Pseudonaja affinis

   1.1 Scientific Name
   1.2 Family
   1.3 Common Names
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
   2.5 Venom apparatus, poisonous parts or organs
   2.6 Main toxins
   3.1 Description of the animal
      3.1.1 Special identification features
      3.1.2 Habitat
      3.1.3 Distribution
   3.2 Poisonous/Venomous Parts
   3.3 The toxin(s)
      3.3.1 Name: Pseudonaja venom; Brown snake venom; BSV
      3.3.2 Description
      3.3.3 Other physico-chemical characteristics
   3.4 Other chemicals in the animal
   4.1 Uses
   4.2 High risk circumstances
   4.3 High risk geographical areas
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
      5.5.1 Bites
      5.5.2 Stings
   5.6 Others
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data Adults Children
      7.2.2 Animal data
      7.2.3 Relevant in vitro data
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analysis
      8.1.2 Storage oflaboratory samples and specimens Toxicological analyses Biomedical analyses
      8.1.3 Transport of laboratory specimens Toxicological analyses
   8.2 Toxicological analyses and their interpretation:
      8.2.1 Tests on toxic ingredient(s) of material Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s)
      8.2.2 Tests for biological specimens Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s) Other dedicated method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their Interpretation:
      8.3.1 Biomedical analyses Blood, plasma or serum Urine Other biomedical specimens
      8.3.2 Arterial blood gas analysis
      8.3.3 Haematological analyses
      8.3.4 Other (unspecified) analyses
      8.3.5 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Summary of most essential biomedical and toxicological analyses in acute poisoning and their interpretation
   9.1 Acute poisoning/envenomation
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin contact
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systemic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological CNS Peripheral nervous system Autonomic Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ear, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic Acid base disturbances Fluid and electrolyte disturbances Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Others
   10.1 General Principles
   10.2 Relevant laboratory analyses and other investigations
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological analysis.
      10.2.4 Other investigations. As indicated medically.
   10.3 Life supportive procedures and symptomatic treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion
   11.1 Case reports from literature
   11.2 Internally extracted case reports
   12.1 Availability of antidotes and antitoxins
   12.2 Specific preventative measures
   12.3 Other
   13.1 Clinical and Toxicological
   13.2 Zoological
    1.   NAME

     1.1  Scientific Name

          (Cogger 1975, 1987; Cogger et al 1983; Mengden & Fitzgerald 1987)
          Pseudonaja affinis

     1.2  Family


          Genus:     Pseudonaja Gunther

     1.3  Common Names

          Scientific name                 Common name

          Pseudonaja affinis affinis      Dugite
                     affinis tanneri      Dugite Tanner's brown snake
                     guttata              Speckled brown snake,
                                          downs tiger snake
                     inframacula          Peninsula brown snake
                     ingrami              Ingrams brown snake
                     modesta              Five ringed snake,
                                          ringed brown snake
                     nuchalis             Gwardar western brown snake
                     textilis             Common brown snake,
                                          eastern brown snake
    2.   SUMMARY

     2.1  Main risks and target organs

          Brown snakes are probably the most common cause of significant 
          snakebites in Australia.  Without appropriate  antivenom 
          treatment, a significant number of cases may be fatal.  

          Main risks are: coagulopathy, acute renal failure, neurotoxic

          Target organs:  neuromuscular junction, coagulation system, 

     2.2  Summary of clinical effects

          Locally: The bite is usually painless, without significant local 
          erythema, bruising or oedema. Bite marks may be difficult to see, 
          and vary from a single puncture to multiple punctures or multiple 

          scratches. Local secondary infection is unusual. Venom may spread 
          to draining lymph nodes with consequent pain and/or tenderness 
          and/or swelling. 

          Systemic: Headache, nausea, vomiting, abdominal pain, impaired 
          conscious state, occasionally loss of consciousness and 
          convulsions. Coagulopathy, rarely with overt bleeding 
          manifestations. Progressive neurotoxic paralysis can occur but is 
          unusual. Acute renal failure. 

     2.3  Diagnosis

          Monitor coagulation to establish the presence and extent of 
          coagulopathy, and as an index of systemic envenomation. This 
          should be performed at presentation, on development of  symptoms 
          or signs of systemic envenomation, regularly thereafter, and 1-2 
          hours after antivenom therapy until sufficient antivenom has been 
          given to reverse coagulopathy. 

          In the absence of a haematology laboratory, whole blood clotting 
          time in a  glass test tube is useful.  If a laboratory is 
          available, prothrombin ratio, activated partial  thromboplastin 
          time,  thrombin clotting  time, fibrinogen level, and 
          fibrin(ogen) breakdown products are most useful. 

          Other useful tests are complete blood picture and platelet count, 
          serum electrolytes, creatinine, urea, serum enzymes, especially 
          creatine kinase, urine output and urine myoglobin, and venom 
          detection using CSL Venom Detection Kit. Best sample is swab from 
          bite site (sample swab stick in kit). If patient  has systemic 
          envenomation urine may also be useful sample. Blood is not a 
          reliable sample. 

     2.4  First-aid measures and management principles

          (a)   If the patient develops evidence of respiratory or cardiac 
                failure, use standard cardiopulmonary resuscitation 
                techniques to maintain life. 

          (b)   The patient should be encouraged to lie still, and 
                reassured to avoid panic. 

          (c)   A broad compression bandage should be applied over the 
                bitten area, at  about the same pressure as for a sprained 
                ankle. This bandage should then be extended distally, then 
                proximally, to cover as much of the bitten limb as 

          (d)   The bandaged limb should be firmly immobilised using a 

          (e)   The bite site wound should not be washed, cleaned, cut, 
                sucked, or treated with any substance. 

          (f)   Tourniquets should not be used.

          (g)   The patient should be transported to appropriate medical 

          (h)   Nil orally unless the patient will not reach medical care 
                for a prolonged period of time in which case only water 
                should be given by mouth. No food should be consumed. 
                Alcohol should not be used. 

          (i)   If the offending snake has been killed it should be brought 
                with the patient for identification. 

          (j)   Remove any rings, bangles etc from the bitten limb.

          Treatment principles

          (a)   Specific: If the patient has systemic envenomation, give 
                brown snake antivenom (CSL). 

          (b)   General: Support  of cardiac and respiratory functions; 
                treatment of shock; maintenance of adequate fluid load, 
                electrolyte balance, and renal output; tetanus prophylaxis; 
                treatment of local sepsis with antibiotics; treatment of 
                significant blood loss with blood transfusion. 

          (c)   Local:  Do not clean or touch local wound until appropriate 
                samples taken for venom detection. Thereafter ensure 
                antisepsis. Early surgical intervention is generally 
                contraindicated, and is only indicated theoretically in the 
                late stages, in the very rare event that significant local 
                necrosis has developed. Such cases have not been described 
                for brown snake bite. 

     2.5  Venom apparatus, poisonous parts or organs

          Venom is produced in paired modified salivary glands, 
          superficially situated beneath the scales, posterior to the eye, 
          and surrounded by muscles, the contraction of which compress the 
          glands, expelling venom anteriorly via venom ducts to the fangs. 
          The paired fangs, situated at the anterior part of the upper jaw, 
          on the maxillary bones. They have an enclosed groove for venom 
          transport, with an exit point near the fang tip. Average fang 
          length in adult brown snakes is 2.8 mm (2.0 - 4.0 mm), and 
          average distance between fangs is 9 mm. Average venom yield is 2-
          6 mg, maximum 167 mg (Pseudonaja textilis). Mean venom injected 
          at first bite (defensive strike) is 4.5 mg (0.03 to 9.10 mg),
          mean venom left on skin is 0.22 mg. 

     2.6  Main toxins

          Pseudonaja venom is a complex mixture of protein and non-protein 
          components, not all of which have been fully evaluated. 

          (a)   Neurotoxins: both presynaptic (eg textilotoxin) and 
                postsynaptic (Pseudonajatoxin a and b). 

          (b)   Procoagulants: principally prothrombin converters( factor 
                Xa analogues), converting prothrombin to thrombin 

          (c)   Nephrotoxins: Not conclusively demonstrated experimentally, 
                but strongly suspected on clinical evidence . 


     3.1  Description of the animal

          3.1.1 Special identification features

          The brown snakes are oviparous, diurnal or crepuscular, and in 
          warm weather may be nocturnal. Food varies with species, 
          subspecies and locality and principally comprises small lizards 
          and small mammals. They do not possess discrete temperature-
          sensing organs. 

          Brown snake dentition is proteroglyphous (maxilla), the paired 
          fangs being situated in the anterior portion of the upper jaw 
          ("front fanged"), on partly mobile maxillae allowing limited 
          elevation for strike (10-15). The fangs have venom transport 
          grooves, enclosed for most of their length. Average fang length 
          2.8 mm (2.0 - 4.0 mm), average distance between fangs 9 mm.
          Pupils are circular. The head is not distinctly triangular. 
          (Cogger 1975) 

                Seven species are currently recognised,  although some 
                taxonomists now believe some species actually comprise a 
                species complex, ie, P. nuchalis may comprise a complex of 
                5 species (Mengden & Fitzgerald 1987). 

                Genus Pseudonaja

                Characterised by a large degree of individual and 
                population variation. Nasal and preocular scales in 
                contact, suboculars absent. Body scales generally smooth; 
                17-21 rows of scales at mid-body; ventral scales 145 to 
                235; anal scale divided, subcaudal scales divided;  (Cogger 
                1975). The scalation posterior to the eye may assist in 
                differentiating Pseudonaja from similar brown coloured 
                snakes, eg, Pseudechis australis, Oxyuranus microlepidotus 
                (Figure ) (Mengden and Fitzgerald 1989). Virtually all 
                Pseudonaja have a distinctive pattern of paired orange 
                spots on each anterior ventral scale, forming a double row 
                ventrally, a feature not seen in other Australian elapid 
                snakes. However, it may not be distinct in P. affinis 
                tanneri & P. inframacula. 

                Pseudonaja affinis

                Scalation: as for genus; mid-body scales 19 rows, ventrals 

                190-230, subcaudals 50-70. 

                Length: 1.5m (up to 2m)
                Colour: grey, olive, or brown dorsally, head often paler 
                than rest of body, sometimes with darker speckling or 
                blotches particularly on the nape.  Some specimens have 
                black scales randomly distributed. 

                Pseudonaja affinis taneri

                Scalation: as above

                Length: 1m

                Colour: Darker (smaller) snake than P. affinis affinis as 
                above, it is usually very dark brown both dorsally and 

                Pseudonaja guttata

                Scalation: as for genus; mid-body scales 19-21 rows, 
                ventrals 190-220, subcaudals 45-70. 

                Length: 0.5m (max.  variously reported as 0.8m and 1.4m).

                Colour: Variable, some specimens uniform pale fawn to 
                orange dorsally, but with a speckled appearance on 
                movement, or with 12-18 broad dark brown to black cross-
                bands or blotches. 

                Pseudonaja inframacula

                Scalation: As for genus; mid-body scales 17 rows, ventrals 
                185-235, subcaudals 45-75. 
                Length: 1.7m
                Colour: Variable, from pale brown to almost black.  Usually 
                has scattered black scales giving patchy speckled 

                Pseudonaja ingrami

                Scalation: As for genus; mid-body scales 17 rows, ventrals 
                190-220, subcaudals 55-70. 
                Length: 1.2m (max 1.7m)
                Colour: Grey-brown to deep brown on dorsal head, and neck 
                black or speckled with dark grey. At least 5 colour morphs 
                noted.  Buccal cavity dark, distinguishing it from closest 
                relative, P. textilis, which has pink buccal cavity. 

                Pseudonaja modesta

                Scalation: As for genus; mid-body scales 17 rows, ventrals 
                145-175; subcaudals 35-55. 
                Length: 0.45m (max 0.6m)
                Colour: Pale grey brown to brown dorsally, with a dark 
                brown to black head, pale nuchal band, followed by a dark 

                nuchal band, and a further 4-7 narrow dorsal bands evenly 
                spaced along the body and tail.  Large specimens may 
                exhibit only very faint banding. 

                Pseudonaja nuchalis

                Scalation: As for genus; mid-body scales 17-19 rows, 
                ventrals 180-230, subcaudals 50-70. 
                Length: 1.5m
                Colour: Very variable, with at least 5 distinct colour 
                morphs probably representing distinct species.  (Mengden & 
                Fitzgerald 1987).  Mostly uniform colour for each specimen, 
                which may be light tan, or grey, orange, brown, dark brown, 
                russet, or almost black.  Some specimens have a black head 
                and nape, sometimes with paler speckling on body, others 
                may have a series of dark brown or black bands on the body 
                and tail, others may have a series of dark brown or black 
                bands on the body and tail, others may lack any dark 
                markings.  There may be randomly placed dark scales, or 
                vertebral blotches.  Some forms may have a pale head. 

                Pseudonaja textilis

                Scalation: As for genus; mid-body scales 17 rows, ventrals 
                185-235, subcaudals 45-75. 
                Length: 1.5m (max. over 2m)
                Colour: Variable, mostly uniform for each specimen, ranging 
                from light tan, or grey, orange, russett, brown, to almost 
                black. There may be darker speckling, banding, blotches, or 
                purely uniform dorsal colour. The head may be uniform with 
                the body, or paler or dark. Juveniles variable but usually 
                with black head dorsally, then a pale orange nuchal band, 
                followed by a black band. The body may be unbanded or with 
                numerous narrow black bands or speckles. 

          3.1.2 Habitat

                Brown snakes occupy a wide variety of habitats from arid 
                dessert, to scrubland, to moister areas. They are not 
                uncommon in association with man's activities, such as in 
                paddocks, around rubbish dumps and farm buildings, and 
                under elevated floors of country homesteads. Principally 
                diurnal, though active on warm nights. 

          3.1.3 Distribution

                Brown snakes are restricted to continental Australia and a 
                few adjacent islands but not Tasmania (Longmore 1986). P. 
                textilis is also reported from Papua New Guinea. (Cogger 
                1975). Distribution for each species based on museum 
                records are shown in Figures . 

     3.2  Poisonous/Venomous Parts

          Venom glands (paired) situated superficially in posterior part of 
          head, connected by ducts to forward placed (paired) fangs.  Fangs 

          small, may leave classic single or double puncture in man, or a 
          more complicated array of scratches and other punctures, the 
          latter by non-fang teeth (White 1987a,c).  Classic bite mark in 
          plaster is shown in Figure .  Actual cases illustrated in 
          Figures . 

     3.3  The toxin(s)

          3.3.1 Name: Pseudonaja venom; Brown snake venom; BSV


                Neurotoxins:Textilotoxin (= Textilon) 

                (Coulter et al 1979, Southcott and Coulter 1979, Coulter et 
                al 1983, SU et al 1983) Tyler et al 1987a) 

                Pseudonajatoxin a
                (Parnett et al 1980)

                Pseudonajatoxin b 

                (Tyler et al 1987b)

                Coagulants:Prothrombin converter (unnamed) from P. 

                (Coulter et al 1983, Masci et al 1987, White et al 1987).

          3.3.2 Description

                Whole venom production based on milking specimens, usually 
                in captivity.  (White 1987b, Fairley & Splatt, 1929). 

                                    Average    Maximum

                Pseudonaja textilis 2 mg       67mg

                Venom components


                Textilotoxin (=Textilon).  A presynaptic neurotoxin, 
                phopholipase A2 protein, with 5 subunits, 20% carbohydrate 
                content including sialic acid, MW approx. 74,000 D (or 
                88,000) LD50 0.001 mg/kg N (mouse) (an LD50 of 0.0006 mg/kg 
                IV mouse has been reported using dilution in BSA).  
                (Coulter et al 1979, Coulter et al 1983, SU et al 1983, 
                Tyler et al 1987). 

                Pseudonajatoxin a.  A postsynaptic neurotoxin, protein, 117 
                amino acids, 7 disulphide bridges, MW 12280), LD50 0.3 
                mg/kg i.p. (mouse), binds strongly (perhaps irreversibly) 
                to acetylcholine receptors.  (Barnett and Holden 1980). 

                Pseudonajatoxin b. A postsynaptic neurotoxin, protein, 71 
                amino acids, MW 7762 D, LD50 0.015 mg/kg i.p. (mouse), 
                binds to acetylcholine receptors on mammalian skeletal 
                muscle only weakly and reversibly, and may be similar to k-
                bungarotoxin which blocks neuronal acetylcholine receptors 
                on sympathetic ganglia (Tyler et al 1987b). 


                The prothrombin-converting activity of brown snake venoms 
                has been noted, and demonstrated for P. textilis, P. 
                nuchalis, P. affinis, and not found in P. modesta venom.  
                (Denson 1969, Chester and Crawford 1982, Marshall and 
                Hermann 1983, Sutherland et al 1981, White et al 1987).  
                The pro-coagulant is complete and independent of factor V. 
                From P. textilis it is a large glycoprotein, approx. MW 
                200,000, comprising approx. 40% of total venom protein, and 
                is lethal in rats at a dose of 0.023 mg/kg.  (Masci et al 

                In a recent report, thrombocytopenia in association with 
                brown snake bite has been documented, with a suggestion 
                that this may be due to a platelet aggregating factor in 
                brown snake venom, apparently discovered by the same group 
                of researchers, from the venom of P. nuchalis and P. 
                affinis.  (Morling et al 1989, Marshall and Hermann 1989).  
                However, there is some doubt about the validity and 
                clinical relevance of these conclusions (White 1990). 

          3.3.3 Other physico-chemical characteristics

                No further data.

     3.4  Other chemicals in the animal

          No data.


     4.1  Uses

          Venom is used both in antivenom production and for laboratory 
          research. The neurotoxins in particular may prove valuable in 
          neuromuscular transmission research, and the procoagulants in 
          further elucidating the mechanism of normal human coagulation. 

     4.2  High risk circumstances

          Children:  when playing in areas were brown snakes are common,
                     either through accidental encounter (ie stepping on 
                     snake) or while trying to emulate naturalists (ie 

                     trying to catch snake). 

          Adults:    when living in areas where brown snakes are common, 
                     and moving around barefoot and without due care, or 
                     while putting hands etc into non-reconnoitred 
                     potential snake retreats (ie hollow logs etc). 

          Farm workers:   when working in areas where brown snakes are 

          Reptile keepers and snake handlers: 

          if due care is not exercised in catching and handling
          snakes, including venom milking.

          Recreation seekers:

                camping or walking or playing sport in areas where brown
                snakes are common.

          Homes:     around homes in brown snake prone areas where water is 
                     seasonally scarce and free water is available in the 
                     garden or home. 

     4.3  High risk geographical areas

          Brown snakes are widely distributed in most habitats of mainland 
          Australia, but are absent form some southern islands and 
          Tasmania.  While no high risk geographic regions have been 
          identified, it is evident that brown snakes may readily enter 
          metropolitan fringes, and country towns, and are frequently found 
          around country rubbish dumps and under the floors of elevated 
          country homesteads, and around farm buildings. 


     5.1  Oral

          No data, but unlikely to be hazardous unless there are open 
          wounds in the gastrointestinal tract. 

     5.2  Inhalation


     5.3  Dermal

          There is no evidence that venom can be absorbed through intact 
          skin. Current first-aid advice is to leave venom on skin for 
          later venom identification. 

     5.4  Eye

          Unlikely, no cases reported.

     5.5  Parenteral

          5.5.1 Bites

                In human envenomation, venom is always inoculated by the 
                snake biting.  Owing to the size of the fangs, venom is 
                most likely to be inoculated cutaneously or subcutaneously. 

          5.5.2 Stings

                Not possible.

     5.6  Others

          Experimentally, venom may be administered to test animals via
          subcutaneous, intramuscular, intravenous, intraperitoneal, and
          intraventricular (CNS) routes.

    6.   KINETICS

     6.1  Absorption by route of exposure

          The rate and amount of absorption will depend on the quantity of 
          venom injected, the depth of injection, site of injection 
          including vascularity, the activity of the victim, and the type, 
          efficiency of application and length of application of first aid. 

          Clinical evidence from human cases of envenomation suggests that 
          much initial venom movement is via the lymphatic pathways. This 
          is supported by work in monkeys. (Barnes & Trueta, 1941; 
          Sutherland et al 1975; Sutherland & Coulter, 1977; Sutherland et 
          al 1981a) 

          Direct intravenous injection, unrecorded in man, obviously allows 
          rapid systemic circulation of venom and may result in different 
          effects from normal routes of inoculation, particularly in regard 
          to coagulation. 

     6.2  Distribution by route of exposure

          It appears that much venom is transported from the bite site via 
          the lymphatic system, then concentrating in draining lymph nodes, 
          before ultimately reaching the systemic circulation.  However, 
          experience with numerous human cases of brown snake envenomation 
          shows that symptoms and signs of envenomation may occur within 
          15-30 minutes of the bite, especially in children.  Such early 
          effects (eg headache, nausea, abdominal pain, collapse) may be 
          due to either rapidly systemically circulating venom toxins, or 
          systemically circulating autocoids released at the bite site by 
          the action of venom on local tissue. 

          Once in the systemic circulation, venom rapidly reaches high 
          concentrations in the kidneys and excreted in the urine.  Such 
          venom must also exit the circulation, to enter the extravascular 
          space where it binds within the neuromuscular junction 

          (presynaptically and/or postsynaptically) and possibly other 
          nerve junction sites (eg autonomic system, perhaps causing 
          abdominal pain). 

          The kinetics of venom distribution, excretion, and detoxification 
          are incompletely understood. Neurotoxic paralysis usually takes 
          at least 2-4 hours to become clinically detectable. Coagulopathy 
          however may become well established within 30 minues of a bite. 

     6.3  Biological half-life by route of exposure

          No data

     6.4  Metabolism

          Little information is available on the metabolism of venom 
          components in man, but most components are fully active in whole 
          venom, requiring no further modification for activity. Venom 
          reaches high concentrations in the kidneys and excreted in urine. 
          (Sutherland & Coulter, 1977 a,b). The fate of specific venom 
          components, particularly neurotoxins and procoagulants, is 
          unclear. It seems likely that these components are progressively 
          detoxified in situ. 

     6.5  Elimination by route of exposure

          Most venom is eliminated via the kidneys in the urine.


     7.1  Mode of action

          Neurotoxic paralysis

          Whole P. textilis venom contains a variable mixture of 
          presynaptic and postsynaptic neurotoxins. The composition of this 
          mixture is apparently not uniform across all populations of brown 
          snakes, and clinically neurotoxic paralysis is not commonly seen 
          with brown snake bite. Neurotoxins have not been described from 
          other species of Pseudonaja, but since research is scant this 
          does not preclude their existence. 

          The following is largely based on work with presynaptic 
          neurotoxins of some other Australian elapid venoms rather than 
          specific work with brown snake venom.The presynaptic neurotoxins 
          (eg  Textilotoxin) appear to bind directly to the cell membrane 
          of the terminal axon, at the neuromuscular junction. After a 
          latent period of approximately 60-80 minutes, the neuromuscular 
          block becomes detectable (in isolated nerve-hemidiaphragm 
          preparations of mouse), and is rapidly established as essentially 
          complete paralysis. This is associated with a reduction in 
          cholinergic synaptic vesicle number, fusion of vesicles, and 
          damage of intracellular organelles such as mitochondria. There is 
          an increase in the level of free calcium in the nerve terminal. 

          Thus the neurotransmitter acetylcholine appears to be 
          progressively removed or made unavailable for release, causing 
          paralysis. (Dowdall et al 1977; Eaker 1978; Cull-Candy et al 
          1976; Datyner & Gage 1973). 

          The postsynaptic neurotoxins cause blockade of the acetylcholine 
          receptor on the muscle end-plate at the neuromuscular junction.  
          As this action is extracellular these toxins are more readily  
          reached by antivenom. 

          A newly described group of neurotoxins, the kappa-bungarotoxins, 
          appear to block the acetylcholine receptor on sympathetic 
          ganglia, and not on the muscle end-plate, and a postsynaptic 
          neurotoxin from brown snake venom may have a similar action 
          (Tyler et tal 1987b). 

          Procoagulants and coagulopathy

          Procoagulants with similar characteristics have been described 
          from P. textilis, P. affinis, and P. nuchalis venom, and may also 
          be present in the venom of P. inframacula, P. ingrami and P. 
          guttata, but probably are not present in P. modesta venom. (White 
          et al 1987). They are proteins, but have not been fully 
          characterized. They cause conversion of prothrombin, through 
          intermediates, to thrombin.  This product then converts 
          fibrinogen to  fibrin clots in vitro. 

          In human envenomation there is widespread consumption of 
          fibrinogen resulting in defibrination and hypocoagulable blood. 
          Any injury to blood vessels then causes increased bleeding, 
          although spontaneous bleeding is not usually seen. Usually 
          platelets are not consumed, but factors V, VIII, Protein C and 
          plasminogen all show acute reductions in human envenomation 
          (White 1983c; White 1987c; White unpublished data). 

          While major clots are not seen in man, some fibrin cross linkage 
          and stabilisation does occur in vivo, as cross-linked fibrin 
          breakdown products (D-dimer) levels rise sharply in human 
          envenomation (White unpublished data). 

          In animal experiments IV bolus doses of venom cause intravascular 
          clotting, which may include intracardiac thrombosis, with lethal 
          effect. Thrombosis of the portal vein was also frequently 
          observed in these studies. Cerebral vascular thrombosis was not 
          noted (Kellaway 1929). 


          Some presynaptic neurotoxins in other snake venoms are also 
          directly myolytic (eg notexin) and cause major destruction of 
          skeletal muscle, locally and systemically, both in experimental 
          animals and occasionally in human envenomation. However, this has 
          not been described for Textilotoxin, and experimental evidence 
          and clinical experience suggests that Pseudonaja venom does not 
          cause rhabdomyolysis (P. textilis), or only to a minor clinically 
          insignificant extent (P. nuchalis, P. affinis; in monkeys only, 

          not shown in man) (Sutherland et al 1981b). 

          Renal damage

          No specific nephrotoxins have been detected in brown snake venom, 
          but several cases of renal function  impairment have been 
          reported in humans envenomed by P. textilis, P. affinis and P. 
          nuchalis. Possible causes include breakdown products of fibrin 
          released secondary to the coagulopathy, and vascular impairment 
          in  the early stages, eg secondary to "shock". There may also be 
          a direct nephrotoxin in the venom (Acott 1988). Acute tubular 
          necrosis appears to be the main renal pathology. 

     7.2  Toxicity

          7.2.1  Human data


                     The human lethal dose for brown snake venom is 
                     unknown. Without antivenom treatment, a few brown 
                     snake bites may be fatal (Fairley 1929a), but even in 
                     the early part of the 20th century, when neither 
                     antivenom nor ICU facilities were available, only 8.6% 
                     of reported brown snake bites were fatal. Despite 
                     this, brown snakes are still thought to be the most 
                     common cause of fatal snakebite in Australia. (Hilton 


                     No data available, but clearly the smaller body mass 
                     of a child compared to available venom ensures that 
                     children are more likely  to receive  a lethal dose 
                     than adults. 

          7.2.2 Animal data

                LD50 subcutaneous injection of dried venom in mice (Broad 
                et al 1979. 

                    Pseudonaja textilis 0.053 
                    Pseudonaja nuchalis 0.473 
                    Pseudonaja affinis  0.660 

          7.2.3 Relevant in vitro data

                No data available

     7.3  Carcinogenicity

          No data.

     7.4  Teratogenicity

          No data.

     7.5  Mutagenicity

          No data.

     7.6  Interactions

          No data of clinical significance.


     8.1  Material sampling plan

          8.1.1 Sampling and specimen collection

       Toxicological analyses

                     For venom detection swab from bite site moistened in 
                     sterile saline. If systemic envenomation also collect 
                     urine (5ml in sterile container). 

                     For venom analysis (research only using 
                     radioimmunoassay): 5ml blood; 5ml urine, frozen. 

                     At autopsy collect vitreous humor, lymph nodes 
                     draining bite area, excised bite site. 

                     (For other laboratory tests see 10.2.1)

       Biomedical 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). 

       Arterial blood gas analysis

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

       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 until 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). 

       Other (unspecified) analysis

                     No data

          8.1.2 Storage oflaboratory samples and specimens

       Toxicological analyses

                For samples for standard venom detection:

                Short term (less than 24 hrs) ordinary fridge is acceptable 
                (4C), in sterile container. 

                Long term, store frozen (-20C or lower).

                For samples for venom analysis (research) store frozen 
                (-200C or lower). 

       Biomedical analyses

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

          8.1.3 Transport of laboratory specimens

       Toxicological analyses

                Use insulated container.

     8.2  Toxicological analyses and their interpretation:

          8.2.1 Tests on toxic ingredient(s) of material

       Simple qualitative test(s)

                     Simple qualitative test for presence of snake venom 
                     and designation of species/genus  group, corresponding 
                     to the most appropriate monovalent anti-venom.  This 
                     test is a commercial test sold by antivenom 
                     manufacturer as a kit (Snake Venom Detection Kit; CSL 
                     Melbourne) (Coulter et al 1980; Chandler & Hurrell 
                     1982; Hurrell & Chandler 1982). 

                (1)  Principle of test

                The kit uses an enzyme linked immunosorbent assay technique 
                with specific antibodies raised to each of the five main 
                venom types in Australia.  If venom is present in the test 
                sample it will cause a colour change in the relevant well 
                of the kit, indicating the presence of venom for that 


                (2)  Sampling

                See section 8.1.  The best samples are a swab from the bite 
                site (swab stick etc. included in kit), or urine (only if 
                patient has systemic envenomation).  Blood has not proved a 
                reliable sample (White 1987d). 

                (3)  Chemicals and Reagents

                All reagents needed for the test are included in the kit.  
                The kit should be kept at 4C (standard fridge) and has a 
                shelf life of 6 months.  A control is built into the kit.  
                If this fails the test results are invalid. 

          (4)   Equipment

                Virtually all equipment required for the test is provided 
                in the kit. The only item not provided is a timer, but an 
                ordinary watch is sufficient, each step taking 
                approximately 10 minutes.  An empty specimen container in 
                which to discard waste fluid at each step is a useful 

          (5)   Specimen preparation

                Not applicable.

          (6)   Procedure

                Refer to instructions in kit.

          (7)   Calibration procedure

                Not applicable.

          (8)   Quality control

                Included in kit.

          (9)   Specificity

                Where testing for snake venom using a bite site swab or 
                urine no interference with a result is expected. If snake 
                venom is present it will react with specific antibody in 
                one of the wells, resulting finally in a colour change in 
                that well. After a further delay all wells will then change 
                colour. It is therefore important to carefully watch the 
                wells in the last stage and note which tube changes colour 
                first. A few snakes may cause simultaneous colour change in 
                two wells initially. Yellow faced whip snakes may cause 
                positive venom detection in either wells indicating brown 
                snake venom or tiger snake venom (Williams and White, 1990) 

          (10)  Detection limit

                The manufacturer states the kit will detect as low as 10ng 
                venom per ml. 

          (11)  Analytical assessment

                Not applicable.

          (12)  Medical interpretation

                If the test is positive, it will indicate the presence of 
                snake venom and the species/genus of snake and therefore 
                the appropriate monovalent antivenom to neutralize the 
                effects of that venom. 

                If the test sample was a bite site swab, a positive result 
                does not indicate either the presence of systemic 
                envenomation, or the need to administer antivenom.  Other 
                clinical criteria are required in this situation (see 
                sections 9 and 10). 

                If the test sample was urine a positive result indicates 
                present or past systemic envenomation and together with 
                other clinical and laboratory criteria may be used to 
                determine the need for antivenom therapy. 

         Advanced qualitative confirmation test(s)

                     As for

       Simple quantitative method(s)

                     Not applicable.

       Advanced quantitative method(s)

                     A radioimmune assay has been developed by staff at the 
                     Commonwealth Serum Laboratories, Melbourne to detect 
                     small quantities of many Australian snake venoms. It 
                     is primarily a research tool, being too time consuming 
                     to be practical in determining emergency treatment of 
                     snakebite victims. It has proved useful in 
                     demonstrating snake venom either at autopsy or after 
                     patient recovery. 

          8.2.2 Tests for biological specimens

       Simple qualitative test(s)


       Advanced qualitative confirmation test(s)


       Simple quantitative method(s)

                     Not applicable.

       Advanced quantitative method(s)


       Other dedicated method(s)

                     No data.

          8.2.3 Interpretation of toxicological analyses

                For venom detection as for subsection (12):
                If the test is positive, it will indicate the presence of 
                snake venom and the species/genus of snake and therefore 
                the appropriate monovalent antivenom to neutralize the 
                effects of that venom. 

                If the test sample was a bite site swab, a positive result 
                does not indicate either the presence of systemic 
                envenomation, or the need to administer antivenom.  Other 
                clinical criteria are required in this situation (see 
                sections 9 and 10). 
                If the test sample was urine a positive result indicates 
                present or past systemic envenomation and together with 
                other clinical and laboratory criteria may be used to 
                determine the need for antivenom therapy. 
                For venom analysis refer to the laboratory performing the 

     8.3  Biomedical investigations and their Interpretation:
          8.3.1 Biomedical analyses

       Blood, plasma or serum

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

                     Urea, creatinine: Look for evidence of renal function

                     CK: If high may indicate rhabdomyolysis, usually 
                     greater than 1000 u/l. 


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

                     Myoglobin: If present indicates rhabdomyolysis, and 

                     may be missed as the red colouration of urine may be 
                     mistaken for haematuria (both may be positive on dip 
                     stick testing). 

                     Electrolytes if indicated (eg. inappropriate ADH 

       Other biomedical specimens

                     No data

          8.3.2 Arterial blood gas analysis

                Impaired respiratory function is usually secondary to 
                neurotoxic paralysis; 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 coagulopathy and if no clot after 15 mins then 
                significant coagulopathy present. If no clot after 30 mins 
                then full defibrination is likely. 

                Coagulation studies: 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. 
                The principal defect likely is a defibrination-type 
                coagulopathy which will render the blood unclottable. This 
                will usually result in the following key results: 

                Prothrombin ratio /INR >12 (normal about 0.8-1.2).
                APTT >150 secs (normal <38 secs).
                Thrombin clotting time (TCT) > 150 secs 
                 (normal <16 secs).
                Fibrinogen <0.1 g/l (normal 1.5-4.0 g/l).
                Fibrin(ogen) degradation products grossly elevated 
                (including D-Dimer). 
                Platelet count normal.

                If the patient exhibits the above picture in the context of 
                a snakebite then they have a defibrination-type 

                This will require specific antivenom therapy (see section 
                10) and repeated tests of coagulation status to define 
                progress of the coagulopathy and titrate antivenom therapy 
                against resolution. The earliest sign of resolution will be 
                a rise in fibrinogen level and this may first be seen as a 
                reduction in the TCT from > 150 secs, often to 80 secs or 
                less. This may occur before there is a detectable rise in 
                fibrinogen titre. It indicates that the pathologic process 
                of venom induced defibrination has ceased implying that all 
                circulating venom has been neutralized, at which point 
                further antivenom therapy can be withheld until the trend 

                of improving results is confirmed, in which case no further 
                antivenom therapy for the coagulopathy is indicated (unless 
                there is a subsequent relapse). 

                In the patient seen late or treated initially elsewhere 
                there may be no abnormal clotting time, with an INR < 2.0, 
                but fibrinogen may be low associated with raised 
                degradation products. In this case the results may indicate 
                a minor or resolved coagulopathy not requiring antivenom 
                Note that the platelet count (complete blood picture) will 
                usually be normal despite the intense defibrination. 
                In a few cases the platelet count may start to fall as or 
                after resolution of the defibrination occurs. This is 
                usually associated with renal damage and renal function 
                should be assessed. In this setting the thrombocytopenia 
                may well be secondary to the renal damage. 

          8.3.4 Other (unspecified) analyses

          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 paralysis, myolysis, 
                coagulopathy and renal damage. 

     8.4  Other biomedical (diagnostic) investigations and their

          While other investigations are not usually required to make the 
          primary diagnosis of snakebite envenomation, they may be 
          indicated in response to secondary effects of envenomation. If 
          there is either renal failure or severe rhabdomyolysis (unlikely 
          with brown snake envenoming) there may be a hyperkalaemia, hence 
          an ECG may be appropriate. If the patient is unconscious, 
          especially in the presence of a severe coagulopathy, then a CT 
          head scan may be appropriate to determine if there is 
          intracranial pathology such as a haemorrhage. 

     8.5  Summary of most essential biomedical and toxicological analyses
          in acute poisoning and their interpretation 

          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. 

          A patient with positive venom detection from either the bite site 
          or urine and a significant coagulopathy clearly is envenomed and 
          will usually require antivenom therapy. 

          A patient with positive venom detection from the bite site only 
          and with no clinical symptoms or signs of envenoming and all 
          other tests negative is not significantly envenomed at that point 

          in time and does not require antivenom therapy. However this 
          situation may change and so careful observation and repeat 
          testing would be indicated. 

          A patient presenting some hours after the bite with positive 
          venom detection from the urine but clinically well and with all 
          other tests either normal or showing a resolved coagulopathy, 
          probably had a minor degree of envenomation, now resolved and 
          will usually not require antivenom therapy. However they should 
          be observed carefully for evidence of relapse. 


     9.1  Acute poisoning/envenomation

          9.1.1 Ingestion

                No data.

          9.1.2 Inhalation

                No data.

          9.1.3 Skin exposure

                Venom not absorbed through intact skin.

          9.1.4 Eye contact

                No data.

          9.1.5 Parenteral exposure

                In practical terms, the only likely route of entry, is by 
                s.c. or i.d. injection. 

                Early symptoms, usually in the first six hours.

                Local: The wound is often painless, without local erythema, 
                oedema, or ecchymosis; persistent bleeding from wound, 
                variable; pain or swelling of draining  lymph nodes (may 
                take 1-4 hours to develop). 

                Systemic: collapse, unconsciousness, convulsions may all 
                occur, especially in children, occasionally as rapidly as 
                15 minutes after the bite. Headache, nausea, vomiting, 
                abdominal pain, and visual disturbance may all occur. Early 
                signs of neurotoxic paralysis such as ptosis, diplopia, 
                dysarthria may develop within 1-3 hours of the bite, or be 
                delayed for 4-12 hours, or may not develop despite other 
                evidence of severe envenomation. 

                Coagulopathy may develop within 30 minutes of the bite.

                Delayed symptoms

                Local: Local bite site necrosis is not generally seen with 
                brown snake bites but possibly might occur, particularly if 
                first aid left in place more than 4 hours, or if a 
                tourniquet  used (Sutherland 1981, 1983a; White 1987d). 


                Paralysis         progressive up to complete paralysis.
                Coagulopathy      bleeding from all puncture wounds.
                Renal impairment  oliguria or anuria.

          9.1.6 Other

                No data.

     9.2  Chronic poisoning

          9.2.1 Ingestion

                No data.

          9.2.2 Inhalation

                No data.

          9.2.3 Skin contact

                No data.

          9.2.4 Eye contact

                No data.

          9.2.5 Parenteral exposure

                No data.

          9.2.6 Other

                No data

     9.3  Course, prognosis, cause of death


          Initially the patient is usually anxious. The subsequent course 
          will depend on (a) amount of venom injected, (b) size of patient 
          relative to venom load (ie children may be worse affected), (c) 
          degree of activity of patient after bite (physical activity 
          hastens venom absorption), (d) timing, type, effectiveness of 
          first aid, (e) speed and nature of specific medical treatment 
          given, if systemic envenomation ensues, (f) pre-existing health 
          factors for each patient (ie past renal problems, allergic 
          problems etc). 

          Minor envenoming: little or no venom injection, no development of 

          system envenomation, no need for antivenom treatment, no likely 
          sequelae or complications. 

          Moderate envenoming: bite may be painless or slightly painful, 
          with no or minor local reactions, subsequent development over 
          next few hours of some or all of the following: headache, nausea, 
          vomiting, abdominal pain, collapse, convulsions (especially in 
          children), occasionally early signs of paralysis, such as ptosis, 
          diplopia, and commonly laboratory evidence of coagulopathy.  
          Antivenom treatment at this stage will usually arrest or reverse 
          the various manifestations of systemic envenomation.  Without 
          antivenom treatment, in most such cases the symptoms and signs 
          will show progressive worsening, with deepening coagulopathy and 
          an increased chance of secondary haemorrhage (beware intracranial 
          haemorrhage), in a few cases progressive paralysis which may 
          ultimately progress to complete respiratory paralysis, about 18-
          24 hours post bite; secondary renal failure; secondary 
          complications of the above, particularly pneumonia; ultimate 
          outcome may be death, more than 24 hours post bite. 

          Severe envenoming: most likely if bite either multiple, or 
          associated with chewing bite and numerous teeth marks.  Local 
          reactions still may be minimal. Rapid development of headache, 
          collapse, convulsions (especially children), sometimes within 30 
          minutes of bite. Subsequent symptoms may include headache, 
          nausea, vomiting, abdominal pain, and evidence of coagulopathy, 
          possibly progressive paralysis, and renal impairment. 
          Coagulopathy may be detectable within 30 minutes of bite; ptosis 
          and diplopia may be evident within 2 hours of bite. Renal damage 
          may occur early. Prompt antivenom treatment required as soon as 
          nature of envenomation evident.  In some circumstances paralysis 
          may be sufficiently advanced at a cellular level that antivenom 
          cannot prevent severe paralysis.  In this situation, intubation 
          and assisted ventilation may be required for a variable period 
          (up to several weeks). The coagulopathy may only reverse 
          following large amounts of antivenom. Renal damage is usually 
          reversible, after a period of haemodialysis. 

          Without antivenom treatment such cases will almost certainly die.

          Special notes

          Children are more likely to develop severe envenomation than 
          adults, and do so more rapidly. 

          Bites to the trunk or face may cause earlier development of 

          Secondary infection of the local bite wound may occur.

          Physical activity after a snakebite increases the rate of 
          absorption of venom and so hastens the onset of envenomation.  
          This situation often occurs in bites to children. 

          Multiple bites nearly always are associated with potentially 
          lethal envenomation. 


          In the past up to 8.6% of all brown snake bites have proved fatal 
          when no antivenom treatment was used (this is based on statistics 
          pre-antivenom era, over 50 years ago: with the use of modern 
          intensive care facilities such figures may be over-pessimistic).  
          No data available on fatality rate with antivenom treatment, but 
          deaths do still occur, and it is thought that most snakebite 
          fatalities in Australia in recent years are due to brown snake 
          bites, at least in part reflecting the commonness of bites by 
          brown snakes compared to the incidence of bites by other species 
          of snakes. 

          Causes of death

          Coagulopathy           primary eg cerebral haemorrhage;
                                 secondary eg renal failure.

          Paralysis              primary eg respiratory failure;
                                 secondary eg pneumonia

          Renal Failure          includes secondary complications such as

          Anaphylaxis            acute allergic reaction to venom is 
                                 possible in a patient previously exposed 
                                 to brown snake venom (e.g. reptile keeper) 
                                 but there are no documented cases.

          Cardiac complications likely to be secondary, and role in brown
                                snake bite fatalities uncertain.

     9.4  Systemic description of clinical effects

          9.4.1 Cardiovascular

                Collapse, presumably due to hypotension, is common in the 
                early stages of systemic envenomation, especially in 
                children.  The mechanism is uncertain but may be due to 
                release of vasoactive substances by or from the venom. 

                Specific cardiac abnormalities due to brown snake 
                envenomation in man are not described, although there has 
                been a suspicion that brown snake venom may cause cardiac 
                anomalies (Sutherland personal communication). 

          9.4.2 Respiratory

                No primary effects of brown snake venom on the respiratory 
                system in man are reported, with the exception of 
                respiratory muscle paralysis (see below). 

          9.4.3 Neurological


                     While no direct CNS toxins have been reported for 
                     brown snake venom, early collapse and convulsions do 
                     occur, especially in children.  Their aetiology 
                     remains uncertain. 

       Peripheral nervous system



                     Abdominal pain.

       Skeletal and smooth muscle

                     The effects of brown snake venom at the neuromuscular 
                     junction, have been documented experimentally. Both 
                     presynaptic and postsynaptic neurotoxins present, 
                     causing progressive neuromuscular paralysis, up to 
                     complete paralysis of all muscles of respiration. 

          9.4.4 Gastrointestinal

                Nausea and vomiting may occur. In the presence of a venom-
                induced coagulopathy, haematemesis and even melaena may 
                occur, though they appear to be rare even in severe 
                envenomation. Abdominal pain is sometimes described. 

          9.4.5 Hepatic

                Direct hepatic effects of brown snake venom have not been 
                noted clinically, or experimentally. 

          9.4.6 Urinary


                     No direct nephrotoxin has been identified in brown 
                     snake venom, but renal failure has been reported in a 
                     number of cases, and is a very serious complication of 
                     envenomation, with a significant mortality, despite 
                     antivenom treatment.  The nature of the renal injury 
                     and its cause are poorly documented, but acute tubular 
                     necrosis seems most likely. Renal cortical necrosis 
                     has not been reported. 


                     No data.

          9.4.7 Endocrine and reproductive systems

                No data.

          9.4.8 Dermatological

                The local bite site is often painless or minimally painful 
                and swelling, and ecchymosis is not usually seen.  Teeth 
                marks are variable, from single fang puncture to multiple 
                tooth punctures and scratches. Local necrosis has not been 
                described.  Secondary infection may theoretically occur 
                (White 1983b). 

          9.4.9 Eye, ear, nose, throat: local effects

                No data.

          9.4.10  Haematological

                Probably the major clinical effect of brown snake 
                envenomation in man is coagulopathy caused by potent 
                procoagulants in the venom, which cause prothrombin 
                activation and secondary fibrinogen consumption.  The 
                resulting defibrination is associated with hypocoagulable 
                blood, and persistent bleeding from any vascular injury, 
                including venepuncture sites.  Without antivenom treatment, 
                this may occasionally resolve. 

                However, as the venom is not apparently vasculotoxic, in 
                the absence of vascular injury bleeding does not occur, 
                thus in many patients the coagulopathy proves relatively 

                An early neutrophil leukocytosis may occur in some 
                patients. Significant depletion of circulating lymphocytes 
                may occur in the early stages of envenomation, with 
                resultant lymphopenia (White et al 1989). 

          9.4.11  Immunological

                No data.

          9.4.12  Metabolic

       Acid base disturbances

                     No changes.

       Fluid and electrolyte disturbances

                     Secondary fluid and electrolyte disturbances due to 
                     renal failure if present. 
                     The possibility of inappropriate ADH (anti-diuretic 
                     hormone secretion) syndrome should be considered.  In 
                     this situation, otherwise acceptable intravenous fluid 
                     loads may result in significant electrolyte imbalance 
                     and other sequelae. 


                     Rise in serum levels of liver enzymes and CK (if 

                     rhabdomyolysis).  A rise in CK to below 1000 U/l is 
                     not indicative of rhabdomyolysis.  True venom-induced 
                     rhabdomyolysis causes CK levels well above 1000 U/l.  
                     This is not a usual feature of brown snake bites. 

          9.4.13 Allergic reactions

                May occur due to allergy to venom or antivenom, and 
                resultant anaphylaxis may prove fatal. 

                Reptile keepers previously bitten by brown snakes are also 
                at potential risk of acute anaphylactic allergic reactions 
                on subsequent bites, which might cause collapse within 
                minutes of the bite. Fatalities have occurred due to this 
                mechanism, with bites by other species, but are not 
                documented for brown snakebites.   (Sutherland 1983; White 
                1987 b,d). 

          9.4.14  Other clinical effects

                Rhabdomyolysis has not been noted clinically. 

          9.4.15  Special risks

                Pregnancy:           no data
                Breast feeding:      no data
                Enzyme deficiencies: no data

     9.5  Others

          No data


     10.1 General Principles

          All patients suspected of having sustained a brown snake bite 
          should be admitted to hospital for observation over the first 24 
          hours.  While all such cases should be treated as potentially 
          fatal not all cases will develop envenomation.  Management of 
          cases with systemic envenomation may be divided into specific, 
          symptomatic, and general treatment. 

          The aims of treatment are:

          (a)   Maintain life through maintenance of vital bodily 
          (b)   Neutralise inoculated venom.
          (c)   Correct venom-induced abnormalities.
          (d)   Prevent or correct secondary complications.

          Specific treatment

          If there is evidence of systemic envenomation, antivenom therapy 

          is the most important treatment.  Once the snake has been 
          identified (eg by venom detection) give specific antivenom (CSL 
          Brown Snake Antivenom). (White 1981; 1987d; Sutherland 1983; 
          Trinca 1963) 

          Symptomatic and general treatment

                Support of cardiorespiratory systems.
                Treatment of shock.
                Maintain adequate renal perfusion.
                Replace major blood loss due to coagulopathy induced 
                haemorrhage (but use blood products only with great caution 
                until coagulopathy resolved ). 
                Tetanus prophylaxis.
                Avoid intramuscular injection while there is a 
                Avoid respiratory depressant medications (eg morphine).
                Avoid antiplatelet medications (eg aspirin).
     10.2 Relevant laboratory analyses and other investigations

          10.2.1 Sample collection

                Venom for venom detection: use CSL Venom Detection Kit; 
                best sample is swab from bite site (swab stick etc in kit); 
                if systemic envenomation present then urine useful; 
                serum/plasma less reliable. If bandage applied over bite 
                site as first aid, keep bandage adjacent to wound, as this 
                may also have venom absorbed, and could be tested for venom 
                (after elution) if all other samples negative in presence 
                of significantly envenomed patient. 

                Blood:  Initially collect for complete blood count (EDTA 
                sample), clotting studies (citrated sample), electrolytes 
                and enzymes (heparin and/or clotted sample) and possibly, 
                group (type) and screen serum (clotted sample).  In 
                anticoagulated blood samples ensure correct ratio of blood 
                to anticoagulant (especially citrate samples) and proper 
                mixing.  If laboratory facilities unavailable, collect for 
                whole blood clotting time (ie 5-10 ml in glass test tube, 
                and measure time to clot).  Samples for clotting studies in 
                particular should be kept cold during transportation. 

                Urine:  Measure urine output, visual check for 
                haemoglobinuria or myoglobinuria (dark red-brown urine); if 
                suspect myoglobinuria collect samples at intervals for 
                subsequent laboratory confirmation (5-10 ml). 

          10.2.2  Biomedical analysis

                Venom detection:  Venom at the bite site confirms only the 
                species of snake, but venom in the urine indicates systemic 

                Coagulation studies:  In the absence of a haematology 
                laboratory, whole blood clotting time is a useful test, for 

                both the presence of a coagulopathy, and its progress and 
                resolution with adequate antivenom therapy. 
                If a laboratory is available, the most useful tests for 
                presence and extent of coagulopathy are: prothrombin 
                time/ratio; activated partial thromboplastin time; thrombin 
                clotting time; fibrinogen assay; fibrin(ogen) breakdown 
                products assay. 
                In addition, a complete blood count should always be 
                performed concurrently, particularly for a platelet count. 

                Other blood tests:

                     Electrolytes (eg Na, K etc);
                     Renal function (eg creatinine, urea);
                     Enzyme levels, especially CK;
                     Arterial blood gas, if appropriate (ie impaired 
                     respiratory function). 

                Urine:For haemoglobinuria and myoglobinuria

          10.2.3  Toxicological analysis.

                Venom detection, see section 8.

          10.2.4  Other investigations.  As indicated medically.

     10.3 Life supportive procedures and symptomatic treatment


          In severe cases of systemic envenomation by brown snakes, where 
          antivenom treatment has been delayed, paralysis may occur and 
          progress to complete or near complete respiratory paralysis.  In 
          this situation early intervention by endotracheal intubation and 
          artificial ventilation is lifesaving. Such respiratory support 
          may be needed for hours, days, or even weeks, until adequate 
          respiratory function returns. 

          Once established, such severe paralysis may not be reversed by 
          antivenom therapy. 


          The principal method of treatment of brown snake envenomation 
          coagulopathy is the neutralisation of all inoculated venom by 
          antivenom. Until this is achieved, use of clotting factor blood 
          products (eg fresh frozen plasma, cryoprecipitate, fibrinogen) 
          may only deepen the degree of coagulopathy, by providing more 
          substrate on which the venom may act. Once all venom is 
          neutralised normal homeostatic mechanisms quickly return 
          coagulation towards normal, without the need of replacement 
          therapy.  The possible exception would be where there is major 
          bleeding as a result of the coagulopathy (eg cerebrovascular 
          accident), when replacement therapy should be considered once 
          adequate antivenom has been given.   Heparin has no proven value 

          in this situation, and there is evidence it may be harmful. 

          In cases of severe envenomation a central venous pressure (CVP) 
          line may be highly desirable for patient management, but in the 
          presence of coagulopathy should be inserted with great caution, 
          due to the likelihood of significant haemorrhage from the 
          insertion site if insertion attempt is unsuccessful. 

          In such cases frequent testing of coagulation will be necessary 
          to titrate antivenom therapy.  A CVP line will allow frequent 
          sampling without further breaches of veins, an important 
          consideration in severe coagulopathy where venepuncture may 
          result in bleeding for hours.  For similar reasons, venepuncture 
          from major veins, such as the femoral, should be avoided, and 
          used only as a last resort. 

          Following resolution of the coagulopathy there may be rebound 
          hyperfibrinogenaemia at about 2-4 days post resolution.  There is 
          a theoretical potential for hypercoagulability at this time, 
          particularly in the immobile paralysed ventilated patient, and 
          the possibility of thrombus formation and emboli, including 
          pulmonary emboli, should not be forgotten. 

          Renal failure

          First priority is to avoid renal injury by ensuring adequate 
          renal perfusion. In all cases of significant systemic 
          envenomation, catheterisation of the bladder to monitor urine 
          output constantly is advisable.  In severe cases of envenomation, 
          the use of a CVP line will assist in adjusting IV fluid load to 
          ensure adequate blood volume and renal perfusion. 

          Once renal injury is established, standard techniques of medical 
          management should apply.  Haemodialysis may be required.  Renal 
          biopsy should be avoided at least until the coagulopathy is 
          completely resolved. 

          Local bite site

          The bite site should be cleaned only after adequate sampling for 
          venom. Local infection may occur, but is rare, and thus 
          prophylactic antibiotic therapy is not appropriate.  Tetanus 
          prophylaxis should be ensured.  In the rare event of minor local 
          necrosis, this could usually be successfully treated 
          conservatively.  Local skin necrosis sufficient to warrant 
          debridement and grafting has not been reported. 



          May be necessary, though most cases will need no more than 
          paracetamol. Morphine should be avoided (CNS depressant effect). 
          Platelet-active drugs should be avoided (eg aspirin). 


          May be useful in treatment or prophylaxis of serum sickness, but 
          their role in the general treatment of brown snake bite is 

     10.4 Decontamination

          Not applicable.

     10.5 Elimination

          Not applicable.

     10.6 Antidote treatment

          10.6.1 Adults

          Brown snake antivenom (CSL, Melbourne) is the specific treatment 
          of brown snake bite.  It should only be used if there is definite 
          systemic envenomation.  (Trinca 1963; Sutherland 1974, 1983b; 
          White 1981, 1987d) 

          The antivenom is a refined horse serum (Fab2 fragments), with all 
          the potential hazards of that product. One ampoule contains 1000 
          units of activity against brown snake venom. This is sufficient 
          to neutralise the "average" amount of venom produced by a single 
          milking of one snake (Pseudonaja textilis). In a severe bite, and 
          multiple bites, several ampoules of antivenom may be necessary. 
          The average volume of antivenom (horse serum) per ampoule is 4.5
          ml, but the precise volume varies from batch to batch. 

          Brown snake antivenom must be given intravenously.

          Since skin testing is unreliable and hazardous, there is no place 
          for pre-therapy sensitivity testing of antivenom.  (Sutherland 
          1983b; White 1987d). 

          Acute allergic reactions up to and including potentially fatal 
          anaphylaxis may occur during antivenom therapy.  Precautions 
          should be taken to reduce the risk to the patient.  These 

          Only give antivenom if staff, drugs and equipment to treat severe 
          anaphylaxis, including intubation facilities are available 
          (preferably in an intensive care unit), unless in extreme 
          Always have adrenaline injection prepared and ready to use.
          Always have a good reliable IV line inserted.
          Always maintain adequate monitoring of patient during and after 
          antivenom therapy, especially blood pressure. 
          Dilute antivenom (1:5 to 1:10) in IV carrier solution (normal 
          saline; dextrose or Hartmann's). 
          Give antivenom initially very slowly, and increase rate if no 
          reaction, aiming to give whole dose over 15-20 minutes. 

          Premedication is proposed by some.  (Sutherland 1983b)  Suggested 
          premedications are subcutaneous adrenaline and intravenous 
          antihistamine.  The author of this monograph does not routinely 
          use such premedication.  (White 1987d)  Antihistamine may make 
          the patient drowsy or irritable, and thus interfere with the 
          ongoing assessment of envenomation, especially in children.  
          Adrenaline is potentially hazardous, especially in older patients 
          or those with coagulopathy, and as acute severe allergic 
          reactions may be delayed up to an hour or more, such 
          premedication is of doubtful value.  A patient with known or 
          likely allergy to horse serum presents a special case, where 
          premedication as above, possibly with the addition of steroids, 
          is worthy of active consideration. Similarly a sole country 
          medical practitioner managing a severe snakebite, where antivenom 
          must be given before an aeromedical evacuation team can arrive, 
          may well consider premedication with subcutaneous adrenaline a 
          worthwhile precaution. 

                In the presence of mild to moderate systemic envenomation 
                (ie no or minor paralysis, no active bleeding from 
                coagulopathy etc) initially give one ampoule of antivenom .  
                Follow up with further ampoule(s) if progression of 
                symptoms and signs, or if no resolution of coagulopathy.  
                Resolution of coagulopathy may be used to titrate antivenom 
                therapy.  (White 1983c; 1987 c,d) 

                In the presence of severe envenomation, initially give 2 
                ampoules of antivenom, and be prepared to give more, as 

                If using the resolution of coagulopathy to titrate 
                antivenom therapy, aim to retest coagulation (see section 
                10.2.1) about 1 to 1.5 hours after completion of antivenom 
                dose.  First evidence of impending resolution may be a 
                reduction in the thrombin clotting time, often accompanied 
                by a slight rise in fibrinogen level.  If there is no 
                significant improvement, give further antivenom.  If there 
                is significant improvement, repeat test in a further 1-2 
                hours and reassess. 

                There is no mandatory upper limit on antivenom dosage, but 
                only rarely will more than 4-5 ampoules be required. 

          10.6.2 Children

                The dosage of antivenom in children is identical to that in 
                adults. However, fluid volume considerations in small 
                children may force lower dilutions of antivenom.  For any 
                given bite the degree of envenomation will be worse in 
                children due to lower body mass. Following antivenom 
                therapy there is a possibility that the patient may develop 
                serum sickness.  This should be explained to the patient so 
                that if symptoms develop, they will seek appropriate 

                If large volumes of antivenom are used (eg 50-100 ml or 
                more) then prophylaxis for serum sickness should be 
                considered (eg oral steroid therapy for 2 weeks).  However, 
                most brown snake bites will be successfully treated with 
                between 1 and 4 ampoules of antivenom, less than 20 ml in 
                total volume. 

     10.7 Management discussion

          Controversies in management exist in several areas:

          First aid

          Tourniquet versus pressure/immobilisation:  the latter is now 
          well accepted as the method of choice.  (Balmain & McClelland 
          1982, Fisher 1982, Murrell 1981, Sutherland 1983b; Sutherland et 
          al 1981 a,b; White 1987d) 

          Suction of wound:  No proven value .

          Cutting or excising wound:  of no practical value and potentially 


          Use of premedication:  not universally accepted.  (Sutherland 
          1975, 1977a, 1977b, 1977c; 1983b; White 1987d) 

          Use of skin pretesting:  not appropriate.


          Use of fibrinogen, fresh frozen plasma etc as primary treatment:  
          No proven benefit and potentially very dangerous.   (White 1987d) 

          Use of heparin:  of no proven benefit and potentially dangerous.

          Non-antivenom treatment

          Based on the assumption that it is paralysis which kills the 
          patient and this can be managed adequately in an intensive care 
          unit by artificial ventilation, therefore antivenom is not 
          required, thus avoiding antivenom allergy problems.  This ignores 
          the danger of coagulopathy, best managed by antivenom therapy, 
          and the fact that early antivenom therapy may avoid severe 
          paralysis and the hazards of artificial ventilation. 


          There are many aspects of brown snake venom worthy of further 
          research, at a basic science level, as well as studies at a more 
          clinical level. 


     11.1 Case reports from literature

          Case 1:  (from Foxton 1914).  A fatal snakebite in a man, age 29 
          years, bitten on the left hand by a brown snake.  First aid was 
          scarification and local ligature.  By one hour he had headache, 
          by 3 hours nausea, vomiting (blood stained) and this continued 
          overnight.  He developed haemorrhage from the gums, and at 18 
          hours post-bite he collapsed, had convulsions, and was comatose.  
          He continued to have convulsions until his death, some 2 hours 
          later.  Autopsy showed mid-brain and brain stem haemorrhages, and 
          small haemorrhagic areas in the stomach, intestines, kidneys, and 
          bladder.  Death was attributed to the haemorrhages in the pons 
          and medulla and was clearly due to the coagulopathy. 

          Case 2:  (from Fairley 1929).  A fatal snakebite in a woman, age 
          29 years, bitten on the leg, through thick riding breeches, by a 
          brown snake which had been milked earlier the same day.  First 
          aid was scarification and ligature.  Initially well, she later 
          developed vomiting, severe abdominal pain, then signs of shock 
          with pallor, sweating, tachycardia and hypotension. She passed 
          bright blood per rectum.  She also developed some paralysis, with 
          dysarthria, but died of "cardiovascular failure" 12 hours post-
          bite.  No autopsy.  The cause of death may well have been due to 
          shock following blood loss associated with the coagulopathy.  
          Fairley comments that significant bleeding problems are common 
          after brown snake bite. 

          Case 3:  (from Schapel et al 1971).  A non-fatal case.  A 19 
          year-old man was bitten on the left wrist by a captive brown 
          snake.  At 15 minutes post-bite he was given a test dose of brown 
          snake antivenom I.V. (with adrenaline, antihistamine pre-
          medication), which resulted in anaphylaxis, successfully treated 
          with adrenaline and steroids.  He had received antivenom on 2 
          previous occasions.  Three hours post-bite he developed extensive 
          generalized submucosal and subcutaneous bruising, oozing of blood 
          from skin puncture wounds, and haematemesis (500 ml). 
          Investigations showed a marked coagulopathy, and 
          thrombocytopenia. Further antivenom was clearly indicated and 
          given under cover of adrenaline and steroids, and in addition he 
          was heparinized.  However, by 12 hours post-bite "bleeding was 
          controlled", although some evidence of coagulopathy was 
          apparently present for several days.  There was a short-lived 
          rise in blood urea level, but urine output remained adequate. 
          There was no evidence of paralysis at any stage.  An eventual 
          complete recovery was made. 

          Hermann et al 1972:  Detailed report of three cases of brown 
          snake bite from Western Australia, with emphasis on haematologic 

          Case 4:  Non-fatal bite to the hand of a 50 year-old man by P. 
          affinis.  At 15 minutes post-bite he developed a severe frontal 
          headache.  He was noted to have persistent oozing from the bite 
          site at two hours, and was given brown snake antivenom, and 
          subsequently made a full recovery. Platelet count remained 

          normal, despite a defibrination type coagulopathy, present for at 
          least 24 hours. 

          Case 5:  Non-fatal bite to the leg of a 35 year-old woman by a 
          presumed P. affinis.  At 30 minutes post-bite she developed 
          severe headache, nausea, visual difficulty, and "weakness", but 
          was not seen medically until 18 hours post-bite.  Antivenom was 
          not given.  Investigations showed a normal platelet count and 
          mild defibrination type coagulopathy. 

          Case 6: Non-fatal bite to the hand of a 45 year-old man by a P. 
          nuchalis. At 20 minutes post-bite he developed severe headache, 
          nausea, and vomiting.  He was given polyvalent antivenom and 
          subsequently recovered. Investigations showed a normal platelet 
          count and a marked defibrination type coagulopathy. 

          The following discussion relates mostly to the therapy of the 
          coagulopathy, with the conclusion that antivenom is the most 
          effective treatment. Neurotoxicity was not noted in these cases. 

          Sutherland et al 1975:  Three cases of snakebite where RIA venom 
          detection was used to prove the diagnosis.  Two were due to brown 

          Case 7:  Non-fatal bite to the leg of a 42 year-old woman by P. 
          textilis. The patient did not believe she had been bitten.  At 20 
          minutes post-bite she developed headache, then collapsed, 
          possibly had a convulsion or cardiac arrest, and was given brown 
          snake antivenom at 30 minutes post-bite.  She promptly improved 
          clinically.  She also developed persistent oozing of blood from 
          the bite site, and at 5 hours post-bite her blood was unclottable 
          (after three ampoules of antivenom).  Fibrinogen was given but 
          the blood remained unclottable for at least several hours.  She 
          subsequently made a full recovery.  Blood taken prior to the 
          first dose of antivenom showed 20 ng/ml of brown snake venom. 

          Case 8:  Non-fatal bite to the ankle of a 66 year-old woman by P. 
          textilis.  She subsequently felt dizzy but this resolved, and no 
          further symptoms developed.  She did not receive antivenom.  A 
          level of 35 ng/ml of brown snake venom was detected in her serum.  
          No comment on tests for coagulopathy is made. 

          Harris et al 1976:  Three cases of brown snake bite with renal 
          failure, from Western Australia. 

          Case 9:  Non-fatal bite to the leg of a 35 year-old man by a 
          presumed P. nuchalis.  Not treated with antivenom and early 
          history not noted.  By 24 hours he developed abdominal pain, 
          vomiting, and oliguria.  Investigation demonstrated acute renal 
          failure (requiring haemodialysis) and an associated micro-
          angiopathic haemolytic anaemia with thrombocytopenia. He 
          subsequently recovered completely, though he was oliguric for 13 


          Case 10:  Non-fatal bite to the leg of a 60 year-old man by a 
          presumed P. affinis.  At one hour post-bite he received brown and 
          tiger snake antivenoms.  At 7 hours he became confused, commenced 
          vomiting, and was oliguric.  This was managed conservatively for 
          five days, then he was transferred to a major hospital.  
          Investigations then showed acute renal failure and a micro-
          angiopathic haemolytic anaemia with thrombocytopenia. There was 
          no evidence at this time of defibrination.  He required 
          haemodialysis and was oliguric for 19 days, but made an almost 
          complete recovery (mild elevation of blood urea at 12 months). 

          Case 11:  Non-fatal bite to the leg of a 53 year-old woman by a 
          presumed P. nuchalis.  Initially she was hypertensive and 
          vomiting, but antivenom was not given.  By the next day she was 
          oliguric, and also developed bleeding problems (epistaxes; per 
          vagina; multiple ecchymoses), and drowsiness. Investigations at 
          four days post-bite showed acute renal failure, a micro-
          angiopathic haemolytic anaemia, and thrombocytopenia.  There was 
          no evidence of defibrination.  She required haemodialysis, and 
          was oliguric for 21 days.  She subsequently made a full recovery. 

          These three cases show a consistent picture of reversible acute 
          renal failure associated haemolysis, but details of the early 
          findings are scant and thus possible association with an early 
          coagulopathy is not apparent. 

          Case 12:  (from Crawford, 1980).  A non-fatal bite to the foot of 
          a 57 year-old man by a juvenile P. nuchalis.  Details of 
          symptomatology are scant, but no neurotoxicity was seen, and 
          bleeding problems were evident, with haemorrhage from 
          venepuncture sites.  A defibrination type coagulopathy was 
          demonstrated, with normal platelet count.  A haemolytic process 
          was also shown.  Brown snake antivenom was given. The importance 
          of this case is principally that it clearly demonstrates juvenile 
          brown snakes are capable of inflicting potentially dangerous 

          Case 13:  (from Pearn et al., 1981).  A non-fatal bite to the 
          hand of an adult male by a P. textilis.  A compression type 
          bandage was applied as first aid, without splint.  During the two 
          hours this first aid was in place, the patient was symptom free, 
          but within five minutes of removal, headache and nausea 
          developed, then pallor, sweatiness, an ache of the face and neck, 
          and dyspnoea.  Previously normal investigations now showed a 
          blood level of brown snake venom of 1.5 ng/ml (peaking at 5 ng/ml 
          at 45 minutes after release of first aid), and a defibrination 
          type coagulopathy.  The latter persisted for at least 24 hours, 
          despite one ampoule of brown snake antivenom, which however 
          relieved the symptomatology.  There was no evidence of 
          neurotoxicity.  This case report is probably the most detailed 
          study of the effectiveness of the compression immobilization type 
          first aid (Sutherland et al 1979) in man. 

          Case 14:  (from Sutherland et al 1982).  A fatal bite to the foot 
          of a 39 year-old, 39-week pregnant woman, by a brown snake 
          (positive venom detection). The snake was small (approx 18cm?), 
          and the bite was initially thought to be trivial. By 30 minutes 
          post-bite she had developed a headache, then sudden collapse 
          while supine on a hospital couch. A cardiac arrest quickly 
          followed and resuscitation failed, the patient dying 1.5 hours 
          post-bite. Brown snake venom was found at the bite site, but not 
          in blood or urine, at autopsy, and no other abnormalities were 
          found. The ensuing discussion concludes that death was due to the 
          supine hypotensive syndrome of pregnancy rather than to 

          Case 15:  (from Acott, 1988).  An important case report, 
          demonstrating isolated renal failure after brown snake bite, 
          without evidence of significant coagulopathy or neurotoxicity. 

          A 51 year-old male was bitten on the right thumb by a small P. 
          textilis. About 2 hours post-bite he developed abdominal pain, 
          nausea, vomiting, and "felt terrible".  Antivenom (one ampoule 
          polyvalent) was given at six hours post-bite.  Investigations on 
          samples taken at that time showed normal renal function, a 
          platelet count of 110 X 109/l, and normal levels of fibrinogen 
          and FDP (XDP), and brown snake venom in the blood.  There was no 
          evidence of neurotoxicity.  He remained apparently stable and 
          well, but at 24 hours post-bite it was realized he was virtually 
          anuric, and retesting showed elevated urea and creatinine, 
          consistent with acute renal failure, a further drop in platelets 
          to 41 X 109/l, but normal coagulation tests. While otherwise well 
          his renal function deteriorated, requiring nine days of 
          haemodialysis.  Renal biopsy showed acute tubular necrosis.  he 
          subsequently had normal renal function. 

          Case 16:  (from Milton, 1989).  A fatal case of brown snake bite 
          in a girl aged 2 years 9 months, found comatose and apnoeic by 
          her parents. There was no history of snakebite. Resuscitation 
          failed. Autopsy revealed possible bite marks on the left leg, 
          from which tissue blocks were taken, and subsequently shown to 
          contain a high concentration of brown snake venom. There was 
          modest congestion and oedema of the lungs with petechial 
          haemorrhages. Further details not provided. 

          From Morling et al 1989:  A paper detailing apparent 
          thrombocytopenia following brown snake bites in Western 
          Australia, presumably due to either P. affinis or P. nuchalis. 10 
          cases of such bites noted, all with evidence of a coagulopathy.  
          All those with sufficient clinical information had some evidence 
          of renal involvement.  Four cases had platelet counts below the 
          normal range. It is suggested by the authors that this may be 
          evidence of a direct platelet aggregating effect of brown snake 
          venom, but some doubt has been cast on the validity of this 
          conclusion (White 1990). 

     11.2 Internally extracted case reports

          Overall case analysis:

          In Australia a significant number of cases of suspected snakebite 
          do not result in identification of the species of snake 
          responsible.  However brown snakes are considered the leading 
          cause of snakebite.  In the author's experience of over 200 cases 
          the snake species was identifiable in 118; 60 were due to brown 

          Of the 60, 19 (32%) showed significant envenomation, however this 
          figure may be biased in favour of severe cases, as mild cases or 
          "dry bites" are less likely to result in identification of the 
          snake responsible. 

          Of the 19 cases with significant envenomation, 16 (+1) had 
          evidence of coagulopathy, 2 (+1) had evidence of neurotoxicity, 5 
          had evidence of renal damage, and none showed evidence of 

          Of the remaining 41 cases, 13 had evidence of possible mild
          envenomation, and 28 had no evidence of envenomation.

          Selected cases:

          Case 1:  (from White 1981).  A two year-old boy was bitten 
          multiply on the left posterior upper thigh by a large brown 
          snake.  Within 30 minutes the child had collapsed, had a possible 
          convulsion, and had developed a severe defibrination type 
          coagulopathy, with unclottable blood, no detectable fibrinogen, 
          gross elevation of FDP, and a normal platelet count. The first 
          dose of antivenom did not change these findings after 2.5  and 4
          hours, but 2 hours after a second dose of antivenom there was 
          substantial improvement, which continued without need of further 
          antivenom.  This child did not show evidence of neurotoxicity, or 
          renal damage.  Evidence of recovery from the coagulopathy 2 hours 
          after the second dose of antivenom correlated with a clinical 
          improvement, the child ceasing to be irritable, and instead 
          happily playing with parents. 

          Case 2:  (from White 1981).  A seven year-old boy bitten once on 
          the thumb by a small (approx 0.6 m) brown snake, proven by venom 
          detection. By 30 minutes post-bite the child was irritable, 
          rousable but drowsy, with non-clottable blood, and a severe 
          defibrination type coagulopathy. A single dose of antivenom was 
          given and resolution of the coagulopathy was less prompt than in 
          the more aggressively treated case 1, despite case 1 being 
          overall less severely envenomed on clinical grounds. There was no 
          evidence of neurotoxicity or renal damage. 

          Case 3:  (from White et al 1989).  A 3.5 year-old boy was bitten 
          twice on the right ankle by an 86 cm P. textilis, and after an 
          early (inappropriate) removal of first aid, collapsed with grand-
          mal convulsions. On arrival at hospital 30 minutes post-bite the 
          child was irritable, awake, with a rash on hands and leg, and 
          normotensive (almost hypertensive, BP 140/90). Unfortunately the 

          seriousness of the envenomation was not initially realized by the 
          treating staff.  Over the next two hours the child became drowsy, 
          more irritable, vomited, complained of abdominal pain, and a 
          severe defibrination type coagulopathy was demonstrated.  Expert 
          advice was sought, and antivenom therapy advised. Over the next 
          few hours five ampoules of brown snake antivenom were given. By 
          2.5 hours after the last dose of antivenom, there was substantial
          improvement in the coagulopathy, which continued to resolve 
          thereafter, associated with a dramatic clinical improvement 
          within two hours, the child ceasing to be irritable, and instead 
          happily playing with parents. There was no evidence of 
          neurotoxicity or renal damage. 

          This case demonstrates clearly the method of titrating antivenom 
          dose against progress of the coagulopathy. 

          Case 4:  (from White and Fassett 1983).  A 26 year-old man was 
          bitten on the right thumb by a large P. nuchalis. He was 
          inebriated at the time and did not apply first aid or seek 
          treatment. The following day he was anuric, and developed a 
          severe DIC with platelet consumption and a micro-angiopathic 
          haemolytic anaemia. He required haemodialysis for 12 days, but 
          made an eventual complete recovery of renal function. Because of 
          his delay in seeking treatment, he did not receive antivenom 
          treatment until the renal and clotting problems were fully 
          established.  Treatment with three ampoules of polyvalent 
          antivenom late on day one did not have a noticeable effect on the 
          coagulopathy. Seven ampoules of brown snake antivenom on days 
          five and six, were associated with resolution of the 
          coagulopathy, though this may have been coincidental. Heparin 
          therapy from day one to six did not appear effective in 
          controlling the coagulopathy. 

          Case 5:  A 27 year-old male was bitten three times while handling 
          a juvenile P. textilis, and at the time was significantly 
          inebriated, with a blood alcohol of 280 mg/100ml. He presented 
          for treatment about 30 minutes post-bite, following a collapse at 
          home, from which he spontaneously recovered, and which was 
          preceded by headache, nausea, vomiting, and confusion.  At 
          hospital he was severely agitated, requiring physical restraint 
          and relaxant medication, which delayed commencement of antivenom 
          therapy.  By 45 minutes post-bite he had a severe defibrination 
          type coagulopathy.  Antivenom therapy was commenced 2.5 hours 
          post-bite. Substantial resolution of the coagulopathy was not 
          apparent until five ampoules of brown snake antivenom had been 
          infused, some 12 hours post-bite, although a trend towards normal 
          was established two hours after the fourth ampoule.  In this case 
          a mild thrombocytopenia was noted, and progressed despite 
          resolution of the coagulopathy.  However, the renal function also 
          deteriorated reaching a peak creatinine level of 0.46 mmol/l on 
          day six, renal function remained impaired for several months, 
          although not sufficient to require dialysis. 

          This case demonstrates the unfortunate combination of alcohol and 
          snakebite, renal failure, and the association of renal failure 
          with thrombocytopenia. 

          Case 6:  (from White 1987c).  A 19 year-old man was bitten on his 
          arm while working under his house in a remote mining town. No 
          snake was seen. He ignored the "sting", but 45 minutes later 
          developed a headache, dizziness, and nausea. By two hours post-
          bite this had worsened, and he had generalized muscle weakness, 
          blurred vision, and hyperaesthesia. A tentative diagnosis of 
          snakebite was made, and appropriate antivenom administered. One 
          hour post antivenom, while on an aeromedical retrieval flight to 
          Adelaide, he developed acute crushing chest pain, cyanosis, and 
          was clammy. This rapidly responded to s.c. adrenaline. On arrival 
          in Adelaide he was awake, but showed general muscle weakness, 
          though without obvious cranial nerve involvement other than 
          blurred vision. The possible bite site was tender, though not 
          swollen, and no bite marks were visible, but a swab for venom 
          detection was positive for brown snake venom. There was no 
          evidence of a coagulopathy, and renal function remained normal. 
          He gradually recovered full muscle power over the next three 

          This case is important in that it represents a case of brown 
          snake bite with apparently significant envenomation, but without 
          the usual coagulopathy. P. nuchalis is found in the area this 
          patient was bitten, in two distinct colour morphs.  The author 
          has seen one similar case with envenomation, generalized muscle 
          weakness, but no coagulopathy or renal damage, caused by what is 
          presumed to be a variant of P. nuchalis. 

          Case 7:  (from White et al 1987).  This represents the only case 
          report to date of envenomation by P. modesta. An 11 year-old girl 
          was bitten on her left foot by a 0.5 m specimen, which was killed 
          and identified. The only initial symptom was nausea, lasting six 
          hours, and then a headache, followed by abdominal pain, lasting 
          16 hours. There was no evidence of neurotoxicity, or a 
          coagulopathy. Renal function was normal. Brown snake venom was 
          detected in the urine confirming systemic envenomation. The 
          patient made a complete recovery without need of antivenom 


     12.1 Availability of antidotes and antitoxins

          Specific brown snake antivenom  and venom  detection kits  
          available directly from  the manufacture,  Commonwealth Serum  
          Laboratories, 45 Poplar  Road,  Parkville,  Victoria  3052,  
          Australia (telephone (03) 389 1911,  telex AA 32789, Fax (03) 389 
          1434, international fax +61 3 389 1434). 

     12.2 Specific preventative measures

          Avoid exposure to brown snakes.  If working in areas where these 
          snakes exist, be alert, wear appropriate footwear and clothing, 
          do not place hands or other parts of body in places where snakes 
          may be present (eg down holes, in rubbish etc).  If handling or 
          catching snakes use appropriate techniques and equipment, 
          regularly checked to ensure peak performance, carry first aid 
          equipment (eg bandages, splint), never work alone, and have an 
          emergency plan documented and tested.  If allergy history or 
          known allergy to horse serum ensure this is documented 

     12.3 Other

          No data.


     13.1 Clinical and Toxicological

          Acott CJ (1988) Acute renal failure after envenomation by the 
          common brown snake; Med. J. Aust. 149 : 709-710. 

          Balmain R & McClelland KL (1982)  Panty-hose compression bandage; 
          first aid measure for snakebite.  Med. J. Aust., 2:  240-241. 

          Barnes JM & Trueta J (1941)  Absorption of bacteria toxins  and 
          snake  venoms  from  the  tissues:    importance  of  the  
          lymphatic circulation. Lancet, 1:  623-626. 

          Barnett D, Howden MEH (1980) A neurotoxin of novel structural 
          type from the venom of the Australian common brown snake; 
          Naturwissenschaften 67;405-406. 

          Broad AJ, Sutherland SK & Coulter AR (1979)   The lethality in 
          mice of dangerous Australian and other snake venoms.  Toxicon, 
          17: 661-664. 

          Chandler HM & Hurrell  JGR (1982)   A new  enzyme immunoassay 
          system suitable for  field use and  its application in  a snake 
          venom detection kit.  Clinica Chimica Acta, 121:  225-230. 

          Crawford GPM (1980) Envenomation by a Juvenile Gwardar; Med. J. 
          Aust., 2:158. 

          Coulter AR, Sutherland SK & Broad AJ (1974) Assay of snake venoms 
          in tissue  fluids.  Journal of Immunological Methods, 4:297-300. 

          Coulter AR, Cox JC, Sutherland SK & Waddell CJ (1978)  A new  
          solid phase sandwich radioimmunoassay and its application to the 
          detection  of snake  venom.   Journal of Immunological Methods, 

          Coulter AR,  Harris RD &  Sutherland  SK  (1980)   Enzyme 
          immunoassay  for the  rapid clinical  identification of  snake 
          venom.  Med. J. Aust., 1: 433-435. 

          Cull-Candy SG, Fohlman J,  Gustavsson D, Lullmann-Rauch R  & 
          Thesleff S (1976)  The effects  of  taipoxin  and  notexin  on  
          the function and  fine structure  of the murine neuromuscular 
          junction.  Neuroscience, 1: 175-180. 

          Datyner ME  &  Gage  PW (1973)   Presynaptic and postsynaptic 
          effects  of  the  venom  of  the   Australian  tiger  snake  at  
          the neuromuscular junction.   British Journal of Pharmacology, 

          Dowdall MH,  Fohlman J & Eaker D (1977)   Inhibition of high 
          affinity choline  transport  in  peripheral  cholinergic  endings  
          by presynaptic snake venom neurotoxins.  Nature, 269:  700-702. 

          Eaker C (1978)  Studies of presynaptically neurotoxic and  
          myotoxic phospholipases A2.  In LI, C.H. Ed. Versatility of 
          Proteins, Academic Press. 

          Fairley NH (1929)a  The present position of snakebite and the 
          snake bitten in Australia.  Med. J. Aust., 1:  296-313. 

          Fairley  NH (1929)b   The   dentition  and  biting  mechanism   
          of Australian snakes.  Med. J. Aust., 1:  313-327. 

          Fairley  NH & Splatt  B (1929)   Venom  yields  in Australian 
          poisonous snakes.  Med. J. Aust., 1:  336-348. 

          Foxton HV (1914) A case of fatal snakebite (with autopsy), Med. 
          J. Aust. 2:108. 

          Fisher M (1982)  First aid in envenomation.  Med. J. Aust., 1: 

          Harris ARC, Hurst PE, Saker BM (1976) Renal Failure after snake 
          bite; Med. J. Aust. 2;409-411. 

          Herrmann RP; Davey MG; Skidmore PH (1972) The coagulation defect 
          after envenomation by the bite of the dugite (Demansia nuchalis 
          affinis), a Western Australian brown snake; Med. J. Aust. 2:183-

          Hilton JMN (1989) A tragic case of snakebite; Med. J. Aust. 

          Hurrell JGR & Chandler HW (1982)  Capillary enzyme immunoassay 
          field kits for the detection of snake venom in clinical 
          specimens:  a review of two years' use.  Med. J. Aust., 2:  236-

          Lloyd CH (1932)  Four  cases of  snake bite.   Med. J.  Aust., 

          Mebs D & Samejima Y (1980)  Purification from  Australian elapid 
          venoms  and properties of phospholipases  A which cause 
          myoglobinuria in mice. Toxicon, 18:  443-454. 

          Morling AC; Marshall LR; Herrmann RP (1989) Thrombocytopenia 
          after brown snake envenomation; Med. J. Aust. 151:627-628. 

          Murrell G (1981) The effectiveness of the pressure/immobilization    
          first aid technique  in the  case of  a tiger  snake bite.   Med. 
          J. Aust., 2:  295. 

          Pearn J, Morrison J, Charles N, Muir V (1981) First aid for 
          snakebite; Med. J. Aust., 2:293-294. 

          Schapel GJ, Utley D, Wilson GC (1971).  Envenomation by the 
          Australian common brown snake - pseudonaja (Demansia) textilis 
          textilis: Med. J. Aust. 1:142-144. 

          Sutherland SK (1974)   Venomous Australian creatures:   the 
          action of their toxins and the care of the envenomated patient.  
          Anaesthesia and Intensive Care, 2(4):  316-327. 

          Sutherland SK (1975) Treatment of snakebite in Australia:  some 
          observations and recommendations.  Med. J. Aust., 1:  30-32. 

          Sutherland SK (1977)a  Serum reactions:  an analysis of  
          commercial antivenoms  and the  possible role  of 
          anticomplementary  activity in de-novo reactions to  antivenoms 
          and antitoxins.  Med. J. Aust.,  1: 613-615. 

          Sutherland SK (1977)b  Antivenoms:   better late than never.   
          Med. J. Aust., 2:  813. 

          Sutherland  SK (1977)c   Acute  untoward  reactions to 
          antivenoms.  Med. J. Aust., 1:  841. 

          Sutherland SK (1981)  When do  you remove first aid measures  
          from an envenomed limb.  Med. J. Aust., 1:  542-543. 

          Sutherland SK (1983)   Prolonged  use of pressure/immobilization 
          after snake bite.  Med. J. Aust., 1:  58. 

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

          Sutherland SK, Campbell  DG & Stubbs AE (1981)  A  study of the 
          major Australian snake venoms in the monkey (Macaca 
          fascicularis), II:  myolytic and haematological effects of 
          venoms.  Pathology, 13:  705-715. 

          Sutherland SK, Coulter AR, Broad AJ, Hilton JMN &  Lane LHD  
          (1975) Human snakebite victims:  the successful detection of 
          circulating  snake venom  by  radioimmunoassay.   Med.  J. Aust., 

          Sutherland SK & Coulter AR (1977) Three instructive cases of 
          tiger snake (Notechis scutatus) envenomation, and how a 
          radioimmunoassay proved the diagnosis.  Med. J. Aust., 2:  177-

          Sutherland SK &  Coulter AR (1977)  Snake bite:  detection  of 
          venom by radioimmunoassay.  Med. J. Aust., 2:  683-684. 

          Sutherland SK,  Coulter  AR  &   Harris RD (1979) Rationalisation  
          of first-aid measures for elapid snakebite.  Lancet, 183-186. 

          Sutherland SK,  Coulter AR,  Harris  RD,  Lovering KE & Roberts 
          ID (1981) A study of the major Australian snake venoms in the  
          monkey  (Macaca fascicularis);  in  the  movement  of  injected 
          venom; methods  which retard this movement,  and the  response to 
          antivenoms.  Pathology, 13:  13-27. 

          Sutherland SK; Duncan AW; Tibballs J (1982); Death from a 
          snakebite associated wit the supine hypotensive syndrome of 
          pregnancy; Med. J. aust., 2:238-239. 

          Sutherland SK & Lovering KE (1979)   Antivenoms:   use and 
          adverse reactions  over a 12 month period  in Australia and Papua 
          New Guinea. Med. J. Aust., 2:  671-674. 

          Trinca JC (1963)  The treatment  of snakebite.  Med. J. Aust.,  

          Tyler MI, Barnett D, Nicholson P, Spence I, Howden MEH, (1987a) 
          Studies on the subunit structure of textilotoxin, a potent 
          neurotoxin from the venom of the Australian common brown snake 
          (Pseudonaja textilis); Biochimica et Biophysica Acta 915;210-216. 

          Tyler MI, Spence I, Barnett D, Howden MEH (1987b); 
          Pseudonajatoxin b; unusual amino acid sequence of a lethal 
          neurotoxin from the venom of the Australian common brown snake, 
          Pseudonaja textilis; Eur. J. Biochem. 166:139-143. 

          White J (1981) Ophidian envenomation; a South Australian 
          perspective. Records of  the  Adelaide  Children's  Hospital,  
          2(3): 311-421. 

          White J (1983)a Patterns of elapid envenomation and treatment in 
          South Australia.  Toxicon, Suppl. 3:  489-491. 

          White J (1983)b  Local tissue destruction and Australian elapid 
          envenomation.  Toxicon, Suppl. 3:  493-496. 

          White J (1983)c  Haematological problems and Australian elapid 
          envenomation.  Toxicon, Suppl. 3:  497-500. 

          White J (1987)a  Elapid snakes: venom production and bite 
          mechanism. In Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic 
          Plants & Animals:  a guide for Australia, Queensland Museum, 504 

          White J (1987)b  Elapid  snakes:  venom toxicity and  actions.  
          In Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic Plants & 
          Animals:  a guide for Australia, Queensland Museum, 504 pp. 

          White J (1987)c Elapid snakes:  aspects of envenomation.  In 
          Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic Plants & 
          Animals:  a guide for Australia, Queensland Museum, 504 pp. 

          White J (1987)d  Elapid   snakes:   management   of  bites.   In 
          Covacevich J, Davie P & Pearn J Eds. Toxic Plants & Animals:  a 
          guide for Australia, Queensland Museum, 504 pp. 

          White J, Fassett R (1983) Acute renal failure and coagulopathy 
          after snakebite; Med. J. Aust., 2:142-143. 
          White J, Williams V, Passehl JH (1987).  The five-ringed brown 
          snake, Pseudonaja modesta (Gunther):  report of a bite and 
          comments on its venom; Med. J. Aust. 147:603-605. 

          White J, Williams V (1989) Severe envenomation with convulsion 
          following multiple bites by a common brown snake, Pseudonaja 
          textilis; Aust. Paediatr. J., 25:109-111. 

          White J (1990) Letter to editor; Med. J. Aust. , 152; 445-446. 

          Williams V and White J (1990) Variation in venom composition and 
          reactivity in two specimens of yellow-faced whip snake (Demansia 
          psammophis) from the same geographic area. Toxicon , 28, 1351-

     13.2 Zoological

          Cogger HG (1975) Reptiles  and Amphibians  of Australia, Sydney, 
          A.H. & A.W. Reed. 

          Cogger HG (1987)   The venomous land  snakes.  In Covacevich,  
          J., Davie,  P. &  Pearn, J.  Eds. Toxic  Plants &  Animals:  a  
          guide for Australia, Brisbane, Queensland Museum, 504 pp. 

          Cogger HG, Cameron EE & Cogger HM (1983) Zoological catalogue of 
          Australia,  Volume I,  Amphibia and  Reptilia, Canberra, 
          Australian Government Publishing Service. 

          Covacevich J (1988)  Australia's dangerous snakes.  In Pearn, J. 
          & Covacevich, J. Eds. Venoms and Victims, Brisbane, Queensland 

          Longmore R (1986) Atlas of elapid snakes of  Australia, Canberra, 
          Australian Government Publishing Service. 

          Schwaner TD,  Baverstock PR,  Dessauer HC & Mengden GA (1985)  
          Immunological evidence for the phylogenetic relationships of 
          Australian elapid snakes.  In Grigg, G., Shine, R. & Ehmann, H.  
          Eds. Biology  of Australasian Frogs  and Reptiles, New  South 
          Wales, Royal Zoological Society. 


     Dr Julian White

     State Toxinology Services
     Adelaide Children's Hospital
     North Adelaide,  South Australia,  5006 
     Phone: 61-8-2047000
     Mobile phone: 61-18-832776
     Fax: 61-8-2046049

     July 1990
     Reviewed by Working Group On Natural Toxins April 1991.
     Revised April 1991, November 1991.

    See Also:
       Toxicological Abbreviations