Analgesia and Procedural Sedation Module

Cite this article as:
Team DFTB. Analgesia and Procedural Sedation Module, Don't Forget the Bubbles, 2020. Available at:
TopicAnalgesia and procedural sedation
AuthorLauren Shearer
DurationUp to 2 hours
Equipment requiredNone
Case: pain assessment and the analgesic ladder
Pain assessment and the analgesic ladder: discussion
Case: other analgesic considerations
Other analgesic considerations: discussion
Advanced case: entonox sedation + adjuncts
Entonox sedation + adjuncts: discussion
Advanced case: ketamine sedation
Ketamine sedation: discussion
  • Pre-reading
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Sim scenario (30-60 mins)
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline for sharing admission criteria.

Lily, 4 years old, presents to the ED with her mother after falling from a scooter whilst in the park. She is holding her arm and not using it. There is no obvious gross deformity.

How would you do a pain assessment in this age category?

What would be the optimum analgesia choice based on a severe pain score?

What other methods or non-pharmacological adjuncts can be used?

When should we reassess the pain?

Pain scores

See RCEM Pain in Children – Best Practice Guidance for a guide on how to assess pain.

Consider different assessment tools:

  • FLACC (Face, legs, activity, cry, and consolability)
  • Wong Baker Faces
  • Visual analogue scale

Analgesic ladder

See the analgesic ladder (RCEM guidance above and the WHO pain ladder).

Adjuvants should be considered in all steps of the ladder.

Bottom of the ladder is the most commonly used paracetamol (at 15mg/kg/dose) and non-steroidal anti-inflammatory drugs (NSAIDs). Paracetamol is an antipyretic and weak analgesic. It is used for the treatment of mild pain and fever associated with a sore throat or illness. But we should avoid oligo-analgesia and use the right drug for the right kind of pain.

Moving up the ladder are weak opioids like codeine. Codeine (an inactive compound of morphine) is no longer recommended for the management of acute moderate pain, particularly in children under 12 years with obstructive sleep apnoea or for post tonsillectomy procedures. Codeine must be metabolised by the cytochrome P450 enzyme 2D6 to the active compound, morphine, to relieve pain. Poor metabolisers of codeine may metabolise only up to 15% of the morphine concentration, receiving little or no analgesia from codeine. Ultra rapid metabolisers may metabolise up to 50% more morphine than normal metabolisers – which is potentially life threatening.

Children with moderate to severe pain should receive opioids together with non opioids. Morphine, oxycodone, hydromorphone are all active compounds that do not require the enzyme conversion to provide analgesia. Fentanyl, a synthetic opioid, has few, if any cardiovascular side effects. This is in contrast to morphine which may exacerbate hypotension with its vasodilatory effects. So in haemodynamically unstable children, fentanyl may be the preferred choice for acute pain management.

What about IN fentanyl?

It’s easy to use, it’s needle-less, and decreases the overall need for utilisation of IV or IM routes which is a positive change in parent and patient satisfaction. It bypasses first pass metabolism permitting rapid and predictable bioavailability (compared with oral and intramuscular routes) and offers direct CSF delivery via the nose- brain pathway route

The maximum volume of IN medication permitted is 1ml per nostril and in cases of nasal trauma or septal defects, IN Fentanyl of course cannot be used. Rule of thumb, the IN dose is 2-3 times the IV dose.

Administer intranasal medications in the sniffing position. Lie the patient flat with occiput posterior, put patient in the sniffing position, seat the mucosal atomizing device cushion in the nostril, aim toward the pinna of the ear, and shoot fast – you have to push the drug as fast as you can to atomize the solution.

IN medication can be used for sedation, anxiolysis, pain control and seizure management. A 2014 Cochrane review on intranasal fentanyl concluded that it can be an effective analgesic for children aged 3 years and above with acute moderate to severe pain. Studies have demonstrated INF to result in decreased time to medication administration and equivalent pain control when compared to IV morphine, oral morphine or IV Fentanyl. IN Fentanyl (1.5mcg/kg) has become an excellent alternative to morphine in the ED, it has a greater safety profile and is easily available in the ED.

What about IN Ketamine?

How does it compare to IN Fentanyl? One study demonstrated a similar pain reduction in children with moderate to severe pain from an isolated limb injury in the Paediatric ED, although the sample size was small and there was no comparator or placebo group. Adverse effects were more frequent with ketamine; however, these were all relatively mild (drowsiness and dizziness). Also, practically speaking, pain control doses for the IN Ketamine route at 1mg/kg mean that volumes for most children weighing above 10kg will exceed 1ml per naris if the ketamine concentration 10mg/ml is used.

What about IN Dexmedetomidine?

An alpha-2 receptor agonist (like clonidine), does not markedly decrease blood pressure. Dexmedetomidine targets receptors in the CNS and spinal cord, and so it provides deep sedation, with very minimal blood pressure effects. It induces a sleep-like state. In fact, EEGs done under dex show the same pattern as seen in stage II sleep. Dexmedetomidine is safe, if titrated, and does not depress airway reflexes or respiration. Dose is 2.5 mcg/kg IN, and can add another 1 mcg/kg if needed. The downside is that it can last 30 minutes or more, but it may be a good choice for an abdominal ultrasound or CT head.Inflicting Pain with an IV to relieve pain is not something that makes sense to young children. IN medication offers pain relief prior to getting intravenous access and can even obviate the need for IV access if definitive care such as a cast, suturing, reduction of bony injuries can be done during the duration of action of the IN medication.

Consider non-pharmacological adjuncts

It is important these are thought about in conjunction with pharmacological techniques. These include:
Play specialists

  • Distraction techniques
  • Music
  • Games
  • Don’t forget the Bubbles

Immobilisation of injuries


  • Right people
  • Right place  
  • Right time

Parental/carer anxiety


Sucrose, and non-nutritive sucking interventions exert analgesic effects independent of the opioid pathway. Swaddling/facilitated tucking (preterm) and skin to skin care significantly increase B-endorphin levels.

Rocking/holding neonates and breastfeeding during minor procedures have all been shown to decrease objective measures of pain such as heart rate and crying.


Pain should be assessed on arrival and then monitored throughout their time in the emergency department and if appropriate beyond. Children in moderate and severe pain should have their pain reassessed within 60 minutes of receiving analgesia.

Frank, 8-years-old, was playing in the street with friends and fell over. He cut his knee on some broken glass and sustained a 4 cm laceration over his patella. An x-ray shows no foreign body and no fractures. The knee is swollen and the laceration requires suturing. On pain assessment he is reporting mild pain.

What are your initial considerations?

What are the options for cleaning and closing?

Don’t forget oral analgesics (as above) and a full assessment for other injuries.

LAT gel (lidocaine, adrenaline and tetracaine)

  • Unsuitable for under 1s
  • Takes 20-30 minutes to work
  • Skin will blanch when ready
  • Max dose: 2 mls for 1 -3 year; 3 mls for >3 years
  • Not for use on: mucous membranes; extremities; wounds >8 hours old
  • Can be used in conjunction with local anaesthetic infiltration
  • Max dose not to exceed 5mg/kg

Local anaesthetic infiltration

  • Inject slowly to reduce pain
  • Small gauge needle to reduce pain
  • Doses: 3mg/kg lidocaine

Other topical agents (not for this case specifically):

EMLA cream (lidocaine 2.5% and prilocaine 2.5%) is effective at numbing the tissue below intact skin to a depth of 6-7mm if left on for 30-60 min but does cause vasoconstriction which can be problematic if looking to cannulate.

LMX4, a topical liposomal 4% lidocaine cream like EMLA has full effectiveness by 30 minutes.


  • Play specialist
    Distraction techniques appropriate to age
  • Preparation of the child and area
  • Quiet setting
  • Parental/carer involvement
  • Using appropriate language

Freddie, 9 years old, attends the emergency department after falling from the monkey bars. He has sustained a displaced and angulated supracondylar fracture. He has some tingling at the fingers in the ulna distribution and therefore requires urgent manipulation. You decide to use nitrous oxide.

Do you need any pharmacological adjuncts?

What about non pharmacological?

What other considerations should be made?

Nitrous oxide – mechanism

Nitrous oxide provides anaesthesia, anoxiolysis and some mild amnesia but offers limited analgesia. Administration of analgesic supplements is recommended. Many papers including the FAN study demonstrate the safety and efficacy of co-administering intranasal fentanyl. Other analgesics can also be safely used.

Delivery methods

There are two methods of delivering nitrous oxide, piped nitrous oxide and Entonox. Piped nitrous oxide can provide variable concentrations and can be titrated to response, whereas entonox is a fixed 50/50 mix of nitrous and oxygen and comes in canisters. The canister is set up with a demand value that needs to be overcome with a deep breath; this can be difficult for under 5’s.  You should see onset of effect in 30-60 seconds with the peak effect at 2-5 minutes. Offset of effects is similar at 2-5minutes, 100% oxygen should be applied during this time post procedure to avoid diffusion hypoxia.

Side effects

Side effects are minor and transient but include:

  • Nausea
  • Vomiting (6-10% children receiving 50% dose). Increases incidence with higher dose, longer duration and concurrent opioid use. Consider prophylactic antiemetic if child has history of nausea or vomiting.
  • Dizziness
  • Nightmares


Nitrous oxide diffuses through tissues more rapidly than nitrogen alone and can expand in air containing spaces within the body, so it is contraindicated in:

  • Pneumothorax
  • Pneumocephalus
  • After diving
  • Gastrointestinal obstruction

Nitrous oxide inactivates the vitamin B12 dependent enzyme, methionine synthase and can deplete the B12 stores.  Therefore caution is advised in those at risk of vitamin B12 deficiency (vegetarians, patients with gastrointestinal disorders and those taking regular H2 receptors and proton pump inhibitors)

Monitoring and staffing

Despite the absence of use of intravenous sedative drugs, it is best practice to manage this patient in a high dependency setting, with monitoring including; respiratory rate, heart rate and oxygen saturations and at least 2 members of staff where one’s job is entirely focused on the sedation and monitoring of the child.

Guided imagery

Guided imagery would work well in this setting with a trained practitioner.  This is a process where a variety of techniques can be used such as simple visualisation, story telling, direct suggestion imagery and fantasy exploration to elicit a physical response such as a reduction in pain, stress or anxiety.

Lola, 2 years old, has fallen in the playground and sustained a laceration to the forehead. Lola had an ice cream after the incident in an attempt to settle her. She has no past medical history and was born at term. Can she have procedural sedation in the department? What are the considerations?

What drugs do you need for the sedation? Should you use any adjuncts with the ketamine? Are there any emergency drugs you should have available?

There are no contraindications and you decide to go ahead with ketamine sedation, during the procedure whilst full monitoring in place the CO2 trace is lost.  What is your structured approach to management of this scenario?


A through pre sedation assessment is required to assess ASA grade, examine airway anatomy and illicit any contraindications listed below


Multiple studies have shown that fasting does not reduce the risk of aspiration or increase the risk of adverse events and the 2020 updated guidelines for ketamine sedation in the ED have echoed this. They advised that the fasting state should be considered in relation to the urgency of the procedure, but recent food intake should not be considered a contraindication to ketamine use. 


RCEM states the procedure should be carried out in an area with immediate access to full resuscitation facilities; three practitioners should be present throughout, one for the sedation, one for the procedure and one for monitoring and assistance. The updated 2020 guidance has included capnography in the mandatory monitoring required along with heart rate, ECG, blood pressure, respiratory rate and oxygen saturations. While there is no evidence that shows that capnography reduces the incidence of adverse events, there are studies that show capnography decreased the incidence of hypoxia and respiratory events. 


Oxygen should be given prior to the procedure if possible and during to reduce the time to de-saturation should an adverse event occur.


Ketamine is a NMDA receptor antagonist. It is a dissociative anaesthetic, a potent analgesic and amnesic. Ketamine induces a trance like state, often with the eyes open. It maintains the airway reflexes and maintains cardiovascular stability.

The RCEM accepted dose is 1mg/kg over 60 seconds. A rate of 60 seconds reduces the incidence of adverse events such as laryngospasm. A top up dose of 0.5mg/kg can be used if necessary. Onset is within 1 minute and will elicit a horizontal nystagmus and a loss of response to verbal stimuli. The HR, BP and RR may increase slightly. Sedation will wear off after 20 minutes and full recovery should occur by 60-120 minutes. RCEM no longer advise the use of IM ketamine as they suggest it is safer to have IV access available from the start of the procedure should an adverse event occur.


Midazolam: a 2018 BestBets review looking at 6 studies including 2 RCTs has shown that prophylactic benzodiazepines do not significantly decrease the incidence of emergence delirium and they in fact can increase the risk of adverse events, so they should not routinely be given prophylactically. However, midazolam can be used to treat severe emergence, especially in older children. (Aliquots of IV 0.05-0.1mg/kg can be given)

Atropine: atropine was previously used prophylactically to reduce secretions however there is no evidence to support its routine use to prevent laryngospasm or other adverse airway events and again it may increase the rate or adverse events. (Green et al)

Ondansetron: may be appropriate for patients at high risk of vomiting due to ketamine’s emetogenic properties. High-risk groups include those with previous nausea/vomiting during sedation/anaesthesia, older children, those who have received opioids or where ketamine is given intramuscularly. Caution should be used in those at risk of long QT.

Emergency drugs: RCEM suggests key resuscitation drug dose calculations should be done prior to the procedure and these should be accessible, however, no specific drugs are recommended. We suggest that WETFLAG dosing should be done along with the dose calculated for suxamethonium (1.5mg/kg for RSI).


Complications are rare with ketamine. A recent study by Bhatt et al in 2017 (6,760 patients across 5 sites in Canada) looking at propofol, ketamine, propofol/ketamine and ketamine/fentanyl, ketamine alone recorded the lowest serious adverse events at 0.4%. Green et al (2009) showed a 1% risk of noisy breathing requiring airway repositioning, a 0.3% risk of laryngospasm and 0.02% risk of intubation being required.

The capnography trace is there to provide early warning of potential or impending airway and respiratory adverse events. A loss of capnography trace indicates apnoea or obstruction. First check the equipment and monitoring is still in place then check for chest wall movement. If the chest wall is not moving then there is central apnoea. If there is chest wall movement there is obstruction. Airway manoeuvres will relieve obstructive apnoea but will not relieve laryngospasm.

10-year-old boy fell from the top of the climbing frame, landed awkwardly on his left ankle. Primary survey shows no other injuries except obvious deformity of the left ankle.


Summary: procedure appropriate for sedation – post procedure simple airway issues due to obesity

Faculty required: operator/Voice of patient/Nurse in scenario

Vitals: HR 120, BP 105/60, Sats 99%, RR 20, ETCO2 4.2, ECG NSR

To establish…

Neurovascular compromise of the foot, CRT delayed

PMH: nil

BH: term, nil complications

DH: nil

NKDA, UTD with immunisations

Last ate 2 hours prior

Candidate should…

  • Check full medical history
  • ASA status
  • Airway assessment (loose tooth, excess body fat)
  • Ensure appropriate setting (RESUS)
  • Appropriate equipment and monitoring (ECG, EtCO2, Sats, HR, RR, BP, suction, tilting table, resuscitation facilities)
  • Describe consent
  • WETFLAG calculations plus emergency drug calculations
  • Choice of appropriate drugs and dosing for sedation
  • Ensure appropriate staff
  • Pre-oxygenation
  • Checks patient during procedure

Post procedure end tidal CO2 trace is lost (due to obesity)

  • Checks equipment
  • Chest wall movement
  • Simple patient positioning and airway manoeuvre opens the airway and CO2 trace returns  
  • Describes post procedure monitoring

Learning points

  1. Emphasis on appropriate preparation
  2. Systematic approach to adverse events and when to anticipate them

Question 1

When should you assess a child’s pain and document a pain score in the emergency department when they present with an injury?

A: Wait until the child is seen by a doctor before assessing pain

B: At triage

C: Immediately after giving oral analgesia

D: Within 60 minutes of receiving analgesia for moderate and severe pain

E: When the child or the child’s parents informs you they are in pain

Answer 1

The correct answer is B + D.

A child’s pain should be assessed on arrival in the emergency department, and should be treated appropriately in a timely manner (within 20 minutes for moderate and severe pain). Pain should also be re-evaluated within 60 minutes of receiving analgesia for moderate and severe pain. This process should be repeated for all subsequent doses of analgesia. Reviewing pain should take into account peak of onset for the analgesia given; as such oral analgesics will not work immediately.

Question 2

Which of the following predict possible airway difficulties in children?

A: C-spine immobilisation

B: Premature birth requiring NICU

C: Trisomy 21

D: Mouth breathing or frequent drooling

E: Reduced mouth opening

Answer 2

All are true.

A through pre assessment prior to sedation should be done to elicit any potential complications and also decide on appropriateness of sedation in the emergency department.

A formal airway assessment should include:

  • Mouth opening
  • Assessment of dentition for loose and protruding teeth
  • Tongue size
  • Presence of soft tissue masses in the mouth
  • Mandible size
  • Neck mobility
  • Tempero-mandibular joint mobility

A review of the child’s medical history should also include, congenital abnormalities, birth complications, previous complications during anaesthetics or sedation, noisy breathing, sleep issues and concurrent upper respiratory tract infections.

Please download our Facilitator and Learner guides

Anaphylaxis Module

Cite this article as:
Kat Priddis. Anaphylaxis Module, Don't Forget the Bubbles, 2020. Available at:
AuthorKat Priddis
DurationUp to 2 hours
Equipment requiredAdrenaline auto-injector if planning a demonstration on a model
Case: anaphylaxis basics
Anaphylaxis basics: discussion
Case: discharging home
Discharging home: discussion
Administering adrenaline
Advanced case: anaphylaxis v allergy
Anaphylaxis v allergy: discussion
Advanced case: anaphylaxis not resolving
Anaphylaxis not resolving discussion
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Sim scenario (30-60 mins)
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

Anaphylaxis is a severe, life-threatening, generalised or systemic hypersensitivity reaction.

Anaphylaxis is described as

  • Sudden onset and rapid progression of symptoms 
  • Life-threatening Airway and/or Breathing and/or Circulation problems 

*Skin and/or mucosal changes (flushing, urticarial, angioedema) are absent 20% of cases*

Angioedema is similar to urticaria but involves swelling of deeper tissues, most commonly in the eyelids and lips, and sometimes in the mouth and throat.

There can also be gastrointestinal symptoms (e.g. vomiting, abdominal pain, incontinence).

Fatality <1%, increased in those with pre-existing asthma. Approximately 20 anaphylaxis-related deaths in the UK every year. 

From a case-series (resus council), fatal food reactions cause respiratory arrest typically after 30–35 minutes; insect stings cause collapse from shock after 10–15 minutes; and deaths caused by intravenous medication occur most commonly within five minutes. Death never occurred more than six hours after contact with the trigger. 


What is an allergy?

It is the body’s response to an external ‘allergen’. An unnecessary immune response to an innocuous substance. 

Common allergens/triggers include: • Food: nuts, milk, fish • Venom: wasp, bee • Drugs: antibiotics, anaesthetic drugs • Contrast media • Latex

Reactions are either delayed type IV or immediate type I. IgE-mediated allergy is broadly characterised as a Type 1 hypersensitivity. Other hypersensitivity reactions (II, III and IV) are mediated by other antibody classes, immune cells or cellular components. Non-IgE mediated reactions typically cause symptoms to appear more slowly, sometimes several hours after exposure. 

Allergy is increasing in prevalence. Theories for this include the ‘Hygiene Hypothesis’, the idea that increased exposure to microorganisms correlates with a decreased tendency to develop allergy and more recently the ‘Old Friends Mechanism’ which links the tendency to develop allergy to an individual’s microbiome (collection of microorganisms living in and on an person’s body). 

Interestingly, kids in developing countries have a decreased allergy prevalence, thought to be because of less sanitation, more exposure to microbes and increased time spent outdoors. 

How do we develop allergic reactions? 

Part 1: Sensitisation

An allergen enters the body and is captured by an antigen presenting cell, that scoops it up and nicely presents it immune cells, particularly T cells (in a similar manner as if the allergen was a foreign invading microbe). Through a number of immune interactions between T cells and B cells, B cells produce allergen-specific IgE antibodies. These get released into the blood, where they bind to mast cells (the major allergy immune cell) as well as other friends like basophils. In some individuals, this can cause a ‘sensitisation’ i.e. the next time their body meets that particular allergen it’s going to go on the offensive. 

Part 2: Re-exposure

Our patient is now carrying allergen-specific IgE bound mast cells. Upon re-exposure, the offensive allergen binds to IgE, causing the mast cells to initiate an aggressive and immediate immune response. 

Mast cells on the attack: 

Mast cells are granular cells, containing many secretory granules that all get released on activation. The binding of IgE causes rapid degranulation, and a shower of inflammatory compounds, including histamine. Result? Local inflammations, and allergy symptoms (see presentation of the patient in anaphylaxis below). 

An 8 year old girl presents after collapsing following attendance at a friend’s birthday party. She was noted to have been eating a sandwich, then promptly developed respiratory distress. On admission with the ambulance crew she is audibly wheezy, with swelling of the tongue and lips.

How would you assess this child?

What is your immediate management?

How much adrenaline do you give and how? Any adjunct therapies to consider?


Usually the parents or child will give a history of exposure to an allergen. This is useful however not essential. If the clinical picture is of anaphylaxis – treat first and seek the provoking agent second!

Life-threatening features of anaphylaxis include:

  • Airway: swelling, hoarse voice, stridor 
  • Breathing: shortness of breath, tachypnoea, wheeze, cyanosis, respiratory arrest 
  • Circulation: pale, clammy, tachycardia, low blood pressure, shock, cardiac arrest
  • Confusion, agitation or decreased level of consciousness can occur due to above problems

Manage according to APLS

  • Remember the ABCDE approach
  • Get senior help 
  • Remove the allergen if possible – remove a stinger, stop IV drugs, but don’t make a patient vomit if suspected food allergy – risk of aspiration. 
  • Maintain oxygen delivery 15l via non-rebreather mask
  • Get monitoring on – and get a BP early
  • If hypotensive then get IV access and bolus 20mls/kg 0.9% sodium chloride

Adrenaline dosing (early and often)

Delayed administration is directly linked with increased morbidity and mortality 

  • Scientific evidence is weak, instead based on what is considered safe and practical. 
  • Adrenaline IM – use 1 in 1000 (or 0.1% – 1mg/ml)
  • The dose is 0.01ml/kg or 0.01mg/kg. Max dose is 0.5ml. 
< 6 years old
150 micrograms IM (0.15 mL)
6 – 11 years old300 micrograms IM (0.3 mL)
>12 years old500 micrograms IM (0.5 mL)
  • Give as an IM injection into the anterolateral thigh. IM provides faster rise in plasma and tissue concentrations than sub-cutaneous route. 
  • Don’t give IV boluses unless there is cardiac arrest. 
  • Can use the patient’s own adrenaline auto-injector if not already used

Adrenaline – mechanism of action

Alpha receptor agonist 

  • Reverses peripheral vasodilation
  • Reduces oedema

Beta receptor agonist

  • Bronchodilation
  • Increased force of myocardiacl contraction
  • Suppresses histamine and leukotriene release
  • Inhibits mast cells – attenuates severity of IgE-mediated allergic reactions. 

Adrenaline – side effects

Normally only occur with IV administration (at which point PICU will be present)

  • Arrythmias
  • Hypertension
  • Pulmonary haemorrhage
  • Intracranial haemorrhage

Adrenaline – duration of action

  • Rapid onset – should see improvement in 5 minutes
  • Duration of action is 15 minutes – beware of rebound

Adrenaline – can I go again?

  • Absolutely – 20% of patients require more than one dose! 
  • By the third dose please call PICU

The patient isn’t getting better. What else do I do?

  • Is the child wheezing? Consider a salbutamol neb 2.5mg/5mg depending on age
  • Antihistamines (H1 and H2 blockers) are a second line treatment and should not delay adrenaline administration! Examples such as chlorpheniramine are useful for urticaria, nasal and ocular symptoms
  • Steroids – think about steroids. 1mg/kg prenisolone (PO) or 4mg/kg hydrocortisone (IV) – but remember slow onset of action. 

Extra tips

  • Keep patient comfortable and minimise distress
  • Ideally have them lying down to aid venous return (hypotension can precipitate cardiac arrest)
  • NICE evidence: Limited evidence from systematic review – consider mast cell tryptase investigations only if reaction is thought to be drug, venom or idiopathic related! Send three timed samples. Immediately after reaction has been treated. 1-2 hours after the start of symptoms. At 24 hours or in convalescence (baseline sample) after the reaction.

A 3 year old presented with a localised erythematous rash after being stung by a bee at a family picnic. His family attended PED where he subsequently developed respiratory distress and he was treated with IM adrenaline. After a couple of hours he was playful and appeared well and his parents want to take him home.

What would you say to the parents?

How would you manage this patient?

What key points make up the discharge planning? 

Biphasic reactions

  • Occur in 6–11% of children.
  • Usually manifest in the first 8 hours after exposure, but may be delayed up to 72 hours.
  • NICE evidence: children who have had emergency treatment for suspected anaphylaxis should be admitted to hospital under the care of a paediatric medical team. No direct evidence from systematic review however in light of risk of biphasic reaction risk, better to keep them in overnight for observation. 
  • All children with suspected anaphylaxis will require risk planning and allergy avoidance advice
  • Corticosteroids have been advocated to prevent protracted and biphasic reactions (no RCT on this). Recent systematic review and meta-analysis (Lee et al) included 27 studies with 4114 anaphylaxis cases, of whom 192 (4.7%) had biphasic reactions. 
  • Steroid administration did not affect the likelihood of a late phase reaction (OR 1.52, 95% CI 0.96 to 2.43). In fact, there was a non-significant trend towards increased risk, (?because steroid use was more common with severe reactions). 
  • Biphasic reactions were more common where hypotension was present at initial reaction (OR 2.18, 95% CI 1.14 to 4.15), but this is unusual in food-induced anaphylaxis. 
  • The median time to onset of biphasic symptoms was 11 (range 0.2–72) hours, that is, 50% of reactions occurred >11 hours after initial reaction. Hence why all children should be admitted. 

Discharging home (RCPCH Pathway)

  • Children and young people at risk of anaphylaxis should be referred to clinics with specialist competence in paediatric allergies. 
  • Children and young people who are at high risk of an anaphylactic reaction should carry an adrenaline auto-injector and receive training and support in its use.
  • They will need 2 auto-injectors – 20% require a second dose
  • Medic-alert bracelet and patient education
  • Further follow up – the most common way to diagnose an IgE-mediated allergy is through a blood test to identify allergen specific IgE or a skin prick test which results in a local inflammatory reaction after administration of the trigger allergen.
  • Oral food challenges – need to have appropriate resus facilities. 
  • AIT – Allergy immunotherapy or ‘Desensitisation’ works by changing the immune system’s response. These changes may include producing less IgE, producing ‘blocking’ IgG antibodies, and producing more regulatory T cells, promoting tolerance and a less active immune response. However, the exact mechanism behind desensitisation is not yet known and it is likely that different patients exhibit different immune profiles following the treatment. Only available for wasps, bees, dust mites and animal dander. Clinical trials for food allergies are on-going.

Can you administer IM adrenaline? (8 minutes)

A 6 year old patient with spina bifida is currently admitted with an LRTI. She has been having a course of amoxicillin for the last week. You are crash bleeped to the ward where she is having her urinary catheter changed by a bank nurse. She is pale and cool to touch, with increased respiratory rate.

What’s going on? Is this allergy? Is this anaphylaxis?

How would you treat it?

What allergy avoidance advice do you give?

  • Initial management: Observations and assess (BP)
  • Initial presentation of anaphylaxis – high safety margin for IM adrenaline
  • Hypotension as a warning sign (absence of a rash) – is it fluid responsive? May require large volumes of fluids. No evidence for crystalline vs colloid. Give 0.9% saline or Hartmanns. 
  • Explore medical history for triggers, explore unusual or uncommon triggers (e.g. exercise as a trigger, consider co-existing triggers e.g. prawns and exercise)

Risk factors for latex allergy

The following are risk factors for latex allergy:

  • Repeated bladder catheterisation 
  • Neural tube defects: Spina bifida 
  • Cloacal abnormalities 
  • Multiple surgical procedures, especially as a neonate 
  • Atopy and multiple allergies 
  • Food allergies: fruit and vegetables including bananas, celery, fig, chestnuts, avocados, papaya and passion fruit are most significant. 
  • Children with a strong or confirmed allergy to banana should be considered allergic to latex and managed accordingly.

Common food triggers for fatal anaphylaxis

The most common food trigger for fatal anaphylaxis in children in the UK is milk, followed by peanut and tree nuts.  While there is broad public recognition of the risks posed by nuts, cow’s milk allergy is often perceived as being less severe. However, milk allergy persisting into school age is often associated with other coexisting atopies (such as asthma) and more severe reactions, particularly in the 30%–40% of milk-allergic children who are unable to tolerate milk in well-baked foods (such as biscuits or cakes). Such exposure often results in delayed reactions which mimic asthma; under such circumstances, it may not be obvious that the child has been exposed to milk. Therefore, always consider anaphylaxis in someone with a known food allergy who has sudden breathing difficulty.

An 8 year old girl presents after collapsing following attendance at a friend’s birthday party. She was noted to have been eating a sandwich, then promptly developed respiratory distress. She has had two epipens with the ambulance crew, and a further dose in PED. You are called as senior support. Her sats are dropping and she is becoming bradycardic.

If the patient isn’t improving after IM adrenaline, what are your next management plans?

How do you prepare for intubation?

What do you do next?

Advanced management

  • Ensure the most senior people are present
  • Contact retrieval services early

Does this child need to be intubated?

  • How would you determine this? 
    • Airway obstruction/cardiovascular collapse
  • Who should be involved in the conversation? Who should perform the intubation?
    • Most senior anaesthetist, ideally with ENT support 
  • What do you do whilst prepping
    • Continue adrenaline – IM and nebulised whilst prepping for intubation
  • What sedation would you use?
    • Choose cardiovascular stable drugs – a drop in BP at this stage can precipitate cardiac arrest. Consider ketamine, fentanyl and rocuronium in 1:1:1 ratios. 
  • What equipment would you use?
    • Have advance and difficult airway trolley prepped and ready
  • What settings would you use?
    • Ventilate as for air trapping/bronchospasm
    • Pressure control (aim PIP <35 cm H2O)
    • Slow respiratory rate (e.g. 10-15 bpm)
    • Long expiratory time (e.g. I:E 1:2)
    • Permissive hypercapnia (aim pH >7.2)
    • PEEP 5 – 10 cm H2O to overcome intrinsic PEEP
    • Consider manual decompression
    • Muscle relax
  • Regular chest physiotherapy and suction for mucus plugging
  • Treat bronchospasm as per asthma guidelines (CATS or local)
  • Watch for pneumothoraces
  • Consider IV adrenaline infusion
  • Consider NaHCO3 for profound/refractory acidosis

IV adrenaline

  • Might need to escalate to IV adrenaline infusion – prescription calculation available on CATS website – ‘in a hurry’ drug chart (see appendix)
  • UK Resus council: No evidence to base a dose recommendation – the dose is titrated to response. Can titrate in presence of continued haemodynamic monitoring. Consider arterial line to enable continuous monitoring. 
  • A child may respond to a dose as small as 1microgram/kg. This requires very careful dilution and checking to prevent drug errors.

Reporting a reaction

All adverse drug reactions should be reported to the Medicine and Healthcare products Regulatory Agency (MHRA) using the “Yellow Card” scheme (found in BNF and MIMS). 

The patient must be referred to an allergist in a defined Regional Allergy Centre. 

All fatal cases of suspected anaphylaxis should be discussed with the coroner.

Question 1

What dose of adrenaline would you give to a 5 year old presenting in suspected anaphylactic shock?

A: 150 micrograms IM (0.15 mL) of 1:1000

B: 150 micrograms IM (0.15 mL) of 1:10000

C: 300 micrograms IV (0.15 mL) of 1:1000

D: 300 micrograms IM (0.15 mL) of 1:10000

Answer 1

The correct answer is A.

IM is always preferred in children owing to its broad safety profile. 1:1000 is the correct concentration. 1ml/kg of 1:10000 IV is the cardiac arrest dose. If the child does arrest then stop using IM and move to the standard APLS arrest dose as per protocol.

Question 2

In order to diagnose anaphylaxis there must be a rash

A: True

B: False

Answer 2

The correct answer is false.

Cutaneous symptoms (most commonly urticaria or ‘hives’) are absent in around 10-20% of anaphylaxis reactions and where present may be delayed in onset. This is consistent with a case series of six paediatric fatalities due to food anaphylaxis, where only one child had evidence of skin involvement: the lack of skin signs may have delayed diagnosis and appropriate treatment with epinephrine, contributing to the fatal outcome.

The Australasian Society of Clinical Immunology and Allergy (ASCIA) recently issued new guidelines, which define anaphylaxis as:

  • Any acute onset illness with typical skin features (urticarial rash or erythema/flushing, and/or angio-oedema), PLUS involvement of respiratory and/or cardiovascular and/or persistent severe gastrointestinal symptoms; or
  • Any acute onset of hypotension or bronchospasm or upper airway obstruction where anaphylaxis is considered possible, even if typical skin features are not present.

These criteria better reflect increasing recognition that cutaneous manifestations are often absent or appear late in near-fatal and fatal anaphylaxis.

Question 3

Antihistamines can be used to treat anaphylaxis initially; epinephrine is only needed if symptoms worsen

A: True

B: False

Answer 3

The correct answer is false.

Histamine is only one of many inflammatory mediators released during anaphylaxis. Oral antihistamines take around 30 min for onset of effect; intravenous chlorphenamine has a faster onset, but can cause hypotension. 

Antihistamines are not effective against anaphylaxis: their prophylactic use during controlled immunotherapy does not prevent anaphylaxis, and any apparent response during acute management of reactions is most likely due to the patient’s own endogenous epinephrine. Antihistamines have now been relegated to third-line therapy in international guidelines; their use is limited to the relief of cutaneous symptoms and should never delay the administration of epinephrine or fluid resuscitation during patient stabilisation.

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Bronchiolitis Module

Cite this article as:
Tessa Davis. Bronchiolitis Module, Don't Forget the Bubbles, 2020. Available at:
AuthorTessa Davis
DurationUp to 2 hours
Equipment requiredNone
Case: treatment options
Treatment options: discussion
Case: escalation to high flow
Escalation to high flow: discussion
Setting up high flow
Advanced case: bronchiolitis vs viral induced wheeze
Bronchiolitis vs viral induced wheeze: discussion
Advanced case: nutrition and intubation
Nutrition and intubation: discussion
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Sim scenario (30-60 mins)
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

A 7 month old infant presents on Day 4 of the illness. He has mild to moderate work of breathing. Sats 95% in air. He is taking around half his normal feeds.

What investigations and treatment options should you consider?

Why doesn’t salbutamol work in this age group?

How do you know when to admit?

See the PREDICT systematic review of all treatments

  • Salbutamol – there is no benefit in using salbutamol in infants with bronchiolitis (and some evidence of adverse effects)
  • Nebulised adrenaline – no clinically useful benefit (there is evidence for temporary effect but not for improvement in outcome)
  • Nebulised hypertonic saline – there is weak evidence of a reduction in length of stay of 0.45 days. However when two studies were removed, both of which used a different discharge criteria than most hospitals, there was no benefit. This is not recommended routinely, although the authors suggest that it should be used only as part of an RCT
  • Glucocorticoids – no benefit
  • Antibiotics – not recommended (The risk of a secondary bacterial infection is very low, and there is potential harm from giving antibiotics)
  • Oxygen – no evidence of benefit in infants with no hypoxia, and low level evidence that maintaining the sats over 91% with oxygen actually prolongs the length of stay. There are no reports of long-term adverse neurodevelopmental outcomes in infants with bronchiolitis, however there is also no data on the safety of targeting sats <92%. Commence oxygen therapy to maintain sats over 91%.
  • Sats monitoring – there is moderate evidence suggesting that continuous sats monitoring increases the length of stay in stable infants
  • High flow – there is low to very-low level evidence of benefit with high flow
  • Chest physiotherapy – not recommended
  • Saline drops – routine saline drops are not recommended but a trial with feeds may help
  • Feeds – both NG and IV are acceptable routes for hydration

See Beta receptor mythbusting (from

A 6 month old infant presents on Day 3 of the illness. She has moderate to severe work of breathing. Sats are 91% in air. She is struggling to feed at home.

What management options would you consider?

Discussion around high flow

See the PARIS Paper

This is the biggest and most robust trial yet done to assess the value of high-flow in bronchiolitis. The primary outcome shows that there is a role for high-flow in the non-ICU management of this disease. Importantly PARIS has shown in a large cohort of children that high-flow, when used within the parameters of the trial protocol, does not lead to an increase in adverse events which in-turn suggests the increased patient:nurse ratios for kids on high-flow that are often mandated by hospital policies may not be necessary (depending on the severity of disease of course). Some caution must be used around the potential for erroneous use of the high-flow circuits themselves and the interpretation of early warning scores in the context of high-flow use.

PARIS was supported with significant nursing education resources potentially reducing errors to a level that were below what could be expected with the standard resourcing of mixed EDs and other environments where high-flow use in children may be infrequent. As with many grey areas in medicine protocols as to how we use high-flow vary by institution with little more than opinion to guide them.

Though neither the intention nor the conclusion of this paper in showing the progress of such a large number of children on high-flow, this trial also provides a basis for more robust decision making around how we use high-flow itself.

Discussion around NG v IV fluids

NICE feeding guidance

  • Give fluids by nasogastric or orogastric tube in children with bronchiolitis if they cannot take enough fluid by mouth.
  • Give intravenous isotonic fluids (see the NICE guideline on intravenous fluids therapy in children) to children who: do not tolerate nasogastric or orogastric fluids; or have impending respiratory failure.

Do you know how to set up high flow? (8 minutes)

How to set up Airvo 2 (Optiflow)  (3.5mins)

How to use Airvo 2 (6 mins)

You have a 12 month old, with two days of coryza and one day of increased work of breathing symptoms.

How do you manage them?

How do you figure out whether they have bronchiolitis or VIW?

Practically speaking, we know that bronchiolitis and viral induced wheeze have two quite different management pathways, but it is not as if a child moves from being 12 months old to 13 months old and therefore cannot have bronchiolitis (or vice versa for viral induced wheeze). These conditions as previously mentioned, exist on a spectrum. 

What would you look for on history and examination to help you decide?

  • What has been the onset of symptoms? Progressive over days is most consistent with bronchiolitis. Onset of wheeze and respiratory distress over hours is most consistent with bronchospasm (viral induced wheeze).
  • What has been the pattern of their work of breathing? 
  • How significant is the work of breathing? 
  • What are the auscultation findings – is there presence of focal findings? Wheeze? Crackles? 
  • Is this affecting the child functionally with feeding or sleeping difficulties?
  • If auscultation is suggestive of possible viral induced wheeze or at least, a component of wheeze that may be responsive to bronchodilators (If wheeze is present and no crackles or focal findings) and presuming the child has more than just mild work of breathing -then we suggest this may be a possible candidate for viral induced wheeze.  

At what age would be appropriate to consider a trial of ventolin for potential viral induced wheeze vs bronchiolitis? 

  • (Note – This is a good opportunity to survey your team and colleagues to see what the practice is at your local department). 
  • Regarding this grey area question, in Australian practice, some clinicians will trial salbutamol for potential viral induced wheeze if the child is 12 months or older. Other doctors may wish to trial if the child is slightly younger (e.g. from 10 months) if they have a strong family history of asthma and atopy or if they have had previous ventolin use reported by their family with good effect. The younger the child is, the less likely that the story and case is to fit viral induced wheeze.

If you have decided to trial ventolin – would you give only an initial 6 puffs and reassess or would you give a burst (x puffs x 20 minutely x 3) ?

It would be prudent to give 6 puffs (or do you use another number?) and reassess following to see if there is any improvement or change.

You’ve started high flow 2L/kg for a four month old with bronchiolitis, moderate work of breathing and saturations of 88% and titrated FiO2 up to 30% to maintain saturations. However they are still intermittently desaturating so you titrate them up to 40% FiO2.

They have ongoing work of breathing with a respiratory rate of 60-70.

What are your next steps?

How would you reassess the patient?

Consider revisiting history, respiratory examination and consider adjuncts to assessment such as a capillary or venous blood gas.

Is their nutrition optimised to minimise work of breathing?

  • For example, Do they have an NG tube on free drainage, are they nil by mouth and on IV fluid support at ⅔ maintenance
  • Are their family actually compliant with this or have also been feeding them via a bottle? 
  • Are they working harder to breathe because they are getting “hangry” and might actually tolerate a continuous NG or comfort feed?

Have you accurately assessed the effect of the intervention (HFNP)?

  • Consider whether the HFNP has led to no change, improvement and then deterioration or simple worsening of symptoms due to patient distress.
  •  If no improvement was observed on commencement – it may be worth de-escalating them – ie. lower flow rates or low flow nasal prongs

What could be missing?

Consider your confidence of whether you have the right diagnosis or if there is need to assess for a secondary pathology such as pneumonia, foreign body, cardiac contribution? Do you need to further investigate with bloods, CXR? Do you need to append your management and provide antibiotic coverage? Do you need to assess for a complication from treatment e.g. pneumothorax.

Escalation options

  • Have you sought a senior review/notified the admitting paediatrician?
  • Do you need an ICU consult, NETS consult or retrieval to a tertiary centre?
  • How long are you comfortable to wait to see if there is a response to high flow?

Non invasive ventilation – switching to CPAP

  • What settings would you start on?
  • Where could you move up to (in terms of peep, FiO2)
  • How soon would you reassess – what are you looking for?

Does this child need to be intubated?

  • How would you determine this?
  • Who should be involved in the conversation? Who should perform the intubation?
  • What sedation would you use?
  • What equipment would you use?
  • What settings would you use?

Question 1

In bronchiolitis, children do not respond to salbutamol because:

A: They don’t have beta receptors until they are older.

B: The beta receptors are immature and do not begin functioning correctly until the child is older.

C: The large amount of secretions interfere with it and prevent it binding to the receptors

D: There is no bronchospasm for the salbutamol to act on.

Answer 1

The correct answer is D.

All humans have beta receptors. Foetuses develop them from around 15 weeks gestation and are therefore born with them. Developing beta receptors after 1 year of age is a common paediatric myth! In fact, in bronchiolitis, there is no bronchospasm in the same way as there is in viral induced wheeze. Bronchiolitis is a illness developing gradually over 4 days and then slowly improving. Patients have increased mucous rather than bronchospasm, which does not respond to a bronchodilator.

Question 2

A 3 month old baby presents to ED with coryza, cough, and poor feeding. Breastfeeding is going ok, but the baby is feeding for shorter periods, more frequently than usual. She is having wet nappies as normal. Saturations are 93% on room air, RR is 62, and there is moderate subcostal recession with some nasal flaring. Which of the following is an indication to admit this baby to hospital?

A: The reduced breastfeeding

B: The oxygen sats

C: The work of breathing

D: The age of the baby

Answer 2

The correct answer is C.

The criteria for admission usually are:

  • feeding less than half of usual, or less wet nappies
  • saturations less than 92% on air
  • increased WOB
  • apnoeic episodes

Risk factors such as:

  • Ex-prem
  • Age less than 12 weeks or less than 37 weeks CGA
  • history of lung disease or congenital heart disease or neurological problems
  • smoke exposure

In clinical practice, you would use your judgement to assess if hospitalisation was necessary. Social concerns should always be considered.

In this case, the baby is maintaining good urine output and the feeds, although shorter, are more frequent. The age alone is not an indication for admission. Obviously, an O2 requirement would be an indication for admission but most units would consider sats of 92% or less as reduced. There is significantly increased work of breathing with recession and nasal flaring, however, so this would be the main indication for admission.

Question 3

You have a 10 month old baby with bronchiolitis who is to be commenced on high flow. Which of the following is false?

A: Nasal prongs size should be estimated based on the width of the patient’s nostrils.

B: Patients can be NG fed immediately once on high flow. 

C: High flow improves the functional residual capacity.

D: The humidified oxygen help clearing mucous secretions.

Answer 3

The correct answer is B.

Patients on high flow will likely need an NG inserted due to abdominal distention, but should usually not be fed for the first couple of hours on high flow. The aim of high flow is to provide humidified, high flow to improve clearance of secretions and to increase the functional residual capacity. Together this should reduce the work of breathing.

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