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- v.19(11); 2019 Nov
- PMC7807856
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BJA Educ. 2019 Nov; 19(11): 350–356.
Published online 2019 Oct 14. doi:10.1016/j.bjae.2019.07.004
PMCID: PMC7807856
PMID: 33456857
J. Challands1,∗ and K. Brooks2
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Key points
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Many paediatric emergencies result from severe respiratory distress or imminent respiratory failure.
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Common causes of paediatric respiratory distress include bronchiolitis, wheeze in the preschool child, asthma and pneumonia.
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Less common causes include interstitial lung disease, pulmonary aspiration and problems associated with tracheostomies.
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Signs of impending respiratory failure warrant involvement of an anaesthetist and, in most cases, tracheal intubation and artificial ventilation.
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Management of paediatric respiratory distress requires meticulous preparation to avoid complications during induction of anaesthesia, intubation and ventilation.
Learning objectives
By reading this article, you should be able to:
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Recognise the paediatric patient in respiratory distress and identify the signs of impending respiratory failure.
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Describe the modifications that may be needed to achieve safe induction of anaesthesia and tracheal intubation in the paediatric patient in respiratory distress.
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See AlsoSigns of Respiratory Distress in ChildrenDyspnea or Respiratory Distress (Pediatric ED)BronchiolitisAcute Respiratory Distress Syndrome (ARDS)Describe the emergency management of children in respiratory distress with a tracheostomy.
Anaesthetists are part of the paediatric emergency response team in hospitals throughout the UK. These teams respond to all paediatric emergencies within the hospital. Respiratory disease is the most common reason for acute hospital admission in children, so it follows that a large number of paediatric emergencies result from severe respiratory distress or imminent respiratory failure. Often, by the time an emergency call is put out or a referral to the anaesthetist is made, the child has deteriorated significantly and usually requires non-invasive or invasive ventilation and transfer to a paediatric ICU (PICU). There are many causes of paediatric respiratory distress with varying treatments and prognoses. A good working knowledge of these diseases and their management can inform and assist with anaesthetic intervention in this stressful situation.
This article summarises the common causes of paediatric respiratory distress and the anaesthetic management thereof. The causes of stridor and respiratory compromise secondary to this have been covered recently in this journal, and will not be discussed here.1
Bronchoconstriction and wheezing
Asthma affects one in 11 children. In 2016 asthma caused 6783 emergency admissions to hospital in patients aged 0–14 yrs. Whilst hospital admissions are common, fatality is fortunately rare with 12 deaths in the same age group in the UK in 2016.2 The pathogenesis is not fully understood. However, variable airflow obstruction and airway hyper-reactivity are involved. Exacerbations may be infective or non-infective; the majority of infective exacerbations are caused by viral infection. The joint British Thoracic Society and Scottish Intercollegiate Guidelines Network guidelines outline the treatment for children admitted to a hospital as follows:3
- (i) Oxygen (method dependent on severity: low-flow nasal cannulae, Hudson face mask, or high-flow nasal cannulae)
- (ii) Nebulised β2-agonists with the addition of an inhaled anticholinergic if response is poor
- (iii) Corticosteroids (i.v. route likely to be required in severe respiratory distress)
- (iv) Magnesium sulphate, salbutamol, and aminophylline (i.v. infusions as required)
Of these treatments, there is some evidence that magnesium sulphate works the fastest, and it should, therefore, be the first choice in patients requiring i.v. treatment. Where there is poor response, artificial ventilation must be considered. In the child in whom medical management is failing, mechanical ventilation must be considered, although it must be noted that this alone does not correct the underlying problem, and these children can be very difficult to manage after tracheal intubation. Non-invasive ventilation is used in some centres. At present, there is no clear evidence of its effectiveness in avoiding intubation.3 However, a 2016 Cochrane review concluded that there was also no evidence of harm.4 A large, single-centre, continuous quality improvement programme in the USA suggests that using bilevel positive airway pressure ventilation in the emergency department reduced the rates of admission to PICU.5 Medical management must be optimised first, and on balance, it is probably advisable to try non-invasive ventilation before tracheal intubation.
Because of the high incidence of wheezing syndromes in those children aged <6 yrs, asthma is not ordinarily diagnosed before this, when more common causes of wheezing include bronchiolitis and ‘preschool wheeze’. Bronchiolitis is the most common disease of the lower respiratory tract in the first year of life, affecting approximately one in three infants. Overall, 2–3% of cases require hospitalisation.6 It is most commonly caused by respiratory syncytial virus, but other viruses are also implicated. Infection of the epithelial cells of the small airways causes inflammation, mucous production, and sloughing of necrotic epithelial cells leading to obstruction of the small airways with resulting hyperinflation, atelectasis, and wheeze.7 Presentation is with coryzal symptoms followed by tachypnoea, cough, crackles or wheeze; apnoea is more common in babies less than 6 weeks old. The prognosis is good and mortality is rare. Risk factors for severe illness are prematurity (especially those babies born at <32 weeks gestational age), bronchopulmonary dysplasia, congenital heart disease, neuromuscular diseases, immunodeficiency, and age <3 months. The initial treatment is suctioning the nostrils, supplemental oxygen if Spo2 persistently is less than 92%, and nasogastric (NG) feeding (which will be stopped in cases of severe respiratory distress). Chest physiotherapy, nebulisers, antibiotics, and steroids are not included in the current guidelines because of a lack of evidence. However, in the context of progressive deterioration, these measures may be considered to avoid invasive ventilation. CPAP should be commenced if there are signs of impending respiratory failure (see Box 1).6 Some units use high-flow oxygen therapy (HFOT) via nasal cannulae instead of CPAP. A recent multicentre trial comparing conventional nasal oxygen therapy with HFOT showed that treatment failure requiring escalation of care occurred less frequently in the HFOT group (12% vs 23%).8
Box 1
Signs of impending respiratory collapse
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Exhaustion: evidenced by listlessness or decreased respiratory effort
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Cyanosis
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Impairment of consciousness
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Spo2 <92% despite supplemental oxygen FIo2 0.6
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Recurrent apnoea
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Worsening hypercarbia
Alt-text: Box 1
The term ‘preschool wheeze’ is used to describe several clinical syndromes, some of which are overlapping. Most cases are transient with only 15% continuing to wheeze after 6 yrs of age. The vast majority of these episodes are managed at home or in primary care, but children may present with this history before surgery, so awareness of the condition is important. If a child is unwell enough with preschool wheeze to be admitted to a hospital, treatment includes supplemental oxygen, inhaled bronchodilators and oral corticosteroids. In cases with poor response, the following can be considered, but have equivocal or no evidence of efficacy: inhaled corticosteroids, leukotriene antagonists, antihistamines and i.v. bronchodilators.9
Pneumonia and sepsis
The incidence of pneumonia in children is 14.4 per 10,000. It affects all age groups, and can be bacterial, viral, or mixed. In those children aged <2 yrs, the ratio of viral:bacterial causes is 50:50, whereas in older children bacterial pneumonia becomes more common, with pneumococcus being the most common organism. Patients present with a history and signs indicating respiratory distress and fever. Treatment is supportive with supplemental oxygen and appropriate antimicrobials. Improvement is usually rapid, and a lack of improvement within 48 h or persistent fever >38°C should prompt a reassessment for complications, such as lung abscesses, pleural effusion, or empyema, which occur in 1% of cases overall, but in 40% of cases admitted to a hospital. Infection with group A streptococcus and Staphylococcus aureus is most likely to progress to these complications or require admission to PICU. The prognosis is generally very good in high-income countries, but it should be noted that pneumonia is the leading infectious cause of paediatric mortality worldwide; in high-income countries, pneumonia kills 3,000 children per year compared with meningitis, which kills 640 children per year.10
Chronic aspiration is a frequent underlying cause of recurrent pneumonia and can be difficult to diagnose. There are many potential causes, including undiagnosed tracheo-oesophageal fistula, laryngeal cleft, craniofacial abnormalities, gastro-oesophageal reflux disease, and neuromuscular diseases (including bulbar palsy). If undiagnosed or untreated, recurrent pneumonia will lead to chronic lung disease (CLD) with the development of bronchiectasis and progressive respiratory failure. Chronic aspiration is the leading cause of death in children with neuromuscular disease. Treatment is supportive during acute episodes of infection with supplemental oxygen and appropriate, targeted antimicrobials. Prevention of recurrent episodes relies on identifying the underlying cause and correcting it where possible.11
It should be remembered that respiratory distress can be a sign of non-respiratory sepsis. In addition, children presenting with decompensated congenital heart disease are likely to be in respiratory distress. Therefore, a thorough assessment of all systems in all children is vital.
Chronic lung disease
Children's interstitial lung disease (chILD) describes a widely varied and poorly understood group of chronic respiratory disorders in children, with an incidence in the region of 0.36 per 100,000. It represents a group of diseases with varying pathophysiologies that are beyond the scope of this article. The patterns of the disease can be either obstructive or restrictive, or both, depending on the cause, and all may be complicated by superimposed infection. Morbidity and mortality are high with an overall mortality of 30% for which the development of pulmonary hypertension is an independent risk factor.12 Chronic lung disease of prematurity, previously termed bronchopulmonary dysplasia, is the most common chILD diagnosis, affecting 20% of neonates born at <30 weeks gestational age with birth weight <1.5 kg. With improved survival of babies born at the limits of viability with extremely low birth weights, children with CLD present frequently to a hospital with respiratory difficulty, which may result from infection or chronic aspiration.13
Patients with a tracheostomy
Tracheostomy is being performed increasingly in children, with an ever-increasing number of patients being cared for at home. Indications for tracheostomy are wide ranging and include neuromuscular disease; respiratory disease; congenital malformations of airway, lungs, or heart; craniofacial syndromes; and acquired subglottic stenosis.14 It follows that we can expect to see an increasing number of paediatric patients with a tracheostomy presenting in respiratory distress to emergency departments. Perhaps more importantly in the case of patients with a tracheostomy, it must be remembered that this may be caused by airway obstruction or tracheostomy problems, such as a large leak, as opposed to, or as well as, primary lung pathology. It has been reported that 43% of patients will have a serious complication with their tracheostomy, and mortality related to tracheostomy complications is 0.7%.15
Emergency management of paediatric respiratory distress: when, who, and how to intubate
There are no evidence-based guidelines on the optimal timing of tracheal intubation in cases of respiratory distress.16 The general approach to the assessment and management of a child in respiratory distress will be discussed in the following paragraphs and boxes, followed by disease-specific alterations to this approach that may be considered.
Assessment
Assessment should be largely clinical, as the signs of impending respiratory failure or severe respiratory distress should be identifiable without the need for blood gas analysis, and should prompt an intervention—either non-invasive or invasive ventilation. Beware of children with myopathy, as they are unable to demonstrate signs of increased work of breathing. Box 1 details the signs of impending respiratory collapse.
General approach
Conduct of the intubation must be determined on a case-by-case basis, looking at the cause of respiratory distress, predicted airway difficulty, equipment and available personnel, and risk of aspiration. Monitoring, including end-tidal carbon dioxide (CO2), should be prepared in advance. Thought must be given to the most appropriate person to lead the induction and intubation, and senior help is called where necessary. Emergency drugs should be prepared in advance in the correct dose for the patient, and these drugs include atropine and suxamethonium with the addition of adrenaline (epinephrine) if the patient is haemodynamically compromised. Prepare a 10–20 ml kg−1 i.v. fluid bolus in advance. Induction of anaesthesia in an unstable child almost always mandates having secured i.v. access, but intraosseous access should not be overlooked if i.v. access fails.
Consideration should be given to the correct drug for induction of anaesthesia. Ketamine confers the benefits of bronchodilatation and relative cardiovascular stability over propofol, the dose of which must be reduced in the haemodynamically compromised or septic child. Thiopental can cause bronchoconstriction and so is a poor choice in a child with obstructive respiratory disease. Inhalation induction with sevoflurane is an option if scavenging is available; sevoflurane also results in bronchodilatation. Neuromuscular block will provide optimal intubating conditions in most cases: rocuronium, suxamethonium, or atracurium is used. The choice of agent can be based on familiarity of the operator. However, it should be noted that atracurium can precipitate histamine release and may therefore worsen bronchoconstriction. Similarly, the addition of fentanyl will help provide optimal intubating conditions.
Straight laryngoscope blades are generally used in babies up to 6 months and curved blades thereafter. Tracheal tube (TT) size and length should be calculated using the standard formulae in Box 2. A cuffed TT is preferable to an uncuffed TT particularly in disease states with high resistance, such as asthma, where high ventilatory pressures will need to be delivered over a prolonged period. Cuff pressure must be monitored. The practice of cutting the TT runs the risk of the tube being too short, requiring reintubation in a critically ill child.
Box 2
Equations for size (internal diameter) and length of tracheal tube (TT)
| Sizes for cuffed TT: | Size for uncuffed TT: |
|---|---|
| >3 kg up to 1 yr: start with size 3.0 mm | <1 yr: 1 kg: size 2.5 mm |
| 1–2 yrs: start with size 3.5 mm | 2 kg: size 3.0 mm |
| >2 yrs: (age/4)+3.5 mm | >3 kg: size 3.5 mm |
| >1 yr (age/4)+4 mm | |
| Depth: | |
| (Age/2)+12 cm OR internal diameter of ETT×3 | |
| Tip of ETT should lie at mid-trachea |
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Alt-text: Box 2
With regard to rapid sequence induction (RSI) in this setting, it must be remembered that the priority is supporting oxygenation and haemodynamic stability whilst securing the airway. The incidence of aspiration in paediatric practice is extremely low.17 Some would argue an RSI increases the risks of haemodynamic instability, hypoxia and awareness. Risk assessment must be performed on a case-by-case basis, but some would argue that RSI has no place in paediatric practice.18
Preoxygenation of the lungs is invaluable if it can be achieved. It may be most appropriate to continue the mode of delivery of oxygen currently in place in settled children, as disturbing them with a tight-fitting face mask may cause distress and increased work of breathing and oxygen demand. In view of the potential inability to preoxygenate, increased oxygen consumption, and closing capacity in small children, the length of apnoea time tolerated before desaturation is low. Oxygenation must remain the priority, and most would advocate continued gentle mask ventilation whilst waiting for adequate neuromuscular block regardless of fasting status.18 In adult practice, the introduction of transnasal humidified rapid-insufflation ventilatory exchange (THRIVE) using high-flow nasal cannulae during apnoea has allowed a significant increase in apnoea times before oxygen desaturation. THRIVE is beginning to be used in paediatric practice with promising results in case reports, and so is an option to prolong apnoea time in carefully selected paediatric patients if equipment is available.19
Post-intubation care
The specific details of care after intubation are determined on a case-by-case basis, but the following points must be considered:
- (i) Sedation and neuromuscular block: midazolam and morphine are commonly used in combination with either vecuronium or atracurium. Fentanyl and ketamine are suitable alternatives. Propofol is avoided in some centres, except in short-term sedation, because of the risk of propofol-related infusion syndrome. The evidence for this is inconclusive20; local guidelines should be followed.
- (ii) NG tube insertion to relieve gastric insufflation and consequently reduce airway pressures
- (iii) Chest X-ray: to check the position of the TT; exclude endobronchial intubation or an inadequately advanced TT that may migrate out during transfers; to rule out pneumothorax, which is a particular risk in bronchoconstriction requiring invasive ventilation
- (iv) Ventilation strategy: there is a much smaller evidence base for specific ventilation strategies compared with adults, but the trend is towards a ‘lung-protective’ strategy with the aim of achieving adequate gas exchange at the lowest possible pressures and volumes to avoid alveolar trauma secondary to stretching. Therefore, the following general principles are advised:21
- (a) Tidal volumes of 5–7 ml kg−1
- (b) Plateau pressure of <30 cmH2O
- (c) Peak inspiratory pressures of <35 cmH2O
- (d) PEEP 5–7 cmH2O
- (e) I:E ratio of 1:2 in most cases (see section ‘Bronchoconstriction’ for further information on this)
- (f) Spo2 >91–92% (with the exception of patients with pulmonary hypertension and brain injury in whom Spo2 should be kept >94%)
- (g) Ventilatory frequency dependent on age of patient and balance between avoiding barotrauma, yet achieving an adequate minute ventilation
- (h) Regular chest physiotherapy and suctioning
- (v) Transfer of patient to PICU: if this involves interhospital transfer, this would be done by a local specialist retrieval service who should be contacted early to facilitate planning.
Disease-specific considerations
Bronchoconstriction
The aforementioned general approach may need to be modified in patients with asthma or other pathologies, in which bronchoconstriction can occur, including bronchiolitis, preschool wheeze and chILD. Ketamine should be considered as an i.v. induction agent because of its direct effects causing bronchodilation. However, it should be remembered that ketamine may also increase respiratory secretion load, and therefore, treatment with an anticholinergic may be useful (e.g. atropine 20 μg kg−1, maximum 600 μg, or glycopyrrolate 4–8 μ kg−1, maximum 200 μg in <12 yrs and 400 μg in >12 yrs).
A cuffed TT is essential in these diseases because of the need for high airway pressures to achieve oxygenation and ventilation.16 High airway resistance and therefore slow expiratory flow can lead to incomplete exhalation, which increases the end-expiratory volume and leads to the development of intrinsic PEEP. Intrinsic PEEP can be identified using an end-expiratory breath-hold manoeuvre on the ventilator. The value at which the pressure settles is the intrinsic PEEP. The addition of further extrinsic PEEP set on the ventilator to this, with an expiratory time that is too short, can lead to breath stacking and further expansion of the alveoli leading to volutrauma, CO2 retention and pneumothorax. The recommended principles for ventilation of a patient with bronchoconstriction are a low ventilatory frequency, extended expiratory time to allow for complete expiration (observe for cessation of flow on the flow–volume loop before inspiration and set I:E ratio accordingly), and a low extrinsic PEEP that does not exceed intrinsic PEEP.22 In the authors' local PICU, a value of 60% of the intrinsic PEEP is commonly used as a starting point. Neuromuscular blocking agents are almost invariably required to achieve adequate oxygenation and ventilation.
The aforementioned ventilator settings may not allow for the removal of enough CO2 to maintain normocapnia. Permissive hypercapnia allows oxygenation whilst reducing the risk of ventilator-associated lung injury caused by excessive pressure or volumes needed to maintain normocapnia. There is no firm consensus on how low to allow the pH to go, but a range of pH 7.15–7.3 was recently recommended by a panel of experts. However, it should be noted that patients with intracerebral pathology, severe pulmonary hypertension, and significant ventricular dysfunction are not appropriate candidates for this technique.23
Pneumothorax must be considered if there is any deterioration in gas exchange or cardiovascular function. The incidence of pneumothorax in patients with asthma requiring mechanical ventilation is approximately 1–3%.16 Pharmacological therapy with i.v. bronchodilators (salbutamol or aminophylline) to treat bronchoconstriction must continue, as without it ventilation will deteriorate. In patients whose lungs are difficult to ventilate adequately, sevoflurane can be considered if scavenging is available.3
Pneumonia and sepsis
The conduct of induction of anaesthesia, tracheal intubation, and mechanical ventilation should be largely the same in patients with pneumonia. However, it should be noted that, if there are signs of sepsis, the dose of induction agent will need to be reduced to prevent a precipitant decrease in arterial blood pressure. Moreover, if there are already signs of circulatory compromise, ensure adequate volume resuscitation, calculate and prepare inotropic agents and vasopressors, and consider starting these before induction of anaesthesia. Post-intubation care in cases of pneumonia will need to include regular suctioning and chest physiotherapy.
Patients with a tracheostomy in respiratory distress
The initial assessment of a patient with a tracheostomy in respiratory distress must include a thorough assessment of the patency of the tracheostomy. The UK National Tracheostomy Safety Project has outlined an emergency algorithm for this purpose (Fig.1). After confirmation of the tracheostomy's patency, if the patient requires positive pressure ventilation, then it may be necessary to upsize or change the tracheostomy tube to a cuffed tube to facilitate this. The management of patients with respiratory distress is otherwise largely similar to those patients without tracheostomy. It should be remembered that they often have a complex medical background, and therefore, the threshold for ventilatory support may be different to the child who is previously fit. Further discussion of this is outside the scope of this article.
Fig 1
Algorithm for the emergency management of paediatric tracheostomies. Reproduced with permission from the National Tracheostomy Safety Project.
Additional strategies to improve gas exchange
In the event of failure of oxygenation despite best-practice ventilation, several other strategies may be considered. The evidence base for all is small, although research is ongoing. A survey conducted in 2013 showed that, despite a lack of strong evidence, the following techniques are considered and used in many centres across North America and Europe, and they are therefore relevant to current PICU practice.24
High-frequency oscillatory ventilation (HFOV) was recently recommended as an alternative strategy in a consensus paper from the Pediatric Acute Lung Injury Consensus Conference in patients with plateau pressures greater than 28 cmH2O. It should be noted that, although there is some evidence that supports a reduction in time on ventilator in paediatric patients, there is none to support a mortality benefit.23
Inhaled nitric oxide has been used in neonatal practice for many years, but there is as yet no evidence to support a mortality benefit in paediatric practice. The mechanism of action is thought to be an improvement of oxygenation via pulmonary vasodilation and improved ventilation/perfusion mismatch. A recent study showed a quicker time to cessation of mechanical ventilation and avoidance of other interventions, such as HFOV and extracorporeal membrane oxygenation (ECMO), when hypoxia had responded to inhaled nitric oxide.25
Prone positioning is one option that can be considered. It has been shown to decrease mortality in adult patients with acute respiratory distress syndrome, but this is yet to be shown in paediatrics. The mechanism of action is thought to be recruitment of previously collapsed dorsal (dependent) areas of lung and subsequent improvement in ventilation/perfusion matching.26 Before using this technique, the potential haemodynamic effects of the prone position, potentially catastrophic loss of a secured airway, and any predicted difficulty in securing the airway whilst maintaining oxygenation must all be considered.
Extracorporeal membrane oxygenation is considered in cases where there is borderline or inadequate gas exchange with high risk of ventilator-induced lung injury (mean airway pressure >20–25 cmH20) and continued severe respiratory failure (Pao2:FIo2 ratio <60–80 or oxygen index >40) despite less invasive therapies, such as those therapies mentioned previously.27 It has been shown to confer a survival advantage in neonates with respiratory failure, and remains an option in paediatric respiratory failure. Presently, there is no evidence of a survival benefit, and a recent small paired cohort study confirmed this and highlighted the need for further research into the benefits of ECMO, which remains an expensive and invasive treatment option.28
Conclusions
Respiratory distress is a common reason to alert the paediatric emergency response team or request input from anaesthetists in the hospital setting. This article has examined some of the more common causes of respiratory distress (bronchiolitis, preschool wheeze and asthma) along with rare, but commonly limiting illnesses, such as chILD. It should be remembered that respiratory distress can also have extrapulmonary causes, such as sepsis (with a source other than pulmonary) and heart disease. Management by the anaesthetist requires meticulous and methodical planning of induction, intubation and ventilation to avoid complications thereof. Senior help is always advised when dealing with these patients. Patients with tracheostomies in respiratory distress represent a special group in whom a careful assessment of tracheostomy patency is the key, in addition to the standard general approach, to paediatric respiratory distress.
Declaration of interest
The authors declare that they have no conflicts of interest.
Acknowledgements
The authors thank Dr Simona Lampariello, consultant in paediatric intensive care, and Dr Chin Nwokoro, consultant respiratory paediatrician and honorary clinical senior lecturer at the Royal London Hospital for their helpful suggestions and comments.
MCQs
The associated MCQs (to support CME/CPD activity) will be accessible at www.bjaed.org/cme/home by subscribers to BJA Education.
Biographies
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Joanne Challands FRCA is a consultant paediatric anaesthetist at the Royal London Hospital.
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Katherine Brooks FRCA is a specialty registrar in anaesthesia at Barts Health NHS Trust and the London School of Anaesthesia.
Notes
Matrix codes: 1C02, 2D01, 3D00
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