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Pseudonaja spp. (Brown Snakes)

Pseudonaja spp. (Brown Snakes)
30.May.2017-Expires: 7 days - Do not archive







Brown snakes



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.[1]


Intervention Level

Child and Adult

Medical observation, preferably in an advanced care facility, is recommended for:
- Any individual suffering a suspected or actual snakebite[2]
Immediately apply pressure immobilization first aid if not already in a medical facility.

Observation Period

Observation at Home

All patients require medical attention.

Medical Observation

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.[3][4]
Patients must be closely observed for the onset of symptoms including:
Bleeding/ooze from bite or venepuncture sites
Bleeding gums
Paralysis (may be subtle)
Ptosis (drooping eyelids)
Ophthalmoplegia (paralysis of motor nerves of the eye)
Acute kidney injury
The coagulation screen and renal function investigations along with a neurological examination must be performed upon presentation and repeated at 6 hours and 12 hours after the bite.[4]
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.[4]
Removal of Pressure Immobilization First Aid
If envenoming is evident, do not remove pressure immobilization first aid until antivenom has been administered.[3]
If there are no clinical or biochemical signs of envenoming only remove pressure immobilization first aid once an IV line has been inserted, a Snake Venom Detection Kit analysis has been performed, and antivenom and advanced resuscitation facilities are at hand.[3][4][5]
Once the pressure bandage is removed repeat blood tests at 1 hour after removal.[4] 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.[4] If clinical signs or biochemical findings indicate systemic envenoming then antivenom should be administered.[6] 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.[4]
Intravenous Fluids
Intravenous hydration is required to reduce the incidence of renal damage.[6]
Normal (0.9%) saline dose
Adjust adult dose to body weight
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:
Snake venom detection kit test
Blood investigations
All patients must then be observed for a minimum of 12 hours.[4]
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.[7] 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.[8] It does not indicate that major envenoming has occurred and is not an indication antivenom is required.[9] The decision to give antivenom should be based on clinical and laboratory evidence of systemic envenoming.[2][8][9][10][11] Conversely, a negative result should not be used to exclude envenoming.[9]
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[9] and should not be tested in patients who do not have evidence of systemic envenoming.[10]
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.[5] 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 concentration
Fibrin degradation products (FDP)/D-dimer immunoassay
If laboratory facilities are not readily available then conduct a whole blood clotting time:[3][12]
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:
White blood cells (especially absolute lymphocyte count)
Serum electrolytes including:
Serum urea
Serum creatinine
Serum creatine kinase (CK)
Collect urine (may be required for subsequent Snake Venom Detection Kit testing)

Admission Criteria

Admission to an intensive care environment is recommended for patients who develop any signs of envenoming or abnormal blood results.



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 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.
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 blow to the head (possibly associated with a post-bite collapse) is a potential source of intracranial hemorrhage. If bleeding is immediately life-threatening, fresh frozen plasma or coagulation factors should be administered. 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 medications likely to depress respiratory function such as opioid analgesics or interfere with platelet function including aspirin. 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
Enhanced Elimination
Supportive Care


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.[13] Avoid insertions in sites where bleeding cannot be easily controlled, such as subclavian, femoral, and jugular veins.[10]

Pressure Immobilization First Aid

- Reassure the patient and ensure they remain still.[10]
- Remove any watch, rings, bracelets, or other jewelery from the bitten limb.[10][1]
- A broad 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,[14] but crepe bandages, clothing strips, towels, or pantyhose will suffice in an emergency.[10][14]
- 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.[1]
- Bandage upward from the lower portion of the bitten limb. Apply the bandage as far as possible up the limb.[1]
- 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.[1]
- 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.[1]
- On the overlying bandage mark the location of the bite.[1]
- Ensure the patient is told not to move at all.[10][1]
- 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.[1]
- 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.[10]
- Transport to hospital.[10]
- Tourniquets should not be used. The bite site should not be washed, cleaned, cut, sucked, or treated with any substance.[10]

Cardiac Arrest

Cardiac arrest or dysrhythmia are likely short-lived as the precipitating blood clot will be dissolved by fibrinolysis.[15] Resuscitation should follow standard procedures for cardiac arrest.


Toxic seizures are generally self-limiting and are unlikely to require specific treatment.


Where the systolic blood pressure is below normal blood pressure ranges for the age group:[16]
Age (years)
Normal Systolic Blood Pressure (mm Hg)
< 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.
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.

Emergency Monitoring

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 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.[3][17][18]


Brown Snake Antivenom (CSL)

Polyvalent Snake Antivenom (CSL)

It may never be too late to administer antivenom and CSL Brown Snake Antivenom is the preferred antivenom. CSL 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.[19]
Antivenom administration is indicated in any patient where there is evidence of developing or established:
Any indication of defibrination (e.g. INR > 1.5)
Renal damage
Any evidence of non-preexistent kidney injury
Any flaccid paralysis including ptosis (unless present without worsening for 6 hours)

Dose and Administration

Only administer if there is clear evidence of envenoming.[8] The dose for a child is the same as that for an adult. Do not remove pressure immobilization first aid prior to administration, only after. Monovalent antivenom is preferable to polyvalent, and pre-testing or pre-medication is not required.[3][7][20]
In most instances of Australian snakebite an adequate initial dose of antivenom will be sufficient and past practices of multiple repeat doses[2][21][22][23][24][25] are both unnecessary and hazardous.[26][27] Nevertheless, it is important that the initial dose of antivenom not be considered the end of treatment and investigation.
Prior to use of snake antivenom ensure adequate resuscitation equipment is available for the management of anaphylaxis, and that an appropriate dose of epinephrine (adrenaline) is prepared for administration if necessary.[1][3][7][28]
Initial Brown Snake Antivenom (CSL) Dose
1 vial IV[26][29][30]
Dilute antivenom up to 1 in 10 in an isotonic solution (e.g. normal [0.9%] saline); dilution should be less for children due to fluid load. Administer intravenously via a drip-set, commence very slowly and increase rate if there is no adverse reaction. Each dose should be given over 15 to 30 minutes.[1][3][10]
Patients must be closely monitored for anaphylaxis during and for 30 minutes after the infusion.[10]
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.[31] 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 clinical 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 (CSL)
For CSL Polyvalent Snake Antivenom, follow the same dosage and administration guidelines 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.[32] Pregnancy is not a contraindication to antivenom administration.[33]
Those at increased risk of severe reaction include patients with history of:[32]
Previous reaction to antiserum

Adverse Effects

Closely monitor the patient for indications of anaphylaxis including:
Airways obstruction
Serum Sickness
Serum sickness may occur some 4 to 14 days following antivenom administration.[3][30][34]
Patients should be observed for, and made aware of, the signs and symptoms of serum sickness including:
Joint aches
If more than 25 mL of CSL Brown Snake Antivenom is administered, prophylaxis with an oral steroid such as prednisolone may be considered, and follow-up arranged.[1][3] Commence prophylaxis on day 2 to 3 post-bite.
Prednisolone dose[35]
1 to 2 mg/kg per day orally for 5 days
50 mg per day orally for 5 days


Enhanced Elimination Not Recommended

Techniques to enhance elimination of venom following envenoming by this creature are not required.



Observe for:
Bleeding/ooze from bite or venepuncture sites
Bleeding gums
Ptosis (drooping eyelids)
Partial ophthalmoplegia (paralysis of motor nerves of eye)
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) or prothrombin time (PT)
Activated partial thromboplastin time (aPTT)
Fibrinogen concentration
Fibrin degradation products (FDP)/D-dimer immunoassay
Full blood count (FBC) including:
White blood cells (especially absolute lymphocyte count)
Serum electrolytes including:
Serum creatine kinase (CK)
Renal function
Serum urea
Serum creatinine
Blood pressure
12 lead ECG
Plasma glucose
Fluid balance (urinary catheterization may be required)


Venom Induced Consumption Coagulopathy

Venom induced consumption coagulopathy (VICC) is due to potent prothrombin activators in the venom.[36] Complete defibrination typically occurs 1 to 2 hours post-envenoming,[13] although in some situations it may develop within 15 minutes.[15] VICC is characterized by rapid development of almost complete deficiencies in fibrinogen, factor V, and factor VIII concentrations along with a partial deficiency in prothrombin.[13][27][37] While a major hemorrhage is the main concern,[21][38][39][40] this appears to be a relatively rare outcome.[10] Intracranial hemorrhage is usually fatal[15][41] and may be more likely in those who have suffered a recent blow to the head, such as from a post-envenoming collapse[39] or in those of older age or with a past medical history of hypertension.[41]
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.[31]
International normalized ratio (INR)
Activated partial thromboplastin time (aPTT)
Fibrinogen concentration
Fibrin degradation products (FDP)/D-dimer immunoassay
Antivenom has been shown to neutralize procoagulant toxins in vitro,[29][42] although due to the rapid depletion of clotting factors (within 1 to 2 hours)[13] it may not be possible to administer antivenom in a timeframe which would be effective at preventing coagulopathy;[13][43] similarly due to rapid inactivation of procoagulant toxins it may not be useful in speeding recovery.[13][43][44] Although this suggests antivenom may have a limited role in venom induced consumption coagulopathy, it is still recommended to ensure neutralization of any circulating toxins, especially where absorption may be delayed, i.e. following the use of pressure bandages.
Following antivenom administration repeat blood tests at 6 hours post-antivenom.[27] 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[13][27][29] with recovery from coagulopathy typically taking 12 to 18 hours.[45] 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.[24] Repeat blood tests at 12 and 18 to 24 hours post-antivenom to determine if the patient has fully recovered.[27]
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 clinical toxicologist.[46] The dose should be the same as used initially followed by factor replacement therapy (fresh frozen plasma [FFP] or cryoprecipitate, or if these are unavailable, fully cross matched fresh whole blood).[47] If there is no evidence of active bleeding repeat blood tests at 9 hours post-antivenom.
The use of factor replacement such as FFP as treatment following Australian snakebite has been controversial.[48][49][50][51][52] It was feared that giving FFP without first administering adequate antivenom may be detrimental as the administered factors will also be consumed by the venom which may lead to an increase in degradation products and further coagulation disturbances.[10][24][52] However, evidence from studies have shown this may not be the case, and FFP may reduce the time to recovery and potentially the risk of bleeding.[43][53] A randomized controlled trial has shown administration of factor replacement after antivenom results in more rapid restoration of clotting function in most patients, but no decrease in discharge time. However, early administration (less than 6 to 8 hours post bite) was found to be less likely to be effective than later administration. Additionally, it could not be determined if administration of FFP could reduce the risk of major hemorrhage.[54] At this stage administration of factor replacement within 6 to 8 hours of a bite should only be given if there is uncontrolled or life-threatening hemorrhage.[54]

Microangiopathic Hemolytic Anemia

Microangiopathic hemolytic anemia may occur following bites and can last 1 to 2 weeks.[37][55][56] The pathogenesis of this condition is not completely understood.[37] If coagulopathic snake envenoming is present, blood films should be monitored, and if abnormal, repeated daily until resolved.[55]
Patients should be monitored for evidence of microangiopathic hemolytic anemia:
Peripheral blood smear
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.[37] It is unknown if further treatment including fresh frozen plasma and/or plasmapheresis is beneficial;[37][55] plasmapheresis did not appear to change the time course of severity in one series of patients.[55] However, as plasmapheresis can be life-saving it should be considered in this setting.[55]


Acute Renal Failure

Renal damage may occur following brown snake envenoming.[57] 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.[58][55] Acute kidney injury typically occurs in the setting of microangiopathic hemolytic anemia.[3] Other contributing factors may include hypotension, myoglobinuria, and coagulopathy.[57][59][60][61][62]
Patients should be monitored for the onset of renal failure:
Urine output
Serum creatinine
Blood urea nitrogen (urea)
Loin pain may occur
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. Catheterization is likely necessary, although caution is required if coagulopathy is evident. Central venous pressure monitoring may be required to maintain optimal fluid balance. If myolysis is present alkalinization of the urine should be considered to prevent renal damage.
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 kidney injury including hemodialysis should be followed.[59][63] In severe cases hemodialysis may be required for an extended period, but the failure is generally reversible.[55][57][62][64]
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 clinical toxicologist.



Sudden loss of consciousness and collapse may occur; thought to be due to immune mediators which can cause hypotension and vasodilatation.[65][66] Direct myocardial depression is also possible.[67] Spontaneous recovery is likely within 10 to 30 minutes[10] unless collapse is associated with cardiac arrest.[26][22][68]
Closely monitor level of consciousness.
Follow standard protocols for the management of coma.


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.[69] 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.[70] Paralysis following snake bite may take days or weeks to resolve.[70]
Observe and examine for onset of cranial nerve signs including:
Ptosis (drooping eyelids)
Partial ophthalmoplegia (paralysis of motor nerves of eye)
Bulbar palsy
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.[28][71][72] For most Australian snakes if paralysis is present it will be partially mediated by presynaptic neurotoxins.[73][74] This has important implications for antivenom therapy as presynaptic paralysis will not respond to even high doses of antivenom or neostigmine.[72][75] 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 clinical 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[76][77] and should also be considered as adjunctive treatment, or in areas where antivenom is not readily obtainable, the use of repeated therapy with neostigmine may permit survival. If the test is negative then paralysis will not respond to further antivenom and giving escalating doses of antivenom to reverse paralysis is inadvisable.
In cases were paralysis cannot be reversed, intubation and artificial ventilation will be required.[40][78]


Cardiac Dysrhythmia

In cases of severe envenoming, venom pro-coagulants may lead to microvascular thrombi, coronary vessel occlusion, cardiac dysrhythmia, and cardiac arrest.[15][22] Such thrombi will dissolve as coagulopathy progresses,[15] and further management is rarely necessary. If required standard advanced life support measures should be undertaken.
Heart rate/rhythm
Blood pressure
12 lead ECG
Manage following standard treatment protocols for cardiac dysrhythmia.


Serum Sickness

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:
Joint aches
Serum sickness may be managed with antipyretics and analgesics, as well as anti-inflammatory agents including antihistamines and corticosteroids:
Prednisone dose
60 mg daily for 7 to 14 days with tapering
Severe cases may require hospitalization.



It is uncommon for an infection to occur at the bite site.[3][79] Prophylactic antibiotics are therefore not required. The bite area should be observed and an appropriate antibiotic administered only if infection becomes evident.[3] The bite site should not be cleaned until after a Snake Venom Detection Kit identification has been made.[17][18]
Observe patient for signs of infection
Bite/sting site for signs of infection
Body temperature
Management of infection should follow standard treatment protocols.

Tetanus Prophylaxis

Tetanus prophylaxis should be provided if indicated by immunologic status.

Do not give tetanus prophylaxis until any coagulopathy is resolved, as a significant hematoma may develop.


Late onset of envenoming is rare.[4] 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.[3][4] If there are no biochemical abnormalities at this time and the patient is asymptomatic on clinical examination, discharge may be allowed.[4]
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.[80] Discharge of those with continuing systemic envenoming, microangiopathic hemolytic anemia, or acute kidney injury is dependent upon their recovery.


Those patients receiving antivenom are at risk of serum sickness occurring 4 to 21 days following administration, and should be made aware of the signs and symptoms of this condition including:
Joint aches
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.[1][3]


Death is a known outcome following snakebite in Australia.[33][58][81] The prognosis is improved if patients are managed in a modern intensive care environment with the appropriate antivenom available, although this does not guarantee a favorable outcome.[39][61] Major hemorrhage associated with venom induced consumption coagulopathy usually carries a grave prognosis; in particular, intracranial hemorrhage can be expected to prove lethal.
In those who recover from envenoming there should be no direct long-term adverse effects. While respiratory paralysis may require artificial ventilation, potentially for over a month, return of full respiratory function can be expected. No permanent neurological defects would be anticipated unless they are from anoxic injury.[70] Acute anuric kidney injury may require hemodialysis for an extended period but is generally reversible.[55][57][62][64]
Individuals may become immunologically sensitized to both the snake venom and snake antivenom.


Following a brown snake bite there is minimal or no local pain at the wound site, rarely swelling or erythema, and as the fangs are small the injury can be virtually invisible;[26][82][83] adults may not even be aware they have been bitten.[25][81]
Initial systemic symptoms can include nausea, vomiting, abdominal pain, headache, and dizziness.[79][84][78][85] Sudden loss of consciousness, typically with spontaneous recovery, may occur early in the course of envenoming.[26][84] There is potential for hypotension, cardiac dysrhythmia, and rarely arrest.[15][26] 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.[26][84] 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.[12][13][55][61][86][87] Although hemorrhage is a major concern, spontaneous bleeding is uncommon to rare.[15] 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.[26] 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.[55] Myolysis is not a feature of brown snake envenoming.[26]

Routes of Exposure

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

Early collapse, if present, is typically the first feature, developing within 5 to 30 minutes.[26][84] Between 30 and 120 minutes there may be lymph node pain and early nonspecific systemic features. Coagulopathy typically develops over 1 to 2 hours post-envenoming,[13] although complete defibrination can occur by 15 to 30 minutes.[15] If neuromuscular paralysis develops the first signs of ptosis may be evident 2 to 6 hours post-bite. Paralysis can be also delayed and may evolve over 12 to 24 hours.[7][28][79][88]
Coagulopathy typically resolves over 12 to 18 hours.[26][45] Paralysis following snakebite may take days or weeks to resolve.[70]

Severity of Envenoming

Mild Pseudonaja EnvenomingModerate Pseudonaja EnvenomingSevere Pseudonaja Envenoming
Abdominal pain
Venom induced consumption coagulopathy
Microangiopathic hemolytic anemia
Intracranial hemorrhage
Acute renal failure
Respiratory failure
Cardiac arrest



Following a bite there may be small puncture wounds or scratches from the fangs.[28][79][89] Local pain, swelling, or erythema are rare.[79][57][82][83]


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.



Venom induced consumption coagulopathy (VICC)
Bleeding or ooze from bite or venepucture site[12][22][26][33][61][81][89][90][91][92][93]
Bleeding gums (classic sign of coagulopathy but rarely seen following brown snake bite)[22][26][39][68]
Major bleeding[21][26][61]
Intracranial hemorrhage[13][21][26][39][81][96][41]
Thrombotic microangiopathy
Microangiopathic hemolytic anemia (MAHA)[26][55][59][62][64][93][94][95]


Ptosis (drooping eyelids)[26][39][88][98]
Respiratory compromise/paralysis[79][68]
Seizure (typically in children,[100] not related to neurotoxin envenoming)[26][81][88][100]
Intracranial hemorrhage (secondary to coagulopathy)[13][21][26][39][81][96]



Coronary ischemia[22]



Lymphadenopathy (if envenoming severe)[84][85][93]
Persistent ooze/bleeding from bite site (indicating coagulopathy)[63]
Bite site edema[84]
Bite site redness[84]


Ophthalmoplegia (paralysis of motor nerves of eye)[68]
Blurred vision[12]


Pulmonary edema[61]
Respiratory compromise/paralysis[79][68]


Anaphylaxis to this snake venom may potentially occur in those previously exposed.[81][103]



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,[104] with the other Pseudonaja species less toxic, and P. modesta less so still.[97] As a group the brown snakes are the most common cause of snakebite and snakebite related death in Australia.[25][33][81]
The majority (75%) of venomous Australian 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 related death in Australia; prior to antivenom development about 18% of all brown snake bites proved fatal.[78] On occasion multiple bites may occur from a single snake with an increased likelihood of effective envenoming.[33][81]



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.[33]


The elderly are at greater risk of severe toxicity than other adults, often due to pre-existing disease.[33]


Serum venom concentrations can be measured by enzyme immunoassays,[105][106] however, these are currently only used in research. Obtaining venom blood concentrations is not necessary for clinical management.



It is unknown if exposure to this creature causes impaired fertility.


A fetus will share the mother’s risk following systemic envenoming. It is unclear if venom crosses the placenta.


It is unknown if exposure to this creature results in excretion of toxic substances into breast milk.


Brown snakes have complex venoms with many different components including pre- and postsynaptic neurotoxins and potent procoagulant toxins. Identified toxins include the neurotoxin textilotoxin.[107]


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,[58][55] though it is possible a nephrotoxic component of the venom may also be responsible. Flaccid paralysis uncommonly emerges[69] and may be due to either pre- or postsynaptic neuromuscular junction neurotoxins. Myolysis is not a feature of brown snake envenoming.[24]
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.[15][86] 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.[13][86] However, prothrombin is only partially depleted suggesting that the prothrombin activator toxins are quickly eliminated or become inactive.[13] 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.[13] There is limited effect on the other coagulation factors.[31]
There is a difference between the onset of coagulopathy between tiger snakes and brown snakes and taipans. The rate of onset of coagulopathy following tiger snake bite may be slower than that of the other snakes due to tiger snake prothrombin activator toxins being factor Xa–like and therefore first require activation of human factor V to factor Va before the conversion of prothrombin to thrombin can occur.[13] In contrast, brown snake and taipan venom contains a factor Xa-Va–like prothrombin activator toxin[42][108][109][110][111] which do not require initial activation so they can more rapidly induce prothrombin activation and coagulopathy.[112][113]
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.[15]
Renal damage following snake envenoming is thought to be a consequence of other effects of envenoming, typically occurring in those with microangiopathic hemolytic anemia[3] other contributing factors may include hypotension, myoglobinuria, and coagulopathy.[57][59][60][61][62] However, it is possible direct nephrotoxins may also be present in venom. An acute tubular necrosis takes place.[64]
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.[73] This may be reversed with adequate doses of antivenom, or repeated doses of cholinesterase inhibitors such as neostigmine.[76][77]
Presynaptic Neuromuscular Junction Neurotoxins
Presynaptic neurotoxins act by causing degeneration of the nerve terminal and intramuscular axons.[73][114] Following a brief period of neurotransmitter discharge, further release halts, with onset of a progressive flaccid paralysis.[73] This paralysis is irreversible due to axonal damage caused by these venoms and may persist for days or weeks.[40][73] Only skeletal muscles (including the muscles of respiration) are affected, not cardiac or smooth muscle.



Brown snakes vary in coloration being either brown, orange-red, grey, or almost black. They may additionally be unbanded, banded, speckled, or black headed.[1] The average adult length is 1.5 m.[10] The fangs are small being only 2.8 mm long in an average adult.[1]


Brown snakes are normally active during the day but may be nocturnal in hot weather. Brown snakes are fast moving and are known to be aggressive when disturbed or threatened. Bites in humans are typically on the extremities and most commonly on the lower extremitries.[2][18][70][78][100][115][116]


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