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AUSTRALIAN SNAKES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Most of the Australian venomous snakes belong to Family Elapidae. The fangs are fixed in the front of the mouth in an erect position.
    B) Elapid snakes of greatest clinical significance in Australia include: Acanthophis, Hoplocephalus, Notechis, Oxyuranus, Pseudechis, Pseudonaja and Tropidechis are discussed in other managements. SEE the following managements:
    1) Australian Black Snakes
    2) Australian Brown Snakes
    3) Australian Death Adders
    4) Australian Taipan Snakes
    5) Australian Tiger Snake Group
    C) This management is limited to OTHER Australian snakes that do not belong to the above described groups, but have been of clinical importance in limited case reports.

Specific Substances

    A) CONSTITUENTS OF THE GROUP
    1) CRYPTOPHIS Genus
    a) Cryptophis Boschmai (Carpentaria snake)
    b) Cryptophis Nigrescens (Small-eyed snake)
    2) DEMANSIA Genus
    a) Demansia atra (black Whip Snake)
    b) Demansia papuensis (black whip snake)
    c) Demansia psammophis (yellow-faced whip snake)
    3) DENISONIA Genus
    a) Denisonia devisi (De Vi's banded snake)
    4) ECHIOPSIS Genus
    a) Echiopsis Curta (previously Notechis curtus)
    b) Echiopsis Curta (Bardick snake)
    5) HEMIASPIS Genus
    a) Hemiaspis damelii (Grey Snake)
    b) Hemiaspis signata (black-bellied swamp snake)
    6) MICROPECIS Genus
    a) Micropechis ikaheka (New Guinean small eyed snake)
    7) SUTA Genus
    a) Suta Punctata (Little spotted snake)
    b) Suta Suta (Curl snake, Myall Snake)
    8) VERMICELLA Genus
    a) Vermicella annulata (bandy-bandy, Ringed snake)

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: Elapids of greatest clinical concern in Australia and New Guinea include 5 major snake groups. These species are discussed in separate managements. See the following managements as appropriate for further information: AUSTRALIAN BLACK SNAKES, AUSTRALIAN BROWN SNAKES, AUSTRALIAN DEATH ADDERS, AUSTRALIAN TAIPAN SNAKES, or AUSTRALIAN TIGER SNAKE GROUP. Although these snakes result in most snake bites and envenomations in Australia and New Guinea, there are a select number of snakes that are not included in these groups but can produce moderate to severe envenomation and death in some cases. This management includes: Micropechis ikaheka (Papua New Guinea small-eyed snake) and Hemiaspis Signata (Black-bellied swamp snake) a black snake with a white line above the eye and one across the lip; they may be misidentified with Pseudechis spp (black snakes). Suta Suta (whip or curl snake) is found in all states of mainland Australia with the exception of Tasmania.
    B) TOXICOLOGY: MICROPECHIS IKAHEKA: The venom of M ikaheka contains neurotoxic (postsynaptic), myotoxic and anticoagulant effects. The venom has high phospholipase A2 (PLA2) enzyme activity, that is likely responsible for the myotoxic and anticoagulant effects. HEMIASPIS SIGNATA: The venom may have a mild procoagulant effect.
    C) EPIDEMIOLOGY: M ikaheka is widely distributed throughout Papua New Guinea, Irian Jaya and Indonesian islands and has caused severe and fatal envenomations. H signata is common in the Hunter and Central Coast regions of New South Wales with limited reports of envenomation. There have been limited case reports for Suta suta.
    D) WITH POISONING/EXPOSURE
    1) MICROPECHIS IKAHEKA (Papua New Guinea small-eyed snake): Local effects include swelling, pain and lymphadenopathy. Systemic effects have included neurotoxicity (including neuromuscular paralysis), myotoxicity (muscle pain and myoglobinuria), coagulopathy, and less frequently hemolysis and hypotension. Deaths have been reported.
    2) HEMIASPIS SIGNATA (Black-bellied swamp snake): Local effects may include significant pain and swelling at the bite site with distal lymphadenopathy. Based on limited reports, it has produced procoagulant effects.
    3) SUTA SUTA (whip or curl snake) is likely to produce progressive neurotoxicity and severe pain has occurred at the bite site. Myotoxic effects have not been observed.
    4) ECHIOPSIS CURTA: Limited data. It has caused localized swelling, but no neurotoxic or coagulopathy effects.
    5) OTHER SPECIES: The following species have no reports OR limited reports of human envenomation, but in vitro studies have found that the venom contains the following:
    a) CRYPTOPHIS BOSCHMAI (Carpentaria snake): Post-synaptic neurotoxic activity and high phospholipase A2 (PLA2) activity and very weak coagulopathic effects;
    b) DENISONIA DEVISI (De vi's banded snake): Post-synaptic neurotoxic activity and very weak coagulopathic effects;
    c) ECHIOPSIS CURTA (Previously Notechis curtus; Bardick snake): Post-synaptic neurotoxic activity and very weak coagulopathic effects;
    d) SUTA PUNCTATA: (Little spotted snake; Spotted-curl snake): The venom was found to have both neurotoxic and myotoxic effects;
    e) VERMICELLA ANNULATA (Bandy-bandy): Post-synaptic neurotoxic activity and very weak coagulopathic effects.
    6) UNKNOWN SPECIES IDENTIFICATION: Symptoms differ slightly depending on the species of snake involved. Some venoms lack presynaptic and myotoxic neurotoxins and do not lead to rhabdomyolysis and renal failure, but have a postsynaptic paralysis which is easily reversed by antivenoms.
    7) If the snake responsible for envenoming cannot be identified either using the venom detection kit or physical appearance, the following clinical findings may help to determine the offending Australian snake involved:
    a) LOCAL TISSUE EFFECTS (Bite Site):
    1) MINIMAL LOCAL TISSUE EFFECTS:
    a) Moderate to severe local pain with no significant redness, swelling or bruising: Consider a death adder.
    b) Minor or no local pain with no significant redness, swelling or bruising: Consider a brown snake or a taipan.
    2) REDNESS, SWELLING, AND BRUISING:
    a) Marked swelling and redness with or without bruising after 3 hours: Consider a mulga snake, red bellied black snake or a yellow faced whip snake.
    b) The presence of mild swelling only after 3 hours: Consider a tiger snake, rough scaled snake, or possible taipan.
    b) SYSTEMIC EFFECTS:
    1) DEFIBRINATION COAGULOPATHY:
    a) Defibrination coagulopathy, low fibrinogen and elevated fibrin degradation products, with paralysis and with or without myolysis: Consider a tiger snake, rough scaled snake or a possible taipan.
    b) Defibrination coagulopathy, low fibrinogen and elevated fibrin degradation products without paralysis or myolysis: Consider a brown snake, broad headed snake or Stephen's banded snake.
    2) COAGULATION NORMAL OR COAGULOPATHY WITH NORMAL FIBRINOGEN AND FIBRIN DEGRADATION PRODUCTS:
    a) Without paralysis: Consider a mulga snake, spotted black snake or Collett's snake.
    b) With paralysis: Consider a death adder or a copperhead.
    3) PARALYSIS:
    a) Paralysis without significant myolysis and with normal coagulation studies: Consider a death adder or a possible copperhead.
    4) MYOLYSIS
    a) Significant myolysis with normal coagulation studies with or without paralysis: Consider mulga snake, spotted black snake, Collett's snake and possibly small eyed snake
    5) NO SYSTEMIC EFFECTS
    a) No evidence of paralysis, coagulopathy or myolysis in the setting of a patient with obvious marked swelling from local effects: Consider a red-bellied black snake, yellow-faced whip snake.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Vital signs may be altered due to anxiety or shock.
    2) Elevated pulse rate may be noted.
    3) Blood pressure may be increased or decreased.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Ptosis may occur as an early sign of paralysis.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Respiratory paralysis may occur due to neurotoxic components of the venom.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Progressive paralysis may occur.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) Hematuria may be present.
    2) The urine may be dark in color from myoglobinuria (muscle pigments being excreted through the kidneys).
    0.2.13) HEMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Coagulopathy is common in significant envenomations.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) The appearance of bite marks is quite variable.
    2) Bite marks are NOT a good predictor of the degree of envenomation. Cases of severe envenomation have occurred without obvious bite marks.
    0.2.15) MUSCULOSKELETAL
    A) WITH POISONING/EXPOSURE
    1) Muscle destruction by myotoxins may cause generalized muscle pain, especially in the movement of some muscle groups.
    0.2.22) OTHER
    A) WITH POISONING/EXPOSURE
    1) UNKNOWN SPECIES IDENTIFICATION
    a) UNKNOWN SPECIES IDENTIFICATION: Symptoms differ slightly depending on the species of snake involved. Some venoms lack presynaptic and myotoxic neurotoxins and do not lead to rhabdomyolysis and renal failure, but have a postsynaptic paralysis which is easily reversed by antivenoms (White, 2005).
    b) If the snake cannot be identified either by physical characteristics or venom detection kit, or was not brought to the healthcare center for identification the following clinical findings may help to determine the offending Australian snake involved (White, 2005):
    1) LOCAL TISSUE EFFECTS (Bite Site) (White, 2005):
    a) MINIMAL LOCAL TISSUE EFFECTS:
    1) Moderate to severe local pain with no significant redness, swelling or bruising: Consider a death adder.
    2) Minor or no local pain with no significant redness, swelling or bruising: Consider a brown snake or a taipan.
    b) REDNESS, SWELLING, AND BRUISING:
    1) Marked swelling and redness with or without bruising after 3 hours: Consider a mulga snake, red-bellied black snake or a yellow-faced whip snake.
    2) Presence of mild swelling only after 3 hours: Consider a tiger snake, rough scaled snake, or a possible taipan.
    2) SYSTEMIC EFFECTS (White, 2005):
    a) DEFIBRINATION COAGULOPATHY:
    1) Defibrination coagulopathy, with low fibrinogen and increased fibrin degradation products, with paralysis and myolysis: Consider a tiger snake, rough scaled snake or a possible taipan.
    2) Defibrination coagulopathy, with low fibrinogen and increased fibrin degradation products, with no paralysis or myolysis: Consider a brown snake, broad headed snake or Stephen's banded snake.
    b) COAGULATION NORMAL OR COAGULOPATHY WITH NORMAL FIBRINOGEN AND FIBRIN DEGRADATION PRODUCTS:
    1) Without paralysis: Consider a mulga snake, spotted black snake or Collett's snake.
    2) With paralysis: Consider a death adder or a copperhead.
    c) PARALYSIS:
    1) Paralysis without significant myolysis and with normal coagulation studies: Consider a death adder or a possible copperhead.
    d) MYOLYSIS
    1) Significant myolysis with normal coagulation studies with or without paralysis: Consider mulga snake, spotted black snake, Collett's snake and possibly small eyed snake
    e) NO SYSTEMIC EFFECTS
    1) No evidence of paralysis, coagulopathy or myolysis in the setting of a patient with obvious marked swelling from local effects: Consider a red-bellied black snake, yellow-faced whip snake.

Laboratory Monitoring

    A) Monitor vital signs, neurologic exam and mental status.
    B) Monitor serial neurologic exams for any evidence of ptosis, ophthalmoplegia, dysarthria, dysphagia, or respiratory or skeletal muscle weakness.
    C) Assess respiratory function; respiratory paralysis may develop secondary to neurotoxicity. Monitor pulse oximetry and ABGs in patients with early signs of systemic envenoming. Monitor for any evidence of difficulty handling secretions. Monitoring negative inspiratory force may provide early evidence of the need for endotracheal intubation and mechanical ventilation
    D) Monitor serum electrolytes, renal function, urinalysis and urine output. Monitor CK if there is clinical evidence of myotoxicity.
    E) 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 can be monitored but may not be necessary in most patients. The whole blood clotting time can also be used to assess for coagulation abnormalities.
    F) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    G) ECG should be monitored, especially in older patients.
    H) 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. Urine may also be utilized with the Venom Detection Kit (VDK).
    I) 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) FIRST AID
    1) Apply first aid immediately (the pressure-immobilization technique). This should be commenced in the field as soon as a snake bite is suspected, or as soon as a patient presents to a healthcare facility. Assume all suspected snake bites may lead to envenomation. The pressure immobilization bandage should not be removed until the patient is at a healthcare facility where antivenom and the capacity to provide ventilatory support are available.
    B) NO OR MILD ENVENOMATION
    1) Patients who are asymptomatic or only have mild symptoms of neurotoxicity should be monitored for a minimum of 12 hours.
    C) SEVERE ENVENOMATION
    1) Patients with severe or progressive neurotoxic symptoms should be treated with antivenom. Patients may require respiratory support including intubation and mechanical ventilation secondary to respiratory paralysis. Coagulopathies may develop following envenomation in certain species.
    D) AIRWAY MANAGEMENT
    1) Airway management is unlikely to be necessary following a mild or moderate envenomation, severe envenomation resulting in progressive neurotoxicity may require airway support and mechanical ventilation due to respiratory muscle paralysis.
    E) ANTIVENOM
    1) SUMMARY: Treat patients with evidence of systemic envenoming (ie, neurotoxicity). If the species of snake responsible is not known, polyvalent antivenom may be used.
    2) POLYVALENT (CSL) ANTIVENOM: DOSE: ADULTS and CHILDREN: The contents of one vial (40,000 units) should be administered slowly by the IV route after being diluted 1 to 10 in crystalloid. The dose is the same for adults and children. In young children, a dilution of 1 to 5 may be used to avoid fluid overload. Do NOT administer by the IM route. MICROPECHIS IKAHEKA: Based on in vitro studies and limited case reports, the CSL polyvalent antivenom has shown some efficacy against Micropechis ikaheka (New Guinea small-eyed snake).
    3) ONLINE ANTIVENOM INDEX: Antivenom for snakes non-native to the US may or may not be available in the US. Zoos maintain antivenoms for venomous snakes in their collections and will generally make them available to providers on a compassionate use basis. The Association of Zoos and Aquariums maintains the Online Antivenom Index website (www.aza.org/ai), where information on appropriate antivenoms for venomous snakebites, their availability, and zoo contact information can be located. Access to the site is restricted to zoos and to regional poison centers, which can be reached at 1-800-222-1222.
    F) 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.
    G) 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. In some cases, early symptoms of paralysis can begin 2 to 4 hours after envenomation followed by progressive paralysis over the next few hours. However, paralysis can be delayed for many hours (12 or more hours) in some patients. If there is no clinical or laboratory evidence of envenomation following the observation period, the patient can be discharged.
    3) ADMISSION CRITERIA: Any patient who develops more than mild clinical signs and symptoms or who develops ANY evidence of neurotoxicity 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.
    H) PITFALLS
    1) The presence of 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 envenomation. The onset of clinical evidence (ie, ptosis, blurred vision) of envenomation can occur 2 to 4 hours after envenomation followed by progressive paralysis over the next few hours. Due to limited case reports for these species, paralysis may be delayed by hours. Patients should be monitored for up 12 hours to rule out neurotoxicity. 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 and ventilatory support can be administered, and the patient should be stabilized and antivenom should generally be administered before the bandage is removed if there is clinical evidence of envenomation.
    I) DIFFERENTIAL DIAGNOSIS
    1) Envenomation by other Australian elapids (eg, tiger snakes or taipan) can also produce neurotoxicity. Myasthenia gravis. Envenomation by tiger snakes, taipan, brown snakes or mulga snakes can cause coagulation abnormalities.

Range Of Toxicity

    A) TOXICITY: Many Australian elapid snakes are capable of causing a fatality with a single bite. MICROPECHIS IKAHEKA: The venom of M ikaheka contains neurotoxic (postsynaptic), myotoxic and anticoagulant effects. The venom has high phospholipase A2 (PLA2) enzyme activity, that likely is responsible for the myotoxic and anticoagulant effects. HEMIASPIS SIGNATA: The venom may have a mild procoagulant effect. SUTA SUTA: The venom is likely to have neurotoxic (postsynaptic mode of action) effects. ENVENOMATION: M ikaheka has caused severe and fatal envenomations. OTHER: Elapids (ie, black, brown, death adders, taipan and tiger snake) of greatest clinical concern in Australia are discussed in separate managements.

Clinical Effects

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Respiratory paralysis may occur due to neurotoxic components of the venom.
    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 Micropechis ikaheka envenomation.
    b) MICROPECHIS IKAHEKA: A 40-year-old man developed difficulty breathing and was intubated about 24 hours after envenomation by a M ikaheka. He was intubated but mechanical ventilation was not available. He was treated with 2 vials of polyvalent antivenom but died of progressive hypotension about 38 hours after envenomation (Warrell et al, 1996).
    c) MICROPECHIS IKAHEKA: A 25-year-old man was bitten by a M ikaheka and within 4 hours developed incoagulable blood, progressive neurotoxicity including, ptosis, difficulty swallowing and paresis of the respiratory muscles. He showed signs of respiratory distress and required frequent suctioning for hypersalivation. A vial of polyvalent antivenom was administered with gradual improvement of some symptoms over the next 48 hours. By day 6, he was transferred out of intensive care with ongoing trismus and myoglobinuria. Two weeks after discharge, the patient continued to have slurring of his speech (Warrell et al, 1996).
    B) RESPIRATORY ARREST
    1) WITH POISONING/EXPOSURE
    a) MICROPECHIS IKAHEKA
    1) CASE REPORT: A 13-year-old girl was bitten on the finger by a probable M ikaheka snake and developed the inability to walk within 2 hours of the bite. She developed further symptoms of neurotoxicity (ie, ptosis, complete ophthalmoplegia and respiratory distress) and myoglobinuria. Two vials of polyvalent antivenom were given with no improvement and died the following day of a cardiorespiratory arrest (Hudson, 1988).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Progressive paralysis may occur.
    3.7.2) CLINICAL EFFECTS
    A) NEUROTOXICITY
    1) WITH POISONING/EXPOSURE
    a) IN VITRO STUDY: In an in vitro study the venom from several species (ie, C boschmai, D devisi, E curta, S punctata and V annulata ) were found to have post-synaptic neurotoxic activity (Pycroft et al, 2012).
    B) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) SUMMARY
    1) Neurotoxic components of the venom may cause muscle paralysis which can lead to ptosis, ophthalmoplegia, and generalized and respiratory paralysis.
    2) Fulminant signs of toxicity may be delayed for many hours.
    b) CASE REPORTS
    1) MICROPECHIS IKAHEKA: A 25-year-old man was bitten by a M ikaheka and within 4 hours developed incoagulable blood, progressive neurotoxicity including, ptosis, difficulty swallowing and paresis of the respiratory muscles and hypersalivation. He was given one vial of polyvalent antivenom and gradually improved over the next 48 hours. By day 6, he was transferred out of intensive care with ongoing trismus and myoglobinuria. Two weeks after discharge, the patient continued to have slurring of his speech (Warrell et al, 1996).
    2) SUTA SUTA: The venom is likely to have neurotoxic (postsynaptic mode of action) effects. Based on limited case reports, envenomation produced progressive neurotoxicity that resulted in flaccid paralysis. Severe pain was also reported (Kuruppu et al, 2007).
    C) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) MICROPECHIS IKAHEKA: Headache has been reported following M ikaheka envenomation (Warrell et al, 1996).
    D) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Drowsiness was observed following M ikaheka envenomation in an adult. However, no alteration in consciousness developed (Hudson, 1988).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) There is a case of suspected neurotoxicity in a dog envenomated by a E curta (Pycroft et al, 2012).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a survey of 27 children with suspected snake bites in southern mainland Australia, symptoms such as headache, vomiting, abdominal pain and abnormal coagulation accurately predicted envenomation (Tibballs, 1992).

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hematuria may be present.
    2) The urine may be dark in color from myoglobinuria (muscle pigments being excreted through the kidneys).
    3.10.2) CLINICAL EFFECTS
    A) BLOOD IN URINE
    1) WITH POISONING/EXPOSURE
    a) Hematuria may be evident.
    b) MICROPECHIS IKAHEKA: A 40 year-old-man was bitten on the foot by a M ikaheka (confirmed by laboratory analysis). At 10 hours, the patient had swelling of the foot, ptosis and pain with swallowing and was transferred to a higher level of care. He was given 2 doses of polyvalent antivenom; the first dose at 20 hours and the second dose at 26 hours. The following day, the patient was oliguric and urinary catheterization showed dark urine that was strongly positive for hemoglobin and myoglobin. The patient appeared to be improving but developed progressive hypotension and died about 38 hours after being bitten (Warrell et al, 1996).
    B) MYOGLOBINURIA
    1) WITH POISONING/EXPOSURE
    a) MICROPECHIS IKAHEKA: Myoglobinuria and hematuria were observed in an adult following M ikaheka envenomation. The effects were noted about 24 hours after being bitten, despite polyvalent antivenom therapy. The patient died about 38 hours after envenomation secondary to progressive hypotension. A second patient also developed myoglobinuria following envenomation, but gradually recovered following polyvalent antivenom administration and supportive care (Warrell et al, 1996).

Hematologic

    3.13.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Coagulopathy is common in significant envenomations.
    3.13.2) CLINICAL EFFECTS
    A) BLOOD COAGULATION PATHWAY FINDING
    1) WITH POISONING/EXPOSURE
    a) MICROPECHIS IKAHEKA (New Guinea Small-eyed Snake): In vitro studies show the venom inhibits platelet aggregation and delays clotting dependent on platelet activation or endothelial cell tissue factor expression (Sundell et al, 2001)
    b) CASE REPORTS: In a study of 11 patients with confirmed envenoming by M ikaheka, 2 patients developed incoagulable blood and 1 patient developed spontaneous bleeding (Warrell et al, 1996).
    1) CASE REPORT: A 25-year-old man was bitten by a M ikaheka and within 4 hours developed incoagulable blood, progressive neurotoxicity including, ptosis, difficulty swallowing and paresis of the respiratory muscles. He was given one vial of polyvalent antivenom and gradually improved over the next 48 hours. By day 6, he was transferred out of intensive care with ongoing trismus and myoglobinuria. Two weeks after discharge, the patient continued to have slurring of his speech (Warrell et al, 1996).
    c) HEMIASPIS SIGNATA (Black-bellied Swamp Snake): Based on limited case reports, envenomation has produced procoagulant effects and significant local symptoms (Isbister et al, 2002).
    d) IN VITRO STUDY: In an in vitro study the venom from several species (ie, C boschmai, D devisi, E curta, and V annulata ) were found to have very weak coagulopathic effects (Pycroft et al, 2012).
    B) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) Thrombocytopenia is not unusual in complicated cases with delayed antivenom therapy. It is not a direct action of the venom.
    b) In one in vitro study, elapid venoms caused fresh platelets to directly and irreversibly aggregate, and this was associated with degranulation. The authors suggest that platelet aggregation and degranulation may contribute to the defibrination syndrome seen in snakebite victims (Marshall & Herrmann, 1989).

Summary Of Exposure

    A) BACKGROUND: Elapids of greatest clinical concern in Australia and New Guinea include 5 major snake groups. These species are discussed in separate managements. See the following managements as appropriate for further information: AUSTRALIAN BLACK SNAKES, AUSTRALIAN BROWN SNAKES, AUSTRALIAN DEATH ADDERS, AUSTRALIAN TAIPAN SNAKES, or AUSTRALIAN TIGER SNAKE GROUP. Although these snakes result in most snake bites and envenomations in Australia and New Guinea, there are a select number of snakes that are not included in these groups but can produce moderate to severe envenomation and death in some cases. This management includes: Micropechis ikaheka (Papua New Guinea small-eyed snake) and Hemiaspis Signata (Black-bellied swamp snake) a black snake with a white line above the eye and one across the lip; they may be misidentified with Pseudechis spp (black snakes). Suta Suta (whip or curl snake) is found in all states of mainland Australia with the exception of Tasmania.
    B) TOXICOLOGY: MICROPECHIS IKAHEKA: The venom of M ikaheka contains neurotoxic (postsynaptic), myotoxic and anticoagulant effects. The venom has high phospholipase A2 (PLA2) enzyme activity, that is likely responsible for the myotoxic and anticoagulant effects. HEMIASPIS SIGNATA: The venom may have a mild procoagulant effect.
    C) EPIDEMIOLOGY: M ikaheka is widely distributed throughout Papua New Guinea, Irian Jaya and Indonesian islands and has caused severe and fatal envenomations. H signata is common in the Hunter and Central Coast regions of New South Wales with limited reports of envenomation. There have been limited case reports for Suta suta.
    D) WITH POISONING/EXPOSURE
    1) MICROPECHIS IKAHEKA (Papua New Guinea small-eyed snake): Local effects include swelling, pain and lymphadenopathy. Systemic effects have included neurotoxicity (including neuromuscular paralysis), myotoxicity (muscle pain and myoglobinuria), coagulopathy, and less frequently hemolysis and hypotension. Deaths have been reported.
    2) HEMIASPIS SIGNATA (Black-bellied swamp snake): Local effects may include significant pain and swelling at the bite site with distal lymphadenopathy. Based on limited reports, it has produced procoagulant effects.
    3) SUTA SUTA (whip or curl snake) is likely to produce progressive neurotoxicity and severe pain has occurred at the bite site. Myotoxic effects have not been observed.
    4) ECHIOPSIS CURTA: Limited data. It has caused localized swelling, but no neurotoxic or coagulopathy effects.
    5) OTHER SPECIES: The following species have no reports OR limited reports of human envenomation, but in vitro studies have found that the venom contains the following:
    a) CRYPTOPHIS BOSCHMAI (Carpentaria snake): Post-synaptic neurotoxic activity and high phospholipase A2 (PLA2) activity and very weak coagulopathic effects;
    b) DENISONIA DEVISI (De vi's banded snake): Post-synaptic neurotoxic activity and very weak coagulopathic effects;
    c) ECHIOPSIS CURTA (Previously Notechis curtus; Bardick snake): Post-synaptic neurotoxic activity and very weak coagulopathic effects;
    d) SUTA PUNCTATA: (Little spotted snake; Spotted-curl snake): The venom was found to have both neurotoxic and myotoxic effects;
    e) VERMICELLA ANNULATA (Bandy-bandy): Post-synaptic neurotoxic activity and very weak coagulopathic effects.
    6) UNKNOWN SPECIES IDENTIFICATION: Symptoms differ slightly depending on the species of snake involved. Some venoms lack presynaptic and myotoxic neurotoxins and do not lead to rhabdomyolysis and renal failure, but have a postsynaptic paralysis which is easily reversed by antivenoms.
    7) If the snake responsible for envenoming cannot be identified either using the venom detection kit or physical appearance, the following clinical findings may help to determine the offending Australian snake involved:
    a) LOCAL TISSUE EFFECTS (Bite Site):
    1) MINIMAL LOCAL TISSUE EFFECTS:
    a) Moderate to severe local pain with no significant redness, swelling or bruising: Consider a death adder.
    b) Minor or no local pain with no significant redness, swelling or bruising: Consider a brown snake or a taipan.
    2) REDNESS, SWELLING, AND BRUISING:
    a) Marked swelling and redness with or without bruising after 3 hours: Consider a mulga snake, red bellied black snake or a yellow faced whip snake.
    b) The presence of mild swelling only after 3 hours: Consider a tiger snake, rough scaled snake, or possible taipan.
    b) SYSTEMIC EFFECTS:
    1) DEFIBRINATION COAGULOPATHY:
    a) Defibrination coagulopathy, low fibrinogen and elevated fibrin degradation products, with paralysis and with or without myolysis: Consider a tiger snake, rough scaled snake or a possible taipan.
    b) Defibrination coagulopathy, low fibrinogen and elevated fibrin degradation products without paralysis or myolysis: Consider a brown snake, broad headed snake or Stephen's banded snake.
    2) COAGULATION NORMAL OR COAGULOPATHY WITH NORMAL FIBRINOGEN AND FIBRIN DEGRADATION PRODUCTS:
    a) Without paralysis: Consider a mulga snake, spotted black snake or Collett's snake.
    b) With paralysis: Consider a death adder or a copperhead.
    3) PARALYSIS:
    a) Paralysis without significant myolysis and with normal coagulation studies: Consider a death adder or a possible copperhead.
    4) MYOLYSIS
    a) Significant myolysis with normal coagulation studies with or without paralysis: Consider mulga snake, spotted black snake, Collett's snake and possibly small eyed snake
    5) NO SYSTEMIC EFFECTS
    a) No evidence of paralysis, coagulopathy or myolysis in the setting of a patient with obvious marked swelling from local effects: Consider a red-bellied black snake, yellow-faced whip snake.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Vital signs may be altered due to anxiety or shock.
    2) Elevated pulse rate may be noted.
    3) Blood pressure may be increased or decreased.
    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) Respiration may be compromised by respiratory paralysis from neurotoxic components of the venom.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) MICROPECHIS IKAHEKA/CASE REPORTS: In a study of 11 patients with confirmed envenoming by M ikaheka, 3 patients developed fever (Warrell et al, 1996).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Hypertension or hypotension may occur.
    2) MICROPECHIS IKAHEKA: A 40-year-old man developed a new onset of hypotension about 30 hours after envenomation by a M ikaheka. He was given 2 vials of polyvalent antivenom at 20 and 26 hours, respectively. The patient died about 38 hours after envenomation secondary to progressive hypotension (Warrell et al, 1996).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) An increase in pulse rate may occur.

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Ptosis may occur as an early sign of paralysis.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) PTOSIS
    a) MICROPECHIS IKAHEKA: In a study of 11 patients with proven envenoming by M ikaheka, 4 patients developed ptosis (Warrell et al, 1996). Bilateral ptosis was observed in 2 other cases of M ikaheka envenomation (Hudson, 1988).
    2) DIPLOPIA
    a) Diplopia has been observed following M ikaheka envenomation (Hudson, 1988).
    3) COMPLETE OPHTHALMOPLEGIA
    a) Complete external ophthalmoplegia has been observed following M ikaheka envenomation (Hudson, 1988).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) DIFFICULTY SWALLOWING
    a) Paralysis of throat muscles may occur.
    b) MICROPECHIS IKAHEKA/CASE REPORTS: A 40-year-old man developed difficulty talking and swallowing saliva about 20 hours after envenomation by a M ikaheka. Another adult also developed difficulty swallowing and a protruding tongue about 12 hours after envenomation (Warrell et al, 1996).
    2) HYPERSALIVATION
    a) MICROPECHIS IKAHEKA: A 25-year-old man was bitten by a M ikaheka and within 4 hours developed incoagulable blood, progressive neurotoxicity including, ptosis, difficulty swallowing and paresis of the respiratory muscles. He showed signs of respiratory distress and required frequent suctioning due to hypersalivation. A vial of polyvalent antivenom was administered with gradual improvement of some symptoms over the next 48 hours (Warrell et al, 1996).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) MICROPECHIS IKAHEKA
    1) In a study of 11 patients with proven envenoming by M ikaheka, 2 patients developed hypotension (Warrell et al, 1996).
    a) CASE REPORT: A 40 year-old-man was bitten on the foot and arrived at the hospital 45 minutes later. At 10 hours, the patient had swelling of the foot, ptosis, pain with swallowing and was transferred to a higher level of care. Polyvalent antivenom was given 20 hours after envenomation, but the patient developed respiratory difficulty and was intubated; mechanical ventilation was not available. The patient was oliguric and urinalysis showed hemoglobinuria and myoglobinuria. The patient appeared to be improving, but on the following day progressive hypotension occurred and he died about 38 hours after envenomation (Warrell et al, 1996).
    B) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) MICROPECHIS IKAHEKA: Bradycardia and tachycardia have been observed after envenomation by a M ikaheka (Warrell et al, 1996).
    1) CASE REPORT: A 25-year-old man was bitten by a M ikaheka and within 4 hours developed incoagulable blood, progressive neurotoxicity including, ptosis, difficulty swallowing and paresis of the respiratory muscles. Shortly after arrival his pulse was weak with hypotension. Approximately, 4 hours after arrival he was given a vial of polyvalent antivenom. Within the first day, he continued to decline and had occasional sinus bradycardia with a heart rate of 60 beats/min. By 48 hours, improvement of some symptoms was observed and he was eventually discharged to home (Warrell et al, 1996).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) The appearance of bite marks is quite variable.
    2) Bite marks are NOT a good predictor of the degree of envenomation. Cases of severe envenomation have occurred without obvious bite marks.
    3.14.2) CLINICAL EFFECTS
    A) SWELLING
    1) WITH POISONING/EXPOSURE
    a) HEMIASPIS SIGNATA: A 7-year-old boy developed localized swelling and pain after being bitten on the thumb by a H. signata. Upon examination 12 hours after exposure, the finger was red and swollen with one small axillary lymph node that was swollen. Neurologic exam, vital signs and laboratory analyses were all normal. Antivenom was not given. Recovery was uneventful (Isbister et al, 2002).
    b) ECHIOPSIS CURTA: A young adult developed localized swelling following envenomation of a E curta, but no systemic events (neurotoxic or coagulopathy effects) (Marshall & Herrmann, 1984).
    B) PAIN
    1) WITH POISONING/EXPOSURE
    a) SUTA SUTA: The venom is likely to have neurotoxic (postsynaptic mode of action) effects. Based on limited case reports, envenomation has produced severe localized pain (Kuruppu et al, 2007).

Musculoskeletal

    3.15.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Muscle destruction by myotoxins may cause generalized muscle pain, especially in the movement of some muscle groups.
    3.15.2) CLINICAL EFFECTS
    A) TOXIC MYOPATHY
    1) WITH POISONING/EXPOSURE
    a) MICROPECHIS IKAHEKA: There is clinical evidence that M ikaheka envenomation has resulted in myotoxicity with or without symptoms of neurotoxicity (Hudson & Pomat, 1988). Severe muscle pain and tenderness were observed in an adult following M ikaheka envenomation (Hudson, 1988).
    b) In vitro studies of Micropechis ikaheka (New Guinea small-eyed snake) demonstrated phospholipase A2-mediated myotoxicity (Kuruppu et al, 2005).
    B) MOTOR DYSFUNCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORTS: In a study of 11 patients with confirmed envenoming by M ikaheka, 3 patients developed generalized muscle pain and tenderness; 1 patient developed trismus (Warrell et al, 1996).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, neurologic exam and mental status.
    B) Monitor serial neurologic exams for any evidence of ptosis, ophthalmoplegia, dysarthria, dysphagia, or respiratory or skeletal muscle weakness.
    C) Assess respiratory function; respiratory paralysis may develop secondary to neurotoxicity. Monitor pulse oximetry and ABGs in patients with early signs of systemic envenoming. Monitor for any evidence of difficulty handling secretions. Monitoring negative inspiratory force may provide early evidence of the need for endotracheal intubation and mechanical ventilation
    D) Monitor serum electrolytes, renal function, urinalysis and urine output. Monitor CK if there is clinical evidence of myotoxicity.
    E) 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 can be monitored but may not be necessary in most patients. The whole blood clotting time can also be used to assess for coagulation abnormalities.
    F) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    G) ECG should be monitored, especially in older patients.
    H) 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. Urine may also be utilized with the Venom Detection Kit (VDK).
    I) Obtain a head CT if altered mentation develops, or if there is any clinical concern for intracranial bleeding.
    4.1.2) SERUM/BLOOD
    A) COAGULATION STUDIES
    1) Monitor clotting factors (PT or INR, PTT, fibrinogen) and platelet count if coagulopathy is present.
    a) In a series of 46 patients bitten by brown snakes, tiger snakes, and taipans, monitoring the PT and aPTT was an effective, clinically available and cost-effective end-point for treating venom-induced consumptive coagulopathy. The addition of fibrinogen did not provide any additional useful information (Isbister et al, 2006).
    2) Some species (ie, tiger snakes) can cause severe coagulopathy. If the species is unknown, 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).
    3) 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).

Methods

    A) MICROPECHIS IKAHEKA
    1) IMMUNOASSAY: A sensitive and specific enzyme immunoassay has been developed for suspected Micropechis ikaheka envenomation (Warrell et al, 1996).
    B) VENOM DETECTION KITS
    1) These kits use microtiter plate strips developed by Commonwealth Serum Laboratories. The strips contain enzyme immunoassays.
    2) These are used to detect venom at the bite site and in other biologic samples. The kits are also used to determine which species-specific antivenom treatment should be administered, rather than a less efficacious polyvalent antivenom. The kits should not be used to determine envenomation, which is based on clinical signs and symptoms plus or minus laboratory evidence of coagulopathy. Instead, once envenomation has been determined, the kits are utilized to determine which antivenom should be administered.
    3) The kits may malfunction (giving false positives in one or more wells) if the quantity of venom detected is much higher than that found in biological samples (Sutherland, 1992a).
    4) In a study of the efficacy of the Snake Venom Detection Kit (SVDK), use of the kit resulted in correct species identification of 30 venom samples from Australian snakes (Clancy et al, 1997).

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, myotoxicity, neurotoxicity, bleeding, 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. In some cases, early symptoms of paralysis can begin 2 to 4 hours after envenomation followed by progressive paralysis over the next few hours. However, paralysis can be delayed for many hours (12 or more hours) in some patients. If there is no clinical or laboratory evidence of envenomation following the observation period, the patient can be discharged.

Monitoring

    A) Monitor vital signs, neurologic exam and mental status.
    B) Monitor serial neurologic exams for any evidence of ptosis, ophthalmoplegia, dysarthria, dysphagia, or respiratory or skeletal muscle weakness.
    C) Assess respiratory function; respiratory paralysis may develop secondary to neurotoxicity. Monitor pulse oximetry and ABGs in patients with early signs of systemic envenoming. Monitor for any evidence of difficulty handling secretions. Monitoring negative inspiratory force may provide early evidence of the need for endotracheal intubation and mechanical ventilation
    D) Monitor serum electrolytes, renal function, urinalysis and urine output. Monitor CK if there is clinical evidence of myotoxicity.
    E) 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 can be monitored but may not be necessary in most patients. The whole blood clotting time can also be used to assess for coagulation abnormalities.
    F) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    G) ECG should be monitored, especially in older patients.
    H) 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. Urine may also be utilized with the Venom Detection Kit (VDK).
    I) Obtain a head CT if altered mentation develops, or if there is any clinical concern for intracranial bleeding.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) Irrigation of the eyes for 15 minutes with water or normal saline should adequately remove any venom in the eye.
    B) Systemic symptoms are NOT expected.

Abstracts

Case Reports

    A) OTHER
    1) SUMMARY: It has been estimated that approximately 3,000 snake bites occur each year in Australia, and of these 200 to 500 receive treatment with antivenom. The low incidence of bites compared to the high proportion of the snake population which is venomous is thought to be due to the relative isolation of most species compared to the major human population centers. With an increased growth in the urban communities, snake habitats will be wiped out; increased leisure and bushwalking will increase contact with snakes.
    2) High Risk Individuals: YOUNG CHILDREN (1 to 3 years old), when playing with snakes in their environment.
    a) LATE PRIMARY SCHOOL CHILDREN (10 to 12 years old), when collecting snake specimens for showing to friends at home and school.
    b) FARM WORKERS who work in snake environments such as pastoral station homesteads, haystacks, swamps, and drainage channels.
    c) AMATEUR REPTILE KEEPERS: It has been estimated that there may be less than 150 private reptile collections in Australia. Special licenses are required to keep venomous snakes.
    d) PROFESSIONAL REPTILE KEEPERS, which includes individuals involved in venom collection for antivenom production and others involved in venom research. A study of 28 herpetologists revealed 119 bites by potentially dangerous snake species, resulting in 17 hospital admissions. There was a median of one bite every 10 years of work (Pearn et al, 1994).
    3) The average age of a snake bite victim is the average age of the population, about 26 years.
    4) Other factors:
    a) Environment: Fields, paddocks, areas with long grass, yards, and gardens;
    b) Time of year: Spring, later winter (August), or early summer;
    c) Time of day: Majority of bites occur in the afternoon;
    d) Sex of victim: Males are involved more than 3 times as commonly as females.

Range Of Toxicity

Summary

    A) TOXICITY: Many Australian elapid snakes are capable of causing a fatality with a single bite. MICROPECHIS IKAHEKA: The venom of M ikaheka contains neurotoxic (postsynaptic), myotoxic and anticoagulant effects. The venom has high phospholipase A2 (PLA2) enzyme activity, that likely is responsible for the myotoxic and anticoagulant effects. HEMIASPIS SIGNATA: The venom may have a mild procoagulant effect. SUTA SUTA: The venom is likely to have neurotoxic (postsynaptic mode of action) effects. ENVENOMATION: M ikaheka has caused severe and fatal envenomations. OTHER: Elapids (ie, black, brown, death adders, taipan and tiger snake) of greatest clinical concern in Australia are discussed in separate managements.

Minimum Lethal Exposure

    A) SUMMARY
    1) Many Australian elapid snakes are capable of causing a fatality with a single bite.
    2) MICROPECHIS IKAHEKA
    a) CASE REPORT: A 40 year-old-man was bitten on the foot and arrived at the hospital 45 minutes later. At 10 hours, the patient had swelling of the foot, ptosis, pain with swallowing and was transferred to a higher level of care. Polyvalent antivenom was given 20 hours after envenomation; however, the patient developed respiratory difficulty and was intubated. Mechanical ventilation was not available. The patient was oliguric and urinalysis showed hemoglobinuria and myoglobinuria. The patient appeared to be improving, but on the following day progressive hypotension occurred and he died about 38 hours after envenomation (Warrell et al, 1996).

Maximum Tolerated Exposure

    A) MICROPECHIS IKAHEKA
    1) CASE REPORT: A 25-year-old man was bitten by a M ikaheka and within 4 hours developed incoagulable blood, progressive neurotoxicity including, ptosis, difficulty swallowing and paresis of the respiratory muscles. Shortly after arrival his pulse was weak with hypotension. Approximately, 4 hours after arrival he was given a vial of polyvalent antivenom. Within the first day, he continued to decline and had occasional sinus bradycardia with a heart rate of 60 beats/min. By 48 hours, improvement of some symptoms was observed and he was eventually discharged to home (Warrell et al, 1996).

Pharmacology Toxicology

Pharmacologic Mechanism

    A) The active components of Australian elapid venoms include neurotoxins, myotoxins, hemolysins, and factors which produce hypocoagulability.

Toxicologic Mechanism

    A) SUMMARY
    1) The venom of various Australian snakes may contain one or more of the following toxins:
    a) NEUROTOXINS: may progress to cause death by respiratory paralysis.
    b) HYPOCOAGULABILITY FACTORS: may cause hemorrhage into the viscera (particularly the gut).
    c) HEMOLYSINS: Can lead to a breakdown of the red blood cells, hemoglobinuria, and/or myoglobinuria.
    d) MYOTOXINS: Can lead to breakdown of the skeletal muscles with congestion and edema of the kidneys, tubular necrosis, and hemoglobinuria.
    B) MICROPECHIS IKAHEKA
    1) SUMMARY: M ikaheka venom contains both neurotoxic and phospholipase A2 (PLA2) activity. Based on an in vitro study, the venom impaired neuromuscular transmission in a concentration dependent manner and appears to have a direct effect on muscle contractility by inhibiting twitch tension when directly stimulated. Myotoxic events are associated with PLA2 activity (Geh et al, 1997).
    2) In animal studies, a long-chain neurotoxin, mikatoxin, has been identified and appears to have no phospholipase A2 activity. In a chick biventer cervicis muscle, likely produced an irreversible antagonism of postsynaptic nicotinic acetylcholine receptors of neuromuscular junction. This could lead to irreversible neuromuscular blockade in skeletal muscle. However, the other components of M ikaheka venom including other postsynaptic neurotoxins, presynaptic neurotoxins as well as myotoxic activity have a role on the muscle membrane (Nirthanan et al, 2002).
    3) Several (MiPLA2, MiPLA3 and MiPLA4) isoenzymes of phospholipase A2 have been identified and produce myotoxic effects The PLA2 activity of the venom effects skeletal muscle and contraction of smooth muscle (Kuruppu et al, 2005; Lok et al, 2005).

Animal Toxicology

Clinical Effects

    11.1.3) CANINE/DOG
    A) Clinical effects in small or large animals are similar to those effects seen in human victims.
    B) Snake bite was diagnosed in 125 dogs and 115 cats over a 10-year period.
    1) Young sporting dogs and young cats were mainly affected. More dogs (48%) were seen in contact with TIGER SNAKES than cats (7%). One hundred and four (48%) dogs and 89 (75%) cats were bitten in the warmer months of the year (October to March).
    2) As the incidence rose in September/October, dogs were bitten on days when the temperature was near 20 degrees C or higher (Barr, 1984).
    C) CASE REPORT: Multiple bites on the buccal mucosa and envenomation of a maned wolf (Chrysocyon brachyrus) by a spotted black snake (Pseudechis guttatus) resulted in collapse, hemolysis, rhabdomyolysis, local tissue necrosis, hepatic and renal failure, and subsequent death despite intensive supportive care, including antivenom, fluid support, and blood transfusion. Necropsy revealed myocardial and intestinal hemorrhage, pulmonary congestion, hepato-splenomegaly, pulmonary and abdominal visceral hemorrhage, acute nephrosis, multifocal hepatic necrosis and splenic congestion (Portas & Montali, 2007).
    D) CASE SERIES: In Australia, there are an estimated 6,200 snakebite cases in domestic animals annually. Brown, tiger, and black snakes account for 76%, 13%, and 6% of these cases, respectively. Antivenom was used in 67% of cases. Ninety-one percent of cats and 75% of dogs survived following administration of antivenom, while 66% of cats and 31% of dogs survived when antivenom was not given (Mirtschin et al, 1998).
    E) The most common presenting signs were dilated pupils and absences of pupillary light reflex. Dyspnea, hypothermia, hindleg ataxia, and glycosuria were common features in cats. Vomiting, tachypnea, hyperthermia and complete flaccid paralysis were often seen in dogs.
    F) The overall recovery rate after administration of antivenom was 90% for cats and 83% for dogs. Dogs treated soon after being bitten recovered more rapidly. There was no correlation between the bite-to-treatment period and the treatment-to-recovery period for cats (Barr, 1984).

Treatment

    11.2.2) LIFE SUPPORT
    A) SUMMARY
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.5) TREATMENT
    A) GENERAL TREATMENT
    1) Treatment is the same as for human victims.

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) SUMMARY
    1) Varies with the type of snake involved. Certainly many of the Australian elapid snakes are capable of producing fatality in patients untreated with antivenin.

References

General Bibliography

    1) American Zoo and Aquarium Association: Antivenom Index. American Zoo and Aquarium Association. Silver Spring, MD. 2009. Available from URL: http://www.aza.org/ai/index.cfm. As accessed 2009-04-13.
    2) Anon: WHO/SEARO guidelines for clinical management of snake bites. So Asian J Trop Med Pub Health 1999; 30 (S1):1-85.
    3) Barr SC: Clinical features therapy and epidemiology of tiger snake bite in dogs and cats. Aust Vet J 1984; 61:208-212.
    4) Baxter Healthcare Corporation: Dear Healthcare Professional Letter for ENLON (edrophonium chloride), and ENLON-PLUS (edrophonium chloride and atropine sulphate). US Food and Drug Administration. Rockville, MD. 2008. Available from URL: http://www.fda.gov/cder/drug/shortages/Enlon.pdf.
    5) Clancy AM, White J, & Wentworth BH: The effect of species and geographical origin of snakes on the identification of their venom using a commercial assay. Med J Aust 1997; 167:56.
    6) 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.
    7) Currie BJ: Treatment of snakebite in Australia: The current evidence base and questions requiring collaborative multicentre prospective studies. Toxicon 2006; 48(7):941-956.
    8) Geh SL, Vincent A, Rang S, et al: Identification of phospholipase A2 and neurotoxic activities in the venom of the New Guinean small-eyed snake (Micropechis ikaheka). Toxicon 1997; 35(1):101-109.
    9) Gold BS: Neostigmine for the treatment of neurotoxicity following envenomation by the asiatic cobra. Ann Emerg Med 1996; 28:87-89.
    10) Hudson BJ & Pomat K: Ten years of snake bite in Madang Province, Papua New Guinea. Trans R Soc Trop Med Hyg 1988; 82(3):506-508.
    11) Hudson BJ: The small-eyed snake (Micropechis ikaheka): a review of current knowledge. P N G Med J 1988; 31(3):173-178.
    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 , Dawson AH , & Whyte IM : Two cases of bites by the black-bellied swamp snake (Hemiaspis signata). Toxicon 2002; 40(3):317-319.
    14) Isbister GK, Williams V, Brown SG, et al: Clinically applicable laboratory end-points for treating snakebite coagulopathy. Pathology 2006; 38(6):568-572.
    15) 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.
    16) Jelinek GA, Rogers IR, & Corkeron MA: Severe multi-system failure following delayed presentation with tiger snake envenomation. Anaesth Intensive Care 1998; 26:584-585.
    17) Kuruppu S , Robinson S , Hodgson WC , et al: The in vitro neurotoxic and myotoxic effects of the venom from the Suta genus (curl snakes) of elapid snakes. Basic Clin Pharmacol Toxicol 2007; 101(6):407-410.
    18) Kuruppu S, Isbister GK, & Hodgson WC: Phospholipase A2-dependent effects of the venom from the New Guinean small-eyed snake Micropechis ikaheka. Muscle Nerve 2005; 32(1):81-87.
    19) Lieberman P, Nicklas R, Randolph C, et al: Anaphylaxis-a practice parameter update 2015. Ann Allergy Asthma Immunol 2015; 115(5):341-384.
    20) 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.
    21) Little M, Hudson DW, & Pereira PL: Antivenoms and helicopter rescue services. Med J Aust 1998; 169:229-230.
    22) Lok SM, Gao R, Rouault M, et al: Structure and function comparison of Micropechis ikaheka snake venom phospholipase A2 isoenzymes. FEBS J 2005; 272(5):1211-1220.
    23) Marshall LR & Herrmann RP: Australian snake venoms and their in vitro effect on human platelets. Thromb Research 1989; 54:269-275.
    24) Marshall LR & Herrmann RP: Cross-reactivity of bardick snake venom with death adder antivenom. Med J Aust 1984; 140(9):541-542.
    25) Mirtschin PJ, Masci P, Paton DC, et al: Snake bites recorded by veterinary practices in Australia. Aust Vet J 1998; 76(3):195-198.
    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) Nirthanan S, Gao R, Gopalakrishnakone P, et al: Pharmacological characterization of mikatoxin, an alpha-neurotoxin isolated from the venom of the New-Guinean small-eyed snake Micropechis ikaheka. Toxicon 2002; 40(7):863-871.
    28) Nocera A, Gallagher J, & White J: Severe tiger snake envenomation in a wilderness environment. Med J Aust 1998; 168:69-71.
    29) Nowak RM & Macias CG : Anaphylaxis on the other front line: perspectives from the emergency department. Am J Med 2014; 127(1 Suppl):S34-S44.
    30) Pearn JH, Covacevich J, Charles N, et al: Snakebite in herpetologists. Med J Aust 1994; 161(11-12):706-708.
    31) Portas TJ & Montali RJ: Spotted black snake (Pseudechis guttatus) envenomation in a maned wolf (Chrysocyon brachyurus). J Zoo Wildl Med 2007; 38(3):483-487.
    32) 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.
    33) Pycroft K , Fry BG , Isbister GK , et al: Toxinology of venoms from five Australian lesser known elapid snakes. Basic Clin Pharmacol Toxicol 2012; 111(4):268-274.
    34) Ryan NM , Kearney RT , Brown SG , et al: Incidence of serum sickness after the administration of Australian snake antivenom (ASP-22). Clin Toxicol (Phila) 2016; 54(1):27-33.
    35) 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.
    36) Sundell IB, Theakston RD, Kamiguti AS, et al: The inhibition of platelet aggregation and blood coagulation by Micropechis ikaheka venom. Br J Haematol 2001; 114(4):852-860.
    37) Tibballs J, Hawdon GM, & Pincus SJ: Severe tiger snake envenomation in a wilderness environment (letter). Med J Aust 1998; 169:228-229.
    38) Tibballs J, Kuruppu S, Hodgson WC, et al: Cardiovascular, haematological and neurological effects of the venom of the Papua New Guinean small-eyed snake (Micropechis ikaheka) and their neutralisation with CSL polyvalent and black snake antivenoms. Toxicon 2003; 42(6):647-655.
    39) Tibballs J: Diagnosis and treatment of confirmed and suspected snake bite: implications from an analysis of 46 paediatric cases. Med J Aust 1992; 156:270-274.
    40) Tibballs J: Fresh frozen plasma after brown snake bite--helpful or harmful?. Anaesth Intensive Care 2005; 33(1):13-15.
    41) 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.
    42) Warrell DA, Hudson BJ, Lalloo DG, et al: The emerging syndrome of envenoming by the New Guinea small-eyed snake Micropechis ikaheka. QJM 1996; 89(7):523-530.
    43) 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, 1995, pp 595-618.
    44) White J: Snake venoms and coagulopathy. Toxicon 2005; 45(8):951-967.
    45) Williams V & White J : Variation in venom composition and reactivity in two specimens of yellow-faced whip snake (Demansia psammophis) from the same geographical area. Toxicon 1990; 28(11):1351-1354.