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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


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][36][37] adults may not even be aware they have been bitten.[25][38]
Initial systemic symptoms can include nausea, vomiting, abdominal pain, headache, and dizziness.[39][40][41][42] Sudden loss of consciousness, typically with spontaneous recovery, may occur early in the course of envenoming.[26][40] 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][40] 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][43][44][45][46] 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.[43] 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][40] 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][39][47]
Coagulopathy typically resolves over 12 to 18 hours.[26][48] Paralysis following snakebite may take days or weeks to resolve.[49]

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


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[2] Jelinek GA, Hamilton T, Hirsch RL. Admissions for suspected snake bite to the Perth adult teaching hospitals, 1979 to 1988. Med J Aust 1991 Dec 2-16; 155 (11-12): 761-4.
[3] Isbister GK. Snake bite: a current approach to management. Aust Prescr 2006; 29 (5): 125-9.
[4] Ireland G, Brown SG, Buckley NA, Stormer J, Currie BJ, White J, Spain D, Isbister GK. Changes in serial laboratory test results in snakebite patients: when can we safely exclude envenoming? Med J Aust 2010 Sep 6; 193 (5): 285-90.
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[6] Pearn J, Morrison J, Charles N, Muir V. First-aid for snake-bite: efficacy of a constrictive bandage with limb immobilization in the management of human envenomation. Med J Aust 1981 Sep 19; 2 (6): 293-5.
[7] Currie BJ. Snakebite in tropical Australia, Papua New Guinea and Irian Jaya. Emerg Med (Fremantle) 2000; 12 (4): 285-94.
[8] Sutherland SK. Treatment of snake bite. Aust Fam Physician 1990 Jan; 19 (1): 21, 24-42.
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[12] Isbister GK, Currie BJ. Suspected snakebite: one year prospective study of emergency department presentations. Emerg Med (Fremantle) 2003 Apr; 15 (2): 160-9.
[13] Isbister GK, Scorgie FE, O'Leary MA, Seldon M, Brown SG, Lincz LF. Factor deficiencies in venom-induced consumption coagulopathy resulting from Australian elapid envenomation: Australian Snakebite Project (ASP-10). J Thromb Haemost 2010 Nov; 8 (11): 2504-13.
[14] Canale E, Isbister GK, Currie BJ. Investigating pressure bandaging for snakebite in a simulated setting: bandage type, training and the effect of transport. Emerg Med Australas 2009 Jun; 21 (3): 184-90.
[15] White J. Snake venoms and coagulopathy. Toxicon 2005 Jun 15; 45 (8): 951-67.
[16] Mackway-Jones K, Molyneux E, Phillips B, Wieteska S, editors. Advanced paediatric life support: the practical approach. 3rd ed. London: BMJ Books; 2001.
[17] Fatovich DM, Hitchcock T, White J. Mild snake envenomation. Emerg Med (Fremantle) 2002 Mar; 14 (1): 85-8.
[18] Jelinek GA, Breheny FX. Ten years of snake bites at Fremantle Hospital. Med J Aust 1990 Dec 3-17; 153 (11-12): 658-61.
[20] White J. Envenoming and antivenom use in Australia. Toxicon 1998 Nov; 36 (11): 1483-92.
[21] Yeung JM, Little M, Murray LM, Jelinek GA, Daly FF. Antivenom dosing in 35 patients with severe brown snake (Pseudonaja) envenoming in Western Australia over 10 years. Med J Aust 2004 Dec 6-20; 181 (11-12): 703-5.
[22] Johnston MA, Fatovich DM, Haig AD, Daly FF. Successful resuscitation after cardiac arrest following massive brown snake envenomation. Med J Aust 2002 Dec 2-16; 177 (11-12): 646-9.
[23] Simes DC. Early and late removal of the pressure bandage in brown snake envenomation: a report of two cases. Crit Care Resusc 2002 Jun; 4 (2): 116-8.
[24] White J. Management of brown snake envenoming. [Editorial] Crit Care Resusc 2002 Jun; 4 (2): 84-6.
[25] White J. Why do people still die from brown-snake bites? Emerg Med (Fremantle) 2000; 12 (3): 204–6.
[26] Allen GE, Brown SG, Buckley NA, O'Leary MA, Page CB, Currie BJ, White J, Isbister GK. Clinical effects and antivenom dosing in brown snake (Pseudonaja spp.) envenoming--Australian snakebite project (ASP-14). PLoS One 2012; 7 (12): e53188.
[27] Isbister GK. Procoagulant snake toxins: laboratory studies, diagnosis, and understanding snakebite coagulopathy. Semin Thromb Hemost 2009 Feb; 35 (1): 93-103.
[29] Isbister GK, O'Leary MA, Schneider JJ, Brown SG, Currie BJ. Efficacy of antivenom against the procoagulant effect of Australian brown snake (Pseudonaja sp.) venom: in vivo and in vitro studies. Toxicon 2007 Jan; 49 (1): 57-67.
[30] Isbister GK, Brown SG, Page CB, McCoubrie DL, Greene SL, Buckley NA. Snakebite in Australia: a practical approach to diagnosis and treatment. Med J Aust 2013 Dec 16; 199 (11): 763-8.
[31] Isbister GK, Williams V, Brown SG, White J, Currie BJ. Clinically applicable laboratory end-points for treating snakebite coagulopathy. Pathology 2006 Dec; 38 (6): 568-72.
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[34] Ryan NM, Downes MA, Isbister GK. Clinical features of serum sickness after Australian snake antivenom. Toxicon 2015 Dec 15; 108 (): 181-3.
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[36] Campbell CH. Clinical aspects of snake bite in the Pacific area. Toxicon 1969 Jun; 7 (1): 25-8.
[37] White J. Local tissue destruction and Australian elapid envenomation. Toxicon 1983; 21 (Suppl 3): 493-6.
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[39] TRINCA GF. The treatment of snakebite. Med J Aust 1963 Feb 23; 50(1) (): 275-80.
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[41] Sutherland SK. Treatment of snake bite in Australia. Some observations and recommendations. Med J Aust 1975 Jan 11; 1 (2): 30-2.
[42] Tibballs J. Diagnosis and treatment of confirmed and suspected snake bite. Implications from an analysis of 46 paediatric cases. Med J Aust 1992 Feb 17; 156 (4): 270-4.
[43] Isbister GK, Little M, Cull G, McCoubrie D, Lawton P, Szabo F, Kennedy J, Trethewy C, Luxton G, Brown SG, Currie BJ. Thrombotic microangiopathy from Australian brown snake (Pseudonaja) envenoming. Intern Med J 2007 Aug; 37 (8): 523-8.
[44] Henderson A, Baldwin LN, May C. Fatal brown snake (Pseudonaja textilis) envenomation despite the use of antivenom. Med J Aust 1993 May 17; 158 (10): 709-10.
[45] Lalloo DG, Trevett AJ, Owens D, Minei J, Naraqi S, Saweri A, Hutton RA, Theakston RD, Warrell DA. Coagulopathy following bites by the Papuan taipan (Oxyuranus scutellatus canni). Blood Coagul Fibrinolysis 1995 Feb; 6 (1): 65-72.
[46] Masci PP, Rowe EA, Whitaker AN, de Jersey J. Fibrinolysis as a feature of disseminated intravascular coagulation (DIC) after Pseudonaja textilis textilis envenomation. Thromb Res 1990 Sep 1; 59 (5): 859-70.
[47] Kellaway CH. The symptomatology and treatment of the bites of Australian snakes. Med J Aust 1942 Aug 29; 2: 171-4.
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[49] CAMPBELL CH, YOUNG LN. The symptomatology, clinical course and successful treatment of Papuan elapine snake envenomation. Med J Aust 1961 Apr 1; 48(1) (): 478-86.

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