Perioperative management of the child with asthma

Learning objectives.

By reading this article, you should be able to:

• •Understand the pathophysiology and classification of asthma.
• •List the common medications used to treat acute and chronic asthma in children.
• •Assess and anaesthetise a child with asthma for elective surgery.
• •Describe the management of a child with an acute exacerbation of asthma and bronchospasm under anaesthesia.

Key points.

• •Asthma is an umbrella term for a heterogeneous group of reactive airway disorders that have a common clinical presentation.
• •Management should focus on symptom control; the majority of patients achieve control with regular inhaled corticosteroids.
• •Poorly controlled asthma is the biggest risk factor for intraoperative bronchospasm and postoperative complications.
• •Understanding asthma in children will help to reduce perioperative complications.

Definition and pathophysiology of paediatric asthma

A total of 1.1 million children in the UK are treated for asthma, and the worldwide prevalence is increasing.¹ Children with asthma have a higher risk of perioperative respiratory adverse events (PRAEs).² Identifying and optimising asthma control in children presenting for elective surgery will reduce harm. Admissions to hospital for asthma are highest in preschool children, with no improvement in admission rates in the past decade despite novel treatments. There is increasing evidence of a close association between poor asthma control and severe life threatening episodes in children, often with associated mortality. Anaesthetists are involved in the management of these patients in the perioperative and emergency settings plus there have been significant changes in asthma guidelines over the past decade.This review outlines the pathophysiology of childhood asthma, common treatments used and the management of bronchospasm under general anaesthesia (GA).

Definition

Asthma is an umbrella term used for a group of heterogeneous disorders characterised by chronic airway inflammation. In susceptible patients this leads to airway hyperreactivity, mucus plugging and bronchospasm causing variable airflow limitation, reversible airway obstruction and respiratory distress. Clinical symptoms include dyspnoea, cough (often nocturnal or exercise-induced) and chest tightness. Signs include wheeze, increased work of breathing, hypoxia and, in life-threatening cases, cyanosis and reduced consciousness.

Pathophysiology

Asthma is a multifactorial disease resulting from interactions between genetic, host (e.g. obesity, prematurity, low birth weight) and environmental factors. Similar clinical manifestations (phenotypes) can have different underlying pathophysiological pathways, which can result in differing responses to treatment. Thus endotypes, the mechanisms underpinning phenotypes, are now being elucidated to help individualised treatments. Endotypes in severe asthma can be classified into Th2 (atopic, aspirin exacerbated respiratory disease [AERD] and late-onset asthma) and non-Th2 (non-atopic).³ Th2 atopic accounts for >85% of paediatric asthma endotypes where sensitisation to aeroallergens cause CD4 activation leading to interleukin (IL)-4, IL-5, IL-13 release causing prolonged eosinophil survival, mucus hyper-secretion, smooth muscle contraction and airway hyperreactivity.

The diagnostic challenge

Children present a unique challenge in the diagnosis of asthma because the diagnosis relies on history, examination, which can differ depending on age, and additional tests, which require a cooperative mature child. Most children with a formal diagnosis of asthma are of school age because they can comply with spirometry. Forty percent of children have one wheezy episode in childhood, but only 25% of children with intermittent cough, wheeze or exerciseinduced symptoms have asthma.⁴ Clusters of signs and symptoms are important: >65% of children with cough, dyspnoea, chest tightness and exercise-induced symptoms have asthma.⁴ Most asthmatic children are managed in primary care.

Preoperative assessment should include questions about the child's general health, growth, exercise tolerance/ability to keep up with their peers, atopy, birth history, significant family history and social history including tobacco smoke exposure. In an otherwise well, thriving child with no significant family or birth history with normal vital observations, an isolated wheezy episode should not be of concern. A child with recurrent wheeze who is failing to thrive, has unusual features in the history or examination should be referred to a paediatrician. If wheeze is auscultated in the preoperative visit, there are clinical signs of respiratory distress or abnormal vital observations, consider rescheduling and refer to a paediatrician or the emergency department.

Preoperative investigations in children with asthma requested by anaesthetists have not been shown to reduce the incidence of PRAEs.⁵ Arterial blood gases are rarely performed in children and capillary gases in well children are unlikely to add useful information.

When encountering a child with recurrent wheeze, consider the following differential diagnoses. Consider bronchiolitis if the child is aged <12 months, the wheeze is seasonal, particularly in the autumn or winter and associated with coryzal symptoms, fever and poor feeding. Consider cardiac causes in the child with recurrent wheeze associated with failure to thrive, heart murmur or hepatomegaly. In a child with wheeze associated with focal chest signs and signs of infection, consider pneumonia. Laryngomalacia or a vascular ring can present as inspiratory wheeze or stridor usually from birth, particularly when crying or feeding. In a toddler with monophonic, localised wheeze, consider foreign body inhalation. Adolescents, particularly girls, who report wheezy episodes not responsive to bronchodilator treatment but are otherwise well may have vocal cord dysfunction.

Investigations and classification of perioperative relevance

Tests

Spirometry and peak expiratory flow rate (PEFR) require a compliant child, usually of school age, who can follow instructions. Spirometry measures forced vital capacity (FVC) and the forced expiratory volume in 1 s (FEV₁) with reference values based on race, age, sex, height and weight. Spirometry is performed before and after bronchodilator therapy. Reversibility is defined by an improvement in FEV₁ >12%. FEV₁/FVC<0.8 and reversibility suggests asthma.⁶ Normal spirometry does not exclude asthma, with sensitivity and specificity of 52% and 73%, respectively.⁴

Peak expiratory flow rate is the maximal rate of expiration after a full inspiration, measured in litres per minute. It reflects larger airway calibre, muscle strength and voluntary effort. The relationship between PEFR and FEV₁ is complex, with some studies showing reasonable correlation; however, PEFR has been shown to underestimate the degree of airflow obstruction in severe disease.⁶ PEFR may be useful when used in conjunction with the clinical picture and other variables.⁶ For example the breathless child who is unable to perform PEFR, but has been able to previously, may indicate a severe attack.

Fraction of exhaled nitric oxide (FeNO) is recommended by the National Institute of Health and Care Excellence (NICE) to diagnose asthma in school-aged children with a value of >35 parts per billion supporting the diagnosis of asthma.⁶ FeNO reflects airway eosinophillic inflammation and is closely linked to atopic status. A chest X-ray and blood tests are not routinely indicated but a blood eosinophil count may be used in severe asthma to help decide whether a child may be eligible for biologic therapy and a chest X-ray may be used to diagnose acute lower respiratory problems.⁴

Classification

Classification of paediatric asthma is conventionally based on spirometry and PEFR. However, their limitations do not exclude asthma, and these tests cannot be performed by children aged <5 yrs; thus, alternative methods of classification may be more useful in the perioperative period. Take a history of the child's level of control over the preceding weeks to months and inhaler use, particularly the short-acting beta agonist (SABA) salbutamol (patients may refer to this as the ‘reliever’ or ‘blue’ inhaler). Using salbutamol more than three times per week or one inhaler per month suggests poor control and warrants review by a paediatrician.⁷ A recent cohort study suggests that using more than three SABA inhalers annually increases mortality risk.⁸ A history of triggers for attacks is also useful. Triggers could include exercise, cold weather, second-hand smoke or aero-allergens (e.g. dust, pollen). Airway instrumentation during GA may also be a trigger.

Completely controlled asthma means that the patient is free from day and nighttime symptoms, no asthma attacks, no need for salbutamol and no activity limitations in the preceding month.⁹ Asthma is suggested with an obstructive spirometry pattern and FEV₁/FVC ratio <70%, a bronchodilator reversibility on spirometry of >12%, or both. Mild asthma includes symptoms two to three times per week with FEV₁ ≥80% without limiting physical activity.⁶ In these categories, as long as the child is as well as they can be, has not had an attack within the past month, has a normal physical examination and unremarkable vital observations, proceed with elective cases.

Children with moderate asthma have daily or nightly symptoms with FEV₁ between 60% and 80% predicted; these children may have reduced exercise capacity compared with their peers. It may be difficult to assess control and consider each case on the risks of proceeding against optimising control. If the child has been well over the past month, compliant with treatment, with good school attendance and a recent paediatrician or primarycare review, ideally within the past month, there is reassurance that it would be safe to proceed with elective surgery.

In severe asthma children have persistent daytime or nighttime symptoms with spirometry FEV₁ <60%.⁶ Severe asthma affects approximately 5% of patients with asthma but accounts for the majority of its health burden.¹⁰ Severe asthma is defined by the European Respiratory Society/American Thoracic Society task force as ‘asthma which requires treatment with high dose of inhaled corticosteroids (ICS) plus a second controller and/or systemic corticosteroids to prevent it from becoming “uncontrolled” or which remains uncontrolled despite this therapy’.¹¹ Severe asthma can be subclassified into difficult asthma, where persistent symptoms result from a failure of basic asthma management, and severe treatment-resistant asthma (STRA), where patients are symptomatic despite maximal therapy and other modifiable factors, such as poor treatment adherence, have been addressed.¹¹

Any child who has undergone tracheal intubation and artificial ventilation for asthma, or has severe asthma, should be under the care of a respiratory paediatrician.⁶ A review preceding elective cases to ensure optimisation of medical management and a plan for perioperative care would be prudent to help reduce perioperative complications. For severe asthma consider performing procedures in a centre with a paediatric high dependency unit (HDU) or paediatric ICU (PICU) facility. If the child requires more than low to moderate dose ICS (>400 μg day⁻¹ for 1–5 yrs or >800 μg day⁻¹ budesonide equivalent for >6 yrs), they should have specialist respiratory input.^6,12,13 If a child with severe asthma presents for an emergency procedure at a district general hospital, consider the risks and benefits and need for PICU before proceeding.

Asthma and comorbidities

Comorbidities in asthma may be coincidental but for children with poorly controlled asthma treatment of comorbidities, including obesity, atopy(e.g., rhinosinusitis, eczema and food allergies), and reducing second-hand smoke exposure may improve control. The effect of treating children with symptomatic reflux or sleep apnoea is unclear.

Management

Chronic management

Good management of asthma requires a multidisciplinary, multimodal approach with medications as outlined in Table 1. All children diagnosed with asthma in the UK should have a printed asthma action plan. It is useful to ask to review this in preoperative assessment as it details their medications, last review and asthma emergency plan.

Table 1.

Medical management of asthma in children. Drug doses from the British National Formulary for Children (BNFC).¹³ CS, Corticosteroids; ICS, inhaled corticosteroids; IVI, intravenous infusion; LABA, long acting beta agonist; LRA, leukotriene receptor agonist; STRA, severe treatment resistant asthma; SABA, short-acting beta-agonist.

Class	Name	Mode of action	Use	Side effects/comments
Acute attack treatment
SABA	Salbutamol	β2 Agonist	Acute asthma dose: Inhaled: 2–10 puffs; can be repeated every 10 mins Nebulised: 1 month–4 yrs: 2.5 mg, repeated every 30 mins >5 yrs: 5 mg repeated every 30 mins	Tachycardia Hypokalemia Tremor Vasodilatation lactic acidosis
SABA	Terbutaline	β2 agonist	Acute asthma dose nebulised: 1 month–4 yrs: 5 mg, repeated every 20 mins. >5 yrs: 10 mg repeated every 20 mins	As salbutamol. Should not be used in conjunction with salbutamol. Considered as efficacious as salbutamol.
Anti-muscarinic agent	Ipatropium bromide	Non-specific muscarinic antagonist causing bronchodilation	Nebulised: 1 month–5 years: 125–250 μg max. 1 mg day−1 6–11 years: 250 μg max 1 mg day−1 12–17 years: 500 μg per dose max 2 mg day−1
CS	Prednisolone Hydrocortisone	Reduction in airway inflammation	2 mg kg−1 max of 60 mg p.o 4 mg kg−1 i.v. max 100 mg usually in 4 divided doses	Give if oral prednisolone not tolerated
SABA	Salbutamol		I.V.: Bolus <2 yrs: 5 μg kg−1 per dose given over 5 mins >2 yrs; 15 μg kg−1 per dose given over 5 mins I.V. Continuous: 1–5 μg kg−1 min−1 depending on response.
SABA	Terbutaline		I.V./s.c. slow bolus: 2–14 yrs: 10 μg kg−1 up to 4 times a day max. 300 μg/dose. 15–17 yrs: 250–500 μg up to 4 times a day. I.V. continuous infusion: 2–4 μg kg−1 bolus then 1–10 μg kg−1 h−1 adjusted based on response.	Should not be used in conjunction with other SABA
Magnesium Sulphate		Bronchial smooth muscle relaxation	2–17 years: 40 mg kg−1 (max 2 g) to be given over 20 mins Inhaled: 40 mg kg−1 (6)	Hypotension if injected rapidly; may prolong neuromuscular block
Aminophylline		Methylxanthine derivative, non-selective phosphodiesterase inhibitor producing smooth muscle relaxation	Only in theophylline naive: 5 mg/kg max 500 mg as a slow bolus followed by an infusion Infusion (after bolus or in patients on theophylline): 1 month–11 yrs: 1 mg kg−1 h−1 12–17 yrs: 0.5 mg kg−1 h−1	Palpitations Arrhythmias Seizure Serious hypokalaemia when used in with B2 agonists
Chronic treatment
SABA	Salbutamol	β2 agonist	Inhaled 2–10 puffs maximum 4 hourly	as above
ICS	Budesonide Beclometasone Ciclesonide Fluticasone propionate	Reduces airway inflammation	All can be given as low, moderate or high dose For more specific dosage information visit (13)	Oral thrush Poor dentition Paradoxical bronchospasm (rare) Adrenal suppression at high doses
ICS+ LABA	Fluticasone and Salmeterol (Seretide) Budesonide and Formoterol (Symbicort) Fluticasone furoate and Vilanterol (Relvar)	Reduced airway inflammation and bronchodilation	Symbicort may be used as maintenance and reliever (single agent) MART regimen Relvar (>12 yrs) used once daily	As above and muscle cramps
LRA	Montelukast	LRA selectively binding to receptors for D4 and E4; reducing airway oedema, bronchoconstriction and inflammation	1–5 yrs: 4 mg OD 5–14 yrs: 5 mg OD >15 yrs: 10 mg OD	Nightmares Neuropsychiatric behaviours Suicidal ideation
rh-DNAse (recombinant human deoxyribonuclease)	Dornase alpha	Used PICU/under specialist supervision as non-evidence based. rh-DNAse is an enzyme that catalyses the hydrolysis of DNA found in respiratory sections thus may reducing mucous plugging and airway obstruction.	2500 units once daily via jet nebuliser
Omalizumab		targets IgE; used in STRA with IgE titres 3–1500 IU/l	>6 yrs dose dependent on IgE level and body weight. Usually 75–600 mg s.c. 2–4 weekly
Mepolizumab		Targets IL5 Severe refractory eosinophilic asthma	6–11 yrs: 40 mg s.c. every 4 weeks 12–17 yrs: 100 mg s.c. every 4 weeks

In children the preferred method of inhaled drug delivery is via a metered dose inhaler (MDI) and spacer with an appropriately sized facemask for toddlers, or a mouthpiece for children aged >4 yrs, for maximal drug delivery.

Children with mild asthma are prescribed low dose ICS or leukotriene receptor antagonists (LRAs) with SABA. Those with moderate asthma require ICS with LRA or long-acting beta agonists (LABAs) and severe asthma are prescribed ICS, LRA and LABA under specialist respiratory input. Treatment is usually started at the most appropriate level for initial severity to achieve good control titrated based on symptoms and attacks. Monoclonal antibodies may be initiated under specialist supervision.

Acute attacks

Acute treatment of asthma aims at relieving bronchoconstriction and airway inflammation and includes oxygen, SABA, ipratropium bromide, corticosteroids (i.v. or oral) and i.v. medications including magnesium, SABA and aminophylline (Fig. 1).

Fig 1.

Summary of the management of an acute paediatric asthma attack. Adapted from the British Thoracic Society⁴. HR, hazard ratio; RR, relative risk.

Asthma and anaesthesia

Risk factors for an asthma attack under GA

Theoretically any child with asthma has an increased risk of a PRAE. Patient factors increasing the risk include previous exacerbations under GA, moderate to severe asthma, respiratory tract infection within the past 4 weeks, age <5 yrs and having previously received artificial ventilation for asthma. Anaesthesia-related factors include airway instrumentation particularly tracheal intubation and positive pressure ventilation and surgical factors include prolonged procedures and airway surgery.

Elective surgery

Children with well-controlled or mild asthma can proceed with elective surgery at district general hospitals as day cases. Ideally, all children should have nurse-led preoperative assessment. Any patient with STRA or a previous exacerbation requiring mechanical ventilation should be assessed by a consultant anaesthetist. This helps to establish rapport, manage expectations, discuss the risks and alternatives to GA, referral to relevant specialties and organisation of a postoperative high-dependency bed.

The perioperative plan for children with moderate to severe asthma may include recommendation for perioperative oral steroids or temporarily increasing the ICS dose. If the child has been receiving >15 mg m⁻² hydrocortisone equivalent for more than 1 month, steroid replacement should be considered.¹⁴ Children on high ICS doses are at risk of adrenal suppression after surgery, and all anaesthetists should be able to diagnose and treat this as a medical emergency.¹⁴ Children with diagnosed adrenal insufficiency should have a perioperative steroid replacement plan by a paediatric endocrinologist. Steroid dosing equivalents can be found in the British National Formulary for Children (BNFC) and from NICE.^12,13

On the day, reassess and confirm the child is fit for surgery. Ensure the child has their usual asthma medications and inhaled or nebulised salbutamol before induction of anaesthesia. Preoperative anxiety should be managed holistically with play specialist input, distraction and, if necessary, sedative premedication. Induction of anaesthesia can be i.v. or via inhalation. Observational studies have suggested i.v. induction is associated with a reduced incidence of PRAE; however, this was not shown in meta-analyses.¹⁵ Common agents include sevoflurane, ketamine and propofol (Table 2). Ensure adequate depth of anaesthesia before proceeding with airway manoeuvres or painful procedures. Consider methods to reduce airway reactivity, bronchospasm and laryngospasm pre-emptively based on the patient, the anaesthesia and the surgery to be performed. Consider whether airway instrumentation is required at all. If airway support is necessary, supraglottic airway devices are associated with lower incidences of laryngo and bronchospasm than tracheal intubation and, if used, consider maintaining spontaneous ventilation. If tracheal intubation is performed, ensure bilateral air entry without wheeze. Use a cuffed tracheal tube to minimise leak, optimise ventilation and monitor cuff pressure to reduce the risk of PRAE's.¹⁵ Intraoperative ventilator settings should be changed only if the child is having an acute attack (see following section). Before extubation, if a neuromuscular blocking drug is used, ensure return of the trainoffour ratio and use a reversal agent as required. Intraoperative multimodal analgesia should include simple analgesics including paracetamol and NSAIDs as per age and weight dosing regimens, and regional anaesthesia or wound infiltration. Most children with asthma can take NSAIDs.¹⁷ NSAIDs should be avoided in children who have a personal or a significant family history of NSAIDs exacerbating asthma symptoms. If opioids are required in certain patients, particularly those with STRA or previous bronchospasm under GA, synthetic opioids or ketamine are preferable as morphine causes more histamine release. Intravenous magnesium may be a useful analgesic adjunct.

Table 2.

Commonly used medications in children receiving GA. Drug doses from BNFC.^12,16 Paracetamol and ibuprofen dosing as per BNFc or local protocols. ∗Propofol and remifentanil TCI have limited evidence in asthma. They can be used to maintain anaesthesia or sedation on ITU. BC, bronchoconstriction; BD, bronchodilatation.

Name	Dose	Clinical Utility in Asthma	Side effects/cautions
Induction agents
Ketamine	1–2 mg kg−1	Maintains airway tone Promotes bronchodilation (BD) through catecholamine release	Caution in volume depleted states as may have a negative ionotropic effect
Propofol∗	2.5–4 mg kg−1	May promote BD	Hypotension
Sevoflurane	0–8%	Promotes BD Maintains spontaneous ventilation	Requires an anaesthetic delivery circuit
Thiopental		Not recommended	May cause BC
Methohexital		Not recommended	Alters airway tone and cause upper airway obstruction
Etomidate		Not recommended	Increased airway resistance
Maintenance of anaesthesia
Ketamine	10–45 μg kg−1 min−1	As above
Volatile agents	Sevoflurane	Promotes BD	Desflurane may cause airway irritability
Opioids
Fentanyl	Induction: 1–5 μg kg−1 Maintenance: 0.2–2 μg kg−1 IVI: 0.5–5 μg kg−1 h−1	Does not promote BC	May cause cough
Alfentanil	Induction 10–20 μg kg−1 Maintenance: 5–10 μg kg−1 IVI: 30–120 μg kg−1 h−1	Does not promote BC	Respiratory depression
Sufentanil	Induction: 0.25-2mcg kg−1 Maintenance: 2.5–10 μg kg−1 IVI: 0.5–1.5 μg kg−1 h−1	Does not promote BC	Respiratory depression
Remifentanil∗	Induction 0.1–1 μg kg−1 Maintenance: 0.2–1 μg kg−1 IVI: 0.1–1 μg kg−1 h−1	Does not promote BC	Skeletal muscle rigidity may occur Respiratory depression
Morphine	I.V.: 0.05–0.1 mg kg−1		May cause BC through histamine release Respiratory depression
Muscle relaxants
Atracurium	0.3–0.6 mg kg−1		May cause BC through histamine release
Vecuronium	0.1 mg kg−1
Rocuronium	0.6–1 mg kg−1		May have a higher risk of anaphylaxis
Suxamethonium	I.V.: 1–2 mg kg−1 IM: 4–5 mg kg−1
Other
Lignocaine	Airway topicalisation I.V.	May relieve BC	Topicalisation increases risk of postoperative airway adverse events11 Increase airway tone
Neostigmine	50 μg kg−1		May cause BC
Glycopyrronium bromide	I.V.: 4–10 μg kg−1 (max 200 μg)	Reduces airway secretions
Dexamethasone	I.V.: 0.3 mg kg−1 day−1	Reduce airway inflammation	Should not be used if the child is already on regular steroids
Ondansetron	I.V.: 0.1–0.15 mg kg−1 (max 4mg)
Paracetamol	Check BNFC for dosing based on weight
Ibuprofen	Check BNFC dosing based on weight		Caution only if the child has known BC induced by NSAIDS.

Postoperatively, if the child is well and meets day-case discharge criteria, they can go home with safety-netting advice.

Specific anaesthetic agents in asthma

There is little evidence for agents other than ketamine and volatiles in asthma. Table 2 presents some of the commonly used drugs and their adverse effects that may affect bronchial reactivity. There is limited evidence for propofol and remifentanil TCI during surgery in children with asthma, but they can be used to maintain anaesthesia or sedation in ICU. All opioids cause respiratory depression and histamine release, and there is some evidence to suggest an increase in asthma/chronic obstructive pulmonary disease (COPD) in the adults with regular opioid exposure¹⁸; however, this has not been investigated in paediatrics. The use of i.v. lidocaine is controversial; lidocaine is thought to decrease airway responsiveness to agents causing bronchoconstriction, however, it itself might increase airway tone, as shown in one small study in adults utilising i.v. lidocaine infusion.¹⁹ Furthermore, aerosol and i.v. lidocaine has been associated with an increase in PRAE in children.²⁰ On balance, we would recommend using other agents first.

Management of severe bronchospasm

The risk of bronchospasm under GA in patients with asthma is between 0.21% and 20%.²¹ Intraoperative bronchospasm can be isolated or as a symptom of anaphylaxis. The pathophysiology of bronchospasm under GA is multifactorial and likely secondary to change in airway tone, vagal stimulation secondary to airway instrumentation, impairment of diaphragmatic function, mucociliary clearance and the cough reflex.

Bronchospasm can present as an increase in peak inspiratory pressure (PIP), decrease in tidal volumes, change in end-tidal CO₂ (‘shark-fin’ trace or loss of end-tidal CO₂) and wheeze. Management includes follows the Association of Anaesthetists’ quick reference guide for the management of bronchospasm and includes calling for help, stopping surgery when safe, giving 100% Fio₂, auscultate to exclude tracheal tube obstruction, displacement or pneumothorax.²² Switch to hand ventilation, which will give you an impression of lung compliance. Exclude anaphylaxis by looking for associated features. Consider deepening anaesthesia (if suitable, consider switching from TIVA or desflurane to sevoflurane). For isolated bronchospasm, treat first line with salbutamol either within the anaesthetic circuit with an MDI or nebuliser (Fig. 2). Second-line treatments include nebulised ipratropium, i.v. salbutamol, magnesium, hydrocortisone and, in extremis, i.v. adrenaline 1 μg kg⁻¹ titrated to response. Bronchospasm under GA requiring i.v. therapies should be treated as severe asthma, and ventilator management is suggested below.

Fig 2.

Nebuliser in circuit.

Mechanical ventilation in a child with acute severe asthma is challenging. Liaise early with PICU or the retrieval team for strategies to improve gas exchange. Use a ventilator that is familiar, ideally one with flowvolume loops and the ability to perform breath holds to help assess lung compliance, the degree of airflow limitation and auto-PEEP. There are proponents for low PEEP (4–5 cmH₂O) to matched PEEP, based on an expiratory hold. Targets include Spo₂ >90%, pH >7.2. The points listed below are some suggestions.23, 24, 25

• 1. Ensure the patient remains under full neuromuscular block (consider a vecuronium infusion).

• 2. Choose a ventilation mode that is familiar and available on your ventilator.

• 3. Choose a PEEP (4–5 cmH₂O) – discuss with local PICU/retrieval team.

• 4. If using pressure-controlled modes, set PIP to <40 cmH₂O. If on a volume control mode, set the PIP limit to 40. Be guided by plateau pressures which should be kept <30 cmH₂O.

• 5. Aim for tidal volumes 5–7 ml kg⁻¹.

• 6. Consider the relationship of the inspiratory to PIP to achieve adequate tidal volumes. High PIP risks baro-trauma.

• 7. Increase expiratory time and aim for an I:E ratio of 1:3–1:4. This can be done by reducing the ventilatory frequency (e.g. 10–15 min⁻¹ for children aged >10 yrs).

• 8. Allow for permissive hypercapnia (pH ≥7.2).

• 9. Multiple methods could be used to assess breath stacking, which can include using the flow trace and ensuring the flow reaches baseline at the end of expiration. If the end-tidal CO₂ trace does not reach plateau, this suggests incomplete expiration.

• 10. Refrain from manually decompressing the chest as this can precipitate a cardiac arrest.

• 11. Consider further i.v infusions of salbutamol, aminophylline, adrenaline or ketamine in addition to sevoflurane.

Conclusions

Paediatric asthma is a common condition and good perioperative care requires a multidisciplinary approach involving primary care, and in severe asthma, secondary and tertiary care. A good understanding of the pathophysiology of asthma, knowledge of the medications used, and national guidelines for the management of asthma and bronchospasm are integral to safe perioperative care.

MCQs

The associated MCQs (to support CME/CPD activity) will be accessible at www.bjaed.org/cme/home by subscribers to BJA Education.

Biographies

Jo Challands FRCA is a consultant paediatric anaesthetist at the Royal London hospital. She has previously published in BJA Education on the management of respiratory distress in children.

Sejal Saglani MD MRCPCH is professor of paediatric respiratory medicine at Imperial College London and a consultant in paediatric respiratory medicine consultant at the Royal Brompton Hospital, specialising in treating and investigating children with severe and difficult-to-treat asthma. Her research programme focuses on investigating mechanisms mediating severe asthma in children using bronchoscopic airway samples and she is currently undertaking a clinical trial of novel biological treatments in children with severe asthma.

Shreya Bali MRCPCH FRCA is a specialty trainee in anaesthesia at St Bartholomew's Hospital. She has previously completed a fellowship in paediatric anaesthesia and has an interest in paediatric asthma.

Matrix codes: 1A02, 2D02

Declaration of interests

The authors declare that they have no conflicts of interest.

Acknowledgements

The authors thank Dr Konstantinos Dimitriades (PICU consultant at the Royal London hospital) for reviewing drafts of this article and giving advice on mechanical ventilation in severe asthma; and Mr. Gecco Navalata, operating department practitioner, and Dr Monica Naik, consultant paediatric anaesthetist, Royal London Hospital, for their support and providing the photograph for Figure 2.