Emergency Management of Snakebites in Children · 2019-09-17 · Venom-induced consumption...

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Emergency Management of Snakebites in Children Document ID CHQ-GDL-00725 Version no. 1.0 Approval date 10/08/2017 Executive sponsor Executive Director Medical Services Effective date 10/08/2017 Author/custodian Director, Paediatric Emergency Department Review date 10/08/2020 Supersedes New Applicable to All CHQ staff involved in the care and emergency management of children with suspected snakebite Authorisation Executive Director Hospital Services Purpose This guideline has been developed to provide an approach for medical officers involved in the emergency investigation and management of snakebites and potential snakebites in children. Scope This guideline applies to all staff involved in the care of children who have sustained or potentially sustained a snakebite presenting to the emergency department. Related documents Forms and templates Snake bite Clinical pathway record https://www.childrens.health.qld.gov.au/wp-content/uploads/PDF/poisons/snake-bite-cp.pdf

Transcript of Emergency Management of Snakebites in Children · 2019-09-17 · Venom-induced consumption...

Page 1: Emergency Management of Snakebites in Children · 2019-09-17 · Venom-induced consumption coagulopathy (VICC) Activation of the clotting pathway by prothrombin activator toxins and

Emergency Management of Snakebites in Children

Document ID CHQ-GDL-00725 Version no. 1.0 Approval date 10/08/2017

Executive sponsor Executive Director Medical Services Effective date 10/08/2017

Author/custodian Director, Paediatric Emergency Department Review date 10/08/2020

Supersedes New

Applicable to All CHQ staff involved in the care and emergency management of children with suspected snakebite

Authorisation Executive Director Hospital Services

Purpose This guideline has been developed to provide an approach for medical officers involved in the emergency investigation and management of snakebites and potential snakebites in children.

Scope This guideline applies to all staff involved in the care of children who have sustained or potentially sustained a snakebite presenting to the emergency department.

Related documents Forms and templates

• Snake bite Clinical pathway record

https://www.childrens.health.qld.gov.au/wp-content/uploads/PDF/poisons/snake-bite-cp.pdf

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Introduction Sea and land snakebites in Australia are potentially fatal and immediate medical attention should be sought. While not all snakes are venomous correct identification of the snake is unreliable. Therefore, all snakebites should be considered potentially life threatening, assessed rapidly and have indicated treatment commenced promptly. Assessment for snakebites should be done in centres supported by 24-hour laboratory services where antivenom is available and trained medical staff are available to provide treatment.

Given the low frequency of snakebite envenomation most medical staff will have limited experience in the treatment. This guideline will help aid emergency medical and nursing staff in the assessment, investigation and management of children with a suspected snakebite.

Envenoming can manifest in localised symptoms, systemic symptoms (nausea, vomiting, headaches, abdominal pain, and diaphoresis), collapse and major toxin syndromes (Table 1). Locally pain, swelling and bruising may occur.

Table 1 Characteristics of clinical syndromes from snakebites in Australia1 Sudden collapse Collapse or syncope occurring within an hour of the bite

• Collapse is associated with hypotension and loss of consciousness • Spontaneous recovery usually occurs within minutes • A minority of patients (about 5%) have a cardiac arrest or seizure

Venom-induced consumption coagulopathy (VICC) Activation of the clotting pathway by prothrombin activator toxins and consumption of clotting factors (fibrinogen, factor V and factor VIII) leads to a consumptive coagulopathy

• INR is high or unrecordable and APTT is prolonged • Fibrinogen level is low or undetectable and D-dimer level is very high

Complete or severe VICC is defined as:

• Undetectable fibrinogen level • INR > 3.0 (most often unrecordable) • Abnormal APTT (outside the laboratory’s reference interval) • Very high D-dimer level (100–1000 × assay cut-off)

Partial VICC (less severe changes) is defined as:

• Low but detectable fibrinogen level (< 1.5 g/L) and INR < 3.0 Neurotoxicity A descending flaccid paralysis that classically first involves the eye muscles (ptosis, diplopia and blurred vision), followed by bulbar muscles, respiratory muscle paralysis and limb paralysis Myotoxicity Local or generalised myalgia and/or muscle tenderness

• CK level is usually normal (within the laboratory’s reference interval) on admission and rapidly rises over 24–48 hours (peak ranges from 1000 U/L in mild cases to > 100 000 U/L in severe cases)

• Potassium level may also be elevated (> 5.0 mmol/L) in severe cases, and renal impairment may develop

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First Aid A pressure bandage with immobilisation (PBI) is recommended as first aid for all suspected snakebites. The bandage should be broad at 15cm and preferably elasticated rather than crepe bandage1. The bandage should be applied to the bite site and should continue up the limb at a pressure commonly used for a sprained ankle. Immobilisation is also important and the limb and patient should remain immobilised from the time of the bite. A PBI applied more than 4 hours after the bite has occurred is unlikely to be effective1. The PBI is removed once the initial exam and first investigations do not suggest envenomation and the patient is in a facility with antivenom. For envenomed patients, the PBI can be removed once the antivenom has been administered. Careful observation of the patient is required for at least one hour following the removal of the PBI to detect the rare cases of delayed envenomation with the application of early PBI1.

Assessment Start with a detailed history of the incident including the patient’s geographical location when the bite occurred, whether the snake was visualised, where they were bitten and first aid since the bite1. It is important to document signs and symptoms experienced prior to arrival in emergency along with any previous medical or surgical history.

Clinically important information associated with severe envenomation is early collapse, most common with brown snake envenoming. Examination should focus on:

Bite site: fang marks, bruising, swelling or local necrosis. Potentially tender draining lymph nodes may support envenomation

Neurological: Cranial nerves especially the ocular and periocular muscles (ptosis, ophthalmoplegia, bulbar weakness), limb weakness and respiratory muscle weakness.

Haematological: evidence of abnormal coagulation (bleeding from IV sites, bite site, oral cavity or occult sites including gastrointestinal, urinary or intracranial) 1.

The following table is a summary of the important Australian snakes and their major clinical effects.

Anticoagulant coagulopathy Provides a good marker of envenoming by all black snakes, including mulga snakes, but is not clinically important

• APTT is moderately abnormal (1.5–2.5 × laboratory’s reference interval), with or without mild elevation of INR (> 1.3)

• D-dimer and fibrinogen levels are generally normal (D-dimer < 1.0 mg/L and fibrinogen > 1.5 g/L [or > 2.0 g/L in some laboratories])

Thrombotic microangiopathy Presence of fragmented red blood cells on blood film (microangiopathic haemolytic anaemia), thrombocytopenia and a rising creatinine level (> 120 mmol/L), which may lead to acute renal failure requiring dialysis Systemic symptoms Non-specific systemic symptoms include nausea, vomiting, abdominal pain, diarrhoea, diaphoresis and headache INR = international normalised ratio. APTT = activated partial thromboplastin time. CK = creatine kinase.

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Table 2: Summary of effects of clinically important venomous Australian snakes1 Coagulopathy Neurotoxicity Myotoxicity Systemic

Symptoms Thrombotic Microangiopathy

Cardiovascular effects

Antivenom

Brown Snake VICC Rare and mild - <50% 10% Collapse (33%), Cardiac arrest (5%)

Brown snake

Tiger snake group : Tiger snake VICC Uncommon Uncommon Common 5% Rare Tiger snake Rough-scaled snake

VICC Uncommon Uncommon Common <5% Rare Tiger snake

Hoplocephalus spp. VICC - - <50% <5% Rare Tiger or Brown snake

Black snake group : Mulga snake Anticoagulant - Common Common - - Black snake Red-bellied black snake

Anticoagulant - Common Common - - Tiger snake

Death Adder - Common - Common - - Death Adder Taipan VICC Common Rare Common 5% Uncommon Taipan Sea Snake Uncommon Common Common Sea Snake

Investigations Coagulation studies

International normalised ratio (INR) and APTT should always be performed. Fibrinogen and D-dimer may help with identifying VICC (to differentiate between VICC and anticoagulant effect) but is not essential. D Dimer levels are usually elevated 100 – 1000 times the assay cut off in VICC and modest increases in the absence of other features of envenoming should be interpreted with caution. Point of care (POC) devices has been shown to have a high false negative rate and is not to be used.

Full Blood Count (FBC)

Thrombocytopenia and red cell fragmentation indicate a diagnosis of thrombotic microangiopathy. Non-specific lymphopenia and leucocytosis can occur with systemic envenomation. Absence of this in death adder bites can help exclude systemic envenomation.

Biochemistry

Creatinine Kinase (CK) – elevates in myotoxicity but compared with clinical muscle injury lags up to 24hrs

LDH – elevation can occur in thrombotic microangiopathy

Electrolytes, urea and creatinine – serial measurements may assist in assessing renal function

Snake Venom Detection Kit (SVDK)

SVDK should not be used to diagnose or exclude envenomation. Even in envenomed patient the SVDK has shown high rates of inaccuracy (14% of bites in snake handlers and false negatives in 25% of envenomed patients) 1. They can be of aid in the identification of the snake once envenomation has been established but due to its high rates of inaccuracy should be used in conjunction with the clinical syndrome and geographical knowledge of the local snakes. Clinical and laboratory findings can be enough to determine the particular snake group and therefore determine the required antivenom.

A swab of the bite site is the most accurate method of SVDK testing however urine can be used. Timing of the urine collection is crucial as urine produced prior to envenomation can lead to a false negative result. Ideally the patient should void on arrival to ED and only the subsequent urine samples are used for the SVDK. SVDK should be performed where possible by trained laboratory staff and not by clinicians.

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Bite swabs can be taken on presentation and kept for testing at a later stage. This can be done by using a dry swab which has been wet with normal saline and then applied to the bite site. This swab is then placed in a sterile specimen container (e.g. urine specimen container).

Management

• All suspected snakebites should be initially managed in a monitored, high dependency bed or treatment space.

• Notify senior emergency doctor.

• Commence documentation on the Snake Bite Clinical pathway (see appendix 1).

• Insert IV cannula and obtain bloods for FBC, UEC, CK, Coagulation studies & D dimer.

• Take swab for SVDK but do not test unless patient is envenomed.

• Ensure antivenom is available (Antivenoms are stored in the green zone fridge)

• Keep PBI in place.

If the patient remains stable and there is no clinical or biochemical evidence of envenomation, PBI can be removed but the patient needs to be monitored in a critical care area. If there is deterioration, immediately reapply PBI and contact the clinical toxicologist on call (via the Poisons Information Centre on 131126), as antivenom may need to be administered. If there are signs of systemic envenomation, administer polyvalent antivenom.

If the patient remains stable, further bloods are obtained (Coagulation studies and CK) 1-hour post-bandage removal. If these results are within normal limits and the patient shows no signs of envenomation, the patient is to be admitted to ESSU for further bloods and observation. These bloods (coagulation test and CK) are to be repeated at 6 hours post bite and 12 hours post bite (not post PBI removal).

If pathology is within normal limits and patient shows no signs of envenomation after the 12 hours bloods are reported, the patient can be discharged home, provided it is during daylight hours, as subtle neurotoxicity can be missed overnight.

Treatment of envenomation

• If the patient shows clinical or biochemical signs of envenomation, notify senior emergency doctor immediately.

• Move patient to resuscitation area, apply full non-invasive monitoring while attending to ABC assessment.

• Contact clinical toxicologist on call regarding choice of antivenom. The choice of antivenom is dependent of the clinical presentation as well as geographical knowledge of local snakes. ALL envenomed patients must be discussed with a clinical toxicologist.

• Notify pathology to process SVDK.

• Administer appropriate antivenom. In cases of severe envenomation, time is critical and SVDK is unlikely to be helpful, consider administration of 1 ampoule of polyvalent antivenom.

• Release PBI after antivenom has been administered.

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• All patients who have received antivenom need admission for further observation and repeat bloods (FBC, UEC, Coagulation studies, CK, D Dimer) at 6, 12, 18 and 24 hours post bite to check for recovery of coagulopathy and development of complications such as renal impairment. Patients who require respiratory support and/or invasive support are admitted to paediatric intensive care unit (PICU). All other patients can be admitted to ESSU, following discussion with clinical toxicologist.

ALERT

All cases of snakebite with signs of envenomation must be discussed with a clinical toxicologist. A clinical toxicologist can be contacted by contacting the Poisons Information Centre on 13 11 26.

ADMINISTRATION OF ANTIVENOM:

• All antivenoms are administered intravenously.

• The dose of antivenom is NOT weight dependent. One vial of the appropriate antivenom is sufficient to treat envenomed patients (4).

• Antivenom is to be diluted 1:10 with sodium chloride 0.9% and is given over 15 to 30 mins. For larger volumes or in small children, dilution can be 1:5.

• There is no role for redosing of antivenom.

ALERT

The use of antivenom is associated with risk of anaphylaxis

Treatment of anaphylaxis and allergic reaction to antivenom The use of antivenom is associated with high rates of acute systemic hypersensitivity (approximately 23% of patients, although it is only severe in 7%). There is no role for use of any premedication such as steroids, antihistamines or adrenaline when administrating antivenom.

In case of anaphylaxis, modification of standard of anaphylaxis guidelines is recommended due to the risk of coagulopathy (see table 4).

Table 3: ABSOLUTE AND RELATIVE INDICATIONS FOR ANTIVENOM1

ABSOLUTE INDICATIONS: • Reported sudden collapse, seizure or cardiac arrest • Abnormal INR • Any evidence of paralysis, with ptosis and/or opthalmoplegia being the earliest

sign RELATIVE INDICATIONS:

• Systemic symptoms (vomiting, headache, abdominal pain, diarrhoea) • Leucocytosis • Abnormal APTT • CK level > 1000 U/L

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All patients who have received antivenom should receive counselling prior to discharge to follow up with their GP. Patients should also be counselled on the risk of serum sickness, which usually presents with a rash and flu-like symptoms approximately 10-14 days post administration of antivenom. The use of steroids (prednisolone 1mg/kg) for 5 days may reduce the risk of serum sickness.

Consultation Key stakeholders who reviewed this version:

Dr Colin Page, Clinical Toxicology Unit, Princess Alexandra Hospital

Dr Katherine Isoardi, Clinical Toxicology Unit, Princess Alexandra Hospital

Dr Deborah Shellshear, Senior Medical Officer, LCCH

Dr Samantha Fairless, Fellow Emergency Services, LCCH

Dr Nandini Choudhury, Fellow Emergency Services, LCCH

Carol Wylie, Manager Queensland Poisons Information Centre

Table 4: MANAGEMENT OF IMMEDIATE REACTIONS TO ANTIVENOM1

1 Stop antivenom infusion. Many reactions will resolve with this step, and the infusion can then be restarted at a slower rate.

2 Lie patient flat, commence high-flow oxygen, support airway and ventilation if required. 3 For hypotension, give rapid infusion of sodium chloride 0.9% (20 mL/kg).

Severe antivenom reactions with hypotension will have reduced venous return; supine posture and fluid resuscitation are essential.

4 For hypotension, hypoxaemia, wheeze or upper airway obstruction, give intramuscular adrenaline (0.01 mg/kg to a maximum of 0.5 mg). Alternatively, those experienced with intravenous infusions of adrenaline may go straight to Step 5.

5 Consider a cautious intravenous infusion of adrenaline — avoid blood pressure surges. Patients with envenoming may be severely coagulopathic, and high blood pressure may cause or worsen intracerebral haemorrhage. Some patients can have exaggerated hypertensive responses to intramuscular bolus adrenaline, especially to second doses. If there is no response to Steps 1–4, consider starting a cautious and closely monitored intravenous infusion of adrenaline, which can be reduced as soon as blood pressure starts to recover, preventing blood pressure surges. Use 1 mg in 100 mL by infusion pump: start at 0.5 mL/kg/h and titrate according to response; monitor blood pressure every 3–5 min (using the arm opposite to the infusion). Be aware that as the reaction resolves, adrenaline requirements will fall, the blood pressure will rise and the infusion rate will need to be rapidly reduced.

6 For persistent hypotension, repeat normal saline bolus. 7 For bronchospasm, consider nebulised salbutamol. 8 For upper airway obstruction, consider nebulised adrenaline. 9 Seek further advice from a National Poisons Information Centre consultant.

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Definition of terms

Term Definition Source PBI Pressure bandage with immobilisation

CK Creatine kinase

SVDK Snake Venom Detection kit

INR International normalise ratio

APTT Activated partial thromboplastin time

ESSU Emergency short stay unit

VICC Venom induced consumptive coagulopathy

IV Intravenous

FBC Full Blood Count

UEC Urea, electrolytes, Creatinine

POC Point of care

References and suggested reading 1. Isbister, G., Brown, S., Page, C., McCoubrie, D., Greene, S. and Buckley, N. (2013). Snakebite in Australia: a

practical approach to diagnosis and treatment. The Medical Journal of Australia, 199(11), pp.763-768.

2. Murray L, Daly F, Little M Cadogan (2015). Toxicology Handbook, 3rd ed.

3. Management of snakebite [revised 2012 June]. In: eTG complete [internet]. Melbourne: Therapeutic Guidelines Limited; 2013 July.

4. Clinical Module, Snakebite Toxicology, Princess Alexandra Hospital Emergency Department, Feb 2017.

Guideline revision and approval history

Version No. Modified by Amendments authorised by Approved by

1.0 Dr Jason Acworth, Director Paediatric Emergency Department

Divisional Director, Critical Care

Executive Director Medical Services

Keywords Snake bite, myotoxicity, SVDK, detection kit, 00725

Accreditation references

NSQHS Standards (1-10): 1, 3, 5, 7 EQuIPNational Standards (11-15): 12, 15

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Appendix 1: Snake bite clinical pathway record

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Appendix 2: Summary management of snake bite

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Reproduced with permission from Toxicology and Wilderness Expert Group. Summary management of snake bite (Figure 17.3) [revised 2012]. In: eTG complete [Internet]. Melbourne: Therapeutic Guidelines Limited; 2017 Mar.

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