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AUSTRALIAN BLACK SNAKES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Australian black snakes are front-fanged elapids that can be found throughout Australia and New Guinea.

Specific Substances

    A) AUSTRALIAN BLACK SNAKES
    1) Australian black snake
    2) Black snake
    3) Collett's snake
    4) King brown snake
    5) Mulga snake
    6) Papuan black snake
    7) Pseudechis australis
    8) Pseudechis butleri
    9) Pseudechis colletti
    10) Pseudechis guttatus
    11) Pseudechis papuanus
    12) Pseudechis porphyriacus
    13) Red bellied black snake
    14) Spotted black snake
    15) Spotted mulga 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: Black snakes are front-fanged elapids; they are found throughout Australia and New Guinea.
    B) TOXICOLOGY: The venoms of Pseudechis australis contains myotoxic, anticoagulant and perhaps neurotoxic activity. The venom of Pseudechis papuanus has neurotoxic activity and causes bleeding. The venoms of Pseudechis porphyriacus, P colletti and P guttatus have myotoxic effects.
    C) EPIDEMIOLOGY: Black snakes are a common cause of bites in some areas of Australia and New Guinea. Dry bites are common, but severe envenomation can occur. Lethal envenomation is rare.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE ENVENOMATION: A significant percent of black snake bites do not result in envenomation. Local effects include pain, swelling, discoloration and tender lymphadenopathy. Nonspecific systemic effects such as nausea, vomiting, diarrhea, abdominal pain, headache, and diaphoresis. Mild coagulopathy and elevations of CK may be noted.
    2) SEVERE ENVENOMATION: Myotoxicity with muscle pain, weakness, severe rhabdomyolysis and renal failure may develop. Moderate coagulopathy may be noted on laboratory evaluation, but life-threatening bleeding is unusual. Pseudechis papuanus envenomation can cause neurotoxic effects such as diplopia, ptosis, dysphagia, dysarthria, diminished strength or reflexes, ophthalmoplegia, and diminished mouth opening; patients may require respiratory support.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes, CK, 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), myotoxicity (muscle pain, tenderness, or weakness) or neurotoxicity (ptosis, dysphagia, weakness, ophthalmoplegia, respiratory insufficiency).
    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) SUPPORT
    1) NO OR MILD ENVENOMATION: Patients who are asymptomatic or only have mild symptoms and no laboratory evidence of envenomation should be monitored for a minimum of 12 hours.
    2) SEVERE ENVENOMATION: Patients with severe symptoms or laboratory evidence of venom-induced coagulopathy or rhabdomyolysis should be treated with antivenom.
    B) ANTIVENOM
    1) Treat patients with venom-induced coagulopathy or myotoxicity secondary to black snake envenomation with black snake antivenom. BLACK SNAKE ANTIVENOM: The antivenom of choice for Pseudechis australis (mulga snakes), it also covers P butleri and P colletti. DOSE: The recommended initial dose is 1 vial given IV (diluted 1 to 10 with an isotonic crystalloid solution administered over 15 to 30 minutes). If there is evidence of severe rhabdomyolysis at the time of presentation a second vial of antivenom may be necessary. TIGER SNAKE ANTIVENOM is often the preferred treatment for Pseudechis guttatus (Spotted- or Blue-bellied black snake) or Pseudechis porphyriacus (Red-bellied Black snake) envenomation, although many patients develop only mild manifestations and do not need antivenom. DOSE: The recommended initial dose is 1 vial given IV (diluted 1 to 10 with an isotonic crystalloid solution administered over 15 to 30 minutes). ALTERNATIVE THERAPY: If Tiger Snake Antivenom is unavailable, initially treat a P guttatus or P porphyriacus envenomation with 1 vial of Black Snake Antivenom (for a small child consider giving 1/3 to 1/2 of a vial) to provide an adequate dose. If a specific antivenom is not available, or the species of snake responsible is not known, polyvalent antivenom may be used. Monitor a patient given antivenom carefully and be prepared to treat anaphylaxis.
    C) 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.
    D) PATIENT DISPOSITION
    1) HOME CRITERIA: There is no role for home management of a possible snake bite.
    2) OBSERVATION CRITERIA: All patients with suspected snake bite should be observed for at least 12 hours, with serial laboratory studies (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.
    3) ADMISSION CRITERIA: 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.
    4) CONSULT CRITERIA: Consult a clinical toxinologist, medical toxicologist or poison center for any patient with severe envenomation or if the diagnosis is unclear.
    E) TOXICOKINETICS
    1) ONSET of envenomation can be quite rapid, with many patients developing pain, swelling and nonspecific systemic symptoms less than an hour after being bitten. The vast majority of patients who develop systemic envenomation have evidence of coagulopathy or myotoxicity on laboratory testing within 12 hours of the bite (generally sooner in patients with severe envenomation).
    F) PITFALLS
    1) The presence of black 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.
    G) DIFFERENTIAL DIAGNOSIS
    1) Envenomation by tiger snakes, taipan or brown snakes can cause coagulation abnormalities. Overdose of anticoagulants such as warfarin or brodifacoum.

Range Of Toxicity

    A) TOXICITY: A single bite from a black snake can cause severe envenomation, but fatalities are not common. Children often develop more severe effects. Some definite bites by black snakes do not result in envenomation, but the percent of "dry" bites is unknown.

Clinical Effects

Summary Of Exposure

    A) BACKGROUND: Black snakes are front-fanged elapids; they are found throughout Australia and New Guinea.
    B) TOXICOLOGY: The venoms of Pseudechis australis contains myotoxic, anticoagulant and perhaps neurotoxic activity. The venom of Pseudechis papuanus has neurotoxic activity and causes bleeding. The venoms of Pseudechis porphyriacus, P colletti and P guttatus have myotoxic effects.
    C) EPIDEMIOLOGY: Black snakes are a common cause of bites in some areas of Australia and New Guinea. Dry bites are common, but severe envenomation can occur. Lethal envenomation is rare.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE ENVENOMATION: A significant percent of black snake bites do not result in envenomation. Local effects include pain, swelling, discoloration and tender lymphadenopathy. Nonspecific systemic effects such as nausea, vomiting, diarrhea, abdominal pain, headache, and diaphoresis. Mild coagulopathy and elevations of CK may be noted.
    2) SEVERE ENVENOMATION: Myotoxicity with muscle pain, weakness, severe rhabdomyolysis and renal failure may develop. Moderate coagulopathy may be noted on laboratory evaluation, but life-threatening bleeding is unusual. Pseudechis papuanus envenomation can cause neurotoxic effects such as diplopia, ptosis, dysphagia, dysarthria, diminished strength or reflexes, ophthalmoplegia, and diminished mouth opening; patients may require respiratory support.

Heent

    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) ANOSMIA
    a) Anosmia or changes in the sense of smell have been reported after black snake envenomation. In some cases, these changes may be permanent (Pearn et al, 2000; Campbell, 1984; Isbister et al, 2006a).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY FAILURE
    1) WITH POISONING/EXPOSURE
    a) Respiratory insufficiency may develop either secondary to severe muscle weakness from myotoxicity or from neurotoxicity.
    b) In a series of 57 patients with Pseudechis porphyriacus (Red-bellied Black snake) envenomation, 7 (12%) developed myotoxicity, one of whom required noninvasive ventilation for muscle weakness secondary to severe myotoxicity (Churchman et al, 2010).
    c) In a series of 9 patients with Pseudechis papuanus (Papuan Black snake) envenomation, one required intubation and mechanical ventilation (Lalloo et al, 1994).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) NEUROTOXICITY
    1) WITH POISONING/EXPOSURE
    a) Neurotoxicity can develop, most commonly with Pseudechis papuanus (Papuan Black snake) envenomation, but less commonly with Pseudechis australis (Mulga) envenomation.
    b) In a series of 9 patients with Papuan black snake envenomation, 5 developed ptosis, 1 complained of diplopia, 3 of dysphagia, 3 of dysarthria, 5 had ophthalmoplegia, 1 had restricted jaw opening, 4 had slurred speech, 1 had diminished reflexes, and 2 had decreased hand grip strength (Lalloo et al, 1994).
    c) In a series of 20 patients with Pseudechis australis (Mulga) envenomation, 3 (15%) had evidence of neurotoxicity, but clinical findings were not detailed by the author (Currie, 2004) .
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache is a fairly common nonspecific systemic manifestation of black snake envenomation (Johnston et al, 2013; Jansen et al, 2007; Mead & Jelinek, 1996; Lalloo et al, 1994).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting are common nonspecific systemic manifestations of black snake envenomation. Symptoms often develop within an hour or two of the bite (Johnston et al, 2013; Jansen et al, 2007; Pearn et al, 2000; Isbister et al, 2006a).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain is a common nonspecific manifestation of black snake envenomation, and is often accompanied by nausea and vomiting, and sometimes by diarrhea (Johnston et al, 2013; Isbister et al, 2006a; Barrett & Little, 2003).
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea can be a nonspecific manifestation of black snake envenomation, but is not as common as nausea and vomiting (Johnston et al, 2013; Isbister et al, 2006a; Campbell, 1984).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Acute renal failure requiring transient hemodialysis has been reported in patients who developed severe rhabdomyolysis after black snake envenomation (Isbister et al, 2006a).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) BLOOD COAGULATION DISORDER
    1) WITH POISONING/EXPOSURE
    a) Coagulopathy is fairly common after envenomation by Australian black snakes (Isbister et al, 2006a; Doherty, 2001). Life-threatening bleeding is uncommon, but minor bleeding may develop. Mild to moderate thrombocytopenia and decreased fibrinogen have been reported, but are not common (Tibballs, 1992; Isbister et al, 2006a).
    b) INCIDENCE: In a series of 20 patients with Pseudechis australis (Mulga) envenomation, 9 (45%) developed coagulopathy (Currie, 2004). In a series of 57 patients with Pseudechis porphyriacus (Red-bellied Black snake) envenomation, 35 (61%) developed an anticoagulant coagulopathy with prolonged aPTT (Churchman et al, 2010).
    c) In a series of 9 patients with Pseudechis papuanus (Papuan Black snake) envenomation, 2 had bleeding from the nose and mouth, and blood stained saliva (Lalloo et al, 1994).
    d) In a series of 13 systemic Pseudechis australis (mulga) envenomations, 10 patients developed anticoagulant coagulopathy with a median aPTT of 82.1 s (range: 38.8 to 95 s). In 4 of 8 patients, fibrinogen and D-dimer assays were performed and the results were normal. There were no reports of clinically significant bleeding (Johnston et al, 2013).
    B) HEMOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Hemolysis is not common, but it has been reported after Pseudechis australis (Mulga) and Pseudechis colletti (Collett's snake) envenomation (Isbister et al, 2006a; Campbell, 1984).
    b) In a series of 13 systemic Pseudechis australis (mulga) envenomations, 6 patients developed acute hemolysis. The median decline in hemoglobin concentration was 52 g/L (range: 26 to 71 g/L). Mild anemia developed in 2 patients (minimum hemoglobin values: 121 and 126 g/L) and 3 had severe anemia (minimum hemoglobin concentrations of 81, 85, and 116 g/L). No patient required a blood transfusion (Johnston et al, 2013).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SWELLING
    1) WITH POISONING/EXPOSURE
    a) Local swelling develops in most patients with systemic envenomation, and a small number of patients have local manifestations only, without developing systemic envenomation. Swelling may be accompanied by discoloration and tender lymphadenopathy is common. Ulceration develops in a minority of patients.
    b) INCIDENCE: In a series of 20 patients with Pseudechis australis envenomation, 19 (95%) developed local swelling and 16 (80%) developed regional lymphadenitis (Currie, 2004). In a series of 57 patients with Pseudechis porphyriacus (red-bellied black snake) envenomation, 55 (96%) had local swelling and 3 (5%) developed local ulceration (Churchman et al, 2010).
    c) Swelling may be less common in Pseudechis papuanus (Papuan Black snake) envenomation. In a series of 9 patients with Pseudechis papuanus envenomation, no patient had significant local swelling, and 6 had tender regional lymph nodes (Lalloo et al, 1994).
    B) PAIN
    1) WITH POISONING/EXPOSURE
    a) Pain generally develops within an hour of envenomation and may be severe (Isbister et al, 2006a; Pearn et al, 2000).
    C) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) Diaphoresis is a fairly common nonspecific systemic manifestation of envenomation (Johnston et al, 2013; Jansen et al, 2007; Pearn et al, 2000).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INJURY OF MUSCLE
    1) WITH POISONING/EXPOSURE
    a) Myotoxicity develops in a significant number of patients with black snake envenomation, and may be severe. Manifestations include elevated CK, myoglobinuria, muscle pain, tenderness and sometimes weakness.
    b) INCIDENCE: In a series of 20 patients with Pseudechis australis (Mulga) envenomation, 12 (60%) developed myotoxicity (Currie, 2004). In a series of 57 patients with Pseudechis porphyriacus (Red-bellied Black snake) envenomation, 7 (12%) developed myotoxicity, one of whom required noninvasive ventilation for muscle weakness secondary to severe myotoxicity (Churchman et al, 2010).
    c) In a series of 13 systemic Pseudechis australis (mulga) envenomations, 7 patients developed myotoxicity. The median creatine kinase was 3100 U/L (range: 1054 to 11258 U/L) and the median time to reach the peak was 38 h (range: 27 to 76.5 h) after envenomation. In addition, elevated urine myoglobin levels were reported in 3 patients. No patient developed significant renal impairment as a result of myotoxicity (Johnston et al, 2013).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes, CK, 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), myotoxicity (muscle pain, tenderness, or weakness) or neurotoxicity (ptosis, dysphagia, weakness, ophthalmoplegia, respiratory insufficiency).
    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, CK, and renal function.
    B) COAGULATION STUDIES
    1) Envenomation with some black snakes can cause 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 snake envenomation (Ireland et al, 2010; 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 and myoglobinuria. Monitor urine output.
    4.1.4) OTHER
    A) OTHER
    1) CLINICAL EXAMINATION
    a) Monitor vital signs 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), myotoxicity (muscle pain, tenderness, or weakness) or neurotoxicity (ptosis, dysphagia, weakness, ophthalmoplegia, respiratory insufficiency).
    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 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).
    3) COMPUTERIZED TOMOGRAPHY
    a) Obtain a cranial CT if there is altered mental status or any other suggestion of intracranial bleeding.

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, 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 and mental status.
    B) Monitor serum electrolytes, CK, 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), myotoxicity (muscle pain, tenderness, or weakness) or neurotoxicity (ptosis, dysphagia, weakness, ophthalmoplegia, respiratory insufficiency).
    E) If there is any question as to the type of snake involved, obtain a swab from the bite site or a urine specimen, and use the venom detection kit to identify the species of snake if any clinical or laboratory evidence of envenomation develop. The presence of venom at the bite site does NOT mean that systemic envenomation has occurred.
    F) Obtain a head CT if altered mentation develops, or if there is any clinical concern for intracranial bleeding.

Range Of Toxicity

Summary

    A) TOXICITY: A single bite from a black snake can cause severe envenomation, but fatalities are not common. Children often develop more severe effects. Some definite bites by black snakes do not result in envenomation, but the percent of "dry" bites is unknown.

Maximum Tolerated Exposure

    A) DRY BITES: Not all black snake bites result in envenomation, although the percent of dry bites is unknown. In a series of 81 patients with definite Red-bellied Black snake bites, 57 patients (70%) had systemic envenomation, one had only local evidence of envenomation, and 23 (29%) had no evidence of envenomation (Churchman et al, 2010).
    B) PSEUDECHIS AUSTRALIS: In a series of 17 Pseudechis australis (mulga) snake bites, the snake was identified by an expert in 11 cases. Most cases occurred in adult males following interference with the snake (10/17). Of the 17 cases, 13 developed systemic envenomation. The following features of systemic envenomation occurred: anticoagulant coagulopathy (n=10), myotoxicity (n=7), acute hemolysis (n=6) and non-specific symptoms ({n=11} nausea (11), abdominal pain (9), vomiting (9), headache (8), diarrhea (4), and generalized diaphoresis (4)). Of the 13 cases, 10 received antivenom therapy. No fatalities were reported (Johnston et al, 2013).

Pharmacology Toxicology

Toxicologic Mechanism

    A) The venom of Pseudechis australis contains myotoxic, anticoagulant and perhaps neurotoxic activity. The venom of Pseudechis papuanus has neurotoxic activity and causes bleeding, though it is not clear if this is from procoagulant or anticoagulant effects. The venoms of Pseudechis porphyriacus, P colletti and P guttatus have myotoxic effects (White, 1995).

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 Centigrade 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) Anon: WHO/SEARO guidelines for clinical management of snake bites. So Asian J Trop Med Pub Health 1999; 30 (S1):1-85.
    2) Barr SC: Clinical features therapy and epidemiology of tiger snake bite in dogs and cats. Aust Vet J 1984; 61:208-212.
    3) Barrett R & Little M : Five years of snake envenoming in far north Queensland. Emerg Med (Fremantle) 2003; 15(5-6):500-510.
    4) Campbell CH: Myotoxic paralysis and hemolytic anemia due to king brown snake bite. Aust N Z J Med 1984; 14(2):169-169.
    5) Churchman A, O'Leary MA, Buckley NA, et al: Clinical effects of red-bellied black snake (Pseudechis porphyriacus) envenoming and correlation with venom concentrations: Australian Snakebite Project (ASP-11). Med J Aust 2010; 193(11-12):696-700.
    6) Currie BJ: Snakebite in tropical Australia, Papua New Guinea and Irian Jaya. Emerg Med Australas 2000; 12(4):285-294.
    7) Currie BJ: Snakebite in tropical Australia: a prospective study in the "Top End" of the Northern Territory. Med J Aust 2004; 181(11-12):693-697.
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