| 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|
| 3.3.3 Other physico-chemical characteristics|
| 3.4 Other chemicals in the animal|
|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|
| 5.6 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|
| 188.8.131.52 Adults|
| 184.108.40.206 Children|
| 7.2.2 Animal data|
| 7.2.3 Relevant in vitro data|
| 7.3 Carcinogenicity|
| 7.4 Teratogenicity|
| 7.5 Mutagenicity|
| 7.6 Interactions|
|8. TOXICOLOGICAL/TOXINOLOGICAL AND BIOMEDICAL INVESTIGATIONS|
| 8.1 Material sampling plan|
| 8.1.1 Sampling and specimen collection|
| 220.127.116.11 Toxicological analyses|
| 18.104.22.168 Biomedical analyses|
| 22.214.171.124 Arterial blood gas analysis|
| 126.96.36.199 Haematological analyses|
| 8.1.2 Storage of laboratory samples and specimens|
| 188.8.131.52 Toxicological analyses|
| 184.108.40.206 Biomedical analyses|
| 8.1.3 Transport of laboratory samples and specimens|
| 220.127.116.11 Toxicological analyses|
| 8.2 Toxicological analyses and their interpretation|
| 8.2.1 Tests on toxic ingredient(s) of the material|
| 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 method(s)|
| 8.2.2 Tests for biological 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 method(s)|
| 126.96.36.199 Other dedicated method(s)|
| 8.2.3 Interpretation of toxicological analyses|
| 8.3 Biomedical investigations and their interpretation:|
| 8.3.1 Biochemical analyses|
| 188.8.131.52 Blood, plasma or serum|
| 184.108.40.206 Urine|
| 220.127.116.11 Other biological specimens|
| 8.3.2 Arterial blood gas analyses|
| 8.3.3 Haematological analyses|
| 8.3.4 Other (unspecified) analyses|
| 8.3.5 Interpretation of biomedical investigations|
| 8.4 Other biomedical (diagnostic) investigations and their interpretation|
| 8.5 Summary of most essential biomedical and toxicological analyses in acute poisoning and their interpretation |
|9. 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 contact|
| 9.2.4 Eye contact|
| 9.2.5 Parenteral exposure|
| 9.2.6 Other|
| 9.3 Course, prognosis, cause of death|
| 9.4 Systemic description of clinical effects|
| 9.4.1 Cardiovascular|
| 9.4.2 Respiratory|
| 9.4.3 Neurological|
| 18.104.22.168 CNS|
| 22.214.171.124 Peripheral nervous system|
| 126.96.36.199 Autonomic|
| 188.8.131.52 Skeletal and smooth muscle|
| 9.4.4 Gastrointestinal|
| 9.4.5 Hepatic|
| 9.4.6 Urinary|
| 184.108.40.206 Renal|
| 220.127.116.11 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|
| 18.104.22.168 Acid base disturbances|
| 22.214.171.124 Fluid and electrolyte disturbances|
| 126.96.36.199 Others|
| 9.4.13 Allergic reactions|
| 9.4.14 Other clinical effects|
| 9.4.15 Special risks|
| 9.5 Other|
| 10.1 General Principles|
| 10.2 Relevant laboratory analyses and other investigations|
| 10.2.1 Sample collection|
| 10.2.2 Biomedical analysis|
| 10.2.3 Toxicological analysis|
| 10.2.4 Other investigations|
| 10.3 Life supportive procedures and symptomatic treatment|
| 10.4 Decontamination|
| 10.5 Elimination|
| 10.6 Antidote treatment|
| 10.6.1 Adults|
| 10.6.2 Children|
| 10.7 Management discussion|
|11. ILLUSTRATIVE CASES|
| 11.1 Cases and reports from literature|
| 11.2 Internally extracted data on cases|
| 11.3 Internal Cases|
|12. ADDITIONAL INFORMATION|
| 12.1 Availability of antidotes|
| 12.2 Specific preventative measures|
| 12.3 Other|
| 13.1 Clinical and Toxicological References|
| 13.2 Zoological References|
|14 AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)|
1.1 Scientific Name
Oxyuranus microlepidotus (McCoy)
Oxyuranus scutellatus (Peters)
subspecies scutellatus scutellatus
subspecies scutellatus canni
Note: Some authors still maintain the junior synonym
Parademansia microlepidota for this species, however it is now
generally accepted as O. microlepidotus. In some early Australian
papers on venomous snakes and snake venom, O. scutellatus is
listed as Pseudechis scutellatus and Oxyuranus maclennani.
1.3 Common Names
Scientific Name Common Name
Oxyuranus microlepidotus Western Taipan, Inland Taipan,
Fierce Snake, Small-scaled Snake
Oxyuranus scutellatus Taipan, Common Taipan
Oxyuranus canni New Guinea Taipan
2.1 Main risks and target organs
Taipans are a relatively minor cause of snakebites in Australia
in relation to numbers of cases, but assume a far more important
position due to the extreme hazard of their bites. Without
appropriate antivenom treatment up to 75% of taipan bites will be
fatal. Indeed, in the era prior to specific antivenom therapy,
virtually no survivors of taipan bite were recorded.
Main risks are: neurotoxic paralysis, coagulopathy,
rhabdomyolysis, acute renal failure.
Target organs: neuromuscular junction, coagulation system,
2.2 Summary of clinical effects
Locally: Local effects appear variable, not all cases being
significantly painful. Bite marks are usually visible, due to
the moderately large fangs, but in some cases local erythema or
oedema may be absent. A complete set of teeth marks including
fangs, post-maxillary teeth, pterygopalatine teeth and mandibular
teeth may be present (Figure ). However, only minor fang marks
may be seen in other cases (Figure ). Local secondary infection
is unusual. Venom may spread to draining lymph nodes with
consequent pain and/or tenderness and/or swelling. Local
symptoms and signs may be made worse by prolonged use of first
Systemic: headache, nausea, vomiting, abdominal pain, impaired
conscious state, occasionally (especially in children) loss of
consciousness and convulsions. Coagulopathy rarely with overt
bleeding manifestations. Progressive neurotoxic paralysis. Muscle
movement pain. Acute renal failure.
Monitor the coagulation profile to establish the presence and
extent of coagulopathy and as an index of systemic envenomation.
Should be performed at presentation, on development of symptoms
or signs of systemic envenomation, and 1-2 hours after antivenom
therapy until sufficient antivenom given to reverse coagulopathy.
In the absence of a clotting laboratory, whole blood clotting
time in a glass test tube is useful. If a clotting laboratory is
available, prothrombin ratio, activated partial thromboplastin
time, thrombin clotting time, fibrinogen level, and fibrin(ogen)
breakdown products (FDP or XDP) are most useful.
Other useful tests include: complete blood picture and platelet
count; serum electrolytes, creatinine, urea; serum enzymes,
especially creatine phosphokinase; urine output and urine
Venom detection using CSL Venom Detection Kit. The best sample is
a swab from the bite site (sample swab stick in kit). If the
patient has systemic envenomation, urine may also be a 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 possible.
(d) The bandaged limb should be firmly immobilised
using a splint.
(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
(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
(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
(a) Specific: If the patient has systemic
envenomation, give taipan snake antivenom (CSL).
(b) General: Support of cardiac and respiratory
functions; treatment of shock; maintenance of
adequate fluid load, electrolyte balance, and
renal output; tetanus prophylaxis; treatment of
local sepsis with antibiotics; treatment of
significant blood loss with blood transfusion.
(c) Local: Do not clean or touch local wound until
appropriate samples taken for venom detection.
Thereafter ensure antisepsis. Early surgical
intervention is generally contraindicated, and is
only rarely indicated in the late stages, in the
unusual event that significant local necrosis has
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.
Fang length in adult taipans is variable and dependent on
species; O. microlepidotus, 3.5 - 6.2 mm; O. scutellatus, 7.9 -
Average venom yield is: O. microlepidotus, 44 mg, max. 110 mg;
O. scutellatus, 120 mg, max. 400 mg. Mean venom injected at first
bite (defensive strike) is: O. microlepidotus, 17.3 mg, range
0.7-45.6 mg, with mean venom left on skin 0.6 mg; O. scutellatus,
20.8 mg, range 0.6-68.9 mg, with mean venom left on skin 0.9 mg.
2.6 Main toxins
Oxyuranus venom is a complex mixture of protein and non-protein
components, not all of which have been fully evaluated.
(a) Neurotoxins: both presynaptic (taipoxin) and
(b) Procoagulants: principally factor Xa analogues,
acting largely independently of cofactors (eg
factor V, calcium, phospholipid), converting
prothrombin to thrombin (meziothrombin).
(c) Myolysins: second action of presynaptic
neurotoxins (eg taipoxin) which contain a
phospholipase A2 component.
3.1 Description of the animal
3.1.1 Special identification features
Taipans are large snakes. Male specimens of O. scutellatus
attain a maximum snout-vent length of 156 cm. The maximum
snout-vent length for females is 144 cm. O. microlepidotus is
only slightly smaller, 132 cm for males, 145 cm for females.
Covacevich et al (1981) describe the colour and pattern of each
species of Oxyuranus: O. scutellatus unmarked light olive to dark
russet brown dorsally (specimens from Tully area, NE Qld, almost
black); head usually lighter coloured, especially in the rostral
and labial regions; ventrally cream, usually with pink or orange
flecking; buccal cavity pink; eye reddish; O. microlepidotus pale
to very dark brown dorsally, often with dark flecks which may
form distinct bands posteriorly; head glossy black in most
freshly collected specimens (this sometimes fades with
captivity); ventrally (behind the black neck region) mustard
yellow without flecks; buccal cavity in dark specimens blue grey
shading to pink, in lighter coloured specimens greyish pink
shading to off-white; eye black.
The heads of Taipans are large, oblong, almost rectangular (in O.
scutellatus) to moderately elongate (in O. microlepidotus). The
canthus rostralis is pronounced in O. scutellatus, but not in O.
The skulls of O. scutellatus and O. microlepidotus are similar,
but they differ in size and proportion and there are minor
differences in dentition (Covacevich et al 1981). The fangs of
O. scutellatus are long (7.9 - 12.1 mm) while those of O.
microlepidotus are of moderate length (3.5 - 6.2 mm). Posterior
to the fangs on the maxilla in O. scutellatus there is a single,
solid tooth. In O. microlepidotus there are several maxillary
teeth posterior to the fangs, and these are structurally
identical to the fangs (ie they are syringe-like for most of
their length) (Figures ).
Oxyuranus microlepidotus: 23 (rarely 25) mid-body scales,
anal single, ventral 211-224, sub-caudals 54-66 paired. Eye
diameter smaller than its distance from the mouth (Figures).
Oxyuranus scutellatus: mid-body scales 21-23, anal single,
ventrals 220-248, sub-caudals 48-76 paired. Eye diameter
greater than its distance from the mouth (Figures ).
O. scutellatus occurs coastally in open forest, dry closed
forests, heathlands, grasslands and cultivated areas. It is
well known in and near sugar-cane plantations.
O. microlepidotus is confined to vast treeless semi-arid and
arid ashy downs remote from the coast.
O. scutellatus is widely distributed in northern and eastern
Australia and in southern Papua New Guinea (O. scutellatus
canni). In Australia it occurs in northwest Western
Australia, in northern parts of the Northern Territory
(including near coastal islands), across Cape York Peninsula
and throughout coastal Queensland as far south as the
Beaudesert area (Figure ___). O. microlepidotus occurs in
the drainage systems of Cooper Creek, the Diamantina River
and the Georgina River in far western Queensland and north
eastern South Australia (Figure ___).
3.2 Poisonous/Venomous Parts
Venom glands (paired) situated superficially in posterior part of
head, connected by ducts to forward placed (paired) fangs (Figure
3.2.1). Fangs moderate in length (see 3.1), sometimes with
multiple reserve fangs (Figure 3.1.1). Fangs may leave small
puncture marks (Figure 2.2.2) through to a complete set of teeth
marks (Figure 2.2.1), or scratches.
3.3 The toxin(s)
Oxyuranus venom; Taipan venom; O. microlepidotus venom; O.
Neurotoxins: Taipoxin (O. scutellatus),
Paradoxin (O. microlepidotus),
O. scutellatus fraction III
O. scutellatus fraction IV
Coagulants: Direct prothrombin converter (O. scutellatus)
Whole venom production based on milking specimens, usually
in captivity, and lethality (LD50 sc mice).
Species Average Maximum LD50
Oxyuranus microlepidotus 44 mg 110 mg 0.025
Oxyuranus scutellatus 120 mg 400 mg 0.099
3.3.3 Other physico-chemical characteristics
Taipoxin - presynaptic neurotoxin, phospholipase A2 based,
moderately acidic sialo-glycoprotein, MW 45,600, as a
ternary complex 1:1:1 with a , b , g subunits. a and b
subunits are 120 amino acids long, with 7 disulphide
bridges. g subunit has 135 amino acids and 8 disulphide
bridges. Only the very basic (pI >10) g-subunit has lethal
neurotoxicity. LD50 of complete molecule is 2 mg/kg (IV
mouse). 17% of venom.
O. scutellatus fraction III - minimal data. Presumed
postsynaptic neurotoxin. LD50 100 mg/kg (IV mouse). 47% of
O. scutellatus fraction IV - minimal data. Presumed
postsynaptic neurotoxin. LD50 100 mg/kg (IV mouse). MW
approximately 8,000. 10% of venom.
Paradoxin - presynaptic neurotoxin, phospholipase A2 based,
essentially identical to taipoxin. It accounts for 12% of
crude venom, is a sialo-glycoprotein with three subunits and
has an LD50 of 2 mg/kg (IV mouse). Amino acid analysis of
paradoxin and taipoxin, both in whole form and as subunits,
shows close homology.
Prothrombin converters from O. scutellatus venom - a large
multichain protein, MW approximately 300,000 D, consisting
of an enzymatic unit of 57,000 D and a cofactor of 220,000
D, the latter promoting the prothrombinase activity of the
former. Structurally resembles factor Xa-Va complex.
Prothrombinase activity is independent of factor V, but
enhanced by phospholipid and calcium. The enzymatic unit
appears to consist of two chains, each approximately 30,000
D, linked by a disulphide bond, while the cofactor has two
chains, 110,000 D and 80,000 D.
No prothrombin converter has been reported for O.
In monkeys, O. scutellatus clearly causes coagulopathy but
O. microlepidotus does not. However, in human envenomation
both species can cause marked defibrination-type
Taipoxin (see above)
In monkeys O. scutellatus venom is myolytic, and O.
microlepidotus only mildly myolytic.
3.4 Other chemicals in the animal
Very little information is available on minor components which
have a weak haemolytic action.
O. microlepidotus has moderate hyaluronidase activity.
4. CIRCUMSTANCES OF POISONING
Venom is used both in antivenom production and for laboratory
research. The neurotoxins in particular have proved valuable in
neuromuscular transmission research, while the procoagulant has
been used in assays of prothrombin level in plasma and other
studies on blood coagulation.
4.2 High risk circumstances
Children: when playing in areas where taipans are common, either
through accidental encounter (ie stepping on snake) or while
trying to emulate naturalists (ie trying to catch snake).
Adults: when living in areas where taipans are common, and moving
around barefoot and without due care, or while putting hands etc
into non-reconnoitred potential snake retreats (ie hollow logs
Farm workers: when working in areas where taipans are common.
Manual labour cane field harvesting may be a particular high risk
Reptile keepers and snake handlers: if due care is not exercised
in catching and handling snakes, including venom milking. Taipans
are particularly fast and agile snakes, and so may be more
difficult to handle safely than most other Australian snakes.
Recreation seekers: camping or walking or playing sport in areas
where taipans are common.
Homes: around homes in taipan prone areas when water is scarce
and free water is available in the garden or home.
4.3 High risk geographical areas
Note distribution of taipans in Australia
(sections 3.1.2, 3.1.3).
Some areas of Australia are known to have high populations of
snakes, and there are many instances of localities where there
are very frequent encounters with potentially dangerous snakes.
These high densities with high incidences of sightings of
specimens usually occur in spring and early summer, when the
snakes emerge from their winter inactivity to search for food or
mates. For example, Pseudechis porphyriacus can be very common in
the Macquarie Marshes, ME New South Wales and Acanthophis
antarcticus is also extremely common in some parts of the
Numinbah Valley, SE Queensland. (Covacevich, unpublished data).
In coastal Queensland, the presence of the introduced cane toad,
Bufo marinus, may have led to an increase in populations of
taipans, O. scutellatus. Shine and Covacevich (1983) have
demonstrated that in the period since the introduction of cane
toads (ie, in 1935), numbers of taipans donated to the Queensland
Museum have increased dramatically in relation to numbers of
donations of other potentially dangerous snakes from the same
area. Of course, this is not conclusive evidence that
populations have increased. Such an inference seems reasonable,
however, because cane toads are known to have deleterious effects
on many species of frog-eating native vertebrates, especially
snakes (Covacevich and Archer, 1975). The highly potent body
toxins of cane toads make them lethal prey. Taipans (Oxyuranus
spp) are not directly affected in this way because they feed
exclusively on mammals, a characteristic unique amongst the
5. ROUTES OF ENTRY
No data, but unlikely to be hazardous unless there are open
wounds in gastrointestinal tract.
No evidence that venom can be absorbed through intact skin.
Current first-aid advice is to leave venom on skin for later
Unlikely, no cases reported.
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. Intramuscular or
intravenous inoculation is much less likely.
Stings: not possible.
Experimentally, venom may be administered to test animals via
subcutaneous, intramuscular, intravenous, intraperitoneal, and
intraventricular (CNS) routes, as well as directly applied to
target tissues or organs (ie muscle, liver, kidney, plasma).
6.1 Absorption by route of exposure
The rate and amount of absorption will depend on the quantity of
venom injected, the depth of injection, site of injection
including vascularity, the activity of the victim, and the type,
efficiency of application and length of application of first aid.
Clinical evidence from human cases of envenomation suggests that
much initial venom movement is via the lymphatic pathways. This
is supported by work in monkeys using RIA to detect whole venom.
Direct intravenous injection, rare in man, obviously allows rapid
systemic circulation of venom and may result in different effects
from normal routes of inoculation, particularly in regard to
coagulation. In sheep given IV tiger snake venom as a bolus,
complete coagulation of blood in the heart occurred within
minutes, causing irreversible cardiac arrest. While similar
experiments with taipan venom have not been performed, this venom
possesses a more potent procoagulant and a similar outcome might
6.2 Distribution by route of exposure
As noted in 6.1, it appears that much venom is transported from
the bite site via the lymphatic system, then concentrating in
draining lymph nodes, before ultimately reaching the systemic
However, experience with a number of human cases of taipan
envenomation shows that symptoms and signs of envenomation may
occur within 15-30 minutes of the bite, especially in children.
Such early effects (eg headache, nausea, abdominal pain,
collapse) may be due to either rapidly systemically circulating
venom toxins, or systemically circulating natural agents 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. Such venom must also exit the circulation, to enter the
extravascular space where it binds within the neuromuscular
junction (presynaptically and/or postsynaptically) and possibly
other nerve junction sites (eg autonomic system, perhaps causing
The kinetics of venom distribution, excretion, and detoxification
are incompletely understood. Neurotoxic paralysis usually
takes 2-4 hours to become clinically detectable. Coagulopathy
however may become well established within 30 minutes of a bite.
6.3 Biological half-life by route of exposure
Substantive data in man are not available.
Little information is available on the metabolism of venom
components in man, but most components are fully active in whole
venom, requiring no further modification for activity. As venom
reaches high concentrations in the kidneys, where it is excreted
in urine, and does not reach equivalent concentrations in the
liver, it could be postulated that little detoxification of venom
components occurs, the body instead relying on direct excretion
of unaltered venom. The fate of specific venom components,
particularly neurotoxins and procoagulants, is unclear. Once
fixed at the nerve terminal, it seems unlikely that the
neurotoxins would then release, return to the circulation, and
exit via the kidney. As the term of paralysis is finite, it seems
more likely that these components are progressively detoxified in
6.5 Elimination by route of exposure
As mentioned previously, most venom is eliminated via the
kidneys, in urine.
7.1 Mode of action
Whole venom contains a variable mixture of presynaptic and
postsynaptic neurotoxins, the latter poorly defined and much less
toxic. Composition of this mixture may or may not be uniform
across all populations of taipans.
The presynaptic neurotoxins (eg taipoxin, paradoxin) appear to
bind directly to the cell membrane of the terminal axon, at the
neuromuscular junction. After a latent period of approximately
60-80 minutes, the neuromuscular block becomes detectable (in
isolated nerve-hemidiaphragm preparations of mouse), and is
rapidly established as essentially complete paralysis. This is
associated with a reduction in cholinergic synaptic vesicle
number, fusion of vesicles, and damage of intracellular
organelles such as mitochondria. There is an increase in the
level of free calcium in the nerve terminal. Thus the
neurotransmitter acetylcholine appears to be progressively
removed or made unavailable for release, causing paralysis.
(Dowdall et al 1977; Eaker 1978; Cull-Candy et al 1976; Datyner &
The postsynaptic neurotoxins cause blockade of the acetylcholine
receptor on the muscle end-plate at the neuromuscular junction.
As this action is extracellular, these toxins are more readily
reached by antivenom.
Procoagulants and coagulopathy
Procoagulants have been isolated from O. scutellatus venom and O.
microlepidotus venom. They are proteins, with a MW of about
200,000 D, and achieve their action in a manner analogous to
factor Xa, causing conversion of prothrombin, through
intermediates, to thrombin. However, they are direct
prothrombin converters, working largely independent of cofactors
in the absence of factor V, calcium and phospholipid. The
thrombin product then converts fibrinogen to fibrin clots in
vitro. (Walker et al, 1980, Speijer et al, 1986)
In human envenomation there is widespread consumption of
fibrinogen resulting in defibrination and hypocoagulable blood.
Any damage to blood vessels then causes increased bleeding,
although spontaneous bleeding is not often seen. Usually
platelets are not consumed, but factors V, VIII, Protein C and
plasminogen all show acute reductions in human envenomation.
While major clots are not seen in man, some fibrin cross linkage
and stabilisation does occur in vivo, as XDP levels rise sharply
in human envenomation. (White 1983c; White 1987c; White
Some of the presynaptic neurotoxins are also directly myolytic
(eg taipoxin) and cause major destruction of skeletal muscle,
locally and systemically, both in experimental animals and
occasionally in human envenomation. The phospholipase A2
components of these toxins may hydrolyse muscle cell surface
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 phosphokinase (CK
or CPK) peaking at between 10 to 20 hours post-bite. Myoglobin
levels also rise and are excreted in the urine, causing the
typical dark brown discolouration. (Sutherland et al, 1981b,
Brigden & Sutherland, 1981).
No specific nephrotoxins have been detected in taipan venom, but
a few cases of renal function impairment have been reported in
humans envenomed by O. scutellatus (Brigden & Sutherland, 1981;
White unpublished data). In one case this was apparently
secondary to renal damage by myoglobin. Other possible causes
include: breakdown products of fibrin released secondary to the
coagulopathy; breakdown products of red cells secondary to venom-
induced haemolysis; deposition of venom and immunoglobulin
complexes in the kidney; vascular impairment in the early stages,
eg secondary to "shock".
7.2.1 Human data
The human lethal dose for taipan venom is unknown.
However, without antivenom treatment, a significant
number of taipan bites may be fatal.
No data available, but clearly their smaller body mass
ensures that children are more likely to receive a
lethal dose than adults.
7.2.2 Animal data
LD50 mg/kg (18-20g mice), subcutaneous injection of dried
venom in mice (Broad et al, 1979, Sutherland 1983b)
Saline Bovine Serum
Oxyuranus microlepidotus 0.025 0.010
Oxyuranus scutellatus 0.099 0.064
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 BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
188.8.131.52 Toxicological analyses
For venom detection: swab from bite site moistened in
sterile saline. If systemic envenomation also collect
urine (5ml in sterile container).
For venom analysis (research only using
radioimmunoassay). 5ml blood; 5ml urine, frozen.
At autopsy collect vitreous humor, lymph nodes draining
bite area, excised bite site.
(For other laboratory tests see 10.2.1)
184.108.40.206 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).
220.127.116.11 Arterial blood gas analysis
Collect arterial blood by sterile arterial puncture
into a container as issued by the laboratory.
18.104.22.168 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; EDTA will be used for complete blood
8.1.2 Storage of laboratory samples and specimens
22.214.171.124 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).
126.96.36.199 Biomedical analyses
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
188.8.131.52 Toxicological analyses
Use insulated container.
8.2 Toxicological analyses and their interpretation
8.2.1 Tests on toxic ingredient(s) of the material
184.108.40.206 Simple qualitative test(s)
Simple qualitative test for presence of snake venom and
designation of species/genus group, corresponding to
the most appropriate monovalent anti-venom. This test
is a commercial test sold by antivenom manufacturer as
a kit (Snake Venom Detection Kit; CSL Melbourne)
(Coulter et al 1980; Chandler & Hurrell 1982; Hurrell &
(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. Yellow faced whip snakes may cause
positive venom detection in either wells indicating
brown snake venom or tiger snake venom (Williams and
(10) Detection limit
The manufacturer states the kit will detect as low as
10ng venom per 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.
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
220.127.116.11 Advanced qualitative confirmation test(s)
As for 18.104.22.168
22.214.171.124 Simple quantitative method(s)
126.96.36.199 Advanced quantitative method(s)
A radioimmune assay has been developed by staff at the
Commonwealth Serum Laboratories, Melbourne to detect
small quantities of many Australian snake venoms. It is
primarily a research tool, being too time-consuming to
be practical in determining emergency treatment of
snakebite victims. It has proved useful in
demonstrating snake venom either at autopsy or after
8.2.2 Tests for biological specimens
188.8.131.52 Simple qualitative test(s)
184.108.40.206 Advanced qualitative confirmation test(s)
220.127.116.11 Simple quantitative method(s)
18.104.22.168 Advanced quantitative method(s)
22.214.171.124 Other dedicated method(s)
8.2.3 Interpretation of toxicological analyses
For venom detection as for 126.96.36.199 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
188.8.131.52 Blood, plasma or serum
Electrolytes: Look for imbalance, particularly evidence
of dehydration, hyponatraemia (inappropriate ADH
syndrome?), hyperkalaemia (renal damage,
Urea, creatinine: Look for evidence of renal function
CK: If high may indicate rhabdomyolysis, usually
greater than 1000 u/l.
Output: Low output may indicate renal damage or poor
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
184.108.40.206 Other biological specimens
8.3.2 Arterial blood gas analyses
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 likely is a defibrination-type
coagulopathy which will render the blood unclottable. This
will usually result in the following key results:
Prothrombin ratio /INR >12 (normal about 0.8-1.2).
APTT >150 secs (normal <38 secs).
Thrombin clotting time (TCT) > 150 secs (normal <16 secs).
Fibrinogen <0.1 g/l (normal 1.5-4.0 g/l).
Fibrin(ogen) degradation products grossly elevated
Platelet count normal.
If the patient exhibits the above picture in the context of
a snakebite then they have a defibrination-type
This will require specific antivenom therapy (see section
10) and repeated tests of coagulation status to define
progress of the coagulopathy and titrate antivenom therapy
against resolution. The earliest sign of resolution will be
a rise in fibrinogen level and this may first be seen as a
reduction in the TCT from > 150 secs, often to 80 secs or
less. This may occur before there is a detectable rise in
fibrinogen titre. It indicates that the pathologic process
of venom-induced defibrination has ceased implying that all
circulating venom has been neutralized, at which point
further antivenom therapy can be withheld until the trend of
improving results is confirmed, in which case no further
antivenom therapy for the coagulopathy is indicated (unless
there is a subsequent relapse).
In the patient seen late or treated initially elsewhere
there may be no abnormal clotting time, with an INR < 2.0,
but fibrinogen may be low associated with raised degradation
products. In this case the results may indicate a minor or
resolved coagulopathy not requiring antivenom therapy.
Note that the platelet count (complete blood picture) will
usually be normal despite the intense defibrination.
In a few cases the platelet count may start to fall as or
after resolution of the defibrination occurs. This is
usually associated with renal damage and renal function
should be assessed. In this setting the thrombocytopenia may
well be secondary to the renal damage.
8.3.4 Other (unspecified) analyses
8.3.5 Interpretation of biomedical investigations
The interpretation of the above tests should be made in the
context of total patient assessment including clinical
evidence of pathology such as paralysis, myolysis,
coagulopathy and renal damage.
8.4 Other biomedical (diagnostic) investigations and their
While other investigations are not usually required to make the
primary diagnosis of snakebite envenomation, they may be
indicated in response to secondary effects of envenomation. If
there is either renal failure or severe rhabdomyolysis there may
be a hyperkalaemia, hence an ECG may be appropriate. If the
patient is unconscious, especially in the presence of a severe
coagulopathy, then a CT head scan may be appropriate to determine
if there is intracranial pathology such as a haemorrhage.
8.5 Summary of most essential biomedical and toxicological
analyses in acute poisoning and their interpretation
Overall interpretation of the results of the above tests will
depend on the clinical setting. Results should never be
interpreted in isolation from an overall clinical assessment.
A patient with positive venom detection from either the bite site
or urine and a significant coagulopathy clearly is envenomed and
will usually require antivenom therapy.
A patient with positive venom detection from the bite site only
and with no clinical symptoms or signs of envenoming and all
other tests negative is not significantly envenomed at that point
in time and does not require antivenom therapy. However this
situation may change and so careful observation and repeat
testing would be indicated.
A patient presenting some hours after the bite with positive
venom detection from the urine but clinically well and with all
other tests either normal or showing a resolved coagulopathy,
probably had a minor degree of envenomation, now resolved and
will usually not require antivenom therapy. However they should
be observed carefully for evidence of relapse.
9. 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, this is the only likely route of entry,
by s.c. or i.d. injection.
Early symptoms, usually in the first six hours.
Local: pain, mild to severe; oedema, mild; ecchymosis,
variable, mild; persistent bleeding from wound, variable;
pain or swelling of draining lymph nodes (may take 1-4 hours
Systemic: collapse, unconsciousness, convulsions may all
occur, especially in children, occasionally as rapidly as 15
minutes after the bite. Headache, nausea, vomiting,
abdominal pain, and visual disturbance may all occur.
Early signs of neurotoxic paralysis such as ptosis,
diplopia, dysarthria may develop within 1-3 hours of the
Coagulopathy may develop within 30 minutes of the bite.
Local: rarely a small area of superficial necrosis may
develop, particularly if first aid left in place more than 4
hours, or if a tourniquet used (Sutherland 1981, 1983a;
Paralysis: progressive up to complete paralysis.
Coagulopathy: bleeding from all puncture wounds.
Myolysis: muscle weakness and movement pain. Dark urine.
Renal impairment: oliguria or anuria.
No data available.
9.2 Chronic poisoning by:
No data available.
No data available.
9.2.3 Skin contact
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
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).
Minor envenoming: little or no venom injection, no development of
system envenomation, no need for antivenom treatment, no likely
sequelae or complications.
Moderate envenoming: bite usually at least slightly painful, with
some local reactions, subsequent development over next few hours
of some or all of the following: headache, nausea, vomiting,
abdominal pain, collapse, convulsions (especially in children),
early signs of paralysis, such as ptosis, diplopia, and
laboratory evidence of coagulopathy. Antivenom treatment at this
stage will usually arrest or reverse the various manifestations
of systemic envenomation. Without antivenom treatment, in most
such cases the symptoms and signs will show progressive
worsening, with deepening coagulopathy and an increased chance of
secondary haemorrhage (beware intracranial haemorrhage),
progressive paralysis which may ultimately progress to complete
respiratory paralysis, about 18-24 hours post-bite; progressive
myolysis and muscle movement pain; secondary renal failure;
secondary complications of the above, particularly pneumonia;
ultimate outcome may be death, more than 24 hours post-bite.
Severe envenoming: most likely if bite either multiple, or
associated with chewing bite and numerous teeth marks. Local
reactions such as ecchymosis, oedema and pain likely. Rapid
development of headache, collapse, convulsions (especially
children), sometimes within 30 minutes of bite. Subsequent
symptoms may include headache, nausea, vomiting, abdominal pain,
and evidence of progressive paralysis, coagulopathy, myolysis and
renal impairment. Ptosis and diplopia may be evident within 2
hours of bite; coagulopathy may be detectable within 30 minutes
of bite; myolysis may take several hours to develop. Renal damage
may occur early. Prompt antivenom treatment required as soon as
nature of envenomation evident. In some circumstances paralysis
may be sufficiently advanced at a cellular level that antivenom
cannot prevent severe paralysis. In this situation, intubation
and assisted ventilation may be required for a variable period
(up to several weeks). The coagulopathy may only reverse
following large amounts of antivenom. The myolysis may not be
preventable, and may result in widespread muscle damage, which
will eventually resolve. Renal damage is usually reversible,
after a period of haemodialysis.
Without antivenom treatment such cases will almost certainly die.
Children are more likely to develop severe envenomation than
adults, and do so more rapidly.
Bites to the trunk or face are harder to manage with first aid,
and so may cause earlier development of envenomation.
Secondary infection of the local bite wound may occur.
Physical activity after a snakebite increases the rate of
absorption of venom and so hastens the onset of envenomation.
This situation often occurs in bites to children.
Multiple bites nearly always are associated with potentially
As noted above. Overall up to 75% of all taipan bites will prove
fatal if no antivenom treatment is used (based on statistics from
cases prior to specific taipan antivenom becoming available;
modern intensive care facilities may improve this figure
significantly). Insufficient data are available on fatality rate
with antivenom treatment, but deaths do still occur.
Causes of death
Coagulopathy primary eg cerebral haemorrhage;
secondary eg renal failure.
Paralysis primary eg respiratory failure;
secondary eg pneumonia
Renal Failure includes secondary complications such as
Anaphylaxis acute allergic reaction to venom in a
patient previously exposed to taipan
snake venom (eg reptile keeper).
Cardiac complications likely to be secondary
9.4 Systemic description of clinical effects
Collapse, presumably due to hypotension, is common in the
early stages of systemic envenomation, especially in
children. The mechanism is uncertain but may be due to
release of vasoactive substances from or by the venom.
Specific cardiac abnormalities due to taipan snake
envenomation in man have not been described.
No primary effects of taipan snake venom on the respiratory
system in man are not reported, with the exception of
respiratory muscle paralysis (see below).
While no direct CNS toxins have been reported for
taipan snake venom, early collapse and convulsions do
occur, especially in children. Their aetiology remains
220.127.116.11 Peripheral nervous system
Effect of venom uncertain and of little clinical
18.104.22.168 Skeletal and smooth muscle
Best documented effects of taipan snake venom are at
the neuromuscular junction, both experimentally and
clinically. Both presynaptic and postsynaptic
neurotoxins present, causing progressive neuromuscular
paralysis, up to complete paralysis of all muscles of
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 taipan snake venom have not been
No direct nephrotoxin has been reported from taipan
venom, but renal failure has been reported in a few
cases, and is a very serious complication of
envenomation, with a significant mortality, despite
antivenom treatment. The nature of the renal injury and
its cause are poorly documented, but acute tubular
necrosis seems most likely. Renal cortical necrosis
has not been reported, but has been seen in one case
(White unpublished records).
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
The local bite site may be painful, though not significantly
so in all cases. Similarly, while local oedema and even
ecchymosis may occur, it is not universal. 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 taipan envenomation in man is
coagulopathy caused by potent procoagulants in the venom,
which cause prothrombin activation and secondary fibrinogen
consumption. The resulting defibrination is associated with
hypocoagulable blood, and persistent bleeding from any
vascular injury, including venepuncture sites. Without
antivenom treatment, this may occasionally resolve.
However, as the venom is not apparently vasculotoxic, in the
absence of vascular injury bleeding does not occur, thus in
many patients the coagulopathy proves relatively benign.
An early neutrophil leukocytosis may occur in some patients.
Significant depletion of circulating lymphocytes may occur
in the early stages of envenomation, with resultant
22.214.171.124 Acid base disturbances
126.96.36.199 Fluid and electrolyte disturbances
Secondary fluid and electrolyte disturbances due to
renal failure if present. Inappropriate ADH (anti-
diuretic hormone secretion) syndrome should be
considered. In this situation, otherwise acceptable
intravenous fluid loads may result in significant
electrolyte imbalance and other sequelae.
Rise in serum levels of liver enzymes, cardiac enzymes,
plus CK (if rhabdomyolysis). A rise in CK to below 1000
IU/l is not indicative of rhabdomyolysis. True venom-
induced rhabdomyolysis causes CK levels well above 1000
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 taipans 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 (Sutherland
1983; White 1987 b,d).
9.4.14 Other clinical effects
Due to direct action of presynaptic neurotoxins (eg
Taipoxin) 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 frank 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 taipan bite should
be admitted to hospital for observation over the first 24 hours.
While all such cases should be treated as potentially fatal not
all cases will develop envenomation. Management of cases with
systemic envenomation may be divided into specific, symptomatic,
and general treatment.
The aims of treatment are:
(a) Maintain life through maintenance of
vital bodily functions.
(b) Neutralise inoculated venom.
(c) Correct venom-induced abnormalities.
(d) Prevent or correct secondary
If there is evidence of systemic envenomation, antivenom therapy
is the most important treatment. Once the snake has been
identified (eg by venom detection) give specific antivenom (CSL
Taipan Snake Antivenom). ( White 1981; 1987d; Sutherland 1983;
Symptomatic and general treatment
Support of cardiorespiratory systems.
Treatment of shock.
Maintain adequate renal perfusion.
Replace major blood loss due to
coagulopathy induced haemorrhage (but use blood
products only with great caution until
Avoid respiratory depressant
medications (eg morphine).
Avoid antiplatelet medications (eg aspirin).
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
Venom for venom detection: use CSL Venom Detection Kit; best
sample is swab from bite site (swab stick etc in kit); if
systemic envenomation present then urine useful;
serum/plasma less reliable. If a bandage has been applied
over the bite site as first aid, keep the bandage adjacent
to wound because this may have absorbed venom; it can be
tested to identify venom (after elution) if all other
samples negative in presence of significantly envenomed
Blood: Initially collect for complete blood count (EDTA
sample), clotting studies (citrated sample), electrolytes
and enzymes (heparin and/or clotted sample) and possibly,
group (type) and screen serum (clotted sample). In
anticoagulated blood samples ensure correct ratio of blood
to anticoagulant (especially citrate samples) and proper
mixing. If laboratory facilities unavailable, collect for
whole blood clotting time (ie 5-10 ml in glass test tube,
and measure time to clot). Samples for clotting studies in
particular should be kept cold during transportation.
Urine: Measure urine output, visual check for
haemoglobinuria or myoglobinuria (dark red-brown urine); if
suspect myoglobinuria collect samples at intervals for
subsequent laboratory confirmation (5-10 ml).
10.2.2 Biomedical analysis
Venom detection: Venom at the bite site confirms only the
species of snake, but venom in the urine indicates systemic
Coagulation studies: In the absence of a haematology
laboratory, whole blood clotting time is a useful test, for
both the presence of a coagulopathy, and its progress and
resolution with adequate antivenom therapy.
If a laboratory is available, the most useful tests for
presence and extent of coagulopathy are: Prothrombin
time/ratio; Activated partial thromboplastin time; Thrombin
clotting time; Fibrinogen assay; Fibrin(ogen) breakdown
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 haemoglobinuria and myoglobinuria
10.2.3 Toxicological analysis
Venom detection, see section 8.
10.2.4 Other investigations
As indicated medically.
10.3 Life supportive procedures and symptomatic
In severe cases of systemic envenomation by taipans, where
antivenom treatment has been delayed, paralysis may progress to
complete or near complete respiratory paralysis. In this
situation early intervention by endotracheal intubation and
artificial ventilation is lifesaving. Such respiratory support
may be needed for hours, days, or even weeks, until adequate
respiratory function returns.
Once established, such severe paralysis may not be reversed by
The principal method of treatment of taipan envenomation
coagulopathy is the neutralisation of all inoculated venom by
antivenom. Until this is achieved, use of clotting factor blood
products (eg fresh frozen plasma, cryoprecipitate, fibrinogen)
may only deepen the degree of coagulopathy, by providing more
substrate on which the venom may act. Once all venom is
neutralised normal homeostatic mechanisms quickly return
coagulation towards normal, without the need for replacement
therapy. The possible exception would be where there is major
bleeding as a result of the coagulopathy (eg cerebrovascular
accident), when replacement therapy should be considered once
adequate antivenom has been given. Heparin has no proven value
in this situation and there is evidence it may be harmful.
In cases of severe envenomation a central venous pressure (CVP)
line may be highly desirable for patient management, but in the
presence of coagulopathy should be inserted with great caution,
due to the likelihood of significant haemorrhage from the
insertion site if the insertion attempt is unsuccessful.
In such cases frequent testing of coagulation will be necessary
to titrate antivenom therapy. A CVP line will allow frequent
sampling without further breaches of veins, an important
consideration in severe coagulopathy where venepuncture may
result in bleeding for hours. For similar reasons, venepuncture
from major veins, such as the femoral, should be avoided, and
used only as a last resort.
Following resolution of the coagulopathy there may be rebound
hyperfibrinogenaemia at about 2-4 days post resolution. There is
a theoretical potential for hypercoagulability at this time,
particularly in the immobile paralysed ventilated patient, and
the possibility of thrombus formation and emboli, including
pulmonary emboli, should not be forgotten.
Apart from antivenom therapy, maintenance of adequate renal
throughput and, in the latter stages during recovery, appropriate
diet (high protein) and physiotherapy.
First priority is to avoid renal injury by ensuring adequate
renal perfusion. In all cases of significant systemic
envenomation, catheterisation of the bladder to monitor urine
output constantly is advisable. In severe cases of envenomation,
the use of a CVP line will assist in adjusting IV fluid load to
ensure adequate blood volume and renal perfusion.
Once renal injury is established, standard techniques of medical
management should apply. Haemodialysis may be required. Renal
biopsy should be avoided at least until the coagulopathy is
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. Taipan bites do not apparently cause sufficient local
reaction to justify surgical decompression. If compartment
syndrome is suspected, then it should be confirmed by
intracompartmental pressure measurement prior to any surgical
May be necessary, though most cases will need no more than
paracetamol. Morphine should be avoided (CNS depressant effect).
Platelet-active drugs should be avoided (eg aspirin).
May be useful in treatment of severe allergic reactions, or in
the prophylaxis of serum sickness, but their role in the general
treatment of taipan snake bite is doubtful.
10.6 Antidote treatment
Taipan snake antivenom (CSL, Melbourne) is the specific treatment
of taipan snake bite. It should only be used if there is definite
systemic envenomation. (Trinca 1963; Sutherland 1974, 1983b;
White 1981, 1987d)
The antivenom is a refined horse serum (Fab2 fragments), with all
the potential hazards of that product. One ampoule contains
12,000 units of activity against taipan snake venom. This is
sufficient to neutralise the "average" amount of venom produced
by a single milking of one snake (Oxyuranus scutellatus). In a
severe bite, and multiple bites, several ampoules of antivenom
may be necessary. The average volume of antivenom (horse serum)
per ampoule is 40 ml, but the precise volume varies from batch to
Taipan antivenom is used to counter the potentially life-
threatening systemic effects of venom and must be given
Since skin testing is unreliable and hazardous, there is no place
for pre-therapy sensitivity testing of antivenom. (Sutherland
1983b; White 1987d).
Acute allergic reactions up to and including potentially fatal
anaphylaxis may occur during antivenom therapy. Precautions
should be taken to reduce the risk to the patient. These include:
Only give antivenom if staff, drugs and equipment to treat severe
anaphylaxis, including intubation facilities are available
(preferably in an intensive care unit), unless in extreme
Always have adrenaline injection prepared and ready to use.
Always have a good reliable IV line inserted.
Always maintain adequate monitoring of patient during and after
antivenom therapy, especially blood pressure.
Dilute antivenom (1:5 to 1:10) in IV carrier solution (normal
saline; dextrose or Hartmann's).
Give antivenom initially very slowly, and increase rate if no
reaction, aiming to give whole dose over 15-20 minutes.
Premedication is proposed by some. (Sutherland 1983b) Suggested
premedications are subcutaneous adrenaline and intravenous
antihistamine. The author of this monograph does not routinely
use such premedication. (White 1987d) Antihistamine may make the
patient drowsy or irritable, and thus interfere with the ongoing
assessment of envenomation, especially in children. Adrenaline is
potentially hazardous, especially in older patients or those with
coagulopathy, and as acute severe allergic reactions may be
delayed up to an hour or more, such premedication is of doubtful
value. A patient with known or likely allergy to horse serum
presents a special case, where premedication as above, possibly
with the addition of steroids, is worthy of active consideration.
Similarly a sole country medical practitioner managing a severe
snakebite, where antivenom must be given before an aeromedical
evacuation team can arrive, may well consider premedication with
subcutaneous adrenaline a worthwhile precaution.
In the presence of mild to moderate systemic envenomation
(ie no or minor paralysis, no active bleeding from
coagulopathy etc) initially give one ampoule of antivenom
(dependent on species of tiger snake, see table below).
Follow up with further ampoule(s) if progression of symptoms
and signs, or if no resolution of coagulopathy. Resolution
of coagulopathy may be used to titrate antivenom therapy.
(White 1983c; 1987 c,d)
In the presence of severe envenomation, initially give 2
ampoules of antivenom, and be prepared to give more, as
above. If using the resolution of coagulopathy to titrate
antivenom therapy, aim to retest coagulation (see section
10.2.1) about 1 - 1.5 hours after completion of antivenom
dose. First evidence of impending resolution may be a
reduction in the thrombin clotting time, often accompanied
by a slight rise in fibrinogen level. If there is no
significant improvement, give further antivenom. If there is
significant improvement, repeat test in a further 1-2 hours
There is no mandatory upper limit on antivenom dosage, but
only rarely will more than 4-5 ampoules be required (also
dependent on species/subspecies of taipan snake).
The dosage of antivenom is identical in children to adults.
However, in small children fluid volume considerations may
force lower dilutions of antivenom. For any given bite the
degree of envenomation will be worse in children due to
lower body mass.
Following antivenom therapy there is a possibility that the
patient may develop serum sickness. This should be explained
to the patient so that if symptoms develop, they will seek
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
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.
Use of fibrinogen, fresh frozen plasma etc as primary treatment:
No proven benefit and potentially very dangerous. (White 1987d)
Use of heparin: of no proven benefit and potentially dangerous.
Based on the assumption that it is paralysis which kills the
patient and this can be managed adequately in an intensive care
unit by artificial ventilation, therefore antivenom is not
required, thus avoiding antivenom allergy problems. This ignores
the danger of coagulopathy, best managed by antivenom therapy,
and the fact that early antivenom therapy may avoid severe
paralysis and the hazards of artificial ventilation.
There are many aspects of taipan snake venom worthy of further
research, at a basic science level, as well as studies at a more
11. ILLUSTRATIVE CASES
11.1 Cases and reports from literature
General paper on snakebite, including 3 cases of definite or
probable taipan bite.
(i) A 49 year-old man was bitten on the right hand by a large
snake, thought to be a taipan. He was initially treated by
incision and tourniquet. At 1.5 hours post-bite he developed
nausea and vomiting, but remained otherwise well, except for the
bitten limb. This remained with a tourniquet in place for 7.5
hours, leaving the arm swollen and numb. He remained drowsy and
weak for several days, without paralysis being noted, and lost
both taste and smell, neither of which returned to normal. He
made an otherwise complete recovery. No antivenom treatment.
(ii) A 35 year-old Aboriginal man was bitten on the leg while on
a bicycle, by a snake thought to have been a taipan. Shortly
thereafter he had a convulsion from which he recovered, but then
commenced vomiting and 6 hours post-bite had 3 more convulsions,
and died. No antivenom treatment.
(iii) A 39 year-old man was bitten on the leg while fishing.
On presentation at hospital 5 hours later he was cyanosed,
comatose, with severe paralysis and dilated pupils. Death
occurred 6 hours post-bite. No antivenom treatment.
(i) Adult male bitten through trousers on right leg by 2.3 m
taipan, applied tourniquet, and remained symptom free until 1.1/2
hours after the bite, when he suddenly had a seizure, followed by
continual seizures and profuse perspiration, continuing until his
death, 5 hours after the bite.
(ii) Adult male bitten on the leg, while working in cane fields,
by a large brownish snake thought to be a taipan (never
confirmed). Initially symptom-free, but after a few hours (time
not stated) became unwell, with vomiting, then paralysis of
tongue and pharynx, then had convulsions and died.
(iii) A 20 year-old female Aborigine was bitten at 11 pm
while walking down a town street, by a large brown snake thought
to be a taipan. She was bitten on the dorsal aspect of the foot,
immediately ran for home, and collapsed unconscious 90 seconds
later, and had convulsions. She died shortly afterwards. Death
was reported due to asphyxia, with blood issuing from nose and
Reid and Flecker, 1950
A detailed case report with recovery. A 19 year-old Aboriginal
boy bitten on the right ankle while stacking timber. Snake killed
and confirmed as taipan. Bite occurred through boot and thick
socks, initially treated with tourniquet and incision. Between
15-30 minutes post-bite was unable to open eyes, then developed
nausea (?vomiting), dyspnoea, and drowsiness. By 4 hours post-
bite he was semiconscious, shocked, restless, and tiger snake
antivenom was sought and used without great success. By the
following day he was drowsy, restless, not shocked, breathing
spontaneously, but with ptosis, facial weakness, dysphagia, and
tongue paresis, although no ocular paresis was detected, and
pupils were reactive to light. DTRs sluggish, and limb weakness
was present. He made little improvement over the next 24 hours,
and thereafter a slow improvement until on day 7 he developed
serum sickness, from which he recovered over several days, being
discharged 19 days after the bite.
A 20 year-old amateur herpetologist was bitten on his left hand
by a taipan (identity confirmed), the bite initially treated with
a tourniquet. He remained well initially, with continued use of
a tourniquet, and received tiger snake antivenom. About 2 hours
post-bite the tourniquet was removed and at 4.5 hours post-bite
he developed blurred vision, vomiting, headache, ptosis, and
facial weakness. At this time the hand was red and swollen.
Paralysis extended over the next 4 hours, with medial rectus
palsy and severe ptosis, tongue paralysis, dysphagia,
dysarthria, and some decreased intercostal movement, and by 9.5
hours post-bite there was complete facial paralysis and minimal
respiratory capacity, requiring attempts at artificial
respiration (in a respirator). The patient resisted this
treatment, and maintained some respiration overnight, but with
developing cyanosis. At 23 hours post-bite he had a rigor. At 26
hours post-bite respiratory movements ceased, and he was again
put in the respirator. At 27 hours post-bite he died, possibly of
cardiac arrest. At autopsy the only finding noted was an area of
dry gangrene around the bite site.
(i) A detailed report, with the first successful use of the
newly available taipan antivenom. A 10 year-old boy was bitten
on the right knee by a snake thought to be a taipan (not
confirmed). He became unconscious almost immediately, recovering
consciousness spontaneously within 30 minutes, at which time he
was noted as pale, drowsy, without paralysis, and was given tiger
snake antivenom. He remained apparently stable until 19 hours
post-bite, when severe ptosis, dilated pupils, marked drowsiness,
abdominal pain, vomiting, and blood oozing from the wound were
noted. The paralysis progressed such that by 24 hours post-bite
he had almost complete ptosis, almost complete ophthalmoplegia,
dilated pupils almost unreactive to light, dysarthria, but no
respiratory distress. At 24.5 hours post-bite he received taipan
antivenom, suffering an allergic reaction controlled by
adrenaline. Within 1.5 hours a definite clinical improvement was
apparent, though marked ptosis remained. The bite site wound
continued to ooze. The ophthalmoplegia and ptosis had virtually
resolved by day 5 post-bite, though the wound still oozed, this
resolving the following day. He made a complete recovery.
(ii) An adult male, aged 19 years, suffered a bite from a
taipan (identity confirmed), subsequently developing vomiting of
"coffee grounds and bright blood", then ptosis, generalised
weakness, and finally respiratory paralysis ending fatally.
(iii) An adult male, aged 52 years, suffered a bite from a
possible taipan (identity not confirmed), remaining symptom-free
for 4 hours, then developing respiratory distress, dysarthria,
and ptosis, progressing to death some 12 hours post-bite.
Sutherland et al, 1980
A 4 year-old boy sustained multiple bites from a taipan (positive
identification of venom), with rapid development of drowsiness,
vomiting, then collapse, death occurring within 60 minutes. No
specific findings were noted at autopsy, other than evidence of
multiple fang punctures (12), and venom in tissues (2 mg/g of
Brigden and Sutherland, 1981
A 39 year-old man presented with a one hour history of nausea and
vomiting, at no stage believing he might have been bitten by a
snake. Six hours later he developed fixed dilated pupils, ptosis,
and progressive paralysis, ultimately requiring intubation and
artificial ventilation. No snake bite marks were found.
Coagulation studies revealed a severe coagulopathy. He was
hypertensive. He was given 4 ampoules of polyvalent antivenom.
Over the ensuing 12 hours he developed oliguria, and a grossly
elevated creatine kinase (19,600 IU/L), but the coagulopathy
reversed. He required ventilatory support for 19 days, and
peritoneal dialysis for renal failure, but made a complete
recovery, being discharged 27 days post-bite. Subsequent testing
of early urine samples was positive for taipan venom and
myoglobin (serum samples negative for venom).
Details of experience with six taipan bites in Port Moresby,
Papua New Guinea.
(i) A male, aged 10 years, bitten on leg, developed vomiting at
1.5 hours post-bite, then tender groin nodes, then mild
paralysis. Given taipan antivenom, with slight worsening of
paralysis but eventual recovery.
(ii) A man, aged 20 years, bitten on the ankle, did not develop
any evidence of envenomation, though was given antivenom.
(iii) A man, aged 35 years, bitten on the ankle, became
unconscious 30 minutes post-bite, with recovery, then later
vomiting and abdominal pain, bleeding problems, and severe
paralysis. Given antivenom, but paralysis progressed requiring
tracheostomy and artificial ventilation for 10 days, with
(iv) A man, aged 20 years, bitten on the foot, developed
epigastric pain and tenderness, and vomiting, without paralysis
being noted, received antivenom, and made a complete recovery.
(v) A man, aged 40 years, bitten on the ankle, developed a
headache at 30 minutes, nausea at 1 hour, tender groin nodes,
haemoglobinuria, albuminuria, and a coagulopathy. Recovered after
(vi) A woman, aged 20 years, bitten on the leg, developed
vomiting, headache, dysarthria, groin pain, and generalised
muscular paralysis. Antivenom was given with "no response", and
the patient required a tracheostomy and artificial ventilation,
with eventual recovery.
Trinca, 1969, and Sutherland et al, 1978
A detailed case report of a bite by what was subsequently shown
to be O. microlepidotus. A 46 year-old male amateur
herpetologist was bitten by a 1.5 m brownish snake in a remote
part of south-west Queensland, while catching the snake. He
sustained 2 bites to the right thumb. He incised the wounds and
applied a tourniquet. 50 minutes post-bite he collapsed,
unconscious, with faecal and urine incontinence. He regained
consciousness within 15 minutes. He remained stable, but with
muscle pain for several hours, then developed nausea and
vomiting. By 6 hours post-bite he had dysphagia and dysarthria,
and the bite site was swollen and cyanosed (tourniquet still in
place, with intermittent release). During the next 3 hours he
became agitated, confused, (while in transit in a Flying Doctor
aircraft) and on landing, about 9 hours post-bite, suffered a
cardiac arrest, from which he was successfully resuscitated. As
he had (incorrectly) identified the snake as a brown snake
(Pseudonaja) he was given brown snake antivenom (which is not
protective for taipan bites). He had a past history of severe
allergy to horse serum, though no anaphylaxis developed on
antivenom administration. He was subsequently placed on a
ventilator. Ptosis and ophthalmoplegia were present, but he
could move all limbs. At 17.5 hours post-bite he had a
hypotensive episode, with haematuria and bloody diarrhoea. By 24
hours post-bite the bleeding had subsided. He developed episodes
of frequent ventricular extrasystoles during aspiration of his
endotracheal tube, which continued intermittently, along with
transient hypertension. He made a slow recovery, requiring
ventilator support for several (unspecified) days. Subsequently
the dead snake was identified as a taipan (Oxyuranus
scutellatus) and later as a western taipan (O. microlepidotus).
Mirtschin et al, 1984
A 37 year-old amateur herpetologist was bitten on his left middle
finger by a juvenile O. microlepidotus (between 445 and 490 mm in
length, less than 1 month old) while attempting to force feed the
snake. At 20 minutes post-bite he complained of severe headache,
feeling flushed, and chest discomfort. No paralysis was noted.
Shortly thereafter he received one ampoule of taipan antivenom,
and made an uneventful recovery. There is no indication that
either coagulopathy or myolysis were tested for in this case.
11.2 Internally extracted data on cases
Case 1 (from White, 1987)
A 10 year-old boy was bitten on his left middle finger by a large
snake (later shown to be a taipan by identification of the venom
from bite site). Pressure/immobilisation first aid was applied 40
minutes later. By 1.5 hours post-bite he complained of nausea,
the bite site was swollen and black, but no evidence of paralysis
was found. At 4.5 hours post-bite he commenced vomiting, had
axillary adenopathy, and a marked defibrination type coagulopathy
was noted. He was given polyvalent antivenom at 5 hours and 7
hours post-bite, but by 10 hours post-bite the coagulopathy
had worsened, now with thrombocytopenia. At 13 hours post-bite he
was given one ampoule each of taipan and polyvalent antivenom. At
15 hours post-bite the coagulopathy showed substantial
resolution, and platelets were now normal. The child made a
continued recovery, the swelling and discolouration of the bitten
finger settling after 24 hours. Paralysis was not detected at any
stage. Of importance in this case is testing for venom. Initially
blood was tested for venom, without success. Later the bite site
was tested, giving a positive result for taipan venom. Blood is
often unreliable as a test sample for venom detection using the
CSL Venom Detection Kit. Using the VDK to test blood for systemic
envenomation is not advisable practice.
Case 2 (from Covacevich, Pearn, White, 1988)
A 65 year-old herpetologist was bitten on the chest by a large O.
microlepidotus, while attempting to catch same for his reptile
park. He had a past history of numerous snakebites and allergy to
antivenom. He used "cut and suck" as first aid, then attempted to
walk for assistance, suffering headache, nausea, and collapse
shortly thereafter. He spontaneously recovered from the collapse
and unconsciousness, and when seen medically 3.5 hours post-bite
was stable, but with vomiting and slight ptosis. At this time he
was approximately 1,000 km from hospital and, in view of this,
his history of antivenom allergy, and stable condition, antivenom
therapy was postponed until he was in a medical facility well
able to manage complications. During the medical evacuation
flight to hospital in Adelaide he became hypertensive and
recommenced vomiting, but no worsening of his then minimal
paralysis occurred until arrival in Adelaide some 7 hours post-
bite. At this stage testing revealed a severe defibrination type
coagulopathy and worsening ptosis (figure 11.2.1), with slight
dyspnoea not sufficient to require ventilation. He was promptly
treated with taipan antivenom, which totalled 6 ampoules over
the next few hours, ultimately reversing his coagulopathy, and
with lessening of degree of paralysis. He suffered the expected
allergic reaction to initial antivenom therapy, with rash (figure
11.2.2), bronchospasm, and hypotension, well-controlled by IV
adrenaline and subsequent steroid therapy. The only other
problems noted were development of non-anuric renal impairment
(rise in creatinine) and progressive mild thrombocytopenia, both
of which resolved over the next few days. He was discharged at
one week post-bite, on steroid therapy, and did not suffer serum
sickness. A mild rise in CPK, with myoglobinuria, was noted in
the first few days, possibly indicative of mild venom-induced
A 29 year-old female amateur herpetologist was bitten on her
right thenar eminence (figure 2.2.1) by a 1.7 m newly purchased
O. scutellatus. No first aid was used. On presentation to
hospital about 15-30 minutes later she was vomiting, with frank
haematemesis (note removal of wisdom teeth 2 days previously) and
agitated, with developing ptosis. Shortly thereafter she
lapsed into unconsciousness, despite normal BP (130 systolic),
lasting 30-40 minutes, by which time she had been intubated and
taipan antivenom commenced. Samples taken at 30 minutes post-
bite already showed severe defibrination type coagulopathy, and
she continued to have significant blood loss from failed IVT
insertion sites (figure 11.2.3) and her mouth over the next 3-4
hours until the coagulopathy was reversed by sufficient taipan
antivenom (6 ampoules). Shortly thereafter, about 7 hours post-
bite, urine was negative for venom (VDK). Despite prompt
aggressive specific antivenom therapy she developed severe
paralysis requiring artificial ventilation for 4 weeks. Ptosis
and ophthalmoplegia resolved after 2 weeks, with return of limb
muscle power, respiratory muscle power being the last to
satisfactorily resolve. A mild degree of myolysis was noted. No
renal problems developed. After resolution of the coagulopathy,
and not before, a mild thrombocytopenia developed, resolving
within one week. Due to significant blood loss in the early
stages as described above, a significant anaemia developed,
requiring transfusion. Steroids were given to reduce the chance
of serum sickness, which did not occur. Intermittent chest pains
during the third to fifth week were thought possibly due to mild
pulmonary embolism, hence the patient was commenced on a three
month course of warfarin. Eventual recovery was complete. The
patient was discharged after 5 weeks.
A 72 year-old female amateur herpetologist was bitten on the
right index finger by a 2.1 m O. scutellatus while feeding the
snake. She arrived in hospital shortly thereafter, apparently
well, and at 30 minutes post-bite no coagulopathy was present.
She was observed over the next 2 hours by staff who noted
development of a headache and vomiting, but no paralysis, and as
she also had a "flu" like illness, the significance of the
symptoms was not appreciated. At 4 hours post-bite, when further
advice was sought, she was hypertensive (170 systolic), with mild
ptosis, intractable vomiting, and tests revealed a mild
coagulopathy. She was promptly treated with taipan antivenom (2
ampoules), with rapid resolution of the coagulopathy. However it
was then noted she was anuric, and over the next 24 hours anuric
renal failure was clearly established. This became her major
problem, necessitating prolonged dialysis and hospital stay.
Renal biopsy showed renal cortical necrosis. However, over a
period of 6 months, she showed a slow resolution, with return of
sufficient renal function to allow cessation of dialysis. At no
stage was significant paralysis or myolysis noted, the
coagulopathy was mild, and apart from the severe renal failure,
this case would be described as minor envenomation for a taipan
bite. As she had no past history of renal dysfunction the cause
of the renal failure remains uncertain, though a primary effect
of the venom would have to be considered. More likely is a
combined effect of dehydration, influenza, possible mild shock,
and a local angiopathic effect of the mild venom induced
11.3 Internal Cases
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes
Specific taipan antivenom and venom detection kits available
directly from the manufacturer, Commonwealth Serum Laboratories,
45 Poplar Road, Parkville, Victoria 3052, Australia (telephone
(03) 389 1911, telex AA 32789, Fax (03) 389 1434, International
Fax +61 3 389 1434).
12.2 Specific preventative measures
Avoid exposure to taipans. 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 adequately.
No data available.
13.1 Clinical and Toxicological References
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.
Benn KM (1951) A further case of snakebite by a taipan ending
fatally. Med. J. Aust, 1: 147-149.
Brigden MC & Sutherland SK (1981) Taipan bite with myoglobinuria.
Med. J. Aust., 2: 42-43.
Broad AJ, Sutherland SK & Coulter AR (1979) The lethality in mice
of dangerous Australian and other snake venoms. Toxicon, 17: 661-
Broad A, Sutherland SK, Tanner C & Covacevich J (1978)
Electrophoretic enzyme and preliminary toxicity studies of the
venom of Parademansia microlepidotus (the Small-scaled Snake),
with additional data on its distribution (Serpentes: Elapidae).
Mem. Qld. Mus., 19(3): 319-329.
Campbell CH (1964) Venomous snake bite and its treatment in the
territory of Papua and New Guinea. Papua New Guinea Medical
Journal, 7(1): 1-11.
Campbell CH (1964) Venomous snakebite in Papua and its treatment
with tracheostomy, artificial respiration, and antivenene.
Transactions of the Royal Society of Tropical Medicine & Hygiene,
Campbell CH (1967) The taipan (Oxyuranus scutellatus) and the
effect of its bite. Med. J. Aust., 1: 735-739.
Campbell CH (1967) Antivenene in the treatment of Australian and
Papuan snake bite. Med. J. Aust., 2: 106-110.
Campbell CH (1979) Snake bite and snake venoms: their effects on
the nervous system. In: Vinken, P.J. & Bruyn, G.W. Eds. Handbook
of Clinical Neurology, Vol. 37, Intoxications of the Nervous
System, North Holland Publishing Co.
Campbell CH (1979) Symptomatology, pathology, and treatment of
the bites of elapid snakes. In Handbook of Experimental
Pharmacology, Vol. 52, Snake Venoms, Springer Verlag.
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.
Chester A & Crawford GPM (1982) In vitro coagulant properties of
venoms from Australian snakes. Toxicon, 20(2): 501-504.
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 SJ & Waddell CJ (1978) A new
solid phase sandwich radioimmunoassay and its application to the
detection of snake venom. Journal of Immunological Methods, 23:
Coulter AR, Harris RD & Sutherland SK (1980) Enzyme immunoassay
for the rapid clinical identification of snake venom. Med. J.
Aust., 1: 433-435.
Covacevich J (1987) Two taipans. In Covacevich J, Davie P &
Pearn J Eds. Toxic Plants and Animals: A Guide for Australia, The
Covacevich J, Pearn J & White J (1988) The world's most venomous
snake. In Pearn J & Covacevich J Eds. Venoms and Victims, The
Queensland Museum and Amphion Press.
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. Denson KWE (1969) Coagulant and
anticoagulant action of snake venoms. Toxicon, 7: 5-11.
Doery HM & Pearson JE (1961) Haemolysins in venoms of Australian
snakes. Biochem. J., 78: 820-827.
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 D (1978) Studies of presynaptically neurotoxic and myotoxic
phospholipases A2. In LI, C.H. Ed. Versatility of Proteins,
Fairley NH (1929) The present position of snakebite and the snake
bitten in Australia. Med. J. Aust., 1: 296-313.
Fisher M (1982) First aid in envenomation. Med. J. Aust., 1: 198.
Flecker H (1940) Snake bite in practice. Med. J. Aust., 2: 8-13.
Flecker H (1944) More fatal cases of bites of the Taipan
(Oxyuranus scutellatus). Med. J. Aust., 2: 383-384.
Fohlman J, Eaker D, Karlsson E & Thesleff S (1976) Taipoxin, an
extremely potent presynaptic neurotoxin from the venom of the
Australian taipan. European Journal of Biochemistry, 68: 457-469.
Fohlman J (1979) Comparison of two highly toxic Australian snake
venoms: the taipan (Oxyuranus scutellatus) and the fierce snake
(Parademansia microlepidotus). Toxicon, 17: 170-172.
Fohlman J, Eaker D, Dowdall MJ, Lullmann-Rauch R, Sjodin T &
Leander S (1979) Chemical modification of taipoxin and the
consequences for phospholipase activity, pathophysiology, and
inhibition of high-affinity choline uptake. European Journal of
Biochemistry, 94: 531-540.
Harris JB & Maltin CA (1982) Myotoxic activity of the crude
venom and the principal neurotoxin, taipoxin, of the Australian
taipan, Oxyuranus scutellatus. Br. J. Pharmac., 76: 61-75.
Harris JB (1983) Myotoxicity of Animal Toxins. In Mebs,
Habermehl Eds. Proceedings of the 5th European Symposium on
animal, plant and microbial toxins, Hanover.
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: 236-237.
Karlsson E (1979) Chemistry of protein toxins in snake venoms. In
Handbook of experimental pharmacology, Vol. 52, Snake Venoms,
Kellaway CH & Williams FE (1929) The venoms of Oxyuranus
maclennani and Pseudechis scutellatus. Amer. J. Exp. Biol. & Med.
Sci., 6: 155-174.
Lee CY & Ho CL (1982) The pharmacology of phospholipases A2
isolated from snake venoms, with particular reference to their
effects on neuromuscular transmission. In Yoshida, Hagihara &
Ebashi Eds. Advances in pharmacology and therapeutics II, Vol.
4, Biochemical Immunological Pharmacology, Oxford, Pergamon
Lester IA (1957) A case of snake bite treated by specific taipan
antivenene. Med. J. Aust., 2: 389-391.
Marshall LR & Herrmann RP (1983) Coagulant and anticoagulant
actions of Australian snake venoms. Thrombosis & Haemostasis
Research (Stuttgart), 50(3): 707-711.
Mebs D (1978) Pharmacology of Reptilian Venoms. In Gans, C. Ed
Biology of the Reptilia, Vol. 8, Physiology B, London, Academic
Mebs D & Samejima Y (1980) Purification from Australian elapid
venoms and properties of phospholipases A which cause
myoglobinuria in mice. Toxicon, 18: 443-454.
Mirtschin PJ, Crowe GR & Thomas MW (1984) Envenomation by the
inland taipan, Oxyuranus microlepidotus. Med. J. Aust., 141:
Morrison JJ, Pearn JH & Coulter AR (1982) The mass of venom
injected by two elapidae: the taipan (Oxyuranus scutellatus) and
the Australian tiger snake (Notechis scutatus). Toxicon, 20: 739-
Morrison JJ, Pearn JH, Covacevich J & Nixon J (1983) Can
Australians identify snakes? Med. J. Aust., 2: 66-70.
Morrison J, Pearn J, Covacevich J, Tanner C & Coulter A (1983-84)
Studies on the venom of Oxyuranus microlepidotus. Clinical
Toxicology, 21(3): 373-385.
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.
Reid CC & Flecker H (1950) Snake bite by a taipan with recovery.
Med. J. Aust., 1: 82-83.
Speijer H, Govers-Riemslag JWP, Zwaal RFA & Rosing J (1986)
Prothrombin activation by an activator from the venom of
Oxyuranus scutellatus (Taipan Snake). J. Biol. Chem., 261(28):
Su MJ & Chang CC (1984) Presynaptic effects of snake venom
toxins which have phospholipase A2 activity (B-Bungarotoxin,
Taipoxin, Crotoxin). Toxicon, 22: 631-640.
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 snake bite in Australia: some
observations and recommendations. Med. J. Aust., 1: 30-32.
Sutherland SK (1977) 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.,
Sutherland SK (1977) Antivenoms: better late than never. Med. J.
Aust., 2, 813.
Sutherland SK (1977) Acute untoward reactions to antivenoms.
Med. J. Aust., 1: 841.
Sutherland SK, Broad AJ, Tanner C & Covacevich J (1978)
Australia's potentially most venomous snake, Parademansia
microlepidotus. Med. J. Aust., 1: 288-289.
Sutherland SK, Coulter AR & Harris RD (1980) Rapid death of a
child after a taipan bite. Med. J. Aust., 1: 136.
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 Animals Toxins, Melbourne, Oxford
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 snake-bite victims: the successful detection of circulating
snake venom by radioimmunoassay. Med. J. Aust., 1: 27-29.
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.
Theakston RDG, Lloyd-James MJ & Reid HA (1977) Micro-Elisa for
detecting and assaying snake venom and venom antibody. Lancet, 2:
Thesleff S (1979) Reptile neurotoxins and neurotransmitter
release. In Chubb IW & Geffen LB Eds. Neurotoxins: fundamental
and clinical advances, Adelaide University Union Press.
Trinca JC (1963) The treatment of snakebite. Med. J. Aust., 1:
Trinca JC (1969) Report of recovery from Taipan bite. Med. J.
Aust., 1: 514-516.
Walker FJ, Whyte GO & Esmon CT (1980) Characterization of the
Prothrombin Activator from the Venom of Oxyuranus scutellatus
scutellatus (Taipan Venom). Biochemistry, 19: 1020-1023.
White J (1981) Ophidian envenomation: a South Australian
perspective. Records of the Adelaide Children's Hospital, 2(3):
White J (1983) Patterns of elapid envenomation and treatment in
South Australia. Toxicon, Suppl. 3: 489-491.
White J (1983) Local tissue destruction and Australian elapid
envenomation. Toxicon, Suppl. 3: 493-496.
White J (1983) Haematological problems and Australian elapid
envenomation. Toxicon, Suppl. 3: 497-500.
White J, Pounder D, Pearn JH & Morrison JJ (1985) A perspective
on the problems of snakebite in Australia. In Grigg, G., Shine,
R. & Ehmann, H. Eds. Biology of Australasian Frogs and Reptiles,
Royal Zoological Society of New South Wales.
White J (1987) Elapid snakes: venom production and bite
mechanism. In Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic
Plants & Animals: a Guide for Australia, Brisbane, Queensland
White J (1987) Elapid snakes: venom toxicity and actions. In
Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic Plants &
Animals: a Guide for Australia, Brisbane, Queensland Museum.
White J (1987) Elapid snakes: aspects of envenomation. In
Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic Plants &
Animals: a Guide for Australia, Brisbane, Queensland Museum.
White J (1987) Elapid snakes: management of bites. In
Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic Plants &
Animals: a Guide for Australia, Brisbane, Queensland Museum.
White J & Pounder DJ (1984) Fatal snakebite in Australia.
American Journal of Forensic Medicine & Pathology, 5(2): 137-143.
Wiener S (1961) Snakebite in a subject actively immunized against
snake venom. Med. J. Aust., 1: 658-661.
13.2 Zoological References
Cogger HG (1975) Reptiles and Amphibians of Australia, Sydney,
Reed, A.H. & A.W.
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.
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
Covacevich J & Wombey J (1976) Recognition of Parademansia
microlepidotus (McCoy) (Elapidae), a dangerous Australian Snake.
Proc. Roy. Soc. Qld., 87: 29-32.
Covacevich J & Archer M (1975) The distribution of the Cane
Toad, Bufo marinus, in Australia and its effects on indigenous
vertebrates. Mem. Qld Mus., 17(2): 305-310, pl. 41.
Covacevich J, McDowell SB, Tanner C & Mengden G (1981) The
relationship of the taipan (Oxyuranus scutellatus) and the
small-scaled snake (Oxyuranus microlepidotus), Serpentes:
Elapidae. In Banks, C.B. & Martin, A.A. Eds. Proceedings of the
Melbourne Herpetological Symposium, Zoological Board of Victoria.
Longmore R (1986) Atlas of elapid snakes of Australia, Canberra,
Australian Government Publishing Service.
McDowell SB (1985) The terrestrial Australian elapids: general
summary. In Grigg G, Shine R & Ehmann H Eds. Biology of
Australasian Frogs and Reptiles, Royal Zoological Society of New
Mengden GA (1985) Australian elapid phylogeny: a summary of the
chromosomal and electrophoretic data. In Grigg G, Shine R &
Ehmann H Eds. Biology of Australasian Frogs and Reptiles, Royal
Zoological Society of New South Wales.
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, Royal Zoological
Society of New South Wales.
Shine R (1985) Ecological evidence on the phylogeny of Australian
elapid snakes. In Grigg G, Shine R & Ehmann H Eds. Biology of
Australasian Frogs and Reptiles, Royal Zoological Society of New
Shine R & Covacevich J (1983) Ecology of highly venomous snakes:
the Australian genus Oxyuranus (Elapidae). J. Herpetology, 17(1):
Storr GM (1985) Phylogenetic relationships of Australian elapid
snakes: external morphology with emphasis on species in Western
Australia. In Grigg G, Shine R & Ehmann H Eds. Biology of
Australasian Frogs and Reptiles, Royal Zoological Society of New
Wallach V (1985) A cladistic analysis of the terrestrial
Australian elapidae. In Grigg G, Shine R & Ehmann H Eds. Biology
of Australasian Frogs and Reptiles, Royal Zoological Society of
New South Wales.
Wilson SK & Knowles DG (1988) Australia's Reptiles, Sydney,
14 AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)
Author(s): Dr Julian White
State Toxinology Services
Adelaide Children's Hospital
North Adelaide 5006
Mobile phone: 61-18-832776
Ms Jeanette Covacevich
Senior Curator (Vertebrates)
PO Box 300
South Brisbane 4101
Date: June 1989
Date: November 1989
Peer Review: Singapore, November 1991