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AUSTRALIAN TIGER SNAKE GROUP

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Tiger snakes are a group of elapids that can be found in the subtropical and temperate regions of Australia. Their venoms have neurotoxic (both pre- and postsynaptic), procoagulant and myotoxic effects. The Australian copperheads, the rough scale snakes, pale-headed snakes, broad-headed snakes and Stephen's banded snake are not tiger snakes but are classified with this group because of similarities in clinical presentation and because they are treated with tiger snake antivenom.

Specific Substances

    A) AUSTRALIAN TIGER SNAKES AND RELATED
    1) Austrelaps labialis
    2) Austrelaps ramsayi
    3) Austrelaps superbus
    4) Australian tiger snake
    5) Adelaide Hills copperhead
    6) Black tiger snake
    7) Broad-headed snake
    8) Common copper head.
    9) Eastern tiger snake
    10) Highlands copperhead
    11) Hoplocephalus bungaroides
    12) Hoplocephalus bitorquatus
    13) Hoplocephalus stephensi
    14) Notechis ater
    15) Notechis ater occidentalis
    16) Notechis scutatus
    17) Pale-headed snake
    18) Rough scale snake
    19) Stephen's banded snake
    20) Western tiger snake
    21) Tropidechis carinatus

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Tiger snakes are a group of elapids that can be found in the subtropical and temperate regions of Australia. The Australian copperheads, the rough scale snakes, and the members of the genus Hoplocephalus, the pale-headed snake, broad-headed snake and Stephen's banded snake, are not tiger snakes but are classified with this group because of similarities in clinical presentation and treatment.
    B) TOXICOLOGY: The venom of these snakes have neurotoxic (both pre- and postsynaptic), procoagulant and myotoxic effects.
    C) EPIDEMIOLOGY: Tiger snakes are a common cause of envenomation in some areas of Australia. Dry bites are fairly common, but severe envenomation and death can occur. Only brown snakes cause more lethal bites in Australia.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE ENVENOMATION: A significant percent of tiger snake bites do not result in envenomation. Local effects include pain, swelling, discoloration and tender lymphadenopathy. Nonspecific systemic effects can include nausea, vomiting, diarrhea, abdominal pain, headache and diaphoresis. Mild coagulopathy and CK elevations may be noted.
    2) SEVERE ENVENOMATION: Myotoxicity with muscle pain, weakness, severe rhabdomyolysis and renal failure may develop. Coagulopathy can be severe, and life threatening bleeding, most often intracranial, can develop. Cranial nerve palsies, generalized weakness and respiratory failure can develop from neurotoxic effects of the venom.

Laboratory Monitoring

    A) Monitor vital signs, neurologic exam and mental status.
    B) Monitor serum electrolytes, renal function, urinalysis and urine output.
    C) 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.
    D) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    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) MILD OR NO 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) Patients with severe symptoms or laboratory evidence of venom-induced consumptive coagulopathy or renal injury should be treated with antivenom and, if coagulopathy is severe, fresh frozen plasma or cryoprecipitate. Patients with severe neurotoxicity may require endotracheal intubation and mechanical ventilation.
    C) ANTIVENOM
    1) For tiger snake or rough scaled snake bites, treat patients with venom-induced consumptive coagulopathy, rhabdomyolysis, paralysis, or renal failure with tiger snake antivenom. If specific antivenom is not available, or the species of snake responsible is not known, polyvalent antivenom may be used. The optimum dose of antivenom is not known. For tiger snake bites, administer at least 2 vials, increase to 4 vials, if coagulopathy, severe neurotoxicity or multiple bites. Treat patients bitten by a broad-headed snake, Stephen's banded snake or pale-headed snake who develop coagulopathy with 2 to 4 vials of antivenom. For copperhead bites, start with 1 vial of antivenom, use 2 to 4 vials if severe envenomation develops or there are multiple bites. Dilute each vial of antivenom in 1 to 10 in crystalloid, and infuse each vial over 15 to 30 minutes. Monitor patient carefully and be prepared to treat anaphylaxis.
    D) VENOM INDUCED CONSUMPTIVE COAGULOPATHY
    1) In addition to antivenom, fresh frozen plasma and/or cryoprecipitate should be considered early in patients with severe consumptive coagulopathy.
    E) 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.
    F) MONITORING OF PATIENT
    1) Monitor vital signs, perform a careful neurologic exam and mental status. Monitor serum electrolytes, renal function, CK, urinalysis and urine output. 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. Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, bruising, epistaxis, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding). 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 develops. The presence of venom at the bite site does NOT mean that systemic envenomation has occurred. Obtain a head CT if altered mentation develops, or there is any clinical concern for intracranial bleeding.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: There is no role for home management of possible snake bite.
    2) OBSERVATION CRITERIA: All patients with suspected snake bite should be observed for at least 12 hours, with serial laboratory studies (ie, coagulation studies, serum electrolytes, renal function) on admission and every 6 hours thereafter, and careful clinical evaluation. If there is no clinical or laboratory evidence of envenomation, coagulopathy, or renal insufficiency 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 ANY evidence of coagulopathy, bleeding, 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.
    H) TOXICOKINETICS
    1) ONSET: Onset of envenomation can be quite rapid, with some patients collapsing shortly after being bitten. The vast majority of patients who develop systemic envenomation have evidence of coagulopathy on laboratory testing within 12 hours of the bite (generally sooner in patients with severe envenomation). DURATION: Once venom-induced consumptive coagulopathy has developed, recovery of normal coagulation generally does not occur until 12 to 18 hours after the administration of antivenom.
    I) PITFALLS
    1) The presence of tiger 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.
    J) DIFFERENTIAL DIAGNOSIS
    1) Envenomation by brown snakes, taipan or mulga snakes can cause coagulation abnormalities. Disseminated intravascular coagulation. Overdose of anticoagulants such as warfarin or brodifacoum.

Range Of Toxicity

    A) TOXICITY: A single bite from a tiger snake can be lethal. Children often develop more severe effects. Some definite bites by tiger snakes do not result in envenomation, it is estimated that about 50% of tiger snake bites result in significant envenomation.

Summary Of Exposure

    A) BACKGROUND: Tiger snakes are a group of elapids that can be found in the subtropical and temperate regions of Australia. The Australian copperheads, the rough scale snakes, and the members of the genus Hoplocephalus, the pale-headed snake, broad-headed snake and Stephen's banded snake, are not tiger snakes but are classified with this group because of similarities in clinical presentation and treatment.
    B) TOXICOLOGY: The venom of these snakes have neurotoxic (both pre- and postsynaptic), procoagulant and myotoxic effects.
    C) EPIDEMIOLOGY: Tiger snakes are a common cause of envenomation in some areas of Australia. Dry bites are fairly common, but severe envenomation and death can occur. Only brown snakes cause more lethal bites in Australia.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE ENVENOMATION: A significant percent of tiger snake bites do not result in envenomation. Local effects include pain, swelling, discoloration and tender lymphadenopathy. Nonspecific systemic effects can include nausea, vomiting, diarrhea, abdominal pain, headache and diaphoresis. Mild coagulopathy and CK elevations may be noted.
    2) SEVERE ENVENOMATION: Myotoxicity with muscle pain, weakness, severe rhabdomyolysis and renal failure may develop. Coagulopathy can be severe, and life threatening bleeding, most often intracranial, can develop. Cranial nerve palsies, generalized weakness and respiratory failure can develop from neurotoxic effects of the venom.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 68-year-old man presented with hypotonia, atrial fibrillation with rapid ventricular response (130 beats/min), coagulopathy, rhabdomyolysis, acute renal failure, respiratory insufficiency, and hypotension after a tiger snake bite. Hypotension required an epinephrine infusion for 3 days to maintain a mean arterial pressure above 70 mmHg. He required continuous veno-venous hemodiafiltration for 16 days and mechanical ventilation for 18 days but eventually recovered (Jelinek et al, 1998).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY FAILURE
    1) WITH POISONING/EXPOSURE
    a) Respiratory failure from either neurotoxicity or severe myopathy, but is not common.
    b) INCIDENCE: In a series of 23 patients with tiger snake envenomation, 3 (13%) patients developed neurotoxicity, and one of those had a respiratory arrest (Scop et al, 2009).
    c) CASE REPORT: A 44-year-old man was bitten on the left ankle. He developed weakness, dysarthria, respiratory insufficiency, severe rhabdomyolysis, compartment syndrome of the upper extremities, coagulopathy and renal failure. Urine testing was positive for tiger snake venom. He was treated with antivenom, transfusion, hemodialysis and mechanical ventilation. He required about 2 weeks of mechanical ventilation but recovered (Jolles et al, 1998).
    d) CASE REPORT: A 44-year-old man was bitten by an unseen animal. He developed severe envenomation, with blurred vision, ptosis, weakness, respiratory failure, renal failure, severe rhabdomyolysis and compartment syndrome, and mild coagulopathy. Urine test was positive for tiger snake venom. He was bitten in a remote area in bad weather, so evacuation was complicated and he did not reach the hospital until nearly 24 hours after the bite. He required mechanical ventilation for 13 days and hemodialysis for 32 days but eventually recovered (Nocera et al, 1998).
    e) CASE REPORT: A 68-year-old man presented with hypotonia, ptosis, ophthalmoplegia, and fixed pupils, coagulopathy, rhabdomyolysis, acute renal failure, respiratory insufficiency, and hypotension after a tiger snake bite. He required continuous veno-venous hemodiafiltration for 16 days and mechanical ventilation for 18 days for respiratory muscle weakness (Jelinek et al, 1998).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headaches is common after tiger snake envenomation, and are often one of the earliest clinical manifestations.
    b) INCIDENCE: In a series of 23 patients with tiger snake envenomation 17 (74%) patients complained of headache (Scop et al, 2009)
    B) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) Paralysis can develop after envenomation by tiger snakes, rough scaled snakes, and probably copper heads. It is not expected after envenomation by Stephen's banded snakes (White, 2005). Manifestations can include generalized weakness, respiratory insufficiency, and cranial nerve palsies with ptosis, ophthalmoplegia, dysphagia or dysarthria. Recovery of neuromuscular function can be slow, requiring 2 to 3 weeks in some cases.
    b) INCIDENCE: In a series of 23 patients with tiger snake envenomation, 2 (9%) patients developed ptosis and 1 (4%) had a respiratory arrest (Scop et al, 2009) .
    c) CASE REPORT: A 44-year-old man was bitten on the left ankle. He developed weakness, dysarthria, respiratory insufficiency, severe rhabdomyolysis, compartment syndrome of the upper extremities, coagulopathy and renal failure. Urine testing was positive for tiger snake venom. He was treated with antivenom, transfusion, hemodialysis and mechanical ventilation. He required about 2 weeks of mechanical ventilation but recovered (Jolles et al, 1998).
    d) CASE REPORT: A 44-year-old man was bitten by an unseen animal. He developed severe envenomation, with blurred vision, ptosis, weakness, respiratory failure, renal failure, severe rhabdomyolysis and compartment syndrome, and mild coagulopathy. Urine test was positive for tiger snake venom. He was bitten in a remote area in bad weather, so evacuation was complicated and he did not reach the hospital until nearly 24 hours after the bite. He required mechanical ventilation for 13 days and hemodialysis for 32 days but eventually recovered (Nocera et al, 1998).
    e) CASE REPORT: A 67-year-old man was unconscious in a barn, and presented to the ED with severe epistaxis, mid-face trauma, hypoxia, coagulopathy, and rhabdomyolysis. He was intubated and treated with fresh frozen plasma. Puncture wounds were later noted on the right thigh and tiger snake venom was detected at the bite site. He was treated with 7 vials of tiger snake antivenom and 3 days later was extubated. At that time he complained of diplopia and blurred vision and was noted to have limitations of horizontal and vertical gaze. He gradually improved over a week (Ferdinands et al, 2006).
    f) CASE REPORT: A 38-year-old woman was bitten on the right ankle. She developed nausea, abdominal pain, lightheadedness and numbness of the hands and feet. Bite site swab was positive for tiger snake venom. Her initial coagulation screen was normal. About 26 hours after the bite she had difficulty opening her jaw, and at 32 hours she had dysphagia and rhabdomyolysis (which peaked at a CK of 153,400 at 68 hour after the bite). She was unable to move her tongue, swallow, open her eyes or cough and had myalgias. She was treated with antivenom 36 hours after the bite and required at total of 5 vials of antivenom. She had ptosis and swallowing difficulties requiring NG feeding for 5 days but gradually recovered; she was discharged on day 27 (Gavaghan & Sparkes, 2003).
    g) CASE REPORT: A 68-year-old man presented with hypotonia, ptosis, ophthalmoplegia, and fixed pupils, coagulopathy, rhabdomyolysis, acute renal failure, respiratory insufficiency, and hypotension after a tiger snake bite. He required continuous veno-venous hemodiafiltration for 16 days and mechanical ventilation for 18 days. Recovery of neuromuscular function was slow. Strength was 4/5 by the end of the 4th hospital day, distal motor strength recovered faster than proximal. Tendon reflexes were still depressed after 19 days. Ptosis, ophthalmoplegia and fixed pupils persisted through day 12 and were partly recovered by day 19 (Jelinek et al, 1998).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain develops in many patients with tiger snake envenomation and may be severe (Casamento & Isbister, 2011; Gavaghan & Sparkes, 2003).
    b) INCIDENCE: In a series of 23 patients with tiger snake evenomation, 11 (48%) patients developed abdominal pain (Scop et al, 2009).
    B) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting are common after tiger snake envenomation, and are often some of the earliest signs of envenomation (Parkin et al, 2002).
    b) INCIDENCE: In a series of 23 patients with tiger snake evenomation, 17 (74%) patients developed nausea and/or vomiting (Scop et al, 2009).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) MYOGLOBINURIA
    1) WITH POISONING/EXPOSURE
    a) Myoglobinuria is often noted in patients who develop severe myopathy and rhabdomyolysis (Sutherland & Coulter, 1977; Hood & Johnson, 1975). Urine will be dark, and is positive for blood on dipstick without evidence of hematuria on microscopic examination.
    B) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Acute renal failure can develop in patients with severe myopathy and rhabdomyolysis. Patients often require hemodialysis but generally renal function recovers over several weeks.
    b) CASE REPORT: A 44-year-old man was bitten by an unseen animal. He developed severe envenomation, with neurologic toxicity, respiratory failure, acute renal failure, severe rhabdomyolysis and compartment syndrome, and mild coagulopathy. Urine test was positive for tiger snake venom. He was bitten in a remote area in bad weather, so evacuation was complicated and he did not reach the hospital until nearly 24 hours after the bite. He required mechanical ventilation for 13 days and hemodialysis for 32 days but eventually recovered (Nocera et al, 1998).
    c) CASE REPORT: A 68-year-old man presented with hypotonia, atrial fibrillation with rapid ventricular response (130 beats/min), coagulopathy, rhabdomyolysis, acute renal failure, respiratory insufficiency, and hypotension after a tiger snake bite. He required continuous veno-venous hemodiafiltration for 16 days and mechanical ventilation for 18 days but eventually recovered (Jelinek et al, 1998).
    d) INCIDENCE: In a series of 23 patients with tiger snake envenomation, 1 (4%) patient developed acute renal failure (Scop et al, 2009).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) METABOLIC ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Metabolic acidosis can develop with severe envenomation but is not common.
    b) CASE REPORT: A 44-year-old man was bitten by an unseen animal. He developed severe envenomation, with neurologic toxicity, respiratory failure, renal failure, severe rhabdomyolysis and compartment syndrome, and mild coagulopathy. Urine test was positive for tiger snake venom. He was bitten in a remote area in bad weather, so evacuation was complicated and he did not reach the hospital until nearly 24 hours after the bite. Laboratory findings on admission included metabolic acidosis with a pH of 7.16, pCO2 44 mmHg, bicarbonate 15 mmol/L, and base excess of negative 13. He required mechanical ventilation for 13 days and hemodialysis for 32 days but eventually recovered (Nocera et al, 1998).
    c) CASE REPORT: A 68-year-old man presented with hypotonia, atrial fibrillation with rapid ventricular response (130 beats/min), coagulopathy, rhabdomyolysis, acute renal failure, respiratory insufficiency and hypotension. Laboratory studies revealed metabolic acidosis with a pH of 7.13, a base excess of negative 10 and a lactate concentration of 6.1 mmol/L; tiger snake venom was detected in urine. He required continuous veno-venous hemodiafiltration for 16 days and mechanical ventilation for 18 days but eventually recovered (Jelinek et al, 1998).
    B) RESPIRATORY ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Respiratory acidosis can develop in patients with respiratory failure from either neurotoxicity or severe myopathy.

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) BLOOD COAGULATION DISORDER
    1) WITH POISONING/EXPOSURE
    a) Coagulopathy often develops in severe envenomation. Characteristic findings include markedly prolonged INR and aPTT, markedly decreased fibrinogen concentrations, elevated D-dimer, normal platelet counts, and decreased concentrations of factors V, VIII, and protein C (Parkin et al, 2002).
    b) ONSET: In a study of 90 patients with venom induced consumptive coagulopathy (45 definite brown snake and 45 definite tiger snake), patients bitten by tiger snake had almost complete depletion of fibrinogen, and factors V and VIII within 2 hours, compared to within 1 hour for the brown snake group (Isbister et al, 2010).
    c) DURATION: Once venom-induced consumptive coagulopathy develops, it generally does not resolve for 12 to 18 hours after antivenom administration, because of the time required for resynthesis of clotting factors and fibrinogen (Isbister, 2010).
    B) BLEEDING
    1) WITH POISONING/EXPOSURE
    a) Spontaneous bleeding is not common, but bleeding at venipuncture sites or other areas of trauma is common in patients who develop coagulopathy (White, 2005).
    b) INCIDENCE: In a series of 23 patients with tiger snake envenomation, 6 (26%) patients developed bleeding, 4 from the bite site, 1 epistaxis and 1 hematemesis (Scop et al, 2009).
    C) MICROANGIOPATHIC HEMOLYTIC ANEMIA
    1) WITH POISONING/EXPOSURE
    a) Microangiopathic hemolytic anemia has been reported after tiger snake envenomation but is not common. It is characterized by acute renal failure, anemia, thrombocytopenia, and evidence of fragmented red cells on peripheral smear. Onset is generally 2 or 3 days after the bite, after recovery from the initial consumption coagulopathy.
    b) CASE REPORT: A 55-year-old woman was bitten on the left small toe. She develop headache, nausea, vomiting, decreased fibrinogen, elevated aPTT and INR and the bite site swab was positive for tiger snake venom. She was treated with tiger snake antivenom and coagulopathy resolved at 19 hours after envenomation. Over the next 2 days she developed anemia, thrombocytopenia, renal failure with fragmented red cells on blood smear. She was treated with plasma exchange and hemodialysis and recovered over 19 days (Casamento & Isbister, 2011).
    c) CASE REPORT: A 46-year-old man was bitten on the right thumb by his pet tiger snake. He developed headache, nausea and vomiting, and coagulopathy. He was treated with tiger snake antivenom and coagulopathy improved 17 hours post bite. Over the next 2 days he developed renal failure, and thrombocytopenia and had fragmented red cells on blood smear. He received continuous renal replacement therapy from day 4 to day 10 after the bite and then intermittent hemodialysis for 7 weeks (Casamento & Isbister, 2011).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) PAIN
    1) WITH POISONING/EXPOSURE
    a) Pain at the bite site develops in many patients with tiger snake envenomation and may be severe.
    b) INCIDENCE: In a series of 23 patients with tiger snake evenomation, 10 (43%) patients developed pain at the bite site (Scop et al, 2009).
    B) SWELLING
    1) WITH POISONING/EXPOSURE
    a) Bites from tiger snakes and the rough scaled snake generally result in mild swelling, erythema and bruising after 3 hours (White, 2005).
    C) NECROSIS
    1) WITH POISONING/EXPOSURE
    a) Local tissue necrosis is not common but has occurred.
    b) CASE REPORT: A 20-month-old boy was bitten by an unseen reptile on the right leg and wrist. Shortly, thereafter he collapsed and had an apparent seizure. On arrival to the hospital he was drowsy, and blood tested positive for tiger snake venom. He developed coagulopathy and rhabdomyolysis, and was treated with tiger snake antivenom and fresh frozen plasma. The following day an area of necrotic skin was noted around the leg bite. The area was surgically explored, revealing necrotic skin and some underlying devitalized fat, and pale somewhat mottled underlying muscle that was not necrotic with no compartment syndrome. Pathology revealed extensive necrosis of the skin and underlying fat with thrombosis of small to medium sized vessels. The child required skin grafting but recovered (Penington & Johnstone, 1997).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) TOXIC MYOPATHY
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: In a series of 23 patients with tiger snake envenomation, 6 (26%) patients developed rhabdomyolysis (Scop et al, 2009).
    b) CASE REPORT: A 47-year-old man was bitten on the hand by a tiger snake. He was treated with 3,000 units of tiger snake antivenom. Over the next 2 days he developed severe myopathy with rhabdomyolysis and focal necrotizing myopathy on biopsy, anuric renal failure and hyperkalemia. He was intubated and mechanically ventilated for about 10 days, and required hemodialysis for about a month. He had severe weakness and muscle wasting but eventually recovered (Hood & Johnson, 1975).
    B) COMPARTMENT SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Compartment syndrome is rare but has been reported. It has occurred as a complication of severe diffuse myopathy in muscles remote from the location of the bite.
    b) CASE REPORT: A 44-year-old man was bitten on the ankle by an unseen animal. He developed severe envenomation, with neurologic toxicity, respiratory failure, renal failure, mild coagulopathy, severe rhabdomyolysis, and compartment syndrome requiring fasciotomy of both forearms and hands. Urine test was positive for tiger snake venom. He was bitten in a remote area in bad weather, so evacuation was complicated and he did not reach the hospital until nearly 24 hours after the bite. He required mechanical ventilation for 13 days and hemodialysis for 32 days but eventually recovered (Nocera et al, 1998).
    c) CASE REPORT: A 44-year-old man was bitten on the ankle and developed weakness, dysarthria, respiratory failure, severe rhabdomyolysis (CK 287,000 units/L), renal failure and coagulopathy. On presentation his muscles were tense and edematous, and he required bilateral forearm fasciotomies (right forearm pressure 67 mmHg and left forearm pressure 56 mmHg) (Jolles et al, 1998).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, neurologic exam and mental status.
    B) Monitor serum electrolytes, renal function, urinalysis and urine output.
    C) 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.
    D) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    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) Tiger snake envenomation can cause severe coagulopathy. 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).
    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, 1995).
    c) In an in vitro study, the venom or saliva of other Australian snakes that are considered venomous, mildly venomous, and non-venomous were found to yield positive results for tiger snake venom on the venom detection kit. The venomous Black snakes mulga (Pseudoechis asutralis) and spotted mulga (Pseudoechis butleri), the mildly venomous Gould's hooded snake (Parasuta gouldii) and the non-venomous Black-headed python (Aspidites melanocephalus) all yielded positive results for tiger snake venom (Jelinek et al, 2004).

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, with serial laboratory studies (ie, coagulation studies, serum electrolytes, CK, renal function) on admission and every 6 hours thereafter, and careful clinical evaluation. If there is no clinical or laboratory evidence of envenomation, coagulopathy, myotoxicity, neurotoxicity or renal insufficiency after this time, the patient can be discharged (Ireland et al, 2010).

Monitoring

    A) Monitor vital signs, neurologic exam and mental status.
    B) Monitor serum electrolytes, renal function, urinalysis and urine output.
    C) 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.
    D) Monitor for clinical evidence of bleeding (eg, hematuria, GI bleeding, epistaxis, bruising, bleeding from venipuncture sites or gums, altered mentation suggesting intracranial bleeding).
    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.

Summary

    A) TOXICITY: A single bite from a tiger snake can be lethal. Children often develop more severe effects. Some definite bites by tiger snakes do not result in envenomation, it is estimated that about 50% of tiger snake bites result in significant envenomation.

Minimum Lethal Exposure

    A) Tiger snakes are the second most lethal snakes in Australia, only brown snakes are responsible for more deaths.
    B) CASE REPORTS
    1) A 14-year-old boy was bitten in the arm by a tiger snake. He was in respiratory distress and required assisted ventilation when paramedics arrived, and suffered a cardiac arrest 30 minutes after the bite. He was treated with CPR and 12 DC shocks in the prehospital setting, followed by 1 vial of polyvalent antivenom and 5 vials of tiger snake antivenom, 10 units of fresh frozen plasma and 8 units of cryoprecipitate once he was admitted. His coagulopathy corrected but he died of anoxic brain injury 30 hours after envenomation (Ferguson et al, 2002).
    2) An 11-year-old boy was bitten on the wrist by a tiger snake. A loose bandage was applied. He developed nausea 10 minutes after the bite, and was pale, drowsy and vomiting and complained of abdominal pain and weakness upon hospital arrival 25 minutes after the bite. He was treated with a vial of tiger snake antivenom. About 10 hours after envenomation his pupils were dilated and nonreactive, he had small fundal hemorrhages but could move all limbs. He received 2 more vials of tiger snake antivenom and 1 vial of brown snake antivenom. He was transferred to tertiary care center and was noted to be unresponsive with a dilated unreactive left pupil, with bruising and petechial hemorrhages on his right arm and left thigh. Cranial CT showed a large right frontal hemorrhage with midline shift. He lost all motor response 26 hours after envenomation and care was withdrawn (Tibballs et al, 1991).
    3) A 40-year-old man was bitten on the heel. He arrived at hospital an hour after the bite, pale and diaphoretic with headache, vomiting, and mild confusion. Tiger snake venom was detected at the bite site. He had a coagulopathy, and was treated with a vial of tiger snake antivenom after pretreatment with hydrocortisone, promethazine and epinephrine intravenously. He had transient hypertension of 195/105 mmHg. About 75 minutes after antivenom infusion he developed left-sided partial motor seizures and left-sided paresis and hemianopsia. He was treated with more tiger snake antivenom, fresh frozen plasma, mannitol and dexamethasone but continued to deteriorate neurologically. A CT showed a massive right intracerebral hemorrhage and care was withdrawn when brain death was confirmed; an autopsy confirmed the findings (McGarity et al, 1991).
    4) A 22-month-old boy fell and was semiconscious almost immediately. On arrival at a clinic 5 minutes later he was pale and unconscious, then developed fixed dilated pupils, had a generalized seizure and a respiratory arrest. He was brought to an ED, where he was intubated and CPR was started. Fang marks were noted on the right foot and swabs from the site were positive for tiger snake venom. He was treated with tiger snake and brown snake antivenom, fresh frozen plasma, atropine and epinephrine and had return of spontaneous circulation. However, his condition continued to deteriorate and he died the next day of DIC with pulmonary, abdominal and intracranial hemorrhages (Sutherland, 1992).
    5) A 62-year-old woman with multiple sclerosis was bitten while in the hospital. She developed severe coagulopathy, intravascular hemolysis, acute renal failure and pulmonary edema and died 6 days later (Sutherland, 1992).

Maximum Tolerated Exposure

    A) Not all bites by tiger snakes result in envenomation, it is estimated that about 50% of tiger snake bites result in significant envenomation (Scop et al, 2009).

Toxicologic Mechanism

    A) Tiger snake venoms have neurotoxic, procoagulant and myotoxic effects. Notexin is believed to be the primary neurotoxin. It is a presynaptic blocker of transmission across the cholinergic neuromuscular junction that causes paralysis that can be prolonged and is resistant to antivenom once established (Ferguson et al, 2002). Notexin also has myotoxic effects. The procoagulant effects are produced by an enzyme that converts prothrombin to thrombin (Ferguson et al, 2002).

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.

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