IDENTIFICATION
SPECIES NAME
Scientific Name | Common Name(s) |
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| Speckled brown snake | | Downs tiger snake |
| Ringed brown snake | | Five ringed snake | | Five ringed brown snake |
| Gwardar | | Western brown snake |
| Common brown snake | | Eastern brown snake |
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INTERVENTION CRITERIA
Any individual suffering a suspected or actual snake bite requires admission for medical observation and treatment as necessary.
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In all cases of suspected snake bite conduct: Snake venom detection kit Blood investigations All patients must then be observed. Snake Venom Detection Kit identification Conduct testing with the CSL Snake Venom Detection Kit. The opinion of the patient or a witness, no matter how experienced in snake identification, should not be accepted without question. The Snake Venom Detection Kit must be used to establish the correct antivenom to administer - if required. A positive snake venom detection result from the bite site (preferred sample site) indicates venom is present and the type of venom. It does not indicate that major envenoming has occurred and is not an indication antivenom is required. The decision to give antivenom should be based on clinical and laboratory evidence of systemic envenoming. Urine may be tested using the snake venom detection kit if there is evidence of significant systemic envenoming and a bite site swab is either unavailable, or has tested negative. Urine may sometimes give false positives and should not be tested in patients who do not have evidence of systemic envenoming. If pressure-immobilization first aid has been applied, do not remove the bandage, rather, cut away a section immediately over the bite area and swab for venom detection. Retain the cut section of bandage as it may later be used for further venom identification. Blood Investigations Insert a secure intravenous line and take blood for: Coagulopathy screen: International Normalized Ratio (INR) or prothrombin time (PT) Activated Partial Thromboplastin Time (aPTT) Fibrinogen level Fibrin Degradation Products (FDP)/D-dimer Immunoassay If laboratory facilities are not readily available then conduct a whole blood clotting time: Collect 5 to 10 mL of venous blood in a GLASS test tube and measure the time required for the blood to clot Time to clot > 10 minutes Suspicious of coagulopathy >20 minutes and no clot Indicative of severe coagulopathy - Determine if the patient is taking any pharmaceuticals likely to interfere with coagulation function, as this will influence interpretation of the coagulation tests. - If possible a control should be run using normal blood from a person taking no anticoagulant drugs (such as a staff member). Full blood count (FBC) including: Platelets White blood cells (especially absolute lymphocyte count) Serum electrolytes including: Potassium Serum urea Serum creatinine Serum creatine kinase (CK) Collect urine (may be required for subsequent Snake Venom Detection Kit testing) |
Intravenous FluidsIntravenous hydration is required to reduce the incidence of renal damage:
Normal (0.9%) SalineNormal (0.9%) saline dose
CHILD
Adjust adult dose to body weight
ADULT
| Initial fluid load |
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| 1 L IV over 2 to 3 hours |
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| Continue infusion at |
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| 100 to 150 mL IV per hour for 6 to 12 hours |
Be circumspect when inserting IV lines, as there will be continued oozing from all sites until the coagulopathy reverses, which will be at least 3 hours, usually more. Avoid insertions in sites where bleeding cannot be easily controlled, such as subclavian, femoral and jugular veins.
ObservationEven trivial looking bites may result in severe envenoming, asymptomatic patients must not therefore be discharged prior to 12 hours following possible envenoming; and should be observed overnight.
Patients must be closely observed for the onset of symptoms including; Paralysis |
| Ptosis (drooping eyelids) |
| Ophthalmoplegia (paralysis of motor nerves of the eye) | Renal failure |
Blood tests should then be repeated at the end of the period of observation, and the patient eligible for discharge if results are normal.
Removal of pressure immobilization first aidDo not remove pressure immobilization first aid unless there are no clinical or biochemical signs of envenoming; and, antivenom and advanced resuscitation facilities are at hand.
If envenoming is evident, do not remove pressure immobilization first aid until antivenom has been administered.
Only remove pressure immobilization first aid once an IV line has been inserted; a Snake Venom Detection Kit analysis has been performed; and blood test results have been reported and show no indication of envenoming.
Blood tests should be repeated 2 to 3 and 5 to 6 hours later. If clinical signs or biochemical findings indicate systemic envenoming then antivenom should be administered.
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Any patient with symptoms or abnormal blood results must be admitted to a medical facility with antivenom and an intensive care environment.
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TREATMENT
TREATMENT SUMMARY
Rapid and effective diagnosis is imperative. While 75% of brown snake bites do not lead to systemic envenoming, all cases should be considered potentially lethal, and all must be admitted. Application of pressure immobilization first aid prior to initial patient movement is life-saving in conjunction with subsequent antivenom administration. Cardiac dysrhythmia/arrest and seizure or collapse may require immediate management. IV fluids are required to ensure renal perfusion and, if there is evidence of systemic envenoming, administration of sufficient quantities of appropriate antivenom is crucial. Hemorrhage should be managed with antivenom. However, if immediately life-threatening, fresh frozen plasma or coagulation factors may be considered. Renal failure is managed using standard procedures but may be associated with disseminated intravascular coagulation. Should the latter occur, circulating venom must be fully neutralized with antivenom before standard management of disseminated intravascular coagulation is employed. Avoid medications likely to depress respiratory function or interfere with platelet function, and ensure tetanus status is adequate (do not give any IM injections until coagulopathy is reversed - to avoid iatrogenic intramuscular hematoma). |
EMERGENCY STABILIZATION
Ensure Adequate Cardiopulmonary Function |
Ensure the airway is protected if compromised (intubation may be necessary). |
Immediately establish secure intravenous access. |
Pressure-Immobilization First Aid |
- Reassure the patient and ensure they remain still.  - Remove any watch, rings, bracelets or other jewellery from the bitten limb. - A broad compression bandage should be applied over the bitten area about as firmly as that used for a sprained ankle. Elasticized bandages are preferable, but crepe bandages, clothing strips or pantyhose will suffice in an emergency. - It is very important that the patient is not moved. If clothing cannot be cut from a bitten limb then a compression bandage should be applied over the clothing - rather than move an arm or leg. - A second bandage should then be applied, starting from the tip of the limb (fingers or toes) and heading toward the body, as firmly as used for a sprained ankle. Elasticized bandages are ideal for this purpose, but crepe bandages, strips of clothing or towels may be used. - Immobilize the arm with a sling; or the leg with a splint and then bandage the split to the limb to prevent movement. Ensure the patient is told not to move at all. - Transport (preferably an ambulance) should be brought to the patient to prevent movement. If this cannot be done, the patient should be carried rather than walk. - Do not give alcohol, fluid, or food by mouth. If the patient will not reach medical care for a long period, only water should be given by mouth. - Transport to hospital. - Tourniquets should not be used. The bite site should not be washed, cleaned, cut, sucked, or treated with any subsatnce. |
Be circumspect when inserting IV lines, as there will be continued oozing from all sites until the coagulopathy reverses, which may take at least 3 hours, usually more. Avoid insertions in sites where bleeding cannot be easily controlled, such as subclavian, femoral and jugular veins.
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Cardiac arrest or dysrhythmia are likely short-lived as the precipitating blood clot will be dissolved by fibrinolysis. Resuscitation should follow standard procedures for cardiac arrest.
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Toxic seizures are generally self-limiting and are unlikely to require specific treatment.
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CHILD Where the systolic blood pressure is below normal blood pressure ranges for the age group: Age (years) | Normal Systolic Blood Pressure (mmHg) | <1 | 70 to 90 | 1 to 2 | 80 to 95 | 2 to 5 | 80 to 100 | 5 to 12 | 90 to 110 | >12 | 100 to 120 |
Administer normal (0.9%) saline 10 mL/kg IV over 5 to 10 minutes If the systolic blood pressure does not return to the normal range, give a further 10 mL/kg body weight normal saline over 5 to 10 minutes. If intravenous access cannot be obtained consider intra-osseus access ADULT Administer a bolus of normal saline if systolic blood pressure is less than 100 mmHg. Normal (0.9%) saline dose: 10 mL/kg IV over 5 to 10 minutes If the systolic blood pressure does not return to the normal range, give a further 10 mL/kg body weight normal saline over 5 to 10 minutes. |
Blood pressure 12 lead ECG
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DECONTAMINATION
Decontamination Not Recommended |
Do not clean the wound prior to use of a Snake Venom Detection Kit. This will remove venom which otherwise might allow identification of the culprit.
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ANTIVENOM
ANTIVENOM USE
Brown Snake Antivenom (CSL) |
Polyvalent Snake Antivenom (CSL) |
In the majority of cases of brown snake bite, antivenom will not be required. However, Brown Snake Antivenom (CSL) or Polyvalent Snake Antivenom (CSL) is indicated in any patient where there is evidence of developing or established: Coagulopathy Any indication of defibrination (e.g. INR > 1.5) Renal damage Any evidence of non-preexistent renal failure Paralysis Any flaccid paralysis including ptosis (unless present without worsening for 6 hours) |
Initial Brown Snake Antivenom (CSL) dose CHILD and ADULT 1 vial IV Patients must be closely monitored for anaphylaxis during and for 30 minutes after the infusion. Further Brown Snake Antivenom (CSL) doses Current evidence indicates it may take at least 6 hours for evidence of recovery to become reliably detectable following antivenom. Therefore, unless there is clear clinical indication for earlier testing, repeat blood tests and conduct a careful neurological examination at 6 hours post-antivenom. If measured parameters are stable or are improving further antivenom is not immediately required. If there is evidence of worsening paralysis, coagulopathy, myolysis, or renal failure, it is recommend that advice from a clinical toxicologist is obtained regarding whether further antivenom therapy is required. Further blood testing and an ongoing schedule of repeat examinations every 12 hours is appropriate for at least 24 hours post antivenom or longer if envenoming has not completely resolved. Polyvalent Snake Antivenom (CSL) Follow the same dosage and administration guidelines for CSL Polyvalent Snake Antivenom as for CSL Brown Snake Antivenom outlined above. Each vial of CSL Polyvalent Antivenom carries the same neutralizing capacity as one vial of CSL Brown Snake Antivenom. Note that polyvalent antivenom is a greater volume of sera and therefore more likely to precipitate an adverse reaction; it is also more expensive than monovalent antivenom. In small children, high doses of polyvalent antivenom may be impractical because of fluid overload issues. |
There is no absolute contra-indication to this potentially life-saving intervention. Those at increased risk of severe reaction include patients with history of: Previous reaction to antiserum Asthma Atopy |
Closely monitor the patient for indications of anaphylaxis including: Rash Erythema Pruritus Urticaria Rhinitis Conjunctivitis Vomiting Diarrhea Wheeze Dyspnea Hypotension Angioedema Shock Airways obstruction |
Serum sickness may occur some 4 to 14 days following antivenom administration.
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Patients should be observed for, and made aware of, the signs and symptoms of serum sickness including: Rash Fever Joint aches Pains Malaise |
If more than 4 vials of Brown Snake Antivenom CSL or greater than 25 mL of antivenom are administered prophylaxis with an oral steroid such as prednisolone may be considered, and follow-up arranged. Commence prophylaxis on day 2 to 3 post-bite. Prednisolone dose ADULT 30 to 50 mg per day orally for 5 days |
ENHANCED ELIMINATION
Enhanced Elimination Not Recommended |
Techniques to enhance elimination of venom following envenoming by this creature are not required. |
SUPPORTIVE CARE
Supportive care after snake bite should follow administration of appropriate antivenom in sufficient quantity to neutralize circulating venom. The patient must also receive intravenous fluid hydration to reduce likelihood of renal damage. Tetanus status should be reviewed, and a booster administered if required (after full reversal of coagulopathy). Pain is unlikely to be a feature; avoid respiratory depressants such as opioid analgesics, and drugs with anti-platelet function including aspirin.
Coagulopathy is characteristic of Australian brown snake envenoming, but may not be clinically apparent unless bleeding from a traumatic injury. Any blow to the head (possibly associated with a post-bite collapse) is a potential source of intracranial hemorrhage. Antivenom should be used to halt bleeding rather than blood products; and any factor potentially causing hypertension should be avoided. Renal damage is a second concern and should be managed following standard protocols if antivenom does not prove adequate. Disseminated intravascular coagulation can develop in association with renal failure. Paralysis is uncommon but may be heralded by onset of ptosis and ophthalmoplegia several hours after a bite. Myolysis is not a feature of this envenoming.
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Observe for: Coagulopathy: Persistent bleeding from bite site or venepucture wounds Paralysis (early signs): Ptosis (drooping eyelids) Partial ophthalmoplegia (paralysis of motor nerves of eye) Repeat blood investigations at 2 to 3 and 5 to 6 hours after initial testing; or at 3 hours after antivenom administration, include: Coagulopathy screen: International Normalized Ratio (INR) or Prothrombin Time (PT) Activated Partial Thromboplastin Time (aPTT) Fibrinogen level Fibrin Degradation Products (FDP)/D-dimer Immunoassay Full Blood Count (FBC) including: Platelets White Blood Cells (especially absolute lymphocyte count) Serum Electrolytes including: Potassium Sodium Chloride Serum Urea Serum Creatinine Serum Creatine kinase (CK) Monitor: Blood pressure 12 lead ECG Plasma glucose Fluid balance (urinary catheterization may be required) |
In cases of severe envenoming, venom pro-coagulants may lead to thrombi, coronary vessel occlusion, cardiac dysrhythmia, and cardiac arrest. Such thrombi will dissolve as coagulopathy progresses, and further management is rarely required. |
Monitor: Heart rate/rhythm Blood pressure 12 lead ECG |
Manage following standard treatment protocols for cardiac dysrhythmia. |
Sudden loss of consciousness may occur with spontaneous recovery likely within 5 to 20 minutes – unless associated with cardiac arrest.
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Development of progressive flaccid paralysis is rare following brown snake bite, and restricted to those not receiving antivenom for many hours. Onset is hours after envenoming and may be missed in the early stages (while still treatable) without careful cranial nerve examination. Antivenom may not fully reverse established paralysis, but may prove beneficial. An anticholinesterase (Tensilon) test can be undertaken, and if paralysis is reduced, further antivenom administration may lead to improvement.
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Observe and examine for onset of cranial nerve signs including: Ptosis (drooping eyelids) Partial ophthalmoplegia (paralysis of motor nerves of eye) Dysarthria |
Follow standard protocols for the management of paralysis.
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Renal damage is the second most commonly seen feature of brown snake envenoming, and the leading cause of snake-bite related renal failure in Australia.
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Acute renal failure, due to acute tubular necrosis, is most common in adults, and in those who have consumed alcohol around the time of the bite. Onset may be in the absence of major coagulopathy. If the only feature is elevated or increasing urea/creatinine in the absence of oliguria/anuria then intravenous fluids should be maintained; fluid balance should be closely monitored and renal function reviewed twice daily. Creatinine may peak at 2 to 5 days and decline with no further requirement for intervention. However, if a rise continues, or there is onset of oliguria/anuria, standard protocols for management of acute renal failure (including hemodialysis) should be followed. In severe cases hemodialysis may be required for an extended period, but the failure is generally reversible. Disseminated intravascular coagulation may occur subsequent to acute renal failure. |
Patients should be monitored for the onset of renal failure: Urine output Creatinine Blood urea nitrogen (urea) Proteinuria Hematuria Loin pain may occur |
Manage following standard treatment protocols for acute renal failure. |
Coagulopathy is characteristic following bites from brown snake species and complete defibrination possible within 15 to 30 minutes; or, may evolve over 6 or more hours. Platelet function is initially unaffected; however thrombocytopenia can develop due to disseminated intravascular coagulation (or possibly other factors) about 12 or more hours after envenoming.
While a major hemorrhage is the main concern following brown snake envenoming, they rarely occur unless the patient is predisposed by recent trauma, laceration, surgery, etc.
Intra-cranial hemorrhage is usually fatal and is more likely in those who have suffered a recent blow to the head, such as from a post-envenoming collapse.
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Antivenom is indicated for the reversal of coagulopathy, large quantities may be necessary. Except in cases of life-threatening hemorrhage Fresh Frozen Plasma (FFP) or coagulation factor replenishment is contra-indicated until all venom has been neutralized by antivenom (otherwise factors will be consumed leading to further coagulation disturbance).
Once antivenom has effectively neutralized circulating venom, clotting function should return to safe, if not normal levels within 6 hours (increasing fibrinogen levels being the first indication of recovery). Further therapy is therefore not usually required.
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Repeat blood investigations at 2 to 3 and 5 to 6 hours after initial testing; or at 3 hours after antivenom administration, include: Coagulopathy screen International Normalized Ratio (INR) Activated Partial Thromboplastin Time (aPTT) Fibrinogen level Fibrin degradation Products (FDP)/D-dimer Immunoassay |
Should coagulopathy be worsening, or not improving, administer a further dose of antivenom, and reassess.
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Disseminated Intravascular Coagulation |
Disseminated intravascular coagulation may appear as a consequence of acute renal failure; with thrombocytopenia indicative of onset (platelets are not directly affected by this venom). It is unusual for platelet count to drop within the first 12 hours following a bite. It is important to ensure the patient has received adequate quantities of antivenom to neutralize all venom prior to managing the disseminated intravascular coagulation.
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Monitor: Full blood count Blood film looking for; Schistocytes Fragmented red blood cells White blood-cell count; Platelet count International normalized ratio (INR) (a)PTT ([activated] Partial thromboplastin time) Fibrinogen level; or, preferably, D-dimer immunoassay |
Follow standard protocols for the management of disseminated intravascular coagulation.
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Serum sickness may occur 4 to 21+ days following antivenom administration. It may therefore develop after recovery from the initial envenoming and after the patient has gone home. It is essential all patients receiving antivenom are fully informed of the possibility and symptoms of serum sickness, and instructed to return for treatment if such symptoms develop following discharge. |
Patients should be observed for, and made aware of, the signs and symptoms of serum sickness including: Rash Fever Joint aches Pains Malaise |
Serum sickness may be managed with antipyretics and analgesics, as well as anti-inflammatory agents including antihistamines and corticosteroids: Prednisone dose ADULT 60 mg daily for 7 to 14 days with tapering Severe cases may require hospitalization. |
While it is possible for an infection to occur at the bite-site, this is most uncommon, therefore prophylactic antibiosis is not required. The bite area should be observed and an appropriate antibiotic administered if infection becomes evident. The bite site should not be cleaned until after a Snake Venom Detection Kit identification has been made.
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Observe patient for signs of infection Monitor: Bite/sting site for signs of infection Body temperature |
Management of infection should follow standard treatment protocols. |
Tetanus prophylaxis should be provided if indicated by immunologic status.
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DO NOT give tetanus prophylaxis until any coagulopathy is resolved, as a significant hematoma may develop.
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DISCHARGE CRITERIA
Late onset of envenoming does uncommonly occur.
Even asymptomatic patients with a normal series of blood investigations should be observed for a minimum of 12 hours, and preferably overnight; and then have full investigations repeated. If there are no abnormalities at this time, and the patient is asymptomatic on clinical examination, discharge may be allowed.
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FOLLOW UP
Those patients receiving antivenom are at risk of developing serum sickness after 4 to 14 days, and should be made aware of the signs and symptoms of this condition including: Rash Fever Joint aches Pains Malaise All patients should be advised to return for review should signs of serum sickness occur. If more than 4 vials or greater than 25 mL of antivenom are administered: prophylaxis with an oral steroid such as prednisolone may be considered; and follow-up arranged. |
PROGNOSIS
Acute anuric renal failure may require hemodialysis for an extended period but is generally reversible.
Individuals may become immunologically sensitized to both the snake venom and snake antivenom.
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SIGNS AND SYMPTOMS
Following a brown snake bite there is minimal or no local pain at the wound, rarely swelling or erythema, and as the fangs are small the injury can be virtually invisible; adults may not even be aware they have been struck. Initial symptoms can include nausea, vomiting, headache, abdominal pain. Sudden loss of consciousness may occur in adults, and seizure in children. There is potential for cardiac dysrhythmia, and rarely arrest.
Bleeding and/or ooze from the bite site (or subsequent venepuncture) is an early indication of coagulopathy, characteristic of brown snake envenoming. Paralysis is uncommon and heralded by ptosis and ophthalmoplegia. Primary or secondary renal failure can develop, but myolysis does not occur.
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Onset/Duration of Symptoms |
Onset of systemic envenoming can occur within 5 to 15 minutes, or may be delayed by many hours.
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The majority (75%) of venomous Australian brown snake (Pseudonjaja sp.) bites do not produce an effective envenoming. However, brown snakes are the most common cause of snake-bite related death in Australia; 10 to 20% of successful envenomings proving fatal without treatment. Prior to antivenom being developed about 8% of all brown snake bites were fatal. |
ACUTE EFFECTS (ORGAN SYSTEM)
Coagulopathy is the hallmark of brown snake envenoming, with potentially complete defibrination and non-clotting blood. International Normalized Ratio (INR) and activated Partial Thromboplastin Time (aPTT) will be prolonged, fibrinogen low to absent, and Fibrin Degradation Products (FDP) and D-dimer Immunoassay elevated. Disseminated intravascular coagulation, with thrombocytopenia, may occur as an indirect effect, but is not common, platelet counts being normal in most cases. Coagulopathy Bleeding or ooze from bite or venepucture site Bleeding gums (classic sign of coagulopathy but rarely seen following brown snake bite) Hematuria Major bleeding Intracranial hemorrhage Disseminated Intravascular Coagulation Thrombocytopenia |
Acute renal failure is least common in children, and most common in adults drinking alcohol around the time of envenoming. The cause is likely secondary, but there is suspicion the venom may be nephrotoxic.
Oliguria Anuria Polyuria Acute Renal failure
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While flaccid paralysis is reported, it is rare. Seizure may occur, more commonly in children, but is not related to neurotoxins.
Headache Vertigo Ptosis (drooping eyelids) Ophthalmoplegia (paralysis of motor nerves of eye) Blurred vision Diplopia Dysarthria Peripheral muscle impairment Respiratory embarrassment Seizure (in children, no t related to neurotoxin envenoming) Intracranial hemorrhage (secondary to coagulopathy)
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Following massive envenoming the following may occur, thought due to an early thrombotic phase of coagulopathy:
Dysrhythmia Coronary ischemia Cardiac arrest
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There is minimal or no local pain at the bite site, rarely swelling or erythema, and as the fangs are small a bite may be virtually invisible; adults may not even be aware they have been bitten.
Lymphadenitis (if envenoming severe) Persistent ooze/bleeding from bite site (indicating coagulopathy)
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Nausea Vomiting Abdominal pain Diarrhea (rare) |
Anaphylaxis to this snake venom may potentially occur in those previously exposed.
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TOXICITY
HUMAN
Brown snakes (Pseudonaja spp.) possess small fangs and relatively small quantities of venom. However, the venom of the eastern brown snake (P. textilis) is considered the second most potent in the world, with the other Pseudonaja species less toxic, and P. modesta less so still. As a group the brown snakes are the most common cause of snakebite and snakebite related death in Australia.
Only 20 to 25% of bites produce envenoming; of those perhaps 10 to 20% will prove fatal without treatment. Prior to antivenom development about 8% of all brown snake bites proved fatal. Approximately 80% of bites will produce no, or only minor, symptoms. On occasion multiple bites may occur from a single snake with an increased likelihood of severe envenoming. Onset of symptoms may be within minutes following major envenoming.
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Children are at greater risk of severe envenoming as they receive the same quantity of venom in a bite, but have a smaller body mass relative to an adult.
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The elderly are at greater risk of severe toxicity than other adults, often due to pre-existing disease.
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REPRODUCTION
PREGNANCY
A fetus will share the mother’s risk following systemic envenoming. It is unclear if venom crosses the placenta. |
TOXIC MECHANISM
Australian Brown Snakes (Pseudonaja spp.)
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Brown snake envenoming is characterized by defibrination coagulopathy. Renal damage may occur, likely secondary to coagulopathy or hypotension, though a nephrotoxic component of the venom may also be responsible. An acute tubular necrosis takes place, which may be associated with a subsequent disseminated intravascular coagulation. Flaccid paralysis uncommonly emerges, in those not receiving antivenom for many hours, and may be due to either pre- or post-synaptic neuromuscular junction neurotoxins. Myolysis is not a feature of brown snake envenoming.
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Snake venom procoagulants act to convert fibrinogen to fibrin with resultant cross-linking and micro-clot formation. However, fibrinolysis is also activated, and the fibrin rapidly destroyed. Such is the ferocity of this reaction that all circulating fibrinogen may be consumed within 15 to 30 minutes, leaving the victim profoundly anticoagulated. At least theoretically, in cases of severe procoagulant envenoming, thrombi may form and embolize prior to fibrinolysis. Various sequelae may occur including coronary artery occlusion and cardiac arrest. These thrombi are then rapidly dissolved. |
Renal damage following snake envenoming may be a consequence of hypotension, coagulopathy, or myolysis. Direct nephrotoxins may also be present in venom.
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Postsynaptic Neuromuscular Junction Neurotoxins |
These toxins reversibly bind to the acetylcholine receptor at the postsynaptic muscle end plate of the neuromuscular junction, resulting in a flaccid paralysis. This action can be reversed with adequate doses of antivenom, or repeated doses of cholinesterase inhibitors such as neostigmine.
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Presynaptic Neuromuscular Junction Neurotoxins |
These toxins damage the terminal axon at the neuromuscular junction. Following a brief period of neurotransmitter discharge, further release halts, with onset of a progressive flaccid paralysis. This paralysis is irreversible due to axonal damage caused by these venoms and may persist for days, weeks, or potentially months. Only skeletal muscles (including the muscles of respiration) are affected, not cardiac or smooth muscle.
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Do Not Archive. This document is current on day of issue,
NZ: 18.May.2012 |
