IDENTIFICATION
HABITAT
Brown snakes ( Pseudonaja spp.) are distributed throughout mainland Australia. They are not found in Tasmania or on the islands off the southern coast of Australia. They may be found in essentially all habitats, including urban and metropolitan areas.  |
INTERVENTION CRITERIA
Medical assessment and observation, preferably in an advanced care facility, is recommended for: - Any individual bitten or suspected to have been bitten by a snake |
All patients require medical attention. |
Even trivial looking bites may result in severe envenoming; asymptomatic patients following possible envenoming must be observed for a minimum of 12 hours and should be observed overnight.   Patients must be closely observed for the onset of symptoms including: Coagulopathy Bleeding/ooze from bite or venepuncture sites Bleeding gums Hematuria Paralysis (may be subtle) Ptosis (drooping eyelids) Ophthalmoplegia (paralysis of motor nerves of the eye) Bulbar palsy Descending flaccid paralysis Acute kidney injury |
The coagulation screen and blood investigations along with a neurological examination must be performed upon presentation, 1 hour after removal of the pressure bandage, and repeated at 6 hours and 12 hours after the bite.  If at 12 hours post-bite all the blood tests are normal and there is no clinical signs of neurotoxicity the patient is eligible for discharge.  The patient should be advised to return if there is any indication of illness including change in their urine color or if they develop any muscle pain, tenderness, or weakness. Removal of Pressure Bandage with Immobilization First Aid If envenoming is evident, do not remove pressure bandage with immobilization first aid until antivenom has been administered.  If there are no clinical or biochemical signs of envenoming only remove pressure bandage with immobilization first aid once an IV line has been inserted and antivenom and advanced resuscitation facilities are at hand.    A bite site swab can be saved for possible venom detection kit (VDK) testing if evidence of envenoming becomes evident. However, VDK analysis is not always necessary. Determination of the appropriate antivenom required to treat an envenomed patient can often be determined through clinical and laboratory features of envenoming and the geographical location of the snakebite. Once the pressure bandage is removed repeat blood tests at 1 hour after removal.  If these results are normal and there are no signs of neurotoxicity repeat blood tests again at 6 hours (unless already > 6 hours) and 12 hours after the bite.  If clinical signs or biochemical findings indicate systemic envenoming then antivenom should be administered.  If at 12 hours post-bite all the blood tests are normal and there is no clinical signs of neurotoxicity the patient is eligible for discharge.  Adequate hydration is required to reduce the incidence of renal damage.  Hydration should be maintained through administration of oral or intravenous fluid to ensure a good urine output. Normal (0.9%) saline dose CHILD Adjust adult dose to body weight ADULT Initial fluid load 1 L IV over 2 to 3 hours Continue infusion at 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 6 hours, usually more. Avoid insertions in sites where bleeding cannot be easily controlled, such as subclavian, femoral, and jugular veins. |
In all cases of suspected snakebite conduct: Blood investigations Snake venom detection kit test depending on geographical location of snakebite All patients must then be observed for a minimum of 12 hours.  Snake Venom Detection Kit Identification 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 bandage with 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. Insert a secure intravenous line and take blood for: Coagulopathy screen: International normalized ratio (INR) Activated partial thromboplastin time (aPTT) Fibrinogen concentration Quantitative D-dimer/Fibrin degradation products Point of care testing devices for coagulation studies have been shown to produce false positive results in cases of snakebite, and should not be used. Full blood count (FBC) including: Platelets White blood cells (especially absolute lymphocyte count) Serum electrolytes including: Potassium Sodium Serum urea Serum creatinine Serum creatine kinase (CK) Collect urine Visually check for hemoglobinuria/myoglobinuria (dark-red/brown coloration) May be required for subsequent Snake Venom Detection Kit testing |
Admission to an intensive care environment is recommended for patients who develop any signs of envenoming or abnormal blood results. |
TREATMENT
TREATMENT SUMMARY
Consultation with a medical toxicologist (at the bedside or through a Poison Center) is advised for this poisoning as toxicity can be life-threatening. |
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 to a hospital capable of providing definitive care. Application of pressure bandage with immobilization first aid prior to initial patient movement can be life-saving in conjunction with subsequent antivenom administration. Cardiac dysrhythmia/arrest and seizure or collapse may require immediate management. If there is evidence of systemic envenoming, administration of appropriate antivenom to neutralize circulating venom is crucial. Further supportive care may be required. Venom induced consumptive coagulopathy is characteristic of Australian brown snake envenoming, although hemorrhage may not be clinically apparent unless bleeding from a traumatic injury. Any injury to the head (possibly associated with a post-bite collapse) is a potential source of intracranial hemorrhage. Routine administration of blood products including fresh frozen plasma is not indicated, unless there is uncontrolled life-threatening bleeding. Any factor potentially causing hypertension should be avoided. Intravenous fluid hydration is required to ensure renal perfusion; renal damage is a concern and should be managed following standard protocols if antivenom does not prove adequate. Paralysis is uncommon but may be heralded by onset of ptosis and ophthalmoplegia several hours after a bite. Antivenom may prove beneficial but may not fully reverse established paralysis. Pain is unlikely to be a feature; avoid drugs with anti-platelet function including aspirin and NSAIDs. Potent analgesics including opioids that potentially produce respiratory depression are usually not required, but can be used in monitored clinical environments. Infection is uncommon and therefore prophylactic antibiotics are not required; if infection becomes evident then an appropriate antibiotic should be administered. Tetanus status should be reviewed, and a booster administered if required; to avoid iatrogenic intramuscular hematoma do not give any IM injections until coagulopathy is reversed. Myolysis is not a feature of brown snake envenoming. Serum sickness may occur following antivenom administration; follow up and/or steroid treatment may be required. |
EMERGENCY STABILIZATION
Ensure Adequate Cardiopulmonary Function |
Ensure the airway is protected if compromised (intubation may be necessary). |
Immediately establish secure intravenous access. |
Be circumspect when inserting IV lines, as there will be continued oozing from all sites until the coagulopathy reverses, which may take at least 6 hours, usually more.  Avoid insertions in sites where bleeding cannot be easily controlled, such as subclavian, femoral, and jugular veins.  |
Pressure Bandage with Immobilization First Aid |
- Reassure the patient and ensure they remain still.  - Remove any watches, rings, bracelets, or other jewelry from the bitten limb.   - A broad elasticized compression bandage should be applied over the bitten area about as firmly as that used for a sprained ankle but not so tight that circulation is compromised. Elasticized bandages are preferable,  but crepe bandages, clothing strips, towels, or pantyhose will suffice in an emergency.   - It is very important that the patient is not moved. A compression bandage should be applied over clothing - rather than move an arm or leg.  - Bandage upward from the lower portion of the bitten limb. Apply the bandage as far as possible up the limb.  - If bite is on the arm, bandage the arm with the elbow bent and leave the tips of the fingers unbandaged to allow circulation to be checked. Bind a splint to the forearm and immobilize the arm with a sling.  - If the bite is on the leg, leave the tips of the toes unbandaged to allow circulation to be checked. Immobilize the leg by bandaging a splint to the limb to prevent movement.  - On the overlying bandage mark the location of the bite.  - Ensure the patient is told not to move the affected limb 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 substance.  |
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. |
Toxic seizures are generally self-limiting and are unlikely to require specific treatment.
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CHILD Hypotension in children is determined by age and systolic blood pressure Age | Hypotension if Systolic Blood Pressure (mm Hg) is: | 0 to 28 days | < 60 | 1 to 12 months | < 70 | 1 to 10 years | < 70 + (age in years x 2) | > 10 years | < 90 |
Administer an isotonic crystalloid fluid 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 of the isotonic crystalloid over 5 to 10 minutes. The intraosseous route can be used if IV access is difficult or delayed. ADULT Administer a bolus of isotonic crystalloid fluid if systolic blood pressure is less than 100 mmHg. Isotonic crystalloid fluid dose: 20 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. The intraosseous route can be used if IV access is difficult or delayed. |
Coagulopathy screen Full blood count Serum electrolytes Serum urea Serum creatinine Serum creatine kinase (CK) Heart rate Blood pressure Respiratory function 12 lead ECG Fluid balance Plasma glucose Head CT scan (if altered mental status) |
DECONTAMINATION
Decontamination Not Recommended |
ANTIVENOM
Australian Polyvalent Snake Antivenom |
Antivenom is most effective when administered early following snakebite, and is less likely to be beneficial once major envenoming syndromes have been established.  Brown Snake Antivenom is the preferred antivenom. Polyvalent Snake Antivenom is an alternative if a suitable monovalent antivenom is not available. |
In the majority of cases of brown snake bite, antivenom will not be required.  Antivenom administration is indicated in any patient where there is: History of unconsciousness, collapse, seizure, or cardiac arrest Coagulopathy INR > 1.3, prolonged bleeding from wounds or venepunctures Neurotoxic paralysis Any flaccid paralysis including ptosis, opthalmoplegia, limb or respiratory muscle weakness (unless present without worsening for 6 hours) Antivenom administration may be indicated in the following circumstances. In these instances discussion with a medical toxicologist is recommended. Renal damage Elevated creatinine and urea Any abnormality of APTT, INR, D-dimer, FBC Significant symptoms including headache and vomiting Any patient who appears systemically unwell |
In most instances of Australian snakebite an adequate initial dose of antivenom will be sufficient and past practices of multiple repeat doses are both unnecessary and potentially hazardous.  Nevertheless, it is important that the initial dose of antivenom not be considered the end of treatment and investigation. |
Initial Brown Snake Antivenom Dose CHILD and ADULT Patients must be closely monitored for anaphylaxis during and for 30 minutes after the infusion.  Further Brown Snake Antivenom 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 kidney injury, it is recommend that advice from a medical toxicologist is obtained regarding whether further antivenom therapy is required. Further blood testing and an on-going 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 For Polyvalent Snake Antivenom, follow the same dosage and administration guidelines as for Brown Snake Antivenom outlined above. Each vial of Polyvalent Antivenom carries the same neutralizing capacity as one vial of 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. Pregnancy is not a contraindication to antivenom administration.  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 |
Patients should be made aware of the signs and symptoms of serum sickness including: Rash Fever Joint aches Pains Malaise |
If more than 25 mL of Brown Snake Antivenom is 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 CHILD 1 mg/kg (up to 50 mg) per day orally for 5 days ADULT 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
Observe for: Coagulopathy Bleeding/ooze from bite or venepuncture sites Bleeding gums Hematuria Paralysis Ptosis (drooping eyelids) Ophthalmoplegia (paralysis of motor nerves of the eye) Bulbar palsy Descending flaccid paralysis Myolysis Myalgia Myoglobinuria Repeat blood investigations at 6 and 12 hours after the bite or at 6 hours after antivenom administration, include: Coagulopathy screen: International normalized ratio (INR) Activated partial thromboplastin time (aPTT) Fibrinogen concentration Quantitative D-dimer/Fibrin degradation products Point of care testing devices for coagulation studies have been shown to produce false positive results in cases of snakebite, and should not be used. Full blood count (FBC) including: Platelets White blood cells (especially absolute lymphocyte count) Serum electrolytes including: Potassium Sodium Chloride Serum creatine kinase (CK) Renal function Myoglobinuria (measurement of myoglobin concentrations in urine is expensive and not usually justified) Serum urea Serum creatinine Monitor: Blood pressure 12 lead ECG Plasma glucose Fluid balance (urinary catheterization may be required) |
Venom Induced Consumption Coagulopathy |
Repeat blood investigations at 6 and 12 hours after the bite or at 6 hours after antivenom administration. In the absence of sensitive fibrinogen assays, measurement of INR and aPTT are a good indicator of return of clotting function.  |
Monitor: International normalized ratio (INR) Activated partial thromboplastin time (aPTT) Fibrinogen concentration Quantitative D-dimer/Fibrin degradation products |
Following antivenom administration repeat blood tests at 6 hours post-antivenom.  If coagulopathy (defibrination) was present at the time of initial antivenom administration it will not likely be fully reversed after 6 hours as recovery relies on the synthesis of new clotting factors    with recovery from coagulopathy typically taking 12 to 18 hours.  However, at 6 hours post-antivenom there may be some improvement such as a slight trend towards lower INR/aPTT or slight increase in fibrinogen. If there has been such an improvement there is no need to give further antivenom.  Repeat blood tests at 12 and 18 to 24 hours post-antivenom to determine if the patient has fully recovered.  If there has been no improvement or worsening following antivenom, check to see if there is active bleeding (bleeding from the bite site, venepuncture, gums, etc), and if there is, consider discussing a further dose of antivenom with a medical toxicologist.  The dose should be the same as used initially, possibly followed by factor replacement therapy (fresh frozen plasma [FFP] or cryoprecipitate depending on the severity of the bleeding, or if these are unavailable, fully cross matched fresh whole blood).  If there is no evidence of active bleeding repeat blood tests at 9 hours post-antivenom. |
Microangiopathic Hemolytic Anemia |
Patients should be monitored for evidence of microangiopathic hemolytic anemia: Jaundice Pallor Hemoglobinuria Anemia Peripheral blood smear Reticulocytosis Heinz bodies Cell fragments Whole blood hemoglobin (may be decreased) Free plasma hemoglobin (may be increased) Serum haptoglobin (may be decreased) Spherocytes (may be present) Red cell glucose-6-phosphate dehydrogenase testing may be indicated |
The optimum treatment has not been determined. Antivenom should be administered early to neutralize any circulating toxins.  It is unknown if further treatment including fresh frozen plasma and/or plasmapheresis is beneficial;   plasmapheresis did not appear to change the time course of severity in one series of patients.  However, as plasmapheresis can be life-saving it should be considered in this setting.  |
Patients should be monitored for the onset of acute kidney injury: Urine output Serum creatinine Blood urea nitrogen (urea) Proteinuria |
If the only feature is elevated or increasing urea/creatinine in the absence of oliguria/anuria then intravenous fluids should be administered to maintain renal perfusion; fluid balance should be closely monitored and renal function reviewed twice daily. If myolysis is present, aggressive hydration is paramount to prevent renal injury. Urinary alkalinization may also be considered. The role of antivenom therapy in preventing or treating snakebite associated kidney injury is not established. For Australian snakebite it appears that most, possibly all cases of acute kidney injury are not primarily caused by venom nephrotoxicity. Therefore, the role of antivenom in managing acute kidney injury is unproven and follow up doses of antivenom for this complication of envenoming are rarely justified; further antivenom should only be considered after consultation with a medical toxicologist. |
Closely monitor level of consciousness. |
Manage coma following standard treatment protocols. |
Development of progressive flaccid paralysis is rare following brown snake bite, perhaps due to brown snake venom neurotoxins being less potent and only making up a relatively small percentage of brown snake venom.  Paralysis is typically restricted to those not receiving antivenom for many hours. Onset can be hours after envenoming and may be missed in the early stages (while still treatable) without careful cranial nerve examination. If present, flaccid paralysis may progress to the point of respiratory compromise.  Paralysis following snake bite may take days or weeks to resolve.  |
Observe and examine for onset of cranial nerve signs including: Ptosis (drooping eyelids) Partial ophthalmoplegia (paralysis of motor nerves of eye) Bulbar palsy Dysarthria |
Antivenom should be administered at the earliest sign of paralysis, even just mild ptosis, as it will halt further progress and should, theoretically, reverse the condition. However, it may not fully reverse established paralysis.    For most Australian snakes if paralysis is present it will be partially mediated by presynaptic neurotoxins.   This has important implications for antivenom therapy as presynaptic paralysis will not respond to even high doses of antivenom or neostigmine.   If there is no significant improvement in paralysis following initial antivenom administration consider performing an anticholinesterase (Tensilon) test to determine if the paralysis is predominately postsynaptic or presynaptic. In the situation of a positive Tensilon test, paralysis may respond to further antivenom and additional antivenom administration should be considered after consultation with a medical toxicologist; if further antivenom is to be given, administer the same dose as used in initial therapy. Neostigmine and atropine have also been used successfully in this situation   and should also be considered as adjunctive treatment. In cases were paralysis cannot be reversed, intubation and artificial ventilation will be required.   |
In cases of severe envenoming, venom pro-coagulants may lead to microvascular thrombi, coronary vessel occlusion, cardiac dysrhythmia, and cardiac arrest.   Such thrombi will dissolve as coagulopathy progresses,  and further management is rarely necessary. If required standard advanced life support measures should be undertaken. |
Monitor: Heart rate/rhythm Blood pressure 12 lead ECG |
Manage cardiac dysrhythmia following standard treatment protocols. |
Serum sickness may occur 4 to 14 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 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: Prednisolone dose CHILD 1 mg/kg (up to 50 mg) per day orally for 5 days ADULT 50 mg per day orally for 5 days Severe cases may require hospitalization. |
It is uncommon for an infection to occur at the bite site.   Prophylactic antibiotics are therefore not required. The bite area should be observed and an appropriate antibiotic administered only if infection becomes evident.  |
Observe patient for signs of infection Monitor: Bite/sting site for signs of infection Body temperature |
Manage infection following 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. |
DISCHARGE CRITERIA
Late onset of envenoming is rare.  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 blood investigations repeated.   If there are no biochemical abnormalities at this time and the patient is asymptomatic on clinical examination, discharge may be allowed.  Envenomed patients should be monitored for 24 hours following antivenom before discharge is considered. If at the end of that time they are clinically well and the INR is < 2 and blood counts and renal function remain stable they can be discharged.  Discharge of those with continuing systemic envenoming, microangiopathic hemolytic anemia, or acute kidney injury is dependent upon their recovery. |
FOLLOW UP
Those patients receiving antivenom are at risk of serum sickness occurring 4 to 14 days following administration, 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 there was a major envenoming, follow up should be organized. |
If greater than 25 mL of antivenom is administered prophylaxis with an oral steroid such as prednisolone may be considered and follow-up arranged.   |
PROGNOSIS
Individuals may become immunologically sensitized to both the snake venom and snake antivenom. |
SIGNS AND SYMPTOMS
Initial systemic symptoms can include nausea, vomiting, abdominal pain, headache, and dizziness.     Sudden loss of consciousness, typically with spontaneous recovery, may occur early in the course of envenoming.   There is potential for hypotension, cardiac dysrhythmia, and rarely arrest.    Bleeding and/or ooze from the bite site or subsequent venepuncture is an early indication of venom induced consumption coagulopathy (VICC), which is the hallmark of brown snake envenoming.    This coagulopathy may potentially lead to 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.       Although hemorrhage is a major concern, spontaneous bleeding is uncommon to rare.   Thrombotic microangiopathy with thrombocytopenia and microangiopathic hemolytic anemia may additionally occur,  but is not common; platelet counts typically remaining normal in most cases. Neurotoxicity is rare and typically only results in mild effects such as ptosis.  Seizure may occur, more commonly in children, but it does not appear to be related to neurotoxins. Acute kidney injury may occur  and it more commonly develops in adults. It appears that most, possibly all cases of acute kidney injury are not primarily caused by venom nephrotoxicity but likely secondary to other effects of envenoming such as thrombotic microangiopathy.  Myolysis is not typically a feature of brown snake envenoming.   |
Clinical effects usually develop following a dermal exposure (bite). Snakebite to the eye or contamination of the eye with snake venom is an unlikely route of exposure. |
Onset/Duration of Symptoms |
Coagulopathy typically resolves over 12 to 18 hours.   Paralysis following snakebite may take days or weeks to resolve.  |
The following are typical features indicating severity in patients known to be envenomed, but it is important to note that the isolated presence of (particularly mild) features does not always indicate that envenoming has occurred. Mild Pseudonaja Envenoming | Moderate Pseudonaja Envenoming | Severe Pseudonaja Envenoming | Nausea Vomiting Abdominal pain Headache Confusion Drowsiness | Pallor Sweating Ptosis Ophthalmoplegia Tachycardia Hypotension Oliguria | Venom induced consumption coagulopathy Microangiopathic hemolytic anemia Intracranial hemorrhage Acute renal failure Paralysis Respiratory failure Cardiac arrest |
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ACUTE EFFECTS (ROUTE OF EXPOSURE)
There does not appear to have been any reported cases of contamination of the eye with snake venom or bites to the eye from Australian snakes. |
Ingested snake meat or snake venom is not likely to cause any adverse effects. |
ACUTE EFFECTS (ORGAN SYSTEM)
Venom induced consumption coagulopathy (VICC) Thrombotic microangiopathy |
Agitation  Dysarthria  Dysphonia  Respiratory compromise/paralysis   |
Coronary ischemia  Dysrhythmia  |
Persistent ooze/bleeding from bite site (indicating coagulopathy)  Bite site edema  Bite site redness  |
Ophthalmoplegia (paralysis of motor nerves of eye) Blurred vision  |
Dyspnea  Pulmonary edema  Respiratory compromise/paralysis   |
Anaphylaxis to this snake venom may potentially occur in those previously exposed.   |
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.  On occasion multiple bites may occur from a single snake with an increased likelihood of effective envenoming.   The majority (75%) of brown snake ( Pseudonjaja spp.) bites do not produce an effective envenoming, producing no, or only minor, symptoms. However, brown snakes are the most common cause of snakebite and snakebite related death in Australia.     Prior to antivenom development, about 18% of all brown snake bites proved fatal.  A more modern case series of brown snake envenomings in Australia over a 10-year period reported 15 deaths in 296 hospital treated cases (5%).  |
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.  |
The elderly are at greater risk of severe toxicity than other adults, often due to pre-existing disease.  |
BIOLOGICAL LEVELS - TOXIC
Serum venom concentrations can be measured by enzyme immunoassays,   however, these are currently only used in research. Obtaining venom blood concentrations is not necessary for clinical management. |
REPRODUCTION
FERTILITY
It is unknown if exposure to this creature causes impaired fertility.
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PREGNANCY
A fetus will share the mother’s risk following systemic envenoming. It is unclear if venom crosses the placenta. |
LACTATION
It is unknown if exposure to this creature results in excretion of toxic substances into breast milk. |
VENOM COMPOSITION
Brown snakes have complex venoms with many different components including pre- and postsynaptic neurotoxins and potent procoagulant toxins. Identified toxins include the neurotoxin textilotoxin.  |
TOXIC MECHANISM
Brown snake envenoming is characterized by venom induced consumption coagulopathy. Renal damage may occur, likely secondary to other effects of envenoming including microangiopathic hemolytic anemia, hypotension, and coagulopathy,   though it is possible a nephrotoxic component of the venom may also be responsible. Flaccid paralysis uncommonly emerges  and may be due to either pre- or postsynaptic neuromuscular junction neurotoxins. Myolysis is not a feature of brown snake envenoming.  |
Snake venom procoagulants are prothrombin activators which 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 minutes, leaving the victim profoundly anticoagulated.   The conversion of prothrombin to thrombin additionally provides positive feedback which results in the activation of factor V to factor Va and factor VIII to factor VIIIa which eventually also leads to complete consumption of these factors.   However, prothrombin is only partially depleted suggesting that the prothrombin activator toxins are quickly eliminated or become inactive.  As venom can be detected in blood for up to 24 hours after envenoming, inactivation would appear to be a more reasonable explanation for the toxins lack of continued activity, although the mechanism remains unclear.  There is limited effect on the other coagulation factors.  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.  |
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 may be reversed with adequate doses of antivenom, or repeated doses of cholinesterase inhibitors such as neostigmine.   |
Presynaptic Neuromuscular Junction Neurotoxins |
Presynaptic neurotoxins act by causing degeneration of the nerve terminal and intramuscular axons.   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 or weeks.   Only skeletal muscles (including the muscles of respiration) are affected, not cardiac or smooth muscle. |
DESCRIPTION
Brown snakes vary in coloration being either brown, orange-red, grey, or almost black. They may additionally be unbanded, banded, speckled, or black headed.  The average adult length is 1.5 m.  The fangs are small being only 2.8 mm long in an average adult.  |
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NZ: 23.May.2022 |