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AUSTRALIAN TAIPAN SNAKES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Taipan snakes are considered the most dangerous snakes in Australia and can cause significant envenoming. They are found throughout various regions of Australia and New Guinea.

Specific Substances

    1) Australian taipan snake
    2) Taipan snake
    3) Common snake
    4) Inland taipan
    5) New Guinea taipan
    6) Oxyuranus scutellatus
    7) Oxyuranus scutellatus canni
    8) Oxyuranus microlepidotus

Available Forms Sources

    A) SOURCES
    1) In coastal Queensland and coastal Papua New Guinea, the increase in poisonous bufo toads (introduced to the area in the 1940s) may have led to a decrease in frog-eating elapids, such as black snakes and death adders, allowing an increase in the number of taipans, who prey on mammals only and not frogs, and an increase in the relative number of taipan bites (Currie et al, 1991a).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Three species of taipan snakes have been identified as being among the world's most venomous snakes and include: Australian coastal taipan (Oxyuranus scutellatus), inland taipan (Oxyuranus microlepidotus), and Papuan taipan (Oxyuranus scutellatus canni). These species are found in the northern coastal region of Australia, central Australia and in the low lying and mountainous regions of Papua New Guinea. Taipan snakes are mammal feeders. They have the longest fangs of any Australian snake.
    B) TOXICOLOGY: Taipan venom is among the most potent venoms of all snakes. The venom has both pre- and post-synaptic neurotoxins, procoagulant (ie, a prothrombin activator) and myotoxic effects. Envenomation can produce rapid defibrination coagulopathy and progressive systemic neuromuscular paralysis. Taipoxin, a trimeric phospholipase A2 neurotoxin, is the predominant toxin that produces clinical effects, and is able to inhibit the release of acetylcholine from presynaptic cholinergic nerve terminals and produces structural changes in the nerve terminal. Other toxins identified have included other phospholipase neurotoxins and a postsynaptic neurotoxin.
    C) EPIDEMIOLOGY: Taipan snakes are among the most dangerous snakes in Australia and remain the most severe cause of envenomation. Bites can be fatal, if treatment is not provided in a timely manner.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE ENVENOMATION: Early symptoms may include nausea, vomiting, abdominal pain and headache.
    2) SEVERE ENVENOMATION: The major features of envenomation are coagulopathy and neurotoxicity. Coagulopathies may begin within minutes (up to 2 hours) of being bitten by a taipan. Ptosis and diplopia and muscle palsies may be early signs of neurotoxicity and typically occur a few hours later. Myolysis and renal damage are unlikely with a taipan envenomation. Progressive coagulation abnormalities and paralysis leading to respiratory failure may occur. Clinically, paralysis can resemble myasthenia gravis because it typically involves muscles innervated by cranial nerves, neck flexors, and proximal limb muscles.

Laboratory Monitoring

    A) Monitor vital signs, careful neurologic exam and mental status. Monitor for evidence of respiratory depression.
    B) Monitor coagulation studies on presentation, after removing pressure immobilization if it has been used, and approximately every 6 hours thereafter including: CBC with platelet count, INR, and aPTT. Fibrinogen, fibrin degradation products, and D-dimer should also be monitored as necessary. The whole blood clotting time can also be used to assess for coagulation abnormalities.
    C) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    D) Monitor serum electrolytes, renal function, urinalysis and urine output.
    E) If there is any question as to the type of snake involved, obtain a swab from the bite site or a urine specimen, and use the venom detection kit to identify the species of snake if any clinical or laboratory evidence of envenomation develop. The presence of venom at the bite site does NOT mean that systemic envenomation has occurred.
    F) Obtain a head CT if altered mentation develops, or if there is any clinical concern for intracranial bleeding.

Treatment Overview

    0.4.7) BITES/STINGS
    A) NO OR MILD ENVENOMATION
    1) Patients who are asymptomatic or only have mild symptoms and no laboratory evidence of envenomation should be monitored for a minimum of 12 hours.
    B) SEVERE ENVENOMATION
    1) Due to the potency of taipan venom, patients with early evidence of severe envenoming (ie, neurotoxicity {ptosis, paralysis}, coagulopathy {bleeding from gums or bite site} or myolysis) should receive antivenom therapy as soon as possible.
    C) ANTIVENOM
    1) SUMMARY: Treat patients with evidence of systemic envenomation as soon as possible with taipan antivenom, if available.
    2) TAIPAN SNAKE ANTIVENOM: The contents of 1 vial (12,000 units) of taipan antivenom should be administered slowly by the IV route after being diluted 1 to 10 in crystalloid. In general, each vial should be infused over 15 to 30 minutes. Initial Dose: 1 vial of antivenom should be administered for mild envenomation; at least 3 vials should be prepared and given for severe defibrination. Up to 5 to 8 vials may be needed (rarely necessary).
    3) POLYVALENT ANTIVENOM: If the taipan antivenom is not available, or the species of snake responsible is not known, polyvalent antivenom may be used. Monitor a patient given antivenom carefully and be prepared to treat anaphylaxis.
    D) ACUTE ALLERGIC REACTION
    1) Antihistamines, inhaled beta agonists, intramuscular epinephrine as needed for mild to moderate reactions, intravenous epinephrine and endotracheal intubation for severe reactions.
    E) PATIENT DISPOSITION
    1) HOME CRITERIA: There is no role for home management of a possible snake bite.
    2) OBSERVATION CRITERIA: All patients with suspected snake bite should be observed for at least 12 hours, with serial laboratory studies (eg, coagulation studies) on admission and every 6 hours thereafter, and careful clinical evaluation. If there is no clinical or laboratory evidence of envenomation, coagulopathy, neurotoxicity, or myotoxicity after this time, the patient can be discharged.
    3) ADMISSION CRITERIA: Any patient who develops more than mild clinical signs and symptoms or who develops evidence of coagulopathy, bleeding, neurotoxicity, myotoxicity or renal insufficiency, should be admitted to an intensive care setting.
    4) CONSULT CRITERIA: Consult a clinical toxinologist, medical toxicologist or poison center for any patient with severe envenomation or if the diagnosis is unclear.
    F) TOXICOKINETICS
    1) Patients envenomed by a Papuan taipan snake usually develop symptoms (local tender lymphadenopathy, abdominal pain, and systemic consumptive coagulopathy) within 1 to 2 hours of a bite. Evidence of neurotoxicity, including progressive ptosis, external ophthalmoplegia, and muscular and respiratory weakness occurs over the next few hours. Up to 50% of patients may require intubation and mechanical ventilation. The median time to neurotoxicity is approximately 9 hours after a bite; the median time to peak neurologic signs is 17 hours. However, symptoms (ie, fatigue) may still be present up to 12 days later. Based on a multi-compartment model (a semi-mechanistic model) to describe the clotting cascade, the half-life of taipan venom is 10 to 15 minutes and no longer than 1 hour.
    G) PITFALLS
    1) The presence of taipan snake venom at the bite site does not necessarily mean that systemic envenomation has occurred and is not an indication for antivenom treatment in the absence of systemic or laboratory evidence of envenomation. The onset of clinical evidence of envenomation may be delayed; all patients with suspected snakebite should be observed for a minimum of 12 hours. Release of pressure bandages applied as a first aid measure has been associated with abrupt rises in serum venom concentrations and abrupt clinical worsening. Pressure immobilization should not be removed until the patient is at a hospital where antivenom can be administered, and the patient should be stabilized and antivenom should generally be administered before the bandage is removed if there is clinical or laboratory evidence of envenomation. Taipan venom can be rapidly introduced into systemic circulation and start to alter clotting factors; therefore, antivenom should be administered ideally within an hour of evenomation.
    H) DIFFERENTIAL DIAGNOSIS
    1) Envenomation by tiger or brown snakes and some black snakes can cause coagulation abnormalities and neurotoxicity. Overdose of anticoagulants such as warfarin or brodifacoum.

Range Of Toxicity

    A) TOXICITY: A single bite from a taipan snake can be fatal. It is considered potentially the deadliest snake in the world, with a highly potent venom (third most lethal of all snakes) and has the second highest average venom yield (120 mg) of Australian snakes. It has an effective "snap-release" method to deliver venom following a bite. Prior to antivenom and mechanical ventilation survival from a taipan envenomation was rare.

Clinical Effects

Summary Of Exposure

    A) BACKGROUND: Three species of taipan snakes have been identified as being among the world's most venomous snakes and include: Australian coastal taipan (Oxyuranus scutellatus), inland taipan (Oxyuranus microlepidotus), and Papuan taipan (Oxyuranus scutellatus canni). These species are found in the northern coastal region of Australia, central Australia and in the low lying and mountainous regions of Papua New Guinea. Taipan snakes are mammal feeders. They have the longest fangs of any Australian snake.
    B) TOXICOLOGY: Taipan venom is among the most potent venoms of all snakes. The venom has both pre- and post-synaptic neurotoxins, procoagulant (ie, a prothrombin activator) and myotoxic effects. Envenomation can produce rapid defibrination coagulopathy and progressive systemic neuromuscular paralysis. Taipoxin, a trimeric phospholipase A2 neurotoxin, is the predominant toxin that produces clinical effects, and is able to inhibit the release of acetylcholine from presynaptic cholinergic nerve terminals and produces structural changes in the nerve terminal. Other toxins identified have included other phospholipase neurotoxins and a postsynaptic neurotoxin.
    C) EPIDEMIOLOGY: Taipan snakes are among the most dangerous snakes in Australia and remain the most severe cause of envenomation. Bites can be fatal, if treatment is not provided in a timely manner.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE ENVENOMATION: Early symptoms may include nausea, vomiting, abdominal pain and headache.
    2) SEVERE ENVENOMATION: The major features of envenomation are coagulopathy and neurotoxicity. Coagulopathies may begin within minutes (up to 2 hours) of being bitten by a taipan. Ptosis and diplopia and muscle palsies may be early signs of neurotoxicity and typically occur a few hours later. Myolysis and renal damage are unlikely with a taipan envenomation. Progressive coagulation abnormalities and paralysis leading to respiratory failure may occur. Clinically, paralysis can resemble myasthenia gravis because it typically involves muscles innervated by cranial nerves, neck flexors, and proximal limb muscles.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) PTOSIS
    a) Ptosis may be an early neurologic finding of taipan envenomation (Southern et al, 1996; King & Smith, 1991).
    b) CASE REPORTS: In a retrospective review of 5 severe taipan envenomations, ptosis was an early finding of neurotoxicity. Symptoms may persist for several days after treatment, but usually resolves completely (Southern et al, 1996).
    c) INCIDENCE: In a series of 120 to 135 Papuan taipan (Oxyuranus scutellatus canni) envenomations (a clear history could not be obtained for each patient), ptosis was reported in 84 (64.1%) cases. Envenomation was confirmed by laboratory analysis (Lalloo et al, 1995a).
    2) BLURRED VISION
    a) CASE REPORT: A herpetologist was "scratched" by a young taipan (O scutellatus) snake and developed blurred vision within 90 minutes of envenomation (Arthur et al, 1991).
    3) DIPLOPIA
    a) Diplopia may be an early neurologic finding of taipan envenomation (Southern et al, 1996; King & Smith, 1991).
    b) CASE REPORTS: In a retrospective review of 5 severe taipan envenomations, diplopia was an early complaint of patients following envenomation. Diplopia may persist for several days after treatment, but usually resolves completely (Southern et al, 1996).
    c) INCIDENCE: In a series of 120 to 135 Papuan taipan (Oxyuranus scutellatus canni) envenomations (a clear history could not be obtained for each patient), diplopia was reported in 26 (21.1%) cases. Envenomation was confirmed by laboratory analysis (Lalloo et al, 1995a).
    4) OPHTHALMOPLEGIA
    a) Ophthalmoplegia has occurred as an early neurotoxic finding of taipan envenomation (Connolly et al, 1995).
    b) INCIDENCE: In a series of 120 to 135 Papuan taipan (Oxyuranus scutellatus canni) envenomations (a clear history could not be obtained for each patient), ophthalmoplegia was observed in 48 (39%) cases upon admission with most patients (105; 76.6%) eventually developing ophthalmoplegia. Envenomation was confirmed by laboratory analysis (Lalloo et al, 1995a).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) In a prospective study, ECG changes were observed in 36 of 69 patients (52%) following taipan envenomation, 2 of 6 patients (33%) following death adder envenomation, and 1 case following brown snake envenomation. Dysrhythmias and septal T wave inversions were equally common (Lalloo et al, 1995).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Transient episodes of collapse may be related to hypotension that can occur due to the allergenic effects of taipan venom. Of 14 herpetologists, 3 became unconscious within minutes of being envenomated (Pearn et al, 1994).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) WITH POISONING/EXPOSURE
    a) Respiratory paralysis may occur from the neurotoxic components of the venom after a taipan envenomation (Southern et al, 1996). In a study of taipan envenomations, 28% required ventilation (Currie et al, 1991b).
    b) CASE SERIES: In a retrospective review of 5 taipan envenomations, profound respiratory paralysis was transient when patients were given repeated doses of antivenom. One patient developed rapid respiratory deterioration once his compression bandage was removed requiring immediate ventilatory support. A second dose of taipan antivenom was given and he was successfully extubated about 11 hours later (Southern et al, 1996).
    c) CASE REPORTS: Three patients envenomated by the Papuan taipan (Oxyuranus scutellatus canni) snake developed respiratory muscle paralysis requiring intubation and artificial ventilation lasting between 2.5 and 5 days despite initial treatment with a polyspecific antivenom (Connolly et al, 1995).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) Neurotoxic components of the venom may cause muscle paralysis which can lead to ptosis, ophthalmoplegia, slurred speech, decreased reflexes and generalized and respiratory weakness or paralysis (Southern et al, 1996; Connolly et al, 1995; Lalloo et al, 1995a).
    b) Clinically, paralysis can resemble myasthenia gravis because it typically involves muscles innervated by cranial nerves, neck flexors, and proximal limb muscles (Connolly et al, 1995).
    c) CASE REPORTS: Three patients envenomated by the Papuan taipan snake developed respiratory muscle paralysis requiring intubation and mechanical ventilation lasting between 2.5 and 5 days despite initial treatment with polyspecific antivenom (Connolly et al, 1995).
    d) Fulminant signs of toxicity may be delayed for many hours.
    1) ANIMAL DATA: An in vivo rat study of TIGER SNAKE (Notechis) and TAIPAN (Oxyuranus) venom revealed degeneration of motor nerve terminals following exposure requiring 5 days for regeneration and functional reinnervation, with abnormalities of collateral innervation persisting for at least 9 months, perhaps explaining the severity and difficulty in management of neurotoxicity in these envenomations (Harris et al, 2000).
    B) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Neurotoxic effects may produce drowsiness following a taipan envenomation (Lalloo et al, 1995a).
    b) INCIDENCE: In a series of 120 to 135 Papuan taipan (Oxyuranus scutellatus canni) envenomations (a clear history could not be obtained for each patient), drowsiness was observed in 38 (31.7%) patients at the time of admission. Envenomation was confirmed by laboratory analysis (Lalloo et al, 1995a).
    C) CEREBRAL HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) PAPUAN NEW GUINEA: A 14-year-old boy was bitten by a Papuan New Guinea taipan and treated with fresh frozen plasma and a vial of antivenom (only one vial available due to a shortage) for incoagulable blood and bleeding from his gums, mouth and venipuncture sites. His course was complicated by respiratory paralysis requiring intubation. He was subsequently noted to have sustained a cerebrovascular accident, with flaccid paralysis of the left arm, left facial weakness, hemisensory loss of the left arm and dyspraxia. The patient presumably had an intracranial bleed; a head CT was not performed (Trevett et al, 1994).
    D) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may be an early finding of a taipan envenomation (Connolly et al, 1995; Lalloo et al, 1995a; King & Smith, 1991; Arthur et al, 1991; Mirtschin et al, 1984).
    b) CASE REPORT: A 37-year-old snake handler was bitten by a young inland taipan (Oxyuranus microlepidotus) after it became agitated during feeding. The patient sought help immediately and arrived at the hospital within 15 minutes. Twenty minutes after exposure he complained of a severe headache and feeling flushed with difficulty speaking. No muscle weakness was observed and his vital signs were stable. Taipan antivenom was given and the patient recovered completely. He was discharged to home 2 days later (Mirtschin et al, 1984).
    c) CASE REPORT: A herpetologist was "scratched" by a young taipan (O scutellatus) snake and developed severe headache within 90 minutes of envenomation (Arthur et al, 1991).
    d) INCIDENCE: In a series of 120 to 135 Papuan taipan (Oxyuranus scutellatus canni) envenomations (a clear history could not be obtained for each patient), headache was reported in 67 (54.5%) cases. Envenomation was confirmed by laboratory analysis (Lalloo et al, 1995a).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nonspecific gastrointestinal features of taipan envenomation can include nausea and vomiting (Currie, 2006; Southern et al, 1996) and are usually an early finding of envenomation (Southern et al, 1996; Arthur et al, 1991). Abdominal pain can also develop after taipan envenomation (Connolly et al, 1995).
    b) INCIDENCE: In a series of 120 to 135 Papuan taipan (Oxyuranus scutellatus canni) envenomations (a clear history could not be obtained for each patient), vomiting occurred in 85 (64.4%) cases and abdominal pain was reported in 76 (59.8%) patients. Envenomation was confirmed by laboratory analysis (Lalloo et al, 1995a).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) BLOOD IN URINE
    1) WITH POISONING/EXPOSURE
    a) Hematuria can develop after a taipan envenomation (Southern et al, 1996).
    b) CASE REPORTS: In a retrospective review of 5 taipan envenomations, hematuria was observed in patients that developed significant coagulopathies. However, myoglobinuria did not develop (Southern et al, 1996).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) BLOOD COAGULATION PATHWAY FINDING
    1) WITH POISONING/EXPOSURE
    a) TAIPAN: Envenomation may cause severe coagulopathy, including prolonged PT/INR and PTT, depressed fibrinogen concentration and increased fibrin degradation products (Southern et al, 1996).
    b) CASE SERIES: Of 87 patients bitten by the Papuan taipan (Oxyuranus scutellatus canni), 80 (92%) developed coagulopathy. Forty-eight had complete defibrinogenation, with marked reductions in factors V and VIII and reductions in factors II, IX, XII and XIIIA. Following treatment with antivenom, fibrinogen levels rose rapidly and coagulability was restored within 6 to 12 hours in 93% of patients (Lalloo et al, 1995).
    c) INCIDENCE: In a series of 120 to 135 Papuan taipan (Oxyuranus scutellatus canni) envenomations (a clear history could not be obtained for each patient), systemic bleeding was observed in 59 (43.7%) cases at the time of admission. Bleeding from the mouth was common with infrequent reports of hemoptysis or epistaxis. Envenomation was confirmed by laboratory analysis (Lalloo et al, 1995a).
    B) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) TAIPAN (Oxyuranus Spp): Thrombocytopenia, potentially profound, was seen in a series of patients envenomated by a Papuan taipan snake (Lalloo et al, 1995).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) TENDER LYMPH NODE
    1) WITH POISONING/EXPOSURE
    a) Lymph node pain and/or tenderness has been reported after a taipan envenomation (Currie, 2006; Connolly et al, 1995).
    B) SWELLING
    1) WITH POISONING/EXPOSURE
    a) Local swelling may develop following a taipan envenoming; it may be absent in some cases of envenomation (Currie, 2006; King & Smith, 1991).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INJURY OF MUSCULOSKELETAL SYSTEM
    1) WITH POISONING/EXPOSURE
    a) Myotoxicity may develop with taipan envenomation, it is usually not a prominent feature of envenomation (Currie, 2006; White, 1995; Connolly et al, 1995).
    b) LACK OF EFFECT
    1) CASE REPORTS: In a retrospective review of 5 severe taipan envenomations, myonecrotic activity (including myoglobinuria) did not develop in any patient. Clinical events were limited to neurologic toxicity and coagulopathies. Each recovered completely with antivenom therapy (Southern et al, 1996).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, careful neurologic exam and mental status. Monitor for evidence of respiratory depression.
    B) Monitor coagulation studies on presentation, after removing pressure immobilization if it has been used, and approximately every 6 hours thereafter including: CBC with platelet count, INR, and aPTT. Fibrinogen, fibrin degradation products, and D-dimer should also be monitored as necessary. The whole blood clotting time can also be used to assess for coagulation abnormalities.
    C) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    D) Monitor serum electrolytes, renal function, urinalysis and urine output.
    E) If there is any question as to the type of snake involved, obtain a swab from the bite site or a urine specimen, and use the venom detection kit to identify the species of snake if any clinical or laboratory evidence of envenomation develop. The presence of venom at the bite site does NOT mean that systemic envenomation has occurred.
    F) Obtain a head CT if altered mentation develops, or if there is any clinical concern for intracranial bleeding.
    4.1.2) SERUM/BLOOD
    A) Monitor serum electrolytes and renal function.
    B) COAGULATION STUDIES
    1) Taipan snake envenomations can cause severe coagulopathy (Southern et al, 1996). Monitor coagulation studies on presentation, after removing pressure immobilization if it has been used, and approximately every 6 hours thereafter (Ireland et al, 2010) including: CBC with platelet count, INR, and aPTT. While fibrinogen, fibrin degradation products, and D-dimer are monitored in some settings, INR and aPTT appear to provide a good assessment of coagulation status in patients with a snake envenomation (Isbister et al, 2006).
    2) WHOLE BLOOD CLOTTING TIME (WBCT): A method to determine whole blood clotting can be done at the bedside with a few millimeters of venous blood placed in a new, clean, dry, glass tube (or bottle), if the patient has no history of coagulopathies. The steps are as follows and may be useful in a setting where laboratory studies are limited (Anon, 1999):
    a) Place a few millimeters of venous blood in a GLASS tube
    b) Leave undisturbed for 20 minutes at room temperature
    c) Tip the vessel once:
    1) If blood is still liquid and runs out it is indicative of a venom-induced coagulopathy
    2) Inaccurate results may occur if the vessel had been cleaned previously with detergent
    d) FALSE NEGATIVE results could occur if clot identification is read beyond 20 minutes (Stone et al, 2006).
    e) FALSE POSITIVE results could occur if polypropylene or polyethylene tubes are used instead of glass (Stone et al, 2006).
    4.1.3) URINE
    A) Monitor urinalysis for hematuria. Monitor urine output.
    4.1.4) OTHER
    A) OTHER
    1) CLINICAL EXAMINATION
    a) Monitor vital signs, neurologic exam and mental status. Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding). Monitor for evidence of respiratory depression.
    2) VENOM DETECTION
    a) If there is any question as to the type of snake involved, use the venom detection kit on the bite site and/or urine to identify the species involved. The presence of venom at the bite site does NOT mean that systemic envenomation has occurred. Many centers advocate obtaining a swab of the bite site or specimen of urine to be held on presentation, and only using the venom detection kit if there is clinical or laboratory evidence of envenomation develops (Jelinek et al, 2004; Isbister & Currie, 2003; Jelinek et al, 1991).
    b) Venom detection in urine usually is associated with systemic envenomation, but a few cases have been reported where venom was detected in urine or blood in the absence of clinical or laboratory evidence of significant envenomation (Jelinek et al, 1991). Blood samples have been found to be unreliable for testing for the presence of venom and should not be used (White, 1995a).
    3) COMPOUND MUSCLE ACTION POTENTIAL
    a) CMAP: Motor nerve conduction studies have been performed following the envenomation of taipan snakes. The findings suggest that there is significant reduction in amplitude, but there is no significant change in motor conduction velocity (Trevett et al, 1995; Connolly et al, 1995).
    4) REPETITIVE STIMULATION STUDIES
    a) Repetitive stimulation studies have been performed to assess the neuromuscular toxicity of taipoxin, the neurotoxic venom of Papuan taipan (Oxyranus scutellatus canni) snakes (Connolly et al, 1995).

Methods

    A) IMMUNOASSAY: Papuan taipan venom has been detected in serum using an immunoassay (Connolly et al, 1995).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.6) DISPOSITION/BITE-STING EXPOSURE
    6.3.6.1) ADMISSION CRITERIA/BITE-STING
    A) Any patient who develops more than mild clinical signs and symptoms or who develops evidence of coagulopathy, bleeding, neurotoxicity, myotoxicity or renal insufficiency, should be admitted to an intensive care setting.
    6.3.6.2) HOME CRITERIA/BITE-STING
    A) There is no role for home management of a possible snake bite.
    6.3.6.3) CONSULT CRITERIA/BITE-STING
    A) Consult a clinical toxinologist, medical toxicologist or poison center for any patient with severe envenomation, or if the diagnosis is unclear.
    6.3.6.5) OBSERVATION CRITERIA/BITE-STING
    A) All patients with suspected snake bite should be observed for at least 12 hours, with serial laboratory studies (eg, coagulation studies) on admission and every 6 hours thereafter, and careful clinical evaluation. If there is no clinical or laboratory evidence of envenomation, coagulopathy, neurotoxicity, myotoxicity, or renal insufficiency after this time, the patient can be discharged.

Monitoring

    A) Monitor vital signs, careful neurologic exam and mental status. Monitor for evidence of respiratory depression.
    B) Monitor coagulation studies on presentation, after removing pressure immobilization if it has been used, and approximately every 6 hours thereafter including: CBC with platelet count, INR, and aPTT. Fibrinogen, fibrin degradation products, and D-dimer should also be monitored as necessary. The whole blood clotting time can also be used to assess for coagulation abnormalities.
    C) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    D) Monitor serum electrolytes, renal function, urinalysis and urine output.
    E) If there is any question as to the type of snake involved, obtain a swab from the bite site or a urine specimen, and use the venom detection kit to identify the species of snake if any clinical or laboratory evidence of envenomation develop. The presence of venom at the bite site does NOT mean that systemic envenomation has occurred.
    F) Obtain a head CT if altered mentation develops, or if there is any clinical concern for intracranial bleeding.

Range Of Toxicity

Summary

    A) TOXICITY: A single bite from a taipan snake can be fatal. It is considered potentially the deadliest snake in the world, with a highly potent venom (third most lethal of all snakes) and has the second highest average venom yield (120 mg) of Australian snakes. It has an effective "snap-release" method to deliver venom following a bite. Prior to antivenom and mechanical ventilation survival from a taipan envenomation was rare.

Minimum Lethal Exposure

    A) SUMMARY
    1) A single bite from a taipan snake can be fatal. It is considered potentially the deadliest snake in the world, with a highly potent venom (third most lethal of all snakes) and has the second highest average venom yield (120 mg) of Australian snakes. Prior to antivenom and mechanical ventilation survival from a taipan envenomation was rare (Currie, 2000).
    a) It has an effective "snap-release" method to deliver venom following a bite (Currie, 2000). A taipan bite is very efficient (likely related to its long fangs) in that most of the venom is injected into its victims. Taipan snakes appear to be able to increase the volume of venom with each sequential bite (Morrison et al, 1982).
    2) The LD50 for mice is 0.064 mg/kg subQ with an average dose per mouse of 20.2 mg (Morrison et al, 1982).
    3) In the mouse LD50, the average venom yield is highest for the taipan than any other snake in Papua New Guinea (Currie et al, 1991).
    4) The potency of taipan venoms varies by species. The rank order of potency is a follows: O microlepidotus (0.025 mg/kg) is greater than O scutellatus canni (0.0505 mg/kg) is greater than O scutellatus scutellatus (0.099 mg/kg) (Kuruppu et al, 2005).
    5) In coastal Queensland and coastal Papua New Guinea, the increase in poisonous bufo toads (introduced to the area in the 1940s) may have led to a decrease in frog-eating elapids, such as black snakes and death adders, allowing an increase in the number of taipans who prey on mammals only and not frogs (Currie et al, 1991).

Maximum Tolerated Exposure

    A) INLAND TAIPAN
    1) CASE REPORT: A 37-year-old snake handler was bitten by a young inland taipan (Oxyuranus microlepidotus) after becoming agitated during feeding. The patient sought help immediately and arrived at the hospital within 15 minutes. Twenty minutes after exposure he complained of a severe headache and feeling flushed with difficulty speaking. No muscle weakness was observed and his vital signs were stable. Taipan antivenom was given and the patient recovered completely. He was discharged to home 2 days later (Mirtschin et al, 1984).
    B) PAPUAN TAIPAN
    1) CASE REPORT: A 14-year-old boy was bitten by a Papuan New Guinea taipan and treated with fresh frozen plasma and a vial of antivenom (only one vial available due to a shortage) for incoagulable blood and bleeding from his gums, mouth and venipuncture sites. His course was complicated by respiratory paralysis requiring intubation. He was subsequently noted to have sustained a cerebrovascular accident, with flaccid paralysis of the left arm, left facial weakness, hemisensory loss of the left arm and dyspraxia. The patient presumably had an intracranial bleed; a head CT was not performed (Trevett et al, 1994).
    C) CASE SERIES: Of 87 patients bitten by the Papuan taipan (Oxyuranus scutellatus canni), 80 (92%) developed coagulopathy. Forty-eight had complete defibrinogenation, with marked reductions in factors V and VIII and reductions in factors II, IX, XII and XIIIA. Following treatment with antivenom, fibrinogen levels rose rapidly and coagulability was restored within 6 to 12 hours in 93% of patients (Lalloo et al, 1995).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) A large volume of venom can be produced by taipan snakes (White, 1995). The maximal quantity of venom delivered in an average bite is 120 mg compared to 35 mg for the Tiger snake (Morrison et al, 1982).
    2) In a postmortem study, an individual envenomated by a taipan had 2 mg of venom per g of tissue (ie, skin and subcutaneous tissue) (Morrison et al, 1982).

Pharmacology Toxicology

Toxicologic Mechanism

    A) SUMMARY
    1) The venom of Australian taipan contains taipoxin, a phospholipase A2, the principal purified neurotoxin. It acts on mammalian motor nerve endings abolishing transmitter release. This block in neuromuscular transmission is preceded by a latent period in which the toxin binds irreversibly to the nerve (Connolly et al, 1995).
    2) It has an effective "snap-release" method to deliver venom following a bite (Currie, 2000). A taipan bite is very efficient (likely related to its long fangs) in that most of the venom is injected into its victims. Taipan snakes appear to be able to increase the volume of venom with each sequential bite (Morrison et al, 1982).
    B) NEUROTOXICITY
    1) Taipan venoms are made up of predominantly pre-synaptic (Currie, 2006; Isbister et al, 2010) and post-synaptic neurotoxins (White, 1995). Clinically, the most significant neurotoxin of taipan venom is taipoxin, a trimeric phospholipase A2 neurotoxin. It inhibits the release of acetylcholine from presynaptic cholinergic nerve terminals and can alter the structure of nerve terminals (Trevett et al, 1995).
    C) COAGULOPATHY
    1) Taipan species (Oxyuranus scutellatus, O microlepidotus, O S. canni) are likely to produce coagulopathies. Effects may develop rapidly after a bite (ie, within 15 minutes in an active child) (White, 1995). Consumptive coagulopathy has been shown to be predominantly procoagulant with fibrinogen depletion (Isbister et al, 2010; Currie, 2006). It has also been found that taipan venom contains potent prothrombin activators (Isbister et al, 2010).
    2) The coagulation defect induced by taipan venom has been described as a consumptive coagulopathy that is characterized by prolonged clotting times, depletion of fibrinogen and cofactors V and VII, and high concentrations of fibrin degradation products. Clinically, these changes can produce bleeding, and in particular may lead to intracranial hemorrhage. Early antivenom therapy (within an hour) is suggested to minimize consumptive coagulopathy (Tanos et al, 2008).
    D) MYOTOXICITY
    1) Myotoxicity is associated with Taipan species, but it is not a prominent feature of envenomation (Currie, 2006; White, 1995).

References

General Bibliography

    1) Anon: WHO/SEARO guidelines for clinical management of snake bites. So Asian J Trop Med Pub Health 1999; 30 (S1):1-85.
    2) Arthur CK, McCallum D, Loveday DJ, et al: Effects of taipan (Oxyuranus scutellatus) venom on erythrocyte morphology and blood viscosity in a human victim in vivo and in vitro. Trans R Soc Trop Med Hyg 1991; 85(3):401-403.
    3) Clinical Toxinology Department, Women's & Children's Hospital: CSL Polyvalent Snake Antivenom. Clinical Toxinology Department, Women's & Children's Hospital. Adelaide, Australia. 2001. Available from URL: http://www.toxinology.com/generic_static_files/cslavh_antivenom_polyvalen.html. As accessed 2012-10-10.
    4) Connolly S, Trevett AJ, Nwokolo NC, et al: Neuromuscular effects of Papuan Taipan snake venom. Ann Neurol 1995; 38(6):916-920.
    5) Currie B, Theakston D, & Warrell D: Envenomization from the papuan taipan (Oxyuranus scutellatus canni) (abstract 33), 10th World Congress on Animal, Plant, and Microbial Toxins, Singapore, China, 1991b.
    6) Currie BJ, Sutherland SK, & Hudson BJ: An epidemiological study of snake bite envenomation in Papua New Guinea. Med J Aust 1991a; 154:266-268.
    7) Currie BJ, Sutherland SK, Hudson BJ, et al: An epidemiological study of snake bite envenomation in Papua New Guinea. Med J Aust 1991; 154(4):266-268.
    8) Currie BJ: Clinical toxicology: a tropical Australian perspective. Ther Drug Monit 2000; 22(1):73-78.
    9) Currie BJ: Clinical toxicology: a tropical australian perspective. Ther Drug Monitor 2000a; 22:73-78.
    10) Currie BJ: Treatment of snakebite in Australia: The current evidence base and questions requiring collaborative multicentre prospective studies. Toxicon 2006; 48(7):941-956.
    11) Harris JB, Grubb BD, Maltin CA, et al: The neurotoxicity of the venom phospholipases A(2), notexin and taipoxin. Exp Neurol 2000; 161(2):517-526.
    12) Ireland G, Brown SG, Buckley NA, et al: Changes in serial laboratory test results in snakebite patients: when can we safely exclude envenoming?. Med J Aust 2010; 193(5):285-290.
    13) Isbister GK & Currie BJ : Suspected snakebite: one year prospective study of emergency department presentations. Emerg Med (Fremantle) 2003; 15(2):160-169.
    14) Isbister GK, O'Leary MA, Hagan J, et al: Cross-neutralisation of Australian brown snake, taipan and death adder venoms by monovalent antibodies. Vaccine 2010; 28(3):798-802.
    15) Isbister GK, Williams V, Brown SG, et al: Clinically applicable laboratory end-points for treating snakebite coagulopathy. Pathology 2006; 38(6):568-572.
    16) Jelinek GA , Hamilton T , & Hirsch RL : Admissions for suspected snake bite to the Perth adult teaching hospitals, 1979 to 1988. Med J Aust 1991; 155(11-12):761-764.
    17) Jelinek GA , Tweed C , Lynch D , et al: Cross reactivity between venomous, mildly venomous, and non-venomous snake venoms with the Commonwealth Serum Laboratories Venom Detection Kit. Emerg Med Australas 2004; 16(5-6):459-464.
    18) King GK & Smith IM: Taipan envenomation. Med J Aust 1991; 155(11-12):850-.
    19) Kuruppu S, Reeve S, Banerjee Y, et al: Isolation and pharmacological characterization of cannitoxin, a presynaptic neurotoxin from the venom of the Papuan Taipan (Oxyuranus scutellatus canni). J Pharmacol Exp Ther 2005; 315(3):1196-1202.
    20) Lalloo DG, Trevett AJ, Korinhona A, et al: Snake bites by the Papuan taipan (Oxyuranus scutellatus canni): paralysis, hemostatic and electrocardiographic abnormalities, and effects of antivenom. Am J Trop Med Hyg 1995a; 52(6):525-531.
    21) Lalloo DG, Trevett AJ, Owens D, et al: Coagulopathy following bites by the Papuan taipan (Oxyuranus scutellatus canni). Blood Coagul Fibrinolysis 1995; 6(1):65-72.
    22) Lieberman P, Nicklas R, Randolph C, et al: Anaphylaxis-a practice parameter update 2015. Ann Allergy Asthma Immunol 2015; 115(5):341-384.
    23) Lieberman P, Nicklas RA, Oppenheimer J, et al: The diagnosis and management of anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol 2010; 126(3):477-480.
    24) Mirtschin PJ, Crowe GR, & Thomas MW: Envenomation by the inland taipan, Oxyuranus microlepidotus. Med J Aust 1984; 141(12-13):850-851.
    25) Morrison JJ, Pearn JH, & Coulter AR: The mass of venom injected by two elapidae: the taipan (Oxyuranus scutellatus) and the Australian tiger snake (Notechis scutatus). Toxicon 1982; 20(4):739-745.
    26) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    27) Nowak RM & Macias CG : Anaphylaxis on the other front line: perspectives from the emergency department. Am J Med 2014; 127(1 Suppl):S34-S44.
    28) Pearn JH, Covacevich J, Charles N, et al: Snakebite in herpetologists. Med J Aust 1994; 161(11-12):706-708.
    29) Product Information: diphenhydramine HCl intravenous injection solution, intramuscular injection solution, diphenhydramine HCl intravenous injection solution, intramuscular injection solution. Hospira, Inc. (per DailyMed), Lake Forest, IL, 2013.
    30) Southern DA, Callanan VI, & Gordon GS: Severe envenomation by the taipan (Oxyuranus scutellatus). Med J Aust 1996; 165:662-664.
    31) Stone R, Seymour J, & Marshall O: Plastic containers and the whole-blood clotting test: glass remains the best option. Trans R Soc Trop Med Hyg 2006; 100(12):1168-1172.
    32) Tanos PP, Isbister GK, Lalloo DG, et al: A model for venom-induced consumptive coagulopathy in snake bite. Toxicon 2008; 52(7):769-780.
    33) Toxinology Department, Women & Children's Hospital: CSL Antivenom Handbook: CSL Taipan Antivenom. The University of Adelaide Toxinology Department, Women's & Children's Hospital. Adelaide, Australia. 2001. Available from URL: http://www.toxinology.com/generic_static_files/cslavh_antivenom_taipan.html. As accessed 2012-12-18.
    34) Trevett AJ, Lalloo DG, Nwokolo NC, et al: Electrophysiological findings in patients envenomed following the bite of a Papuan taipan (Oxyuranus scutellatus canni). Trans R Soc Trop Med Hyg 1995; 89(4):415-417.
    35) Trevett AJ, Nwokolo NC, Kevau IH, et al: Cerebrovascular accident after taipan bite. Med J Aust 1994; 160(2):94-.
    36) Vanden Hoek,TL; Morrison LJ; Shuster M; et al: Part 12: Cardiac Arrest in Special Situations 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. American Heart Association. Dallas, TX. 2010. Available from URL: http://circ.ahajournals.org/cgi/reprint/122/18_suppl_3/S829. As accessed 2010-10-21.
    37) White J: Clinical Toxicology of sea snake bites In: Meier J & White J (Eds): Handbook of Clinical Toxicology of Animal Venoms and Poisons, CRC Press, New York, NY, USA, 1995, pp 159-170.
    38) White J: Clinical toxicology of snakebite in australia and new guinea, in Meier J & White J (eds): Handbook of Clinical Toxicology of Animal Venoms and Poisons, CRC Press, Boca Raton, FL, 1995a, pp 595-618.