Neurological

               9.4.3.1    CNS

                     Early development of impaired consciousness or coma in 
                     severe cases has been noted, either directly due to 
                     venom effects, or secondarily due to hypoxia 
                     (pulmonary oedema). However, clinical experience shows 
                     that patients do not present with or develop early 
                     coma but are anxious and alert.  Raised intracranial 
                     pressure may develop and may be lethal (experimentally 
                     in monkeys, not shown in man). 

               9.4.3.2    Peripheral nervous system

                     Widespread effect of neurotoxic action of Robustoxin 
                     and analogues with spontaneous transmitter release, 
                     and failure of response to stimuli.  Manifest as 
                     muscle fasciculations, tremors, spasms, and patchy 
                     weakness (which is usually a late manifestation). 

               9.4.3.3    Autonomic

                     Widespread effect of neurotoxic action of Robustoxin 
                     or analogues on synapses in sympathetic and 
                     parasympathetic systems, with spontaneous release of 
                     transmitters.  Manifest as alterations in vascular 
                     tone, and excessive secretions, especially salivation 
                     and lachrymation, and piloerection. 

               9.4.3.4    Skeletal and smooth muscle

                     Widespread effect of neurotoxic action of Robustoxin 
                     or analogues as noted in 9.4.3.2 and 9.4.3.3.

          9.4.4 Gastrointestinal

               Specific effects of toxin not generally noted, although 
               nausea and vomiting common, and gastric distension noted. 

          9.4.5 Hepatic

               No specific effects noted.

          9.4.6 Urinary

               9.4.6.1    Renal

                     No specific effects.

               9.4.6.2    Other


                     Not noted.

          9.4.7 Endocrine and Reproductive System

               Increased catecholamine excretion.  Effects on pregnancy not 
               known. 



          9.4.8 Dermatological

               No specific effects.

          9.4.9 Eye, ear, nose, throat: local effects.

               No specific organ injury noted, but note excessive 
               lachrymation, and fixed dilated pupils. 

          9.4.10 Haematological

               No specific effects noted.  Potential for secondary 
               coagulopathy.  Fluid shifts may cause haemoconcentration.


          9.4.11 Immunologic

               No specific effects noted.

          9.4.12 Metabolic

               9.4.12.1   Acid base disturbances

                     Acute metabolic acidosis early followed by respiratory 
                     acidosis. 

               9.4.12.2   Fluid and electrolyte disturbances

                     Fluid shift out of circulation (note pulmonary 
                     oedema). 

               9.4.12.3   Others

                     Hyperthermia is reported.  Massive rises in serum 
                     creatine phosphokinase may occur and marked 
                     catecholamine excretion in urine (studies in monkeys). 

          9.4.13 Allergic reactions

               Not reported.

          9.4.14 Other clinical effects

               No data.

          9.4.15 Special risks: pregnancy, breast-feeding, enzyme 
                 deficiency 

               Pregnancy:  No data.  Presumed significant risk to both 
               foetus and mother.



               Breast feeding:  No data.  Breast feeding unlikely to be 
               practically possible if severe envenomation, and in the 
               absence of data confirming safety, is contraindicated if 
               envenomation is suspected.

               Enzyme deficiencies:  No data.

     9.5  Others

          No data.


    10.  MANAGEMENT

     10.1 General principles

          All cases of suspected bite by funnel-web spiders occurring in 
          areas inhabited by Atrax robustus, Hadronyche formidabilis, H. 
          infensa and H. versuta should be treated as potentially life-
          threatening emergencies.  This is especially true of bites to 
          children from male A. robustus.  (See refs. sect. 9.3, also Noel 
          1985, Sutherland 1973a, 1978, 1983, Wiener 1978)

          If appropriate first aid has not been applied and it is within 2 
          hours of the bite, or symptoms of systemic envenomation are 
          present, then it should be applied prior to assessment at a 
          funnel-web spider treatment centre.  If first aid has been 
          applied it should be left in place until the patient is at a 
          treatment centre (exception:  arterial tourniquet where viability 
          of limb is at stake, but beware rapid massive envenomation on 
          removal).  For relevant first aid see section 2.4.

          Main principles of medical management are:

          (a)  Maintain life through general measures including life 
               support systems if indicated. 

          (b)  Neutralise venom with specific antivenom (Funnel-web spider 
               antivenom, CSL, Melbourne) if systemic envenomation is 
               present. 

          (c)  Strive to avoid secondary complications, eg hypoxia and 
               hypoxic damage, brain damage, renal failure, coagulopathy. 

     10.2 Relevant laboratory analyses and other investigations

          10.2.1 Sample collection

               Blood and urine for biomedical analysis.
               Request if possible the capture of the spider for 

               confirmation of species and sex.  Dead spiders may be 
               preserved in either ethanol, or methanol, preferably 70% 
               strength. 

          10.2.2 Biomedical analysis

               There are no specific assays for funnel-web spider venoms.

               All tests are to determine the extent of effects of venom 
               systemically, e.g. 

               (a)   Arterial blood gases - extent of hypoxia and response 
                     to treatment. 
               (b)   Serum/plasma electrolytes, acid base, renal function - 
                     extent of metabolic acidosis, secondary renal 
                     impairment. 
               (c)   Serum creatine kinase - secondary elevation.
               (d)   Complete blood picture - early evidence of secondary 
                     coagulopathy, haemoconcentration. 
               (e)   Coagulation studies - required if suspicion of 
                     secondary coagulopathy (rarely present, not usually 
                     seen acutely in the first 8 hours after bite). 
               (f)   Urinary catecholamines - may be significantly 
                     elevated. 

          10.2.3 Toxicological analysis

               No specific venom analysis available.  See Section 8.

          10.2.4 Other investigations 

               Not applicable.

     10.3 Life supportive procedures and symptomatic treatment

          Severe funnel-web spider envenomation is a complex multi-system 
          disease. This is best managed in an ICU setting, preferably in a 
          treatment centre with previous experience in handling such cases.

          (a)  IV line - urgently establish good IV line access.

          (b)  Respiratory - severe pulmonary oedema causing hypoxia and 
               respiratory failure demands urgent ICU management which 
               classically includes intubation and mechanical ventilation 
               (intermittent positive pressure ventilation (IPPV); positive 
               end expiratory pressure (PEEP), oxygen, possibly high dose 
               steroids (now believed to be contraindicated), and later, 
               and possibly diuretics (value uncertain).  CVP line, 
               arterial line, and Swan-Ganz catheter have proved valuable 
               for monitoring.  (Note:  see section 11.1 for detailed 
               review of management of pulmonary oedema in these cases.) 

          (c)  Circulatory - managed in conjunction with respiratory 
               problems.  May require isoprenaline, and volume replacement 
               with SPPS or albumin. Dopamine infusion, suggested by one 
               author, is probably contraindicated. 

     
               In the early stages where hypertension and tachycardia are a 
               problem, sympathetic blockade has been suggested.  While 
               alpha blockade has been used, it requires massive doses, and 
               beta blockade might well prove lethal in this situation, 
               therefore the writers do not advocate the use of either for 
               funnel-web envenomation. 

          (d)  Pharmacologic - atropine has proved valuable, eg for 
               parasympathetic blockade.  Diazepam has also been suggested, 
               but only when ventilation is supported.

     10.4 Decontamination

          No data.  Local suction unlikely to be useful.  There is some 
          suggestion that prolonged immobilisation of venom at the bite 
          site using recommended first aid (see Section 2.4) may allow 
          local destruction of venom. 

     10.5 Elimination

          No data.

     10.6 Antidote

          The availability since 1981 of specific funnel-web spider 
          antivenom (CSL, Melbourne) has dramatically changed the pattern 
          of funnel-web spider bite envenomation sequelae.  In all cases 
          where envenomation has occurred antivenom is the definitive and 
          preferred treatment.  (DIEKMAN et al 1989, Fisher et al 1981, 
          Hartman & Sutherland 1984, Sutherland 1980, 1983, Sutherland et 
          al 1981)

          Sutherland has defined the following as clinical indicators of 
          systemic envenomation by male A. robustus.  The presence of any 
          of the following is an indication for antivenom:

          (a)  Muscle fasciculation in the limb involved or remote from the 
               bite, usually first seen in tongue or lips when systemic 
               spread of venom has occurred.
          (b)  Marked salivation or lachrymation.
          (c)  Piloerection.
          (d)  Significant tachycardia.
          (e)  Hypertension in a previously normotensive patient.
          (f)  Dyspnoea.
          (g)  Disorientation, confusion, or a depressed level of 
               consciousness. 

          In most cases of bites by funnel-web spiders, no symptoms will 
          develop other than local pain of limited duration due to the 
          mechanical trauma of the bite.  These patients do not require 
          antivenom. 

          Funnel-web spider antivenom is prepared by hyperimmunising 
          rabbits with male A. robustus venom, and is therefore a rabbit 
          immunoglobulin.  The average quantity per ampoule is 100 mg of 

          purified rabbit IgG, which is enough to neutralise in vitro the 
          average venom yield from at least 4 adult male A. robustus. 


          Sutherland recommends prophylactic pretreatment with 
          antihistamine and a steroid, about 15 minutes prior to antivenom.  
          Pre-medication with adrenaline is not recommended.  Subcutaneous 
          testing for allergy is not recommended.  The antivenom should be 
          given intravenously, initially very slowly.  The initial dose is 
          a minimum of 2 ampoules, or 4 ampoules for a severe case, and 
          repeated in 15 minutes if no improvement.  As with all 
          antivenoms, everything should be prepared to treat anaphylaxis 
          should it occur; however, anaphylaxis has not been reported in 
          these cases and theoretically it is unlikely it could occur in 
          severe cases due to the neuroendocrine response.  The dosage is 
          the same for children and adults. Serum sickness has not occurred 
          following therapy with funnel-web spider antivenom.  In the 
          unlikely event of occurrence, steroid therapy may be worth 
          consideration.

          10.6.1 Adults

               Minimum 2 ampoules, most cases will require 4 or more 
               ampoules. 

          10.6.2 Children

               As for adults.


     10.7 Management discussion: alternatives, controversies, research 
          needs 

          See also section 11.1

          While systemic envenomation by male A. robustus and some other 
          funnel-web spiders is a severe, potentially fatal complex multi-
          system illness, the advent of specific antivenom has 
          significantly modified the likely outcome and problems 
          encountered.  Its development and dissemination by Sutherland and 
          colleagues at CSL Melbourne has been the crucial step in 
          ameliorating this envenomation syndrome and dramatically reducing 
          the likelihood of fatalities.  As a result, much of the pre-
          antivenom controversy about management practices and medication 
          is now largely redundant.  The important work of Fisher and 
          others had established valuable precedents in the successful 
          treatment of severe envenomation in an ICU setting, prior to 
          antivenom becoming available (see section 11.1 and Fisher et al 
          1980 for a detailed discussion).  Similarly, Sutherland's work on 
          first aid methods, initially controversial, is now widely 
          accepted as the standard, with little active dissent, although 
          tourniquets are still wrongly used as first aid in a disturbingly 
          high number of cases.  Of more importance is the finding that in 
          many cases no first aid has been used, a situation which is most 
          disturbing considering the rapidity of onset of life threatening 
          problems in severe cases and the effectiveness of correct first 

          aid in delaying such problems.  Possibly even more vigorous 
          public education would help. 

          While the development of a venom assay, akin to those developed 
          for Australian snake venoms, might allow further clinical and 
          experimental study of venom actions, because of the nature of 
          funnel-web spider envenomation compared to snakebite, it would 
          not be likely to have the same clinical impact as the snake Venom 
          Detection Kit (CSL Melbourne), and from both a clinical 
          management and economic viewpoint is of quite dubious value.  The 
          antivenom prepared against A. robustus venom has now been shown 
          potent against bites by other species.

    11.  ILLUSTRATIVE CASES

     11.1 Case reports from the literature

          Fisher et al, 1980

          Very detailed report of 2 severe, non-fatal cases, which 
          constitute an excellent guide to successful management if 
          antivenom unavailable.  Both cases are therefore given in some 
          detail. 

          Case 1

          RB, a 23 year old previously healthy man, was bitten twice on the 
          left knee by a male funnel-web spider (Atrax robustus) while 
          rock-climbing.  An arterial tourniquet was applied above the site 
          of the bite immediately.  The spider was killed and kept for 
          identification purposes and the patient assisted to Royal North 
          Shore Hospital by his companions. 

          On arrival, some 30 minutes after the bite, he complained of 
          burning pain on the inside of his left thigh, extending to his 
          groin.  He noticed circumoral paraesthesia, spasms of his tongue 
          and palate, followed by agitation, sweating, lacrimation, 
          salivation and blurred vision.  He vomited twice and complained 
          of increasing dyspnoea.  His blood pressure was 160/100 mmHg, 
          heart rate 120/minute, and his left pupil was fixed and dilated.  
          He had spasm and rigidity of proximal and distal muscles in both 
          upper and lower limbs. 

          He was given atropine 0.6 mg and diazepam 5 mg intravenously and 
          a further 5 mg diazepam and transferred to the Intensive Therapy 
          Unit.  Chest X-ray showed diffuse interstitial pulmonary oedema 
          and a normal cardiac shadow:  blood gases breathing room air were 
          PaO2 56 mmHg, PaCO2 22 mmHg, pH 7.37.  His haemoglobin (Hb) was 
          17.2 g/100 ml. 

          The tourniquet was released and oxygen administered with a Hudson 
          non-rebreathing mask with a flow of 12 litres/minute.  He 
          deteriorated rapidly developing increasing dyspnoea, gross 
          peripheral vascular shutdown and cyanosis while his blood 
          pressure rose to 210/120 mmHg.  There was no response to further 
          increments totalling 45 mg of diazepam intravenously and his 

          ventilation was assisted with a Mapleson D breathing circuit with 
          100% oxygen.  He was given suxamethonium 100 mg.  As muscle 
          relaxation occurred vast quantities of pink frothy oedema fluid 
          poured from his mouth and onto the floor, making endotracheal 
          intubation extremely difficult.  He was paralysed with 
          pancuronium and commenced on intermittent positive pressure 
          ventilation (IPPV) with 100% oxygen and a tidal volume (TV) of 
          one litre and a rate of 14 breaths/minute.  Peak pressure was 45 
          cm H2O and plateau pressure 35 cm H2O (Elema Schonander 900B 
          ventilator). 

          Following the institution of ventilation a positive end-
          expiratory pressure (PEEP) was applied and rapidly increased 
          until the oedema fluid was absent from the tubing.  The PEEP 
          level necessary was 20 cm H2O.  He was given methylprednisolone 2 
          g and frusemide 40 mg.  There was no diuresis.  His right pupil 
          became fixed and dilated.  A central venous catheter was inserted 
          and his central venous pressure (CVP) off the respirator was 25 
          cm H2O (zero reference point mid axillary line).  On each 
          occasion that the patient was disconnected from the ventilator or 
          the PEEP reduced, copious pink frothy fluid poured into the 
          respirator tubing. 

          Analysis of the pulmonary oedema fluid taken four hours after 
          admission showed high levels of protein.  When ventilation (FiO2 
          = 1) was stabilised blood showed PaO2 346 mmHg, PaCO2 68 mmHg, pH 
          7.1.  The minute volume was increased to 22 litres over a period 
          to bring PaCO2 to normal levels and correct the acidosis. 

          After 90 minutes his blood pressure began to fall and PaO2 on 
          100% oxygen fell to 117 mmHg.  He was treated with infusion of 
          25% albumin 500 ml over one hour which reduced the Hb 
          concentration to 16.2 g/100 ml.  Over the next four hours he was 
          given 500 ml of stable plasma protein solution 5% (SPPS) and a 
          further 200 ml of 25% albumin.  The vasoconstriction was not 
          improved by chlorpromazine 25 mg intravenously and an 
          isoprenaline infusion was commenced at the same time as the 
          albumin infusion.  His pulse slowed and peripheral perfusion 
          improved over about 30 minutes. 

          Eight hours after intubation his spontaneous tidal volume was 
          1200 ml and he was fighting the ventilator.  He was extubated and 
          commenced on salt and water restriction and intermittent 
          frusemide to produce a negative salt and water balance. His 
          radiological appearance and alveolar-arterial gradient 
          deteriorated markedly on extubation but over the next few days 
          progressively returned to normal.  He had episodes of high fever 
          over the next five days.  His complement levels and clotting 
          screen were normal, CPK and fibrin degradation products were 
          minimally raised. He was discharged well 13 days after admission. 

          Case 2

          RT, a fit 40 year old woman, was bitten on the distal phalanx of 
          her left index finger by a spider positively identified as a male 
          Atrax robustus.  The spider had to be prised from her finger and 

          the wound bled profusely.  An arterial tourniquet was applied and 
          she was taken to Woy Woy District Hospital.  The tourniquet was 
          released with no untoward effects and she was transferred to 
          Gosford Hospital. 

          On arrival 40 minutes after the bite she complained of perioral 
          tingling, anxiety and nausea.  Her pulse rate on admission was 
          120 and over the next 30 minutes fell to 34 beats/minute with 
          blood pressure 190/110 mmHg.  ECG at this time showed blocked 
          atrial escape which reverted to bi-directional tachycardia after 
          atropine 0.6 mg intravenously. 

          Over the next two hours she became progressively more 
          hypertensive and flushed, her left pupil became fixed and dilated 
          and eyes became puffy.  She developed marked peripheral 
          vasoconstriction.  She was given diazepam 10 mg intravenously 
          with no noticeable effect and transferred to the Intensive Care 
          Unit.  Her chest was clear.  Three and a half hours after the 
          bite she was dyspnoeic with generalised crepitations over all 
          lung fields; blood pressure was now 170/110 mmHg, pulse rate 130.  
          Chest X-ray showed bilateral interstitial and alveolar oedema and 
          blood gases on room air were PaO2 46 mmHg, PaCO2 28 mmHg, pH 7.3. 

          She became progressively more breathless and, four hours post-
          bite, minor muscle spasms developed along with peripheral 
          cyanosis and gross vasoconstriction.  She was given diazepam 20 
          mg, atropine 0.6 mg and suxamethonium 100 mg and an endotracheal 
          tube was inserted with difficulty, due to profuse pulmonary 
          oedema which poured on to the bed and floor.  She was commenced 
          on IPPV and controlled with pancuronium and diazepam.  PEEP was 
          applied until airway flooding ceased at 10 cm. 

          Her haemoglobin was 16.2 g/100 ml.  CVP reading was 16 cm H2O. 
          She rapidly developed hypotension which was treated with albumin 
          infusion and isoprenaline infusion.  As her blood pressure 
          improved her peripheral vasoconstriction decreased.  She was 
          given 2 g hydrocortisone; the albumin infusion was continued for 
          episodes of hypotension.  Over 24 hours she received two litres 
          of 25% albumin which brought her haemoglobin down to 10 g/100 ml 
          and was associated with continuing improvement in arterial blood 
          gases.  In the second 24 hours she received a further 600 ml of 
          albumin and an increase in PEEP to 20 cm was required to maintain 
          oxygenation. 

          Over the next 24 hours she became oliguric.  She was given 500 ml 
          of Ringer's lactate, immediately developing profuse airway 
          flooding in spite of high levels of PEEP.  This ceased within 
          minutes of stopping the infusion.  She was given two doses of 
          frusemide 80 mg with little response.  Forty-eight hours after 
          admission to Gosford she was transferred to Royal North Shore 
          Hospital. 

          On arrival she was stabilised on a Servo volume-cycled ventilator 
          delivering 80% oxygen with 20 cm of PEEP and minute volume 10 
          litres.  Arterial blood gases were PO2 110 mmHg, PCO2 50 mmHg, pH 
          7.42.  A Swan-Ganz catheter was inserted and pressures recorded 

          were pulmonary artery (PA) 40/26 mmHg, and mean pulmonary 
          capillary wedge pressure (PCWP) 23 mmHg, CVP 26 cm H2O. 

          Reduction of PEEP led to immediate airway frothing.  She was 
          given frusemide 250 mg and methylprednisolone 2 g six-hourly for 
          24 hours.  1000 ml of blood was removed by phlebotomy over two 
          hours bringing mean PCWP to 17 mmHg.  A diuresis began and she 
          passed in excess of 40 ml urine hourly over the next 16 hours.  
          She was given 500 ml of packed cells over four hours to restore 
          the haematocrit.  Twenty-four hours after arrival she was on 20 
          cm of PEEP, PCWP (mean) was 13 mmHg, and blood gases on FiO2 0.45 
          were PaO2 101 mmHg, PaCO2 37 mmHg, pH 7.47.  Six hours after 
          admission she developed a high fever which persisted 48 hours.  
          Blood cultures were negative. 

          She became oliguric and unresponsive to increasing dosage of 
          frusemide.  Serum creatinine was 0.31 mmol/l.  She was given 500 
          ml of fresh frozen plasma and mean PCWP increased to 17 mmHg and 
          was associated with a brisk diuresis. She was continued on salt 
          and water restriction and artificial ventilation.  On the 4th day 
          reduction of PEEP was not followed by airway frothing and she was 
          commenced on intermittent mandatory ventilation.  The 
          isoprenaline was ceased. 

          On day 5 she was extubated with radiological deterioration of 
          lung function after extubation.  On day 6 her serum creatinine 
          was normal, she was commenced on a light diet and fluid intake 
          was gradually increased.  She was extremely weak for five days 
          and was gradually mobilised over the next week and discharged 
          well 20 days after the bite. 

          Clotting screen and complement levels were normal throughout the 
          illness, CPK and liver function tests were marginally raised. 

          Discussion (From original paper, edited).

          Pulmonary oedema due to the bite of the male funnel-web spider 
          has been well documented and may be a feature of seriously ill 
          envenomated patients. 

          In the period 1940 to 1978, 33 patients were admitted to Royal 
          North Shore Hospital with a history of spider bite.  Only three 
          had major symptoms and these were all envenomated by male funnel-
          web spiders.  Symptoms were predominantly pulmonary oedema and 
          cardiovascular.  One patient recovered spontaneously and two 
          died. 

          The clinical features in the two patients with definite male 
          Atrax robustus envenomation were: 

          (1) Pulmonary oedema

          Pulmonary oedema is produced when fluid enters the pulmonary 
          interstitium at a rate exceeding pulmonary lymphatic drainage.  
          Clinical features appear when the interstitial volume is six 
          times normal.  The oedema may occur due to disturbance of any of 

          the factors governing fluid movement in the lung. One of these 
          with possible relevance to funnel web spider envenomation is 
          increased pulmonary capillary membrane permeability (PCMP), which 
          is an increasingly recognised form and usually the most severe, 
          although only moderate changes in permeability are required and 
          they may be short-lived.  Under some circumstances increased PCMP 
          may not produce oedema without raised capillary pressure. Both 
          cases described showed a protein content suggestive of increased 
          PCMP oedema. The initial washout of interstitial protein may be 
          beneficial in increasing plasma-tissue osmotic pressure gradient, 
          but the loss from plasma to interstitium promotes greater 
          movement of fluid into the interstitium and leads to reduced 
          clearing and eventual organisation and fibrosis in the alveoli. 
          In hydrostatic pulmonary oedema, PEEP does not retard lung water 
          accumulation although in increased PCMP oedema due to sepsis it 
          protects against the effects of volume loading.  There is no 
          benefit in raising COP in increased PCMP pulmonary oedema. 

          Because of the evidence of massive sympathetic discharge, severe 
          vasoconstriction, high protein oedema and the lack of 
          experimental evidence of an effect of the venom on the pulmonary 
          capillary membrane in animals, it is possible that the mechanism 
          of the pulmonary oedema due to Atrax robustus venom may either be 
          "neurogenic pulmonary oedema" or a direct effect of toxin or 
          mediator on the pulmonary capillary membrane. 

          Our approach to the therapy of the pulmonary oedema in both 
          patients was to control ventilation with increasing levels of 
          PEEP until airway flooding ceased, to restore blood volume with 
          colloid solutions, and to carefully dehydrate the patients when 
          volume was restored and airway flooding ceased, which avoided the 
          dangers of diuretic therapy in the presence of hypovolaemia.  The 
          combination of albumin to raise COP and maintain blood volume 
          with diuretics to reduce extracellular fluid volume has been used 
          successfully to treat pulmonary oedema by a number of authors.  
          Although PEEP may not alter fluid dynamics in the lung and 
          usually improves oxygenation by opening closed alveoli, the PEEP 
          in these circumstances stopped large airway flooding and allowed 
          volume restoration and maintenance of COP.  PEEP may often 
          produce marked improvement in chest radiography due to opening of 
          alveoli and increased functional residual capacity.  The dramatic 
          deterioration in X-ray after institution of spontaneous 
          ventilation and cessation of PEEP in Case 1 we felt was of such 
          magnitude as to represent a true deterioration in oedema over and 
          above the cosmetic effects of PEEP.  The high levels of PEEP 
          required to stop large airway flooding led to over-distension of 
          the lung, and the difficulty in removal of CO2 could have been 
          related to increased dead space as a consequence of excessive 
          PEEP or increased CO2 production. 

          The use of Ringer's lactate solution in Case 2 was associated 
          with prompt appearance of airway frothing which was not 
          controlled by increasing PEEP. Suction was avoided in these 
          patients until airway frothing had ceased to avoid applying 
          negative pressure to the alveoli.  Removing the PEEP to measure 
          central venous pressure was associated with massive airway 

          flooding and is at best a hazardous and probably unnecessary 
          practice.  Both patients required a high minute volume initially 
          to achieve normocarbia. 

          In addition we used high dosage steroids in both patients, in 
          Case 1 once only and in Case 2 for 72 hours.  Sutherland states 
          that there is no evidence that steroids affect the clinical 
          course in Atrax envenomation, and while acknowledging that these 
          patients do not provide such evidence, we believe they should be 
          given for their potential benefit, in producing fall in total 
          peripheral resistance, improvement in oxygenation and pulmonary 
          oedema, stabilisation of pulmonary capillary membrane, shift in 
          haemoglobin dissociation curve to the right and decreased 
          pulmonary vascular resistance. 

          (2) Circulatory changes 

          The venom causes vasoconstriction, potentiation of response to 
          noradrenaline, and a biphasic response in rabbit atria with 
          initial depression followed by stimulation related to 
          noradrenaline release. Both patients showed hypertension and 
          tachycardia on admission.  Case 2 developed a bizarre arrhythmia 
          shortly after admission which responded to atropine.  Case 1 had 
          supraventricular tachycardia for the first four hours. 

          The most marked feature was the gross peripheral vasoconstriction 
          which was associated with hypertension and tachycardia.  This was 
          associated with right and left cardiac failure and 
          haemoconcentration.  The haemoconcentration occurs due to plasma 
          loss, and in the absence of blood loss has been used to 
          quantitate plasma loss. 


          Isoprenaline appeared effective in reducing vasoconstriction and 
          lowering blood pressure in these patients and was initially 
          associated with a slowing of the pulse rate. 

          Hypovolaemia may have contributed to the subsequent development 
          of hypotension in these patients, and in Case 1 treatment of 
          failure and vasoconstriction with isoprenaline and blood volume 
          restoration with albumin and SPPS to normalise haematocrit 
          promptly restored circulation.  In Case 2 oxygenation improved 
          while two litres of 25% albumin was given, but further increments 
          produced a deterioration in lung function which was corrected by 
          venesection and diuresis. 

          Restoration of blood volume in the presence of increased 
          pulmonary capillary membrane permeability (PCMP) is a 
          controversial subject.  Colloid solutions have been used to 
          replace volume and raise colloid osmotic pressure and it has been 
          suggested that albumin and dextran may act to "plug the leak".  
          However, these solutions may leak into the pulmonary interstitium 
          making the situation worse. They have the advantage of restoring 
          volume while avoiding salt and water excess with over-expansion 
          of interstitial water. 


          In Case 1 the use of high level PEEP and albumin in combination 
          enabled restoration of normal haematocrit with continuing 
          improvement of alveolar-arterial gradient which is evidence 
          against loss of albumin into the interstitium.  Case 2 improved 
          in a similar fashion until overloaded, and was improved 
          dramatically by venesection and lowering of PCWP. 

          (3) Pupillary changes 

          Both patients showed unilateral fixed dilated pupils on the side 
          of the bite proceeding to bilateral fixed dilated pupils for a 
          four to six hour period.  At no time was there evidence of 
          papilloedema. 

          (4) Muscle spasms 

          These occurred as an early manifestation in Case 1 and a late 
          manifestation in Case 2.  The recommended treatment for such 
          spasms is diazepam intravenously. Diazepam did not appear 
          effective in Case 1 and its efficacy could not be assessed in 
          Case 2 as a small dosage was given prior to muscle spasms.  The 
          administration of repeated dosages of diazepam to patients who 
          have pulmonary symptoms after Atrax envenomation we would regard 
          as contraindicated in the absence of demonstrated efficacy in 
          humans, because of the hazards of repeated administration of 
          respiratory depressant drugs in respiratory failure.  The use of 
          ventilatory support and non-depolarising relaxants would seem a 
          safer way of blocking the effects of acetylcholine while 
          improving the ventilatory status. 

          (5) Renal function

          Both patients developed elevation of serum creatinine.  Urinary 
          electrolytes were unhelpful in assessing the patients in the 
          early stages due to the use of frusemide. In Case 2 concentrating 
          ability and sodium retention were normal on day 4 in spite of a 
          serum creatinine that rose to 0.33 mmol/l. 

          Case 1 was found to have hyaline casts in his urine and Case 2 
          had no abnormal sediment.  There is no experimental evidence of a 
          nephrotoxic effect of the venom and the renal impairment may well 
          have been related to the circulatory disturbance consequent on 
          the profound vasoconstriction and the well documented effects of 
          high levels of PEEP, or reduced glomerular filtration due to 
          elevated serum protein levels. 

          It was interesting to note that oliguria persisted in Case 2 
          after 500 mg frusemide when there was a mean pulmonary capillary 
          wedge pressure (PCWP) of 13 cm H2O but following subsequent 
          elevation of the PCWP to 16 cm H2O with plasma there was an 
          immediate diuretic response, without changes in blood pressure, 
          pulse rate or CVP. 

          Hyperglycaemia occurred in both patients in the early phase.  
          This may have been due to sympathetic activity or steroids. 


          Perioral tingling was the first symptom in both patients.  
          Excessive salivation occurred in both patients.  Atropine in the 
          dosages given (0.6 mg) did not reduce this and higher dosages 
          should be used.  Intermittent pyrexia occurred in both patients, 
          as a late manifestation. 

          Management of envenomation due to Atrax robustus.  

          The deterioration in Case 1 after tourniquet release was dramatic 
          and we endorse the view of Sutherland and Duncan that a pressure 
          immobilisation bandage should be applied.  An arterial tourniquet 
          is also effective but hazardous and painful. Whatever means are 
          used to delay systemic effects, they should not be released until 
          the patient is in hospital.  We would endorse the use of 
          atropine, in higher dosage than we used, for control of 
          secretions and bradycardia. 

          For reasons outlined earlier we find it difficult to support 
          Sutherland's advocacy of diazepam if there are respiratory 
          symptoms.  We believe that pulmonary oedema and circulatory 
          failure due to envenomation by Atrax robustus should be treated 
          by: 

          1.   artificial ventilation and levels of PEEP sufficient to 
               prevent airway flooding; 
          2.   high dose steroids;
          3.   blood volume replacement with albumin;
          4.   circulatory support and treatment of vasoconstriction with 
               isoprenaline, phentolamine or nitroprusside; 
          5.   fluid restriction and diuretic therapy when the airway 
               flooding phase has ended; 
          6.   during fluid replacement Hb and CVP should be measured and 
               in severe cases Swan-Ganz catheterisation is indicated. 


          However, rather than rigid adherence to protocols of management 
          it is essential for successful outcome in the management of these 
          patients that careful application of modern principles of 
          assessment, therapy and repeated measurements be used in 
          treatment. 

          Musgrave, 1927

          Case 1

          Child (? age 2 years), outcome fatal.  Presumed A. robustus. 
          The boy was bitten on the 5th digit, left hand, at home in 
          Thornleigh (Sydney); he immediately commenced crying.  Tourniquet 
          applied.  When seen medically the child was unconscious, deeply 
          cyanosed, and in a state of chronic convulsive spasm.  Treatment 
          not detailed.  Died 1.25 hours after arrival and "a few hours" 
          after the bite (Sutherland, 1983, lists death as occurring 1.5 
          hours after the bite). This case is apparently the first recorded 
          fatality from funnel-web spider bite in Australia. 

          Case 2


          Adult man, 42 years, non-fatal.  "Male A. robustus".
          Trod on spider, causing bite to foot, with 2 punctures, and local 
          pain "similar to that of a bee-sting"; 35 minutes later developed 
          numbness of tongue, loss of taste, and "twinging pain in the 
          tongue and lips".  By 1.5 hours, pain had extended to both hands 
          and feet and, by 2 hours, he developed excessive salivation, 
          nasal discharge, twitching of facial muscles, especially lips, 
          and facial parasthesiae.  By 3 hours developed lachrymation, 
          could only control eyelids with difficulty, had nausea, a choking 
          feeling in the throat. At about 3.5 hours, blurred vision, 
          difficulty controlling limbs, and peripheral coldness and 
          numbness occurred.  All symptoms became progressively worse over 
          the next 2 hours.  Symptoms continued over the next 12 hours or 
          so, but with some relief by the next day, over 24 hours post-
          bite. Steady improvement over the next 2 days. 

          Case 3

          Adult man, non-fatal.  Male H. formidabilis.
          Bite to the buttock while dressing one night (spider in 
          trousers), then bite to finger. Intense local pain initially, 
          then numbness.  By 3 hours had developed "intense vomiting, 
          profuse perspiration, violent cramps in the limbs and abdominal 
          muscles", delirium, bradycardia (60 bpm), laboured respirations 
          and "coughing up quantities of mucous, saliva trickling from the 
          mouth, and pupils contracted".  No further details though the 
          patient survived (further details in Ingram and Musgrave, 1933). 

          Beazley, 1930

          46 year old woman, outcome fatal.  Male A. robustus.
          Bitten on left thumb; 40 minutes later had a red congested face 
          with cold clammy periphery, thready pulse, and hypotension 
          (systolic BP 55 mm Hg).  She then developed "incessant retching 
          of thick tenacious mucus", then an hour later, dyspnoea, 
          pulmonary oedema, laryngeal spasms, facial cyanosis, and apparent 
          peripheral shutdown.  Atropine had no clinical effect.  About 4 
          hours post-bite she had moderate cyanosis, frothing at lips, 
          clonic contractions of arms and legs every 10-20 minutes, 
          bilateral small fixed pupils, and a tachycardia.  The bite site 
          had 2 minute punctures, without local oedema.  By 6 hours post-
          bite she was comatose. She died at 9 hours post-bite. 

          Autopsy showed oedematous lungs with fine froth throughout the 
          airways, and alveolar distension.  Some congestion was seen in 
          the liver, kidneys and stomach wall.  No cerebral lesions were 
          seen. 

          Ingram and Musgrave, 1933

          Case 1

          Young adult woman (? age 25 years), outcome fatal.  Presumed A. 
          robustus. Bitten on buttock while sitting on grass, causing sharp 
          local pain.  Within 10 minutes was "pale, felt weak and ill, and 

          commenced to perspire freely".  She subsequently collapsed, with 
          "marked dyspnoea and inspiratory stridor".  No local reaction at 
          the bite site.  She produced frothy fluid from the airways, and 
          vomited frequently.  A hyperthermia (38°C) was noted with 
          tachycardia (150 bpm) and tachypnoea (50 bpm).  "Analgesia of the 
          whole body was observed" and the pupils were small and 
          unreactive.  Tendon reflexes sluggish.  She developed progressive 
          cyanosis and "died suddenly from heart failure 13 hours after 
          being bitten". Autopsy revealed acute pulmonary oedema. 

          Case 2

          Boy, 7 years, outcome non-fatal.  Male A. robustus.  Bitten on 
          right hand, causing local pain; 30 minutes later had severe 
          dyspnoea with frothing at the mouth, and shortly thereafter had 
          "signs of acute lung oedema", tachycardia (130 bpm), marked 
          inspiratory stridor, constant vomiting, paralysis of 
          accommodation, unable to open mouth, and apparent right facial 
          weakness.  Morphine and atropine appeared to give temporary 
          relief, but he again developed vomiting, dyspnoea, tachycardia, 
          and abdominal rigidity, priapism, and arreflexia.  A lateral 
          nystagmus was noted, and generalised muscle tenderness.  Cyanosis 
          developed, then coma, and a venesection (200 ml) was performed.  
          This gave rapid relief and within 30 minutes he was able to 
          drink, and he continued to complete recovery. 
     
          Wiener, 1961

          Lists 10 fatal cases (including those in 11.1.2 and 11.1.3) since 
          1927. 

          Torda et al, 1980

          A detailed case report.

          Female, 31 years, outcome fatal.  Male A. robustus.  Bitten on 
          wrist.  Use tourniquet first aid.  At 30 mins noted blurred 
          vision and sweating, and at 60 mins, muscular twitching and then 
          generalised spasms, followed by profuse salivation, nausea and 
          vomiting, and respiratory difficulty (PaO2 46 mmHg while on 
          oxygen at 6 L/min).  By 3 hours post-bite she was stuporous, 
          cyanosed, irritable, tachypnoeic, tachycardic (180 bpm) with 
          frequent ventricular ectopics, hypertensive (160/110), and had 
          generalised muscular spasms.  She had severe pulmonary oedema and 
          at about 3 hours post-bite was paralysed, intubated and 
          ventilated with IPPV and PEEP on 100% O2, giving a PaO2 of 91 
          mm/Hg. 

          She remained stable for 4 hours, then at about 6-7 hours post-
          bite she became severely hypotensive and anuric, with sluggishly 
          reactive dilated pupils.  She was resuscitated with 1.5 L SPPS, 
          dopamine infusion (10 mg/kg/min), and digoxin 0.5 mg IV, with 
          return of urine output, contraction of pupils, and rise in BP (to 
          80-100 mmHg) by 11 hours post-bite. By next day (24 hours post-
          bite) she was awake but falling PaO2 required increased PEEP.  
          She was assessed as having continued pulmonary oedema consistent 

          with adult respiratory distress syndrome.  Further falls in PaO2 
          were initially managed with increased PEEP with secondary 
          pneumomediastinum. 

          By day 3 she developed severe peripheral cyanosis and an apparent 
          DIC-type coagulopathy, and raised liver enzymes and creatinine.  
          Deterioration continued, and by day 4 she was unconscious, and 
          she required PEEP and continuous dopamine infusion, peripheral 
          cyanosis worsened, and heparinisation instituted for the 
          coagulopathy. 

          On the 5th day there was deterioration in cerebral function, with 
          poor response to painful stimuli, papilloedema, and EEG 
          deterioration, and hyperthermia.  By the 6th day she was anuric, 
          developed further unresponsive hypotension, and died in asystole. 

          Fisher et al, 1981

          Report of first 2 cases treated (successfully) with specific 
          funnel-web spider antivenom. 

          Case 1

          Male, 49 years, bitten on foot by a male A. robustus.  
          Compression bandage first aid applied.  15 mins post-bite he had 
          local pain, sweating, piloerection, and perioral tingling, 
          shortly followed by muscle fasciculation of the arms progressing 
          to severe spasm, then nausea, vomiting, marked salivation and 
          lachrymation.  By 25 mins there was evidence of pulmonary oedema 
          and hypertension (240/140).  By 50 mins there was stridor and 
          cyanosis, and he was intubated.  He was then transferred to 
          another hospital, by which time (75 mins post-bite) there was no 
          evidence of pulmonary oedema, but continued hypertension, a 
          metabolic acidosis, tachycardia, and increased muscle tone.  
          Following pretreatment with promethazine and methylprednisolone 
          he received 7.5 ml funnel-web antivenom IV, and 15 mins later a
          second dose.  Over the next hour his BP reduced to normal, HR 
          reduced to 120 bpm, and muscle tone reduced.  The improvement 
          continued and he was discharged less than 2 days post-bite.  His 
          only residual problem was excessive sweating for 3 weeks. 



          This case illustrates a marked beneficial response to antivenom 
          in severe envenomation, with significant reduction in length of 
          hospitalisation and complications. 

          Case 2

          Male, 3 years, bitten on the toe by a male A. robustus.  
          Tourniquet applied as first aid.  Within minutes of removal of 
          first aid, developed acute distress, marked salivation, 
          lachrymation, sweating, piloerection, hypertension, tachycardia, 
          then pulmonary oedema, cyanosis, and disorientation.  He was 
          intubated and ventilated with PEEP, but with continued pulmonary 
          oedema.  Funnel-web spider antivenom was then administered IV 

          following premedication with promethazine and methylprednisolone.  
          Over the next hour there was a steady improvement, and extubation 
          was possible 75 mins later.  He was discharged the following day, 
          and had no further problems. 


          This case again illustrates severe envenomation rapidly resolved 
          by antivenom therapy, with consequent reduction in 
          hospitalisation. 

          Knight and Sutton, 1982

          Male, aged 9 years, bitten on a finger by a male Hadronyche 
          formidabilis.  By 10 mins he was vomiting, sweating, with local 
          pain, and by 15 mins he was pale, sweaty, tachycardic (160 bpm) 
          and hypertensive (140/110).  He was transferred by air to Sydney, 
          and on arrival, 2 hours post-bite, he had fasciculation of 
          tongue, poor peripheral perfusion, with a tachycardia (150 bpm), 
          and hypotension (85 systolic), but no evidence of pulmonary 
          oedema.  After pre-treatment with promethazine and 
          hydrocortisone, he received funnel-web spider antivenom IV (2 
          ampoules), with rapid improvement thereafter.  However symptoms 
          returned, necessitating a further 2 ampoules of antivenom about 
          one hour later.  Again there was rapid improvement but a further 
          relapse 2 hours later, which stabilised spontaneously without 
          more antivenom therapy, and 3 hours later he was substantially 
          well, being discharged 3 days post-bite. 

          Hartman and Sutherland, 1984

          This paper documents 9 cases of funnel-web spider envenomation 
          treated successfully with specific antivenom.  All had severe 
          envenomation, and showed clear improvement following antivenom 
          therapy.  The duration of hospitalisation was 1-3 days, compared 
          to 2-3 weeks prior to antivenom availability. 

          Each case is briefly discussed.  The first three cases are those 
          presented in 11.1.7 and 11.1.8 above. In discussion it is 
          suggested that correct first aid may reduce the incidence of 
          severe envenomation by allowing some local inactivation of the 
          venom. 

          Fisher and Bowey, 1989


          Review of cases of envenomation admitted to one ICU over 12 
          years.  35 patients admitted with funnel-web spider bite.  8 of 
          these had severe envenomation, 6 requiring artificial 
          ventilation, and all showed pulmonary oedema, hypertension, 
          tachycardia, and muscular spasms.  Average duration of 
          hospitalisation in these 8 cases:  9.6 days (no antivenom), and 2 
          days (antivenom therapy).  Diekmann et al 1989. 

          Diekmann et al 1989

          Description of 3 cases of significant envenomation by Hadronyche 

          versuta, H. infensa, and H. cerberea, all successfully treated 
          with funnel-web spider antivenom.

     11.2 Internally extracted data on cases

          See cases listed in 11.1.  (Fisher et al 1980, 1981, 1989, Fisher 
          1989, DieckmanN et al 1989) 

     11.3 Internal cases

    12.  ADDITIONAL INFORMATION

     12.1 Availability of antidotes:

          Specific Funnel-web Spider Antivenom is available from the 
          manufacturer (or agents), Commonwealth Serum Laboratories, 45 
          Poplar Road, Parkville, Vic, 3052 AUSTRALIA.  Current cost in 
          Australia, $491.00 per ampoule.  Advice available from 
          manufacturer, telephone (03) 389 1911, telex AA 32789, Fax (03) 
          389 1434, International Fax +61 3 389 1434. 

     12.2 Specific preventive measures:

          In areas known or likely to have funnel-web spiders, avoid 
          contact with spiders. Do not leave clothing or footwear on the 
          floor or where spiders may enter.  Check gloves, footwear, and if 
          appropriate, clothing, for spiders prior to use. Use care when 
          working in areas where spiders may be common, such as in gardens, 
          rockeries, under materials left lying on the ground (clean them 
          up),and under houses.  Do not place hands in places not visually 
          inspected first.  Don't walk about at night bare-footed or 
          wearing 'thongs' or sandals. Attach draught strips to possible 
          under door entry points and flywire screens to windows and 
          ventilators. Check swimming pools, including filters, for 
          wandering spiders that sometimes fall in, as they can take many 
          hours to drown. If working or living in areas at risk from 
          funnel-web spiders, ensure appropriate first aid materials 
          available (bandages, splints) and methods understood by all those 
          at risk. 

     12.3 Other

          No data



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          robustus.  Toxicon, 14:  185-189.

          Musgrave A (1927)  Some poisonous Australian spiders.  Rec. Aust. 
          Museum, 16: 33-46.

          Musgrave A (1949a)  Spiders harmful to man I.  The Aust. Museum 
          Mag., 9(11):  385-388.

          Musgrave A  (1949b)  Spiders harmful to man II.  The Aust. Museum 
          Mag., 9(12): 411-419.

          Myelcharane EJ, Spence I & Gregson RP (1984)  In vivo actions of 
          atraxin, a protein neurotoxin from the venom glands of the 
          funnel-web spider (Atrax robustus).  Comp. Biochem. Physiol., 
          79(2):  395-399.

          Noel V/Sutherland SK (1985)  Letter to Editor, with reply from 
          S.K. Sutherland. Med. J. Aust., 142:  328.

          Sheumack DD, Carroll PR, Hampson F, Howden MEH, Inglis AS, 
          Roxburgh CM, Skorulis A & Strike PM (1983)  The isolation and n-
          terminal sequence of the lethal neurotoxin from the venom of the 
          male Sydney funnel-web spider, Atrax robustus. Toxicon, Suppl. 3:  

          397-400.

          Sheumack DD, Baldo BA, Carroll PR, Hampson F, Howden MEH & 
          Skorulis A (1984)  A comparative study of properties and toxic 
          constituents of funnel-web spider (Atrax) venoms.  Comp. Biochem. 
          Physiol., 78(1):  55-68.

          Sheumack DD, Claasseens R, Whiteley NM & Howden MEH (1985)  
          Complete amino acid sequence of a new type of lethal neurotoxin 
          from the venom of the funnel-web spider Atrax robustus.  FEBS 
          Letters, 181(1):  154-156.

          Spence I, Adams DJ & Gage PW (1977)  Funnel-web spider venom 
          produces spontaneous action potentials in nerve.  Life Sciences, 
          20:  243-250.

          Sutherland SK (1972a)  The Sydney funnel-web spider (Atrax 
          robustus).  1.  A review of published studies on the crude venom.  
          Med. J. Aust., 2:  528-530.

          Sutherland SK (1972b)  The Sydney funnel-web spider (Atrax 
          robustus). Fractionation of the female venom into five distinct 
          components.  Med. J. Aust., 2: 593-596.

          Sutherland SK (1972c)  The Sydney funnel-web spider (Atrax 
          robustus).  3.  A review of some clinical records of human 
          envenomation.  Med. J. Aust., 2: 642-646.

          Sutherland SK (1973a)  Treatment of funnel-web spider bites.  
          Med. J. Aust., 1: 1016.

          Sutherland SK (1973b)  Isolation, mode of action and properties 
          of the major toxin (Atraxotoxin) in the venom of the sydney 
          funnel-web spider (Atrax robustus).  Proc. Aust. Soc. Med. Res., 
          3:  172.

          Sutherland SK (1978)  The management of bites by the Sydney 
          funnel-web spider, Atrax robustus.  Med. J. Aust., 1:  148-150.

          Sutherland SK (1980)  Antivenom to the venom of the male Sydney 
          funnel-web spider, Atrax robustus.  Med. J. Aust., 2:  437-441.

          Sutherland SK (1983)  Australian Animal Toxins, Melbourne, Oxford 
          University Press.

          Sutherland SK & Duncan AW (1980)  New first-aid measures for 
          envenomation: with special reference to bites by the Sydney 
          funnel-web spider (Atrax robustus). Med. J. Aust., 1:  378-379.

          Sutherland SK, Duncan AW & Tibballs J (1980)  Local inactivation 
          of funnel-web spider (Atrax robustus) venom by first-aid 
          measures.  Med. J. Aust., 2:  435-437.

          Sutherland SK, Tibballs J & Duncan AW (1981)  Funnel-web spider 
          (Atrax robustus) antivenom.  1.  Preparation and laboratory 
          testing.  Med. J. Aust., 2: 522-524.


          Tibballs J, Sutherland SK & Duncan AW (1987)  Effects of male 
          Sydney funnel-web spider venom in a dog and a cat.  Australian 
          Veterinary J., 64(2): 63-64.

          Torda TA, Loong E, & Greaves I (1980)  Severe lung oedema and 
          fatal consumption coagulopathy after funnel-web bite.  Med. J. 
          Aust., 2:  442-444.

          Watkins AM (1939)  A bite by Atrax robustus.  Med. J. Aust., 1:  
          710.

          White J (1987)  Review of clinical and pathological aspects of 
          spider bite in Australia.  In:  Gopalakrishnakone, P., & Tan, 
          C.K. Eds  Progress in venom and toxin research, Singapore, Univ. 
          Sing.

          White J, Hirst D & Hender E (1989)  36 cases of bites by spiders, 
          including the white-tailed spider, Lampona cylindrata.  Med. J. 
          Aust., 150:  401-403.

          Wiener S (1957)  The Sydney funnel-web spider (Atrax robustus).  
          1.  Collection of venom and its toxicity in animals.  Med. J. 
          Aust., 2:  377-382.

          Wiener S & Drummond FH (1956)  Assay of spider venom and 
          antivenene in Drosophila.  Nature (Lond.), 178:  267-268.

          Wiener S (1959)  The Sydney funnel-web spider (Atrax robustus).  
          II.  Venom yield and other characteristics of spider in activity.  
          Med. J. Aust., 2:  678-682.

          Wiener S (1961)  The Sydney funnel-web spider (Atrax robustus).  
          The neutralization of venom by haemolymph.  Med. J. Aust., 1:  
          449-451.

          Wiener S (1961)  Observations on the venom of the Sydney funnel-
          web spider (Atrax robustus).  Med. J. Aust., 2:  693-699.

          Wiener S (1963)  Antigenic and electrophoretic properties of 
          funnel-web spider (Atrax robustus) venom.  In Venomous and 
          Poisonous Animals and Noxious Plants of the Pacific Area, Oxford, 
          Pergamon Press.


          Wiener S, Sutherland SK (1978)  Letter to editor, with reply from 
          S.K. Sutherland.  Med. J. Aust., 2:  104-106. 

     13.2 Zoological references

          Gray MR (1981)  Getting to know funnel web spiders.  Aust. Nat. 
          Hist. 20:265-270.

          Gray MR (1984)  The taxonomy of the Atrax adelaidensis species 
          group (Macrothelinae:  Mygalomorphae) with notes on burrowing 
          behaviour.  Rec. S. Aust. Mus., 18(19):  441-452.


          Gray MR (1984)  A guide to funnel-web spider identification.  
          Med. J. Aust., 2: 837-840.

          Gray M  (1987)  Distribution of the funnel-web spiders.  In: 
          Covacevich, J., Davie, P., & Pearn, J. Eds  Toxic Plants and 
          Animals - A Guide for Australia, Brisbane, Queensland Museum.

          Gray MR (1988)  Aspects of the systematics of the Australian 
          funnel-web spiders (Araneae:Hexathelidae:Atracinae) based upon 
          morphological and electrophoretic data.  In: eds. Austin A.D., 
          Heather N.W. eds; Australian Arachnology; Miscl. Publ. No.5, 
          Aust. Entomol. Soc.; 113-125.

          Raven RJ (1980)  The evolution and biogeography of the 
          Mygalomorph spider family Hexathelidae (Araneae, Chelicerata).  
          J. Arachnol., 8(3):  251-266. 



    14.  AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)

     Authors:  Dr Julian White
               State Toxinology Services
               Adelaide Children's Hospital
               North Adelaide   SA   5006  
               Australia

               Tel: 61-8-2047000
               Mobile tel: 61-18-832776
               Fax: 61-8-2046049

               Dr Michael Gray
               Head, Invertebrate Zoology
               The Australian Museum
               College Street
               Sydney  NSW 2000
               Australia
               Dr Malcolm Fisher
               Head, Intensive Care Unit
               The Royal North Shore Hospital of Sydney
               Pacific Highway
               St Leonards NSW 2065
               Australia

     Date:     July 1989

     Reviewer: Reviewed by Working Group on Natural Toxins November 1991

    See Also:
       Toxicological Abbreviations