| 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|
| 3.3.2 Description|
| 3.4 Other chemical contents|
|4. CIRCUMSTANCES OF POISONING|
| 4.1 Uses|
| 4.2 High risk circumstances|
| 4.3 High risk geographical areas|
|5. ROUTES OF ENTRY|
| 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|
| 18.104.22.168 Adults|
| 22.214.171.124 Children|
| 7.2.2 Relevant animal data|
| 7.2.3 Relevant in vitro data|
| 7.3 Carcinogenicity|
| 7.4 Teratogenicity|
| 7.5 Mutagenicity|
| 7.6 Interactions|
|8. TOXICOLOGICAL/TOXINOLOGICAL AND OTHER BIOMEDICAL INVESTIGATIONS|
| 8.1 Material sampling plan|
| 8.1.1 Sampling and specimen collection|
| 126.96.36.199 Toxicological analyses|
| 188.8.131.52 Biomedical analyses|
| 184.108.40.206 Arterial blood gas analysis|
| 220.127.116.11 Haematological analyses|
| 8.1.2 Storage of laboratory samples and specimens|
| 18.104.22.168 Toxicological analyses|
| 8.1.3 Transport of laboratory samples and specimens|
| 22.214.171.124 Toxicological analyses|
| 8.2 Toxicological analyses and their interpretation|
| 8.2.1 Tests on toxic ingredient(s) of materials|
| 126.96.36.199 Simple qualitative test(s)|
| 188.8.131.52 Advanced qualitative confirmation test(s)|
| 184.108.40.206 Simple quantitative method(s)|
| 220.127.116.11 Advanced quantitative method(s)|
| 8.2.2 Tests for biologicals specimens|
| 18.104.22.168 Simple qualitative test(s)|
| 22.214.171.124 Advanced qualitative confirmation test(s)|
| 126.96.36.199 Simple quantitative method(s)|
| 188.8.131.52 Advanced quantitative methods(s)|
| 184.108.40.206 Other dedicated methods(s)|
| 8.2.3 Interpretation of toxicological analyses|
| 8.3 Biomedical Investigations and Their Interpretation:|
| 8.3.1 Biochemical analyses|
| 220.127.116.11 Blood, plasma or serum|
| 18.104.22.168 Urine|
| 22.214.171.124 Other biological 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 Investigations and Their Interpretation|
| 8.5 Summary of most essential biomedical and toxicological analyses|
|9. CLINICAL EFFECTS|
| 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 by:|
| 9.2.1 Ingestion|
| 9.2.2 Inhalation|
| 9.2.3 Skin exposure|
| 9.2.4 Eye contact|
| 9.2.5 Parenteral exposure|
| 9.2.6 Other|
| 9.3 Course, prognosis, cause of death|
| 9.4 Systematic description of clinical effects|
| 9.4.1 Cardiovascular|
| 9.4.2 Respiratory|
| 9.4.3 Neurological|
| 126.96.36.199 CNS|
| 188.8.131.52 Peripheral nervous system|
| 184.108.40.206 Autonomic|
| 220.127.116.11 Skeletal and smooth muscle|
| 9.4.4 Gastrointestinal|
| 9.4.5 Hepatic|
| 9.4.6 Urinary|
| 18.104.22.168 Renal|
| 22.214.171.124 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|
| 126.96.36.199 Acid base disturbances|
| 188.8.131.52 Fluid and electrolyte disturbances|
| 184.108.40.206 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 analysis and other investigations|
| 10.2.1 Sample collection|
| 10.2.2 Biomedical analysis|
| 10.2.3 Toxicological analysis|
| 10.2.4 Other investigations.|
| 10.3 Life supportive procedures and symptomatic treatment|
| 10.4 Decontamination|
| 10.5 Elimination|
| 10.6 Antidote/antivenin treatment|
| 10.6.1 Adults|
| 10.6.2 Children|
| 10.7 Management discussion|
|11. ILLUSTRATIVE CASES|
| 11.1 Case reports from literature|
| 11.2 Internally extracted data on cases|
| 11.3 Internal cases|
|12. ADDITIONAL INFORMATION|
| 12.1 Availability of antidotes and antitoxins|
| 12.2 Specific preventative measures:|
| 12.3 Other|
| 13.1 Clinical and Toxicological|
| 13.2 Zoological|
|14. AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)|
1.1 Scientific Name
(Cogger 1975, 1987; Cogger et al 1983; Covacevich 1988;
1.3 Common Names
Scientific Name Common Name
Pseudechis australis mulga snake, king brown
butleri Butler's snake
colletti Collett's snake
guttatus spotted black snake,
blue bellied black snake
papuanus Papuan black snake
porphyriacus red bellied black snake
2.1 Main risks and target organs
Black snakes are only a moderately common cause of significant
snakebites in Australia. Severity depends on species, with P.
australis often causing significant envenomation while some other
species, notably P. porphyriacus, only rarely causing severe
envenomation. In the past P. papuanus has been thought to be a
significant cause of snakebites in Papua New Guinea, but there is
some doubt that this is still so.
Main risks are: rhabdomyolysis, acute renal failure, and
possibly coagulopathy and neurotoxic paralysis in some species.
Target organs: skeletal muscle, coagulation system, and possibly
the neuromuscular junction for some species.
2.2 Summary of clinical effects
Locally: usually immediately painful, with subsequent development
of mild to marked local oedema, and sometimes ecchymosis. Bite
marks vary from single puncture, through multiple punctures, to
multiple scratches. Local secondary infection unusual. Venom may
spread to draining lymph nodes with consequent pain, tenderness
Systemic: headache, nausea, vomiting, abdominal pain, impaired
consciousness, occasionally loss of consciousness and possibly
convulsions. Coagulopathy with overt bleeding manifestations is
rare. Neurotoxic paralysis is not well documented clinically.
Muscle movement is painful. Acute renal failure. Rhabdomyolysis
may dominate the clinical picture for P. australis bites and
possibly for P. butleri bites.
Monitor coagulation to establish the presence and extent of
coagulopathy. This should be performed at presentation, on
development of symptoms or signs of systemic envenomation, and 1-
2 hours after antivenom therapy. However, coagulopathy due to
Pseudechis bites is poorly documented and defibrination has not
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 for venom
detection is a swab from the 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.
(a) Specific: If the patient has systemic envenomation, give
specific snake antivenom (CSL).
Pseudechis australis black snake antivenom
butleri black snake antivenom
colletti tiger snake antivenom
guttatus tiger snake antivenom
porphyriacus tiger snake antivenom
papuanus black snake antivenom
(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
(c) Local: Do not clean or touch the local wound until
appropriate samples taken for venom detection. Thereafter
ensure antisepsis. Early surgical intervention is generally
contraindicated, and is only rarely indicated in the late
stages if significant local necrosis has developed.
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 fangs are likewise paired, 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.
2.6 Main toxins
Pseudechis venom is a complex mixture of protein and non-
protein components, not all of which have been fully evaluated.
(a) Neurotoxins: both presynaptic and postsynaptic may be
present, though neither appear to be clinically important
in human envenomation.
(b) Procoagulants: principally anticoagulants.
(c) Myotoxins: second action of presynaptic neurotoxins
which is a phospholipase A2, and also a separate action of
distinct phospholipase toxins without significant
3.1 Description of the animal
3.1.1 Special identification features
The black snakes belong to the Class Reptilia; Order Squamata;
Suborder Serpentes: Family Elapidae. They are oviparous (except
P. porphyriacus which is ovoviviparous), diurnal or crepuscular,
and in warm weather may be nocturnal. Food varies with species,
subspecies and locality, and includes frogs, small lizards, and
Black 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 . The fangs have venom transport
grooves, enclosed for most of their length. For fang details see
Six species are currently recognized.
Scientific Name Common Name
Pseudechisaustralis mulga snake, king brown
butleri Butler's snake
colletti Collett's snake
guttatus spotted black snake,
blue bellied black snake
papuanus Papuan black snake
porphyriacus red bellied black snake
Genus Pseudechis: Characterized by smooth scales, mid-body
scales in 17-19 rows, anal and subcaudal scales variable,
anal usually divided, but anterior subcaudals usually
single, suboculars absent, head usually broad to triangular
in outline with some vertical compression.
Scalation: smooth, 17 rows in mid body, ventrals 185-225,
anal divided (occasionally single), subcaudals 50-75,
usually single anteriorly.
Length: 2 metres (max over 2.7 m)
Colour: Colour usually uniform dorsally, ranging from pale
brown, through russet brown, to dark brown depending on
specimen and location. Scales usually lighter in colour
proximally becoming darker near their tips giving an
overall reticulated pattern on close inspection. Ventrally
cream to pink often with darker blotches.
Scalation: smooth, 17 rows in mid body, ventrals 204-216,
anal usually divided, subcaudals 55-65, usually single
Length: 1.6 metres
Colour: Sides and front of head brown or reddish brown,
rest of head dorsally black or brown black, extending to
nape of neck, body with reticulated appearance as each
scale has a base colour of dark brown to black with a large
central area of pale yellow. Ventrally yellow with black
Scalation: smooth, 19 rows in mid body, ventrals 215-235,
anal usually divided, subcaudals 50-70, single anteriorly.
Length: 1.5 metres (maximum about 2 m).
Colour: Distinctive, with deep brown to black dorsally
with numerous irregular cross bands of pink, or cream
scales, tending to dominance laterally, more vivid in
juveniles where the colour may be deeper and even orange
or red orange, ventrally cream to yellow or orange.
Scalation: smooth, 19 rows in mid body, ventrals 175-205,
anal usually divided, subcaudals 45-65, single anteriorly.
Length: 1.5 metres (maximum about 2 m).
Colour: Variable. Two basic forms, one black to blue black
dorsally with grey to black ventrally (blue bellied black
snake), the other black with brown blotches dorsally and
laterally, grey ventrally (spotted black snake), and in
some specimens the dominant dorsal scale colour may be
cream with black tips.
Scalation: smooth, 19-21 rows in mid body, ventrals 215-
230, anal usually divided, subcaudals 45-65, mostly single
but divided posteriorly.
Length: 2.1 metres.
Colour: Dorsally black (occasionally brown), ventrally
grey or bluish grey.
Scalation: smooth, 17 rows in mid body, ventrals 170-215,
anal usually divided, subcaudals 40-70, single anteriorly.
Length: 1.25 metres (maximum about 2.5 m).
Colour: Dorsally black, ventrally usually red,
occasionally pink, or pale cream to white, or black.
(Cogger 1971, Cogger 1975, Mirtschin & Davis 1983, Smith
Habitat varies with species ranging from arid lands to
Pseudechis australis (mulga snake, king brown)
Found in a diverse range of habitats from arid areas across
central Australia, through to sub-tropical and tropical
regions. Principally diurnal, it is however active on warm
P.butleri (Butler's snake)
Essentially similar to P. australis but with a more limited
range, not encompassing tropical areas.
P. colletti (Collett's snake)
Relatively little known about the ecology of this snake,
but it is found principally in arid and semi-arid areas.
P. guttatus (Spotted black snake, blue bellied black snake)
This species favours wetland areas including riverine and
P. papuanus (Papuan black snake)
The papuan black snake is confined to Papua New Guinea
chiefly in southern and coastal regions. It has been
recorded in savanna woodland, adjacent forrest, and in
swampland. The true distribution and ecology and habitat
preferences of this snake have yet to be defined.
P. porphyriacus (Red bellied black snake)
Essentially a wetlands species favouring swamps, riverine,
and similar habitats.
The distribution for each species based on museum records
and published accounts is 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). The classic bite mark
in plaster is shown in Figure.
3.3 The toxin(s)
P. australis Mulga snake venom
Mulgatoxin a (specific myotoxin)
Pa 10a, Pa 11, Pa 13 (PLA2 [=phospholipase
P. porhyriacus Black snake venom
Pseudexin A,B,C (PLA2 toxins)
P. colletti Colletts snake venom
P. guttatus Spotted black snake venom
P. papuanus Papuan black snake venom
Whole venom production based on milking specimens, usually
in captivity. (White 1987b, Fairley & SPLATT, 1929)
Venom yield and fang length, where known, are listed below
(Fairley 1929b, Kellaway 1929, Kellaway and Thompson 1930,
Martin and Smith 1892, Sutherland 1983, White 1987a,
Worrell 1970, Morrison et al 1982)
Snake: P.aus P.but P.col P.gut P.por P.pap
(mm) 6.5 - - 3.5 4.0 -
(mm) - - - - 12 -
yield (mg) 180 - 30 - 40 -
yield (mg) 600 - 50 - 94 -
Mean venom injected
(mg) 61.6 - - - 1.3 -
Mean venom left
(mg) 0.07 - - - 0.9 -
From P. australis venom: (also as Pa VIIIa,), Basic PLA2
single chain protein, 122 AA, 7 disulphide bridges, MW
13484 D, LD50 200 mg/kg ip mice, a specific myotoxin in
mice causing myoglobinuria, affecting skeletal muscle, and
with death due to probable paralysis at high doses, without
histological evidence of damage to heart or smooth muscle
(Leonardi et al 1979, Mebs & Samejima 1980)
From P. australis venom: Lethal, causes myoglobinuria in
mice, LD50 0.25 mg/kg ip mice. (Leonardi et al 1979)
From P. porphyriacus venom: Initially described as a PLA
single chain polypeptide, MW 16500 D, LD50 0.48 mg/kg ip
mice. Later shown to be a dimer, then a mixture of 3
isomers, A,B,& C,with respective LD50s and MWs of; A= LD50
1.3 mg/kg ip mice, 117 AA, MW 13096D; B= LD50 0.75 mg/kg,
117 AA, MW 13002D; C= non-toxic in mice, not further
elaborated. It was further noted that monoclonal antibody
to Pseudexin neutralized the presynaptic neurotoxin from
tiger snake venom (notexin, Notechis scutatus). Although
principally described as a lethal myotoxin, it is therefore
possible that pseudexin also functions as a neurotoxin.
(Vaughan et al 1981, Moon & Rys 1984, Schmidt & Middlebrook
From P. porphyriacus venom: A lethal myotoxin, basic PLA2
protein, 120 AA, MW 13400D, LD50 6.4 mg/kg sc mice, minimum
dose for myoglobinuria 1.4 mg/kg sc mice. (Mebs & Samejima
From a mixture of P. colletti and P. guttatus venom. Two
lethal myotoxins , both PLA2 basic proteins, II = 127 AA,
MW 14170D, LD50 4.5 mg/kg sc mice; IV = 129 AA , MW 14100D,
LD50 4.3 mg/kg sc mice. For all toxins described in this
study (including Ib and VIIIa above) death occurred in
hours due to respiratory paralysis at high doses, but in
days due to myolysis and renal failure at lower doses.
(Mebs & Samejima 1980)
From P. colletti venom: Lethal PLB protein, dimer, MW
33000D in two chains of 16500D, LD50 approx. 2 mg/g ip
mice. Causes death due to myolysis and also associated
ataxia, respiratory difficulty, possibly neurotoxic, and
also strongly haemolytic. (Bernheimer et al 1987)
From P. australis venom: Lethal single chain PLA2 protein,
LD50 0.1 mg/g iv mice. Produces paralysis by reducing
acetylcholine release from the terminal axon at the
neuromuscular junction, and by direct blockade of muscle
fibre contractility. (Rowan et al 1989)
From P. australis venom: Lethal single chain PLA2 protein,
LD50 0.23 mg/g iv mice, MW 14000D, 118 AA. Action similar
to Pa10a. (Nishida et al 1985, Rowan et al 1989)
From P. australis venom: Single chain PLA2 protein, MW
13500, 118 AA, initially described as non-lethal, later as
lethal at higher doses with an LD50 6.8 mg/g iv mice.
Action similar to PA10a. (Nishida et al 1985, Rowan et al
From P. australis venom: Single chain protein, 62 AA, MW
7100D, LD50 76 mg/kg iv mice. Described as a short chain
neurotoxin with considerable homology to similar sea snake
neurotoxins, presumably post-synaptic in action. (Takasaki
& Tamiya 1985)
From P. australis venom: Single chain protein, 68 AA, non-
lethal to mice, considered a long chain neurotoxin
homologue. (Takasaki 1989)
None isolated. Pseudechis venoms appear to be anticoagulant
in vitro rather than procoagulant. (Sutherland et al 1981,
Marshall & Herrmann 1983, Campbell 1967, Campbell &
Chesterman 1972, Trethewie 1971). They are not noted to
have significant platelet activity. (Marshall & Herrmann
In vitro haemolytic activity of Pseudechis venoms has long
been recognized but few haemolysins have been characterized
specifically. Significant activity has been noted for P.
australis, P. porphyriacus, P. papuanus, P. colletti.
Phospholipase B has been characterized as a haemolytic
fraction of P. colletti venom. (Doery & Pearson 1961,
Bernheimer et al 1986,1987)
3.4 Other chemical contents
There are few data on most of these components, which include L-
amino acid oxidase.
(Trethewie 1971, Takasaki & Tamiya 1982)
4. CIRCUMSTANCES OF POISONING
Venom is used both in antivenom production and for laboratory
4.2 High risk circumstances
Children: when playing in areas where black snakes are common,
either through accidental encounter (ie stepping on snake) or
while trying to emulate noted naturalists (ie trying to catch
Adults: when living in areas where black 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 black snakes are
Reptile keepers & snake handlers: if due care is not exercised
in catching and handling snakes, including venom milking.
Recreation seekers: camping or walking or playing sport (ie
water sports, water skiing) in areas where black snakes are
Homes: around homes in black snake prone areas where water is
seasonally scarce and free water is available in the garden or
4.3 High risk geographical areas
No specific high risk areas for black snake bites have been
documented. P. porphyriacus most likely to be encountered in
wetlands areas and along creeks. P. australis most common in arid
central and north Australia where it may be a major cause of
snakebite. P. papuanus is common in parts of Papua New Guinea.
5. ROUTES OF ENTRY
Venom cannot be absorbed through intact skin.
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.
Experimentally venom may be administered to test animals via
subcutaneous, intramuscular, intravenous, intraperitoneal, and
intraventricular (CNS) routes.
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.
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
6.2 Distribution by route of exposure
It appears that much venom is transported from the bite site via
the lymphatic system, ultimately reaching the systemic
circulation. Experience with human cases of black snake
envenomation shows that symptoms and signs of envenomation may
occur within 60 minutes of the bite, especially in children,
particularly for P. australis bites. 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, whence it is excreted in the
urine. Venom must also exit the circulation and enter the
extravascular space, where it binds within target organs.
The kinetics of venom distribution, excretion, and detoxification
are incompletely understood. Coagulopathy potentially may become
well established within 30 minutes of a bite, although this is
poorly documented for most Pseudechis spp. (P. papuanus is an
exception which may cause significant coagulopathy, but there is
doubt over the validity of the clinical data on which this is
based (Campbell 1967, Campbell & Chesterman 1972).
6.3 Biological half-life by route of exposure
Little information is available on the metabolism of venom
components in man, but most components are fully active in whole
venom and require no further modification for activity. Venom
reaches high concentrations in the kidneys, where it is excreted
in urine. (Sutherland & Coulter, 1977 a,b). The fate of specific
venom components, particularly neurotoxins and procoagulants, is
6.5 Elimination by route of exposure
Most venom appears to be eliminated via the kidneys in the urine.
7.1 Mode of action
Whole venom of at least some species of Pseudechis contains a
variable mixture of presynaptic and postsynaptic neurotoxins.
Composition of this mixture may not be uniform across all
populations of black snakes. However current clinical case data
and some animal experimental work indicates that neurotoxic
envenomation by these snakes is either not seen or is of minor
extent. It should be noted that relatively few case reports are
available for most species thus the issue of paralysis due to
Pseudechis bites remains unresolved.
Procoagulants and coagulopathy
No procoagulants have been isolated from Pseudechis venoms, which
distinguishes these venoms from those of other major Australian
snakes (Notechis, Oxyuranus, Pseudonaja, Tropidechis) which
contain potent procoagulants. Early research suggested that
Pseudechis venoms have a procoagulant action in vitro but it now
appears that its action is anticoagulant.
Early clinical work in Papua New Guinea suggested P. papuanus
caused a defibrination-type coagulopathy in man (Campbell 1967),
but subsequent reviews have indicated that this was probably
false due to misidentification of the snake. Experimental
evidence clearly supports the anticoagulant action of these
venoms (Campbell & Chesterman 1972, Marshall & Herrmann 1983).
P. papuanus has a potent anticoagulant action in vitro with
inhibition of thromboplastin generation, and inhibition of
conversion of prothrombin to thrombin (Campbell & Chesterman
1972). Anticoagulant action and lack of procoagulant action was
shown with in vitro experiments using P. papuanus and P.
australis venom (Marshall & Herrmann 1983). This latter work
showed a slight coagulant effect without apparent anticoagulant
effect for P. porphyriacus venom. In vivo experiments using
monkeys demonstrated an apparent "coagulopathy" using P.
australis venom, with prolongation of partial thromboplastin time
and prothrombin time, but no comment on fibrinogen levels and FDP
were made, thus these results are equally consistent with an
anticoagulant action (Sutherland et al 1981).
While some presynaptic neurotoxins are also directly
myolytic (eg notexin) and cause major destruction of skeletal
muscle, locally and systemically (Harris et al 1975), both in
experimental animals and occasionally in human envenomation, some
Pseudechis venoms contain direct myotoxins which do not appear to
exert significant neurotoxic activity. However these myotoxins,
which have been found in all Pseudechis venoms searched (eg. P.
australis, P. porphyriacus, P. colletti, P. guttatus), do appear
to be mostly PLA2 toxins closely related to the myotoxic
presynaptic neurotoxins. Based on extensive work with these
latter toxins the mode of action of Pseudechis myotoxins may be
inferred. The phospholipase A2 activity of these toxins may
hydrolyse muscle cell membrane phospholipids (Mebs & Samejima
1980). Not all muscle cells are equally affected, skeletal
muscle being most susceptible, and immature muscle cells
appear resistant. In experimental animals muscle cell
destruction may occur in only a few hours; within 3 days the
process is complete and cell regeneration commences, with
complete regeneration taking 3-4 weeks (Harris et al 1975).
Following acute muscle damage there is a progressive rise in
serum levels of creatine kinase (CK) peaking at 10 - 20 hours
post-bite. Myoglobin levels also rise and are excreted in the
urine, causing the typical dark brown discolouration (Sutherland
et al 1981b).
In humans, the peak CK may be extraordinarily high (up to
300,000 U/l or more), and myoglobinuria may continue for many
days (for example, the maximum is 11 days for N. ater niger bite)
(White, unpublished data; Hood and Johnson, 1975). Data on human
cases of Pseudechis envenomation with myolysis is scant, but the
author's experience is that P. australis bites often cause severe
myolysis but bites by P. porphyriacus and P. guttatus do not.
No specific nephrotoxins have been detected in Pseudechis snake
venom, and no clear cases of renal function impairment have been
reported in humans envenomed by Pseudechis. However, a fatal case
of P. australis envenomation did show evidence of renal damage at
autopsy, possibly secondary to extensive myolysis (Rowlands et al
7.2.1 Human data
The human lethal dose for Pseudechis venoms is
unknown. However, without antivenom treatment, a
significant number of P. australis bites will prove
fatal. The same may apply for P. papuanus and possibly
P. butleri (for which there are no human case
reports), but for P. porphyriacus, and possibly P.
colletti and P. guttatus human fatalities are very
rare, and envenomation by these species is very
unlikely to be life threatening, except perhaps in a
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
7.2.2 Relevant animal data
Snake LD50 mg/kg sc mice
P. australis 2.38
P. butleri no data
P. colletti 2.38
P. guttatus 2.13
P. papuanus 1.09
P. porphyriacus 2.52
7.2.3 Relevant in vitro data
No data available.
No data available.
No data available.
No data available.
No data of clinical significance.
8. TOXICOLOGICAL/TOXINOLOGICAL AND OTHER BIOMEDICAL
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
220.127.116.11 Toxicological analyses
For venom detection: swab from bite site moistened in
sterile saline. If there is 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)
18.104.22.168 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).
22.214.171.124 Arterial blood gas analysis
Collect arterial blood by sterile arterial puncture
into a container as issued by the laboratory.
126.96.36.199 Haematological analyses
For whole blood clotting time as a "bedside" test
collect 5-10 ml of venous blood without anticoagulant
(either in the collection syringe or from a central
line or other venous access line that may have
anticoagulant) and place in a glass test tube.
Carefully observe the time till a clot appears.
For standard tests (eg. coagulation studies, complete
blood picture) collect venous blood in appropriate
containers with anticoagulant as issued by the
laboratory ensuring that the right amount of blood is
used (for coagulation studies citrate will usually be
the anticoagulant, and EDTA will be used for complete
8.1.2 Storage of laboratory samples and specimens
188.8.131.52 Toxicological analyses
For samples for standard venom detection:
Short term (less than 24 hrs) ordinary fridge is acceptable
-(4°C), in sterile container.
Long term, store frozen (-20°C or lower).
For samples for venom analysis (research) store frozen (-
200°C or lower).
For samples for standard tests refer to laboratory. In
general keep at 4°C, particularly for samples for
8.1.3 Transport of laboratory samples and specimens
184.108.40.206 Toxicological analyses
Use insulated container.
8.2 Toxicological analyses and their interpretation
8.2.1 Tests on toxic ingredient(s) of materials
220.127.116.11 Simple qualitative test(s)
A simple qualitative test for presence of snake venom
and designation of species/genus group, corresponding
to the most appropriate monovalent anti-venom 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 species.
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 4°C (standard fridge)
and has a shelf life of 6 months. A control is built
into the kit. If this fails the test results are
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 addition.
(5) Specimen preparation
Refer to instructions in kit
(7) Calibration procedure
(8) Quality control
Included in kit
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. This is particularly true for P.
porphyriacus, P. colletti and P. guttatus which may
cause simultaneous colour change in wells for both
mulga snake venom and tiger snake venom.
(10) Detection limit
The manufacturer states the kit will detect
concentrations of venom as low as 10 ng/ml.
(11) Analytical assessment
(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. Note however
that for some species of Pseudechis there may be a
colour change in two tubes simultaneously which may
cause confusion. This most often is manifest by change
in the tubes for both mulga snake and tiger snake
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
18.104.22.168 Advanced qualitative confirmation test(s)
as for 22.214.171.124
126.96.36.199 Simple quantitative method(s)
188.8.131.52 Advanced quantitative method(s)
A radioimmunoassay 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 biologicals specimens
184.108.40.206 Simple qualitative test(s)
220.127.116.11 Advanced qualitative confirmation test(s)
18.104.22.168 Simple quantitative method(s)
22.214.171.124 Advanced quantitative methods(s)
126.96.36.199 Other dedicated methods(s)
No data available.
8.2.3 Interpretation of toxicological analyses
For venom detection as for 188.8.131.52 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 Biochemical analyses
184.108.40.206 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 be due to renal damage or poor
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
Electrolytes: if indicated (eg. inappropriate ADH
220.127.116.11 Other biological specimens
8.3.2 Arterial blood gas analysis
Performed in the setting of impaired respiratory function,
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 is likely to be 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).
time (TCT) > 150 secs (normal <16 secs).
Fibrinogen <0.1 g/l (normal 1.5-4.0 g/l).
products grossly elevated
Platelet count normal.
If the patient exhibits the above picture in the context of
a snakebite then they have a defibrination-type
coagulopathy. 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. This implies that all circulating venom has been
neutralized, at which point further antivenom therapy can
be withheld until the trend of improving results is
confirmed. No further antivenom therapy for the
coagulopathy is indicated (unless there is a subsequent
In the patient seen late or initially treated elsewhere
there may be no abnormal clotting time (INR < 2.0) but
fibrinogen may be low and associated with raised
degradation products. In this case the results may indicate
a minor or resolved coagulopathy not requiring antivenom
therapy. Note that the platelet count (complete blood
picture) will usually be normal despite the intense
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 Investigations and Their Interpretation
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 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. These 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 which is now resolved
and will usually not require antivenom therapy. However they
should be observed carefully for evidence of relapse.
9. CLINICAL EFFECTS
9.1 Acute poisoning/envenomation
No data available.
No data available.
9.1.3 Skin exposure
If skin surface intact, no effects.
9.1.4 Eye contact
No data available.
9.1.5 Parenteral exposure
In practical terms, subcutaneous or intradermal injection
is the only likely route of entry.
Early symptoms (usually in the first six hours).
Local: pain, mild to severe; oedema, mild; ecchymosis,
variable, mild; 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
Local: rarely a small area of superficial necrosis may
develop, particularly if first aid is left in place more
than 4 hours, or if a tourniquet is used (Sutherland 1981,
1983a; White 1987d; Frost, 1981).
Myolysis - muscle weakness and movement pain. Dark urine.
Renal impairment - oliguria or anuria. Paralysis and
coagulopathy not convincingly reported.
9.2 Chronic poisoning by:
No data available.
No data available.
9.2.3 Skin exposure
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
No data available.
No data available.
9.3 Course, prognosis, cause of death
Initially the patient will usually be anxious, knowing they have
sustained a snakebite. 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).
Bites will vary in severity with the species of black snake
involved in addition to the factors mentioned above.
P. australis: Potentially moderate to severe bite,
P. butleri: As above (no human case data).
P. papuanus: As above.
P. porphyriacus: Generally mild bites, not lethal in adults
P. colletti: As for P. porphyriacus (little human case data)
P. guttatus: As for P. porphyriacus (little human case data).
Minor envenoming: little or no venom injection, no development
of systemic envenomation, no need for antivenom treatment, no
likely sequelae or complications.
Moderate envenoming: bite usually at least slightly painful,
with some local reactions usually including local swelling and
sometimes ecchymosis, subsequent development over the next few
hours of some or all of the following: headache, nausea,
vomiting, abdominal pain, collapse, and possibly convulsions
(more likely in children).
On the evidence of current human case data, paralysis is unlikely
to occur following Pseudechis envenomation but caution dictates
that it should at least be sought; early signs include ptosis and
diplopia. The same applies to coagulopathy which, if present, is
most likely due to true anticoagulation rather than
defibrination; however, laboratory evidence of coagulopathy
should be sought.
Antivenom treatment at this stage may arrest or reverse the
various manifestations of systemic envenomation. Without
antivenom treatment, in most cases of P. australis, P. papuanus,
and probably P. butleri envenomation, the symptoms and signs will
show progressive worsening. Progressive myolysis and muscle
movement pain; and secondary renal failure are particular risks;
secondary complications of the above, particularly pneumonia,
should be considered. The ultimate outcome may be death, more
than 24 hours post-bite.
For bites by P. porphyriacus, and probably P. colletti and P.
guttatus, the clinical picture is in general less severe. There
may be quite significant local symptoms (especially swelling and
pain) and some systemic symptoms (headache, nausea, vomiting, and
abdominal pain). It is rare for other problems to occur.
Specifically it appears that significant myolysis and renal
damage are not seen, and most bites with envenomation are not
life-threatening and, at least in healthy adults, may not require
Severe envenoming: most likely if the bite is either multiple,
or associated with a chewing bite and numerous teeth marks. P.
porphyriacus, P. colletti, P. guttatus bites are not likely to be
lethal. Severe envenoming is only likely after bites by P.
australis, P. butleri, P. papuanus. Note that, as with any form
of envenomation, atypical cases may occur which are more severe
than might be expected for that species.
The following applies to bites by P. australis, P. butleri, P.
papuanus. Local reactions such as ecchymosis, oedema and pain
likely. Rapid development of headache, and possibly collapse,
and convulsions (especially children), sometimes within 30
minutes of bite. Subsequent symptoms may include headache,
nausea, vomiting, abdominal pain, and evidence of progressive
myolysis and renal impairment. Paralysis and defibrination-type
coagulopathy are not likely on the evidence of current case data
(although research data suggest that paralysis may be possible).
However, myolysis may mimic some features of paralysis due to
muscle movement pain and intrinsic weakness. Features of
paralysis should be looked for such as ptosis and diplopia.
Myolysis may take several hours to develop. Renal damage may
occur early. Prompt antivenom treatment is required as soon as
nature of envenomation evident. The myolysis may not be
preventable, and may result in widespread muscle damage, which
will eventually resolve. Renal damage is probably reversible,
after a period of dialysis.
Without antivenom treatment patients with severe envenoming may
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
Multiple bites nearly always are associated with more
In the past, perhaps as many as 30% of all P. australis
snake bites have proved fatal when no antivenom treatment
was used. No data are available on the fatality rate
associated with antivenom treatment, but deaths do still
occur.The situation with P. papuanus and P. butleri is
probably similar or less severe. For P. porphyriacus it is
clear that very few deaths have occurred, and probably none
in normal healthy adults, but children and the elderly may
be at more risk. This should be born in mind when deciding
on the merits of antivenom therapy as the subjective
symptomatology for the patient may be worse than the degree
of envenomation actually present. Bites by P. colletti and
P. guttatus are probably similar in severity to those of P.
porphyriacus, although case data are lacking, and there are
no known fatalities.
Causes of death
Myolysis This appears to be the major clinical
problem. Fatal cases poorly
Renal Failure Includes secondary complications such
Anaphylaxis Acute allergic reaction to venom in a
patient previously exposed to
Pseudechis snake venom (eg reptile
Cardiac complications likely to be secondary, and their
role in Pseudechis snake bite
9.4 Systematic description of clinical effects
Collapse, presumably due to hypotension, is seen in the
early stages of systemic envenomation at least by P.
australis, especially in children. The mechanism is
uncertain but may be due to release of vasoactive
Specific cardiac abnormalities due to Pseudechis
envenomation in man are not described.
No primary effects of Pseudechis venom on the respiratory
system in man are reported.
No direct CNS toxins have been reported for Pseudechis
venom, early collapse and convulsions may occur,
especially in children. Their aetiology remains
18.104.22.168 Peripheral nervous system
Effect of venom uncertain and of little clinical
22.214.171.124 Skeletal and smooth muscle
Pseudechis venom has been shown to act at the
neuromuscular junction experimentally but not
clinically. Presynaptic neurotoxins are present but
their clinical significance is uncertain.
Theoretically, they may cause progressive
neuromuscular paralysis, up to complete paralysis of
all muscles of respiration. No documented cases.
Nausea and vomiting may occur. In the presence of a venom-
induced coagulopathy, haematemesis and even melaena may
occur, though they appear rare, even in severe
envenomation. Abdominal pain is sometimes described.
Direct hepatic effects of Pseudechis venom have not been
noted clinically or experimentally.
No direct nephrotoxin has been reported from
Pseudechis venom, nor has renal failure been reported
but in one fatal case there was evidence of renal
damage, and it is potentially a very serious
complication of envenomation. The nature of the renal
injury and its cause are poorly documented, but acute
tubular necrosis seems most likely.
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
The local bite site is often painful, with significant
swelling, and ecchymosis is sometimes seen. Teeth marks
are variable, from single fang puncture to multiple tooth
punctures and scratches. Local necrosis may occur, but is
usually minor if present, unless a tourniquet is used as
first aid. Secondary infection may occur (White 1983b).
9.4.9 Eye, ear, nose, throat: local effects
No data available.
A major clinical effect of most Australian snake
envenomation in man is coagulopathy caused by potent
procoagulants in the venom, which cause prothrombin
activation and secondary fibrinogen consumption. Initially,
this was also thought to be true of Pseudechis bites,
especially P. papuanus and P. australis. It now appears
this is not so and therefore major bleeding is not likely.
However, minor bleeding problems associated with the
anticoagulant effect of the venom may occur.
An early neutrophil leukocytosis may occur in some patients.
Significant depletion of circulating lymphocytes may occur
in the early stages of envenomation, with resultant
No data available.
126.96.36.199 Acid base disturbances
188.8.131.52 Fluid and electrolyte disturbances
Secondary fluid and electrolyte disturbances due to
renal failure (if present), or myolysis may occur.
Beware particularly of hyperkalaemia.
The possibility of inappropriate ADH (antidiuretic
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 occurs). A rise in CK to below 1000
U/l is not indicative of rhabdomyolysis. True venom-
induced rhabdomyolysis causes CK levels well above
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 black snakes are also
at risk of acute anaphylactic allergic reactions on
subsequent bites, which may cause collapse within minutes
of the bite. Fatalities have occurred due to this
mechanism with other species (Notechis), and the author is
aware of severe non-fatal acute allergic type reactions
following bites by P. porphyriacus (Sutherland 1983; White
1987 b,d, White unpublished observations).
9.4.14 Other clinical effects
Due to direct action of myotoxins on muscle cells, causing
widespread muscle damage. This causes muscle weakness,
muscle tenderness, muscle movement pain, diminished deep
tendon reflexes, rise in serum CK, and myoglobinuria (dark
brown urine). If muscle damage is severe, recovery may take
weeks, although full functional recovery is possible.
Severe muscle wasting may be apparent, and intensive
physiotherapy is required to prevent contractures in the
early stages, and to promote rapid muscle regeneration in
the later stages.
9.4.15 Special risks
No data available.
No data available.
10.1 General Principles
All patients suspected of having sustained a Pseudechis 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 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 by supporting vital bodily functions.
(b) Neutralise inoculated venom.
(c) Correct venom-induced abnormalities.
(d) Prevent or correct secondary complications.
If there is evidence of systemic envenomation, antivenom therapy
is the most important treatment. Once the snake has been
identified (eg by venom detection) consider giving specific
antivenom depending on the clinical situation and the species of
snake involved (see section 9). Bites by P. australis, P.
papuanus, and probably P. butleri will require antivenom therapy
(CSL Black Snake Antivenom).
Bites by P. porphyriacus, and probably P. colletti and P.
guttatus often may not require antivenom therapy despite systemic
envenomation (especially in adults, see section 9), and if
antivenom is required then CSL Tiger Snake Antivenom is preferred
(cheaper and of lower volume) (White 1981; 1987d; Sutherland
1983; Trinca 1963).
Symptomatic and general treatment
Support of cardiorespiratory systems.
Treatment of shock.
Maintain adequate renal perfusion.
Avoid respiratory depressant medications (eg morphine).
Avoid antiplatelet medications (eg aspirin).
10.2 Relevant laboratory analysis 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 is useful but
serum or plasma are 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). 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.
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
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
Urine: For 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
Antivenom therapy, maintenance of adequate renal diuresis and, in
the latter stages during recovery, appropriate diet (high
protein) and physiotherapy. Carefully monitor for hyperkalaemia,
both directly, and by ECG changes.
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. Dialysis may be required.
Local bite site
The bite site should be cleaned only after adequate sampling for
venom. Local infection may occur, but is not usual, and thus
prophylactic antibiotic therapy is not appropriate. Tetanus
prophylaxis should be ensured. If there is minor local necrosis,
this can usually be successfully treated conservatively. Only
rarely will local skin necrosis be sufficient to warrant
debridement and grafting, and this is best left until the acute
phase of envenomation is over, and the area of injury clearly
delineated. Pseudechis bites do not apparently cause sufficient
local reaction to justify surgical decompression, although local
swelling can be quite severe, and extend to involve most or even
all of the bitten limb, and occasionally the adjacent trunk
(especially bites by P. australis). If compartment syndrome is
suspected, then it should be confirmed by intracompartmental
pressure measurement prior to any surgical intervention.
The principal method of treatment of defibrination-type
coagulopathy is the neutralisation of all inoculated venom by
antivenom. However, it is unclear whether this applies to the
mild anticoagulant type problems seen with some Pseudechis
envenomations, most notably due to bites by P. australis and P.
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 the attempt is unsuccessful. For similar
reasons, venepuncture from major veins, such as the femoral,
should be avoided, and used only as a last resort.
In severe cases of systemic envenomation by Pseudechis species,
where antivenom treatment has been delayed, it is possible
paralysis may occur and even progress to complete or near
complete respiratory paralysis although there are no documented
human cases (compare with some cases from Papua New Guinea of P.
papuanus envenomation, which may have actually been due to
Oxyuranus scutellatus canni, a species known to cause paralysis).
In this situation early intervention by endotracheal intubation
and artificial ventilation may be lifesaving. Based on experience
with other species from Australia, such respiratory support may
be needed for hours, days, or even weeks, until adequate
respiratory function returns. Once established, severe paralysis
might not be reversible by antivenom therapy.
Analgesia 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).
Steroids may be useful in treatment of severe allergic reactions,
or in the prophylaxis of serum sickness, but their role in the
general treatment of Pseudechis snake bite is doubtful.
10.6 Antidote/antivenin treatment
Antivenom (CSL, Melbourne) is the specific treatment of
Pseudechis snake bite. Two specific antivenoms and Australian
polyvalent antivenom are each effective. The type of monovalent
(specific) antivenom most appropriate depends on the species of
Pseudechis and the two groups will be discussed separately below
(Trinca 1963; Sutherland 1974, 1983b; White 1981, 1987d).
For bites by P. australis, P. butleri and P. papuanus, the
preferred antivenom is CSL Black Snake Antivenom. One ampoule
contains 18,000 units of activity against mulga snake (P.
australis) venom, but is active against venoms of all other
members of the genus. The antivenom is a refined horse serum
(Fab2 fragments), with all the potential hazards of that product.
This is sufficient to neutralise the "average" amount of venom
produced by a single milking of one snake (Pseudechis australis).
In a severe bite, and multiple bites, several ampoules of
antivenom may be necessary. The average volume of Black Snake
antivenom (horse serum) per ampoule is 35 ml, but the precise
volume varies from batch to batch.
For bites by P. porphyriacus, P. colletti and P. guttatus,
antivenom is not often required, even in the presence of general
systemic symptoms, because major envenoming is very rare and the
mortality rate is very low (possibly only one recorded case). The
quantity of venom produced by these snakes is also less than for
the mulga snake and therefore only a third of one ampoule of
Black Snake Antivenom is recommended as a standard dose. However
CSL Tiger Snake Antivenom is also active against the venoms of
these three Pseudechis species, the equivalent dose being one
ampoule. As this will be a lower volume of antivenom, it is
theoretically safer and less likely to result in side effects.
The cost of Tiger Snake Antivenom is also much less than Black
Snake Antivenom, and therefore the current recommendations are
that if a bite by one of these three snakes requires antivenom
therapy, then Tiger Snake Antivenom is the preferred choice, not
Black Snake Antivenom.
Antivenom must be given intravenously.
Since skin testing is unreliable and hazardous, there is no place
for pre-treatment 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
Always have adrenaline drawn up 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 of
admnistration if there is no reaction; try 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,
should be considered. 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
For bites by P. australis, P. butleri and P. papuanus, in the
presence of moderate systemic envenomation (as defined in 9.3)
initially give one ampoule of Black Snake Antivenom Follow up
with further ampoule(s) if progression of symptoms and signs,
(White 1983c; 1987 c,d).
In the presence of severe envenomation, initially give 2 ampoules
of antivenom, and be prepared to give more, as above.
There is no mandatory upper limit on antivenom dosage, but only
rarely will more than 4-5 ampoules be required
Antivenom may not be required even in the presence of envenoming
for bites by P. porphyriacus, P. colletti and P. guttatus, except
possibly in children or the infirm (see above). If antivenom
therapy is indicated, commence with one ampoule of Tiger Snake
Antivenom. Only rarely would further doses be required.
The dosage of antivenom is identical in children to that in
adults. However, in small children fluid volume considerations
may indicate the need for lower dilutions of antivenom. For any
given bite the degree of envenomation will be worse in children
due to their 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
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).
10.7 Management discussion
Controversies in management exist in several areas, and have
already been discussed.
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, 1977 a,b,c; 1983b; White 1987d)
Use of skin pretesting: not appropriate.
There are many aspects of Pseudechis venom worthy of further
research, at a basic science level, as well as studies at a more
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Case 1 (Rowlands et al, 1967)Pseudechis australis
Fatal case of mulga snake bite in a 20 year-old man in Western
Australia. This is the only reported fatality from this species.
Bitten on the hand at least twice by a 1.8m specimen (positive
identification). At 2 hrs post-bite there was nausea and
vomiting. At 4 hrs post-bite he was lethargic with weak limb
movements, dilated but reactive pupils, and red urine (?
myoglobin). Given antivenom (no black snake antivenom available,
ie no specific antivenom therapy). Continued to deteriorate and
at 37 hrs post-bite was irritable, restless, drowsy, had
abdominal pain, little movement of upper part of chest, bilateral
ptosis, limited jaw movement, limited tongue extension, weak
skeletal muscle, decreased tendon jerks, and severe swelling of
the bitten hand and arm up to the axilla. The urine was still
red, and the plasma potassium raised (6.0 mEq/l). there was no
coagulopathy, but there was a thrombocytopenia (19 x 109/l). He
rapidly developed a progressive hypotension and then a fatal
cardiac arrest 39 hrs post-bite. Autopsy performed shortly after
showed severe subcutaneous oedema, haemorrhage and infiltration
with neutrophils at the bite site, two small subepicardial
haemorrhages, many small foci of swollen damaged myocardial
fibres, congested lungs with pulmonary oedema, congested swollen
kidneys, severe liver congestion, no specific brain abnormality
apart from congestion, and all sectioned skeletal muscle showed
swelling and acute coagulative necrosis of muscle fibres
consistent with rhabdomyolysis, worse in the muscles of the
bitten arm, the respiratory muscles, and the extra-ocular
Case 2 (Sutherland 1983)P. australis
A 4 year-old girl was multiply bitten by a 1.8 m mulga snake on
the lower leg. By 15 mins post-bite she was pale, tachycardia
(160 bpm), vomiting, and had enlarged lymph nodes in her groin.
By about 45 mins post-bite she was semi conscious and had ptosis
and required respiratory support with oxygen. She was promptly
given polyvalent antivenom (2 amps), and thereafter made a rapid
improvement. There was no other evidence of a paralytic process,
nor a bleeding diathesis, and urine was normal. She subsequently
developed an abscess at the bite site.
Case 3 (Balmain & McClelland, 1982)P. australis
A 3 year-old boy was bitten on the arm by a snake (later
positively identified as venom of mulga snake). By 20 mins he was
vomiting, but by 2 hrs he was conscious and in no distress
(effective first aid still in place), and had no evidence of
significant envenomation. Therefore no antivenom was given at
this time. He remained well until 20 hrs post-bite when he
developed "haematuria", at which time it was discovered he had
elevated FDP (> 40mg/l), prolonged clotting time (APTT 50 secs.).
A decision was made to give antivenom after review of the
results, commencing at about 26 hrs. post-bite. Subsequent
results showed myolysis (CPK 27500 U/l) and haemolysis (Hb fell
from 122 to 94 g/l). He subsequently made a complete recovery,
and did not develop renal failure.
Case 4 (Vines, 1978; White, 1981)P. australis
A 24 year-old man was bitten on the thenar eminence by a large
mulga snake he was attempting to catch. He used a tourniquet as
first aid, and developed severe local swelling and subsequent
gangrene of the thumb requiring amputation. Prior to antivenom
therapy he had a prolonged clotting time, rectified after
antivenom. There was no evidence of neurotoxic problems, and no
details about the coagulopathy, or about evidence for myolysis or
Case 5 (Campbell, 1967)P. papuanus
A report of experience with snakebite in Port Moresby, Papua New
Guinea with reference to bites by the Papuan black snake. 13
cases are listed, but subsequent experience suggests many or most
of these cases, where the snake was not positively identified,
were more likely due to other species (especially Oxyuranus
scutellatus canni). In only one case was the snake positively
identified. Overall, the series showed 9 of 13 cases with
paralysis (5 severe), 4 with coagulopathy, 4 with severe
haemolysis, and 1 with renal failure.
Case 6 (Sutherland, 1983)P. porphyriacus
A brief review of 5 cases:
(i) 15 year-old male bitten on the finger. Developed local
swelling and axillary tenderness, vomiting, and headache;
required antivenom therapy (6000 U Blacksnake antivenom).
(ii) 23 year-old male bitten on the foot. Developed local pain,
groin pain, but no systemic symptoms, possibly due to early
antivenom therapy (9000 U Blacksnake antivenom).
(iii) 7 year-old boy bitten on the foot. Developed local pain,
swelling, and vomiting and severe abdominal pain. Given
antivenom therapy (6000 U Blacksnake antivenom). Foot still
swollen the next day.
(iv) 23 year-old male bitten on the hand (?). Rapidly developed
vomiting, painful bitten arm and axilla, then abdominal
pain, blood-stained diarrhoea, and by 3 hrs post-bite
twitching of the limbs, mild headache, haematuria, and
faecal incontinence. Subsequent antivenom therapy (6000 U
Blacksnake antivenom) resolved his symptoms.
(v) 20 year-old male bitten on the finger. Developed local pain
and swelling, vomiting, latterly blood stained. antivenom
therapy was therefore given (6000 U Blacksnake antivenom),
with rapid recovery.
Case 7 (Sutherland, 1979)P. porphyriacus
Very brief second hand report of a presumed bite by this snake
which resulted in grand mal convulsions in a previously well non-
epileptic person. Outcome unknown.
Case 8 (Potter & Gaudry, 1988)P. porphyriacus
A 24 year-old male was bitten on the hand. He used a tourniquet
as first aid. He developed severe pain in the bitten arm,
abdominal pain, nausea, vomiting, tender axillary adenopathy, and
there was no evidence of coagulopathy (tests NAD), or myolysis
(CPK 340 U/l). He was given antivenom therapy (3000 U Tiger snake
antivenom), and his symptoms resolved apart from severe pain in
the bitten arm and adjacent axilla, and a rise in CPK (to 1460
U/l on day 4). This settled over the next few days. It was
considered the severe arm pain was due to compartmental syndrome
secondary to local ischaemia caused by the tourniquet.
11.2 Internally extracted data on cases
Mulga Snake bites (P. australis)
Experience with 10 cases has been that most occurred in reptile
keepers or persons trying to catch snakes (7 of 10). 7 showed
some evidence of envenomation, mostly mild. No cases showed
paralytic symptoms or signs, or renal damage. In 3 cases there
was some evidence of a mild disturbance of coagulation, without
evidence of significant defibrination. In 4 cases there was
evidence of myolysis. All cases with significant envenomation
showed obvious local swelling, often involving much of the bitten
limb, and most bites were locally painful.
Case 1 (White, 1987d)P. australis
A 48 year-old man in a remote country area was found unconscious
by his son and taken to the local hospital where he was noted as
drowsy, cold, hypotensive (BP 90/65), and with a swollen hand.
Later questioning revealed that at no time had the patient either
seen a snake or felt a bite. As he had a past history of
myocardial infarction a further episode was assumed. However
serial ECG and enzyme studies were not consistent with such a
diagnosis, and the swollen hand and a peak CPK of 13758 U/l
suggested snakebite. Urine was positive for mulga snake venom. As
he was already recovering well no antivenom was given.
Case 2 (White, 1987d)P. australis
An 11 year-old boy was bitten on the thumb by a small (? 0.9m)
mulga snake he was trying to capture. He rapidly developed
headache, abdominal pain, nausea, vomiting, and local swelling
and pain in the bitten hand. He was given antivenom therapy (1
amp. polyvalent antivenom, then 1 amp. blacksnake antivenom). He
remained drowsy overnight but then made a full recovery, apart
from the bitten hand which remained swollen and painful for
several days. There was no evidence of paralytic problems,
significant coagulopathy (mild elevation of FDP), or renal
damage, and peak CPK was only 400 U/l.
Case 3 (White, unpublished case)P. australis
A 17 year-old male was bitten on the hand by a moderate sized
(approx 1.5-2 m) mulga snake he was trying to catch. He
subsequently developed headache, nausea, vomiting, diarrhoea,
dark urine, generalised aches and a painful swollen bitten hand.
As he was in a remote area retrieval and antivenom therapy were
delayed. By the time he was seen by the author he had a
significantly swollen tender hand, tender axilla, muscle movement
pain, reduced muscle power, but no ptosis, diplopia or other
evidence of classic paralytic envenomation. His urine was dark
red brown and positive for myoglobin. His peak CPK on day 2 was
25658 U/l. His renal function was normal, and FDPs were not
elevated although initially he had a slightly prolonged clotting
time (PR 1.4, APTT 49 secs). His urine remained dark for several
days, and his hand remained swollen and painful for about one
Red Bellied Black Snake bites (P. porphyriacus)
Experience with 20 cases has been that while most show evidence
of envenomation (15 of 20), it is rarely more than mild and is
without significant complications. The only serious case was in a
reptile keeper previously bitten who had a severe anaphylactic-
type reaction on a subsequent bite, with collapse, hypotension,
disseminated intravascular coagulation (DIC) and other secondary
problems. In most cases there was at least mild local pain and
swelling of the bite area, often associated with mild general
symptoms such as headache, abdominal pain, and nausea. None of
the cases showed evidence of paralysis, coagulopathy (compare
with above noted case with secondary DIC), myolysis or renal
Case 4 (White, 1987d)P. porphyriacus
A 24 year-old male was bitten on his finger by his pet snake. He
had been consuming alcohol prior to the accident. About 1 hr
post-bite he became dizzy, short of breath, vomited, then lapsed
into unconsciousness for a brief period. At this time the bitten
hand was painful and swollen. Testing at this time did show any
evidence of coagulopathy or myolysis, and as he was
symptomatically improving and had a history of past antivenom
exposure no antivenom was used. He made a rapid recovery although
the hand remained swollen and painful for several days.
Case 5 (White, 1987d)P. porphyriacus
A 9 year-old boy was bitten on his toe by an adult black snake
while walking near a creek. By 30 mins post-bite he was nauseous,
with abdominal pain, and shortly afterwards started vomiting. The
identity of the snake was confirmed by venom detection. Tests
showed no myolysis or significant coagulopathy (mild prolongation
of clotting time, ie PR 1.45). At 2 hrs post-bite he was
symptomatically improved and antivenom was withheld. At 4 hrs
post-bite he again developed abdominal pain and vomiting lasting
2 hrs, thereafter not recurring. The bitten foot was painful for
about 6 hrs, and was swollen for several days.
Blue bellied black snake
Case 6 (White, unpublished case)P. guttatus
A 33 year-old male was bitten on his hand while handling his pet
blue bellied black snake. By 1 hr post-bite the hand was painful,
starting to swell, and he developed a headache, nausea, and
blurred vision. There was no objective evidence of paralytic
problems, but he was tender in the axilla. There was no evidence
of coagulopathy or myolysis, and his general symptoms rapidly
improved without antivenom therapy. However the hand and arm
became progressively more painful and swollen, and a cellulitis
or compartmental syndrome was considered though not proven.
Antibiotic therapy was commenced but the arm remained swollen and
painful for about a week, then after apparently improving there
was a return of local symptoms which again took several days to
Case 7 (White, unpublished case)P. colletti
A 16 year-old male was bitten on the hand by 3 pet snakes, one
being a small colletts snake. He developed local pain and
swelling, and drowsiness, but was neurologically stable. These
latter symptoms resolved rapidly but the hand remained swollen
for several days. There was no evidence of coagulopathy.
11.3 Internal cases
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes and antitoxins
Specific black snake antivenom, tiger snake antivenom and venom
detection kits are available directly from the manufacturer,
Commonwealth Serum Laboratories, 45 Poplar Road, Parkville,
Victoria 3052, Australia (telephone: 03-3891911, telex: AA
32789, Fax: 61-3-3891434).
12.2 Specific preventative measures:
Avoid exposure to black 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
No data available.
13.1 Clinical and Toxicological
Balmain R & McClelland KL (1982) Pantyhose 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.
Bernheimer AW, Weinstein SA, Linder R (1986) Isoelectric
analysis of some Australian elapid snake venoms with special
reference to phospholipase B and haemolysis. Toxicon 24(8):
Bernheimer AW, Linder R, Weinstein SA, Kim KS (1987) Isolation
and characterization of a phospholipase B from venom of Collett's
snake Pseudechis colletti. Toxicon 25(5): 547-554.
Broad AJ, Sutherland SK & Coulter AR (1979) The lethality in
mice of dangerous Australian and other snake venoms. Toxicon,
Campbell CH (1967) The Papuan black snake (Pseudechis papuanus)
and the effect of its bite. Papua New Guinea Med. J. 10(4):
Campbell CH, Chesterman CN (1972) The effect of the venom of the
Papuan black snake (Pseudechis papuanus) on blood coagulation.
Papua New Guinea Med J.. 15(3); 149-154.
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.
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.
Doery HM, Pearson JE (1961) Haemolysins in venoms of
Australian snakes. Biochem. J., 78: 820-27.
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.
Fisher M (1982) First aid in envenomation. Med. J. Aust.,
Harris JB, Johnson MA, Karlsson E (1975) Pathological responses
of rat skeletal muscle to a single subcutaneous injection of a
toxin isolated from the venom of the Australian tiger snake,
(Notechis scutatus scutatus). Clin. exp. Pharm. Physiol. 2: 383-
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-
Leonardi TM, Howden MEH, Spence I, (1979) A lethal myotoxin
isolated from the venom of the Australian king brown snake
(Pseudechis australis). Toxicon 17: 549-55.
Marshall LR, Herrmann RP (1983) Coagulant and anticoagulant
action of Australian snake venoms. Thrombosis Haemostasis
Marshall LR, Herrmann RP (1989) Australian snake venoms and
their in vitro effect on human platelets. Thrombosis Research
Mebs D, Samejima Y (1980) Myotoxic phospholipases A from snake
venom, Pseudechis colletti, producing myoglobinuria in mice.
Mebs D, Samejima Y (1980) Purification from Australian elapid
venoms and properties of phospholipases A which cause
myoglobinuria in mice. Toxicon, 18: 443-454.
Mebs D, Ehrenfeld M, Samejima Y (1983) Local necrotizing effect
of snake venoms on skin and muscle: relationship to serum
creatine kinase. Toxicon, 21(3):393-404.
Moon KE, Rys A (1984) Amino terminal analysis of Pseudexin from
the venom of the Australian red-bellied black snake (Pseudechis
porphyriacus). Toxicon 22(1): 165-167.
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.
Nishida S, Terashima M, Shimazu T, Takasaki C, Tamiya N (1985a)
Isolation and properties of two phospholipases A2 from the venom
of an Australian elapid snake (Pseudechis australis). Toxicon
Nishida S, Terashima M, Tamiya N (1985b) Amino acid sequences
of phospholipases A2 from the venom of an Australian elapid snake
(Pseudechis australis). Toxicon 23: 87-104.
Potter D, Gaudry P (1988) A case of snakebite with unusual
features. Med. J. Aust., 149: 565.
Rowan EG, Harvey AL, Takasaki C, Tamiya N (1989) Neuromuscular
effects of three phospholipases A2 from the venom of the
Australian king brown snake Pseudechis australis. Toxicon. 27:
Rowlands JB, Mastaglia FL, Kakulas BA, Hainsworth DA (1969)
Clinical and pathological aspects of a fatal case of mulga
(Pseudechis australis) snakebite. Med. J. Aust. 1: 226-229.
Schmidt JJ, Middlebrook JL (1989) Purification sequencing and
characterization of Pseudexin phospholipases A2 from Pseudechis
porphyriacus (Australian red-bellied black snake). Toxicon
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 (1977c) Acute untoward reactions to antivenoms.
Med. J. Aust., 1:841.
Sutherland SK (1979) Epilepsy after envenomation by a red-
bellied black snake. Med. J. Aust. 2:257.
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 & 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.
Takasaki C, Tamiya N (1982) Isolation and properties of
lysophospholipases from the venom of the Australian elapid snake
Pseudechis australis. Biochem J. 203: 269-276.
Takasaki C, Tamiya N (1985) Isolation and amino acid sequence of
a short chain neurotoxin from an Australian elapid snake
Pseudechis australis. Biochem. J. 232: 367-371.
Takasaki C (1989) Amino acid sequence of a long chain neurotoxin
homologue Pa 1D from the venom of an Australian elapid snake
Pseudechis australis. J. Biochem. 106: 11-16.
Takasaki C, Sugama A, Yanagita A, Tamiya N, Rowan EG, Harvey AL
(1990a) Effects of chemical modifications of Pa-11 a
phospholipase A2 from the venom of the Australian king brown
snake (Pseudechis australis) on its biological activities.
Toxicon 28(1): 107-117.
Takasaki C, Suzuki J, Tamiya N (1990b) Purification and
properties of several phospholipases A2 from the venom of
Australian king brown snake (Pseudechis australis). Toxicon.
Takasaki C, Yutani F, Kajiyashiki T, (1990c) Amino acid
sequence of eight phospholipases A2 from the venom of Australian
king brown snake Pseudechis australis. Toxicon 28(3): 329-339.
Trethewie ER (1971) The pharmacology and toxicity of the venoms
of the snakes of Australia and Oceania. In Eds. Bucherl W,
Buckley EE, Venomous Animals And Their Venoms, Academic Press,
New York, : 79-101.
Trinca JC (1963) The treatment of snakebite. Med. J. Aust.,
Vaughan GT, Sculley TB, Tirrell R (1981) Isolation of a toxic
phospholipase from the venom of the Australian red-bellied black
snake (Pseudechis porphyriacus) Toxicon 19: 95-101.
Vines A (1978) Severe local reaction to bite of king brown
snake. Med. J. Aust. 1:657.
White J (1981) Ophidian envenomation; a South Australian
perspective. Records of the Adelaide Children's Hospital,
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.
Cogger HG (1971) The venomous snakes of Australia and Melanesia.
In Eds. Bucherl, W., Buckley, E.E., Venomous Animals And Their
Venoms, Academic Press, New York,: 35-77.
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.
14. AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)
Author: Dr Julian White
State Toxinology Services
Adelaide Children's Hospital
North Adelaide, South Australia 5006
Mobile phone: 61-18-832776
Date: August 1990
Peer review:Singapore, November 1991.