PAEDIATRIC ANAESTHESIA Tutorial 368

Acute upper airway obstruction in

children
Dr. Martin Gray
Anaesthetic Registrar, North Central Thames Deanery, UK

Dr. Linda Chigaru

Anaesthetic and CATS Consultant, Great Ormond Street Hospital, UK

Edited by
Dr. Isabeau Walkeri and Dr. Kate Wilsonii
iConsultant Anaesthetist, Great Ormond Street Hospital, London, UK
iiConsultant Anaesthetist, Sheffield Children’s Hospital, UK

Correspondence to [email protected] 12th Dec 2017

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Key Points

 When assessing a child with a compromised airway, avoid upsetting or stressing the child as it may result in
deterioration of an already compromised airway.
 Utilise available local, regional and national guidelines to help guide management.
 Plan ahead – inform senior anaesthetic and ENT staff or discuss patients with a transfer team at an early stage.

INTRODUCTION
Acute airway obstruction may occur at any age and should be considered an emergency. The causes of airway
obstruction differ between adults and children. This tutorial will focus on acute upper airway obstruction in children;
readers are referred to a recent tutorial by Bryant et al for management of the obstructed airway in adults 1.

Infants and young children are anatomically, physiologically and psychologically different to adults. It is important that
these differences are taken into account when managing the child with acute airway obstruction, particularly in neonates
and infants, as the child has limited reserve, and may rapidly progress to complete airway obstruction2.

ASSESSMENT

Airway obstruction may occur at different anatomical levels and may be partial or complete, and may occur abruptly or
over a more gradual time course. Acute, total airway obstruction may rapidly progress to cardiopulmonary arrest, which
should be managed according to standard resuscitation guidelines 3. The most obvious clinical sign of partial upper
airway obstruction is stridor: a harsh, often high-pitched noise induced by the turbulent flow of air through the narrowed
airway.

Type of obstruction Level of obstruction

Inspiratory stridor Extrathoracic / above the vocal cords
Expiratory wheeze or stridor Intrathoracic / below the vocal cords
Inspiratory & expiratory stridor / wheeze At or below the vocal cords

Table 1 – Relationship between phase of stridor and likely level of airway obstruction

Stridor may be the sign that arouses the clinician or parent’s attention to the problem, the differential diagnosis is wide,
and therefore a comprehensive assessment is necessary to avoid anchoring error. APLS guidelines suggest a method of
airway and breathing assessment that focuses on the effort, efficacy and effort of breathing (table 2). This should then

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ATOTW 368 – Acute upper airway obstruction in children (12th Dec 2017) Page 1 of 9
progress to an assessment of circulation, disability and exposure in order to complete the primary survey in a full A to E
format. An excellent resource available to help those wishing to develop their skills for systematic assessment of the sick
child is available for free at https://www.spottingthesickchild.com.

Parameters evaluated
Effort of breathing Respiratory rate
Added sounds: Stridor / wheeze / grunting
Recession
Accessory muscle usage
Flaring of nostrils
Efficacy of breathing Chest expansion / abdominal excursion
Auscultation: reduced, absent, symmetrical
Oxygen saturation
Effect of respiratory Heart rate
failure on other systems Skin colour
Mental status
Table 2 – APLS suggested assessment of breathing2

Whichever systematic method you use to complete your primary survey of a child with a compromised airway, the golden
rule must be ‘avoid upsetting the child’, as this may result in further clinical deterioration.

During the initial assessment:

 Leave the child with the parent / carer in a comfortable position.
 DO NOT insert a tongue depressor or other device to examine the airway
 DO NOT attempt IV access or blood tests
 DO NOT request X-ray / imaging at this stage
 DO NOT force an oxygen mask on the child
 Remember that pulse oximetry may be falsely reassuring when the child is receiving supplementary oxygen

After completion of your initial assessment, take a comprehensive history before moving on to physical examination and
any appropriate investigations.

 Birth history
 Neonatal history, immunizations history
 Previous respiratory problems
 Current respiratory symptoms
o Duration
o Precipitating / exacerbating events e.g. feeding / crying
 Presence of other current signs / symptoms
o Fever
o Drooling
 Family history
Table 3 – Headings to be considered when taking a history as part of a secondary survey

CAUSES AND MANAGEMENT OF UPPER AIRWAY OBSTRUCTION IN CHILDREN

Causes of acute upper airway obstruction (UAO) can be classified into congenital or acquired and then further sub
classified as infective or non-infective. The congenital causes such as choanal atresia and laryngomalacia tend to
present in the first weeks of life and will not be the focus of this tutorial. Instead we shall focus on the more common
acquired causes of UAO as these will be seen more commonly by the general anaesthetist.

Viral croup
Acute viral layngotracheobronchitis (viral croup) is the commonest form of croup 3. 75% of infections are caused by
parainfluenza virus4, with other pathogens including respiratory syncytial virus and adenovirus. Croup affects
approximately 3% of children each year4, with a peak incidence in the second year of life5. Although this condition can be
seen at any time of year, most cases in the UK present during late autumn.

Croup usually causes UAO in children under 2 years of age. As the subglottic lumen increases in size as children grow,
the effect of any oedema caused by the infection has less impact on the airway. If the child is older than 3, other causes
of airway obstruction are more likely than a diagnosis of viral croup.

A child with croup usually presents with a barking seal-like cough, harsh inspiratory stridor, and hoarse voice and cry,
often starting at night, and commonly preceded by symptoms of a cold with a low-grade fever. The airway symptoms are

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caused by subglottic and tracheal swelling. If the upper airway inflammation is minor, stridor may only be audible when
the child breathes more vigorously, for instance, if they are upset. Stridor may be apparent during both inspiratory and
expiratory phases of respiration, and becomes audible at rest as airway narrowing progresses. There may be signs of
increased work of breathing, such as recession, tachypnoea and tachycardia. Recession is common in smaller children
as they have a soft ribcage; this is an ominous sign in an older child. The child may become wheezy if infection spreads
distally and the bronchi become affected.

The treatment of croup depends on the severity of airway obstruction as indicated by the observed signs and symptoms.
Individual hospitals may have their own guidelines for management of this common condition; however, the Westley
Croup Score and Children’s Acute transport Service (CATS) flow chart may be useful to guide treatment in the absence
of an in-house policy (Figure 1).

Figure 1 - Westley Croup Score and Children’s Acute transport Service (CATS) flow chart to guide the management of a
child with croup6

The mainstay of treatment for croup are glucocorticoids with or without nebulised adrenaline. In most children the
symptoms of croup will resolve within 48hrs. Only1-3% of children admitted to hospital require tracheal intubation4.
A systematic review of the literature in 20134 concluded that:
 In children with mild croup:
o A single dose of dexamethasone improves symptoms compared with placebo
o Although humidification is often used there is no high-quality evidence to support its use in clinical
practice
 In moderate to severe croup:
o Intramuscular or oral dexamethasone, nebulised adrenaline, and nebulised budesonide reduce
symptoms compared to placebo
o Oral dexamethasone is as effective as nebulised budesonide at reducing symptoms, and less
distressing for the child
o A dose of dexamethasone of 0.15 mg/kg may be as effective as a dose of 0.6 mg/kg
o Adding nebulised budesonide to oral dexamethasone does not seem to improve efficacy when
compared with either drug alone
o There is a lack of evidence to know whether heliox or humidification are beneficial

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Steroids are used to treat the airway oedema / inflammation and may result in clinical improvement within 30mins3.
Systemic dexamethasone or nebulised budesonide are equally effective 4.

Parenteral dexamethasone has no advantage over oral dexamethasone 4,7, so administration by the quickest and least
anxiety provoking route for the child would seem the most sensible approach. The dose of dexamethasone in our unit is
chosen according to the severity of the croup8.

Nebulised adrenaline is the other well established treatment in croup. This reduces oedema of the inflamed mucosa via
alpha-adrenoreceptor-mediated vasoconstriction. The effects of nebulised adrenaline can be immediate and dramatic, if
short lived (<2hrs), and repeat administration may be necessary 9. Systemic absorption of the adrenaline may occur and
ECG monitoring should be considered; however, take care not to upset a severely compromised child. The dose of
nebulised adrenaline used in our unit is 0.5mg/kg of 1:1000 solution up to a maximum of 5mg 6,8.

Other suggested treatments for croup include humidification and heliox, although there is no strong evidence for their
effectiveness4. Humidification improves patient comfort, so a pragmatic approach is to consider humidification if
supplementary oxygen is required.

Heliox is a mixture of oxygen and helium. Helium is a low-density gas and theoretically reduces the work of breathing if
there is turbulent flow through a narrowed upper airway. The percentage oxygen in the mixture is generally only 21%
(occasionally 30% or 40%), which may not be sufficient for the clinical situation. A Cochrane review published in 2013
suggested there was a short-term benefit of heliox inhalation in children with moderate to severe croup after
administration of oral or intramuscular dexamethasone’ 10.

A child with croup must undergo serial assessments to determine the response to treatment and the need for further
intervention. Lack of response or deterioration of the patient may be an indication for intubation, which will be discussed
later in the tutorial.

Post intubation croup

Subglottic oedema may occur following instrumentation of the airway, particularly following repeated attempts at
intubation or insertion of an oversized tracheal tube. In such a situation, the child presents with stridor or other signs of
airway compromise post extubation. The child will usually respond well to treatment with dexamethasone and nebulised
adrenaline.

Bacterial tracheitis
Bacterial tracheitis is a serious, life-threatening condition. Over 80% of children with bacterial tracheitis will need to be
intubated3. It affects children between the ages of six months to eight years, with average age range of 4-6 years5.
Children are usually older than those with croup, they look ‘sicker’ and don't respond to treatment with nebulised
adrenaline11. The classical presentation is of a child with a history of upper respiratory tract infection for 2-3 days
followed by rapid deterioration over approximately 8hours, who presents looking toxic with high fever and respiratory
distress. These children have a productive cough with copious secretions that may induce retrosternal pain. The voice
may be hoarse and stridor is common.

Pathogens responsible for bacterial tracheitis include Staphylococcus aureus, Streptococci and Haemophilus influenzae.
The larynx, trachea and bronchi can become acutely obstructed due to inflammation, thick purulent secretions and
mucosal necrosis.

Intubation may be very difficult so an experienced clinical should perform this. There may be thick purulent sections
beyond the vocal cords, which should be suctioned and sent for culture. The tracheal tube may become blocked by
secretions immediately after intubation, so be prepared to remove the tube and replace it with a clean tube. The tube
may need to be changed several times. Once the airway is secured, obtain IV access, take blood cultures and give
antibiotics if this has not been done already. Ceftriaxone is a reasonable first line antibiotic. Vancomycin and or
clindamycin may be indicated if there is a high incidence of community acquired methicillin resistant S. aureus
Tracheal stenosis is unfortunately a late complication of this condition 7.

Abscess
Retropharyngeal or tonsillar abscesses tend to be caused by similar organisms to those responsible for bacterial
tracheitis, namely staphylococcal or streptococcal infections 7. The abscess may cause neck pain and swelling,
dysphagia, trismus and fever. Furthermore, oedema may cause inspiratory stridor. The antibiotics used will be the same
as those for bacterial tracheitis and again, should be given after obtaining the necessary cultures. If surgery is deemed
appropriate, care must be undertaken at the time of airway instrumentation to avoid rupture of the abscess and
contamination of the lower airways. For further information the reader should refer to a previous ATOTW on the
subject12.

Epiglottitis
A child with epiglottis may present with acute severe airway obstruction. The diagnosis is made from the characteristic
history and clinical findings, and if suspected, preparations should immediately be made for intubation.

Epiglottitis is caused by bacterial infection of the epiglottis, aryepiglottis and arytenoids with obstruction of the larynx, and
results in acute presentation with high fever, lethargy, soft inspiratory stridor and rapidly increasing respiratory difficulty

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over a period of 3-6 hours. In contrast to a child presenting with croup, there is usually minimal cough and the child will
sit immobile, with mouth open and tongue protruding in order to keep the airway open. Drooling is common as the child
is unable / unwilling to swallow due to severe throat pain. A child with epiglottis will look much ‘sicker’ than a child with
croup. It is important to avoid attempts to examine the airway or stress the child in any way as worsening airway
obstruction could result in an irretrievable situation with complete airway obstruction.

The mnemonic ‘4Ds’ was described to aid to diagnosis of epiglottitis 13:

1. Drooling
2. Dysphagia
3. Dysphonia
4. Dyspnoea

The pathogen responsible for epiglottitis in children is almost always Haemophilus influenza, and so the condition is
fortunately less common since the introduction of the Hib vaccine in 1992. However, epiglottitis can be caused by other
organisms such as streptococcal or staphylococcal infection 7 and may be seen in those who have not received the Hib
vaccine.

Nebulised adrenaline may be tried whilst preparations are being made for intubation. Since intubation may well be
difficult, an experienced team including a senior anaesthetist and ENT surgeon should ideally be present. In a distressed
child, IV access should only be attempted after the airway is controlled. Blood cultures should be taken and IV antibiotics
administered (ceftriaxone 80mg/kg/day, max 4g/day, or according to local guidance).

Infectious mononucleosis (IM)

Massive tonsillar enlargement and mucosal oedema is an uncommon feature of IM seen in 1-3.5% of cases5. This
complication tends to affect younger children and presents with dyspnoea, sore throat, dysphagia and drooling.
Intubation will bypass the pharyngeal obstruction and act as an effective treatment for these severe cases of IM.

Foreign Body Aspiration

The peak incidence of foreign body aspiration (FBA) is in 1-2 year olds, possibly as they lack molars to chew food
effectively, and play whilst eating. They also tend to explore the world with their mouths, lacking the ability to distinguish
between edible and inedible objects14. Most foreign bodies lodge in the distal airway, although they can occasionally
lodge in the larynx or trachea, with a risk of complete airway obstruction5.

The classic history of FBA is of sudden onset of coughing, choking or stridor, often when the child is eating or playing. A
history of sudden onset respiratory compromise, during waking hours and without any preceding history of fever or
illness should place an inhaled FB very high on the differential diagnosis. APLS suggests clear guidelines for the
management of the acutely compromised choking child 3; in summary, coughing should be encouraged whilst effective
and back blows alternating with chest and abdominal trusts should be commenced if coughing is ineffective.

Many children will not present with such an acute respiratory deterioration and the symptoms may be difficult to
distinguish from asthma. A child who presents with a new history of refractory asthma may occasionally prove to have an
undiagnosed foreign body.

Surgical removal of the FB will usually require rigid bronchoscopy under general anaesthesia by an experienced ENT
surgeon. An effective technique is to perform an inhalational induction of anaesthesia, before ‘topicalization’ of the airway
using lignocaine 3mg/kg, before passing a rigid bronchoscope whilst the child keeps breathing spontaneously. This is a
good example of a ‘shared airway’. Rigid bronchoscopy will allow both confirmation and removal of the foreign body.
Intravenous dexamethasone, with or without nebulised adrenaline, helps to reduce airway oedema. Intubation and
positive pressure ventilation prior to rigid bronchoscopy is generally avoided as it may result in impaction of the foreign
body more distally, and should only be considered with impending airway or cardiovascular collapse.

Anaphylaxis
Anaphylaxis may develop over minutes and may cause potentially life threatening airway, respiratory and circulatory
compromise. Multiple triggers have been identified, with foods (especially nuts), drugs and venoms amongst the most
common causes3. Prodromal symptoms of flushing, itching, facial swelling, and urticaria usually precede airway
compromise and stridor.

As for all life threatening emergencies, a structured ABCDE treatment algorithm should be followed. The key steps in the
management of a patient with a suspected anaphylactic reaction will include 3:
 Call for help
 Remove the allergen
 Administer oxygen via mask
 Administer intramuscular (IM) adrenaline at a dose of 10 micrograms/kg3 or a specified dose adjusted for the
child’s age range as per the CATS guideline15:

Further management includes appropriate monitoring and management of the airway, IV fluid resuscitation, repeat doses
of IM or IV adrenaline, and age specific doses of hydrocortisone and chlorphenamine 15.

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Hereditary angioedema (HAE)
Hereditary angioedema (HAE) has an estimated prevalence of 1:50,000 and results from a deficiency of C1 esterase
inhibitor. It should be considered in the differential diagnosis of any child presenting with angiooedema as symptoms
HAE tend to start in the first or second decade of life, with approximately 75% of affected individuals experiencing their
first attack as a child, before the age of 15 years16.

The condition is either due to impaired production of C1 esterase inhibitor (Type I, 85% of cases) or a reduction in
function of the protein (Type II). This enzyme usually plays a key role in controlling the complement cascade by
preventing auto activation of C1, the first factor in the classical pathway. Lack of C1 esterase inhibitor can lead to
uncontrolled complement activation with the resultant release of vasoactive and chemotactic peptides causing an
increase in vascular permeability, vasodilatation and contraction of vascular smooth muscle. The clinical picture is of
acute, localised, non-pitting, non-pruritic, non-erythematous angioedema, which can involve any part of the body 16. Areas
most commonly affected by swelling include the face (particularly the eyelids, lips & tongue), the extremities and the
genitals.

It is estimated that 50%-70% of HAE sufferers will experience laryngeal oedema at some point in their lifetime. A
common trigger for laryngeal attacks is tooth extraction or oral surgery 5,16. Airway oedema tends to occur at the level of
or above the larynx. As with others causes of laryngeal oedema, symptoms of stridor, voice changes and dysphagia will
alert the clinician.

Although the mode of inheritance of both Type I and II HAE is autosomal dominant, approximately 25% of cases may be
due to spontaneous mutation on chromosome 11. Approximately 5% of carriers don’t display any clinical features, so a
family history of angiooedema may not be present.

Acute management is the same as for any child with acute airway compromise. Immediate airway assessment should be
performed without distressing the child and steps should be taken to secure the airway as necessary. Of note, agents
commonly used to treat allergic angioedema, such as adrenaline, steroids and anti-histamines will not be effective in the
treatment HAE. Treatment requires infusion of C1 esterase inhibitor in either a plasma derived or recombinant form, as
available. Fresh frozen plasma (FFP) has been used to treat acute attacks, but because it also contains C4, it can fuel
further cleavage of complement factors and occasionally exacerbates symptoms.

Airway oedema occurs at the level of, or above the larynx, so tracheostomy should be considered if intubation fails. A
surgical team scrubbed and prepared is therefore mandatory for any child suffering from angioedema secondary to HAE;
in some situations tracheostomy may be considered as the primary means of emergency airway management. Genetic
screening and long-term prophylactic treatment of HAE requires specialist input.

Inhalational injury
Acute airway compromise may occur following thermal injury and associated oedema. If there is a suspicion of thermal
injury, or concern about later deterioration, early preparations should be made for tracheal intubation by an experienced
team2.

Factors indicating potential inhalational injury include:

 History of exposure to smoke in a confined space
 Carbon deposits around the mouth and nose
 Carbonaceous sputum

Trauma
The airway may be compromised due to oedema, sections or blood from traumatic causes. Trauma may be accidental or
iatrogenic (e.g. secondary to tracheal intubation or tracheostomy). It is particularly important to avoid multiple attempts at
intubation in infants as this will result in the rapid development of airway oedema. Assessment and management of
airway compromise due to trauma will depend on the underlying cause.

INDICATIONS FOR INTUBATION

Experience is important when deciding the need for tracheal intubation and the urgency with which this should proceed.
Situations where immediate intubation should be considered include:
 Suspected epiglottitis
 Inhalational injury
 Falling conscious level
 Increasing respiratory failure, indicated by:
o Rising PaCO2
o Exhaustion
o Hypoxia (SpO2 <92% despite high flow oxygen administered via mask)

An early decision should also be made regarding whether a surgeon experienced in performing an emergency
tracheostomy is required.

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MANAGEMENT OF INTUBATION

Planning should start at an early stage, particularly with regard to the personnel required as it may take time to assemble
an appropriately experienced skilled team. Good communication is essential throughout the process of anaesthetising,
stabilising and transferring the patient. Everyone needs to be kept informed and aware of the plan at all times.

The most experienced anaesthetist must be present at the intubation. Ideally two experienced anaesthetists should be
present, with one identified to lead the procedure. A skilled anaesthetic assistant will be required, and a surgeon
experienced in performing an emergency tracheostomy. If present, the surgeon should be scrubbed and ready to
perform an immediate tracheostomy if intubation is unsuccessful.

All necessary equipment and drugs should be assembled, drawn up and available. Prepare an age appropriate tracheal
tube, and smaller sizes in case of airway oedema/narrowing. A ‘croup tube’ may be useful - these are longer than
standard tracheal tubes. Ideally, difficult intubation should be anticipated in advance. The APA/DAS guidelines will help
with management of difficult situations 17. A back up plan for oxygenation of the patient must be available. In many cases
this will include emergency surgical access to the airway.

Most anaesthetists favour an inhalational/gas induction using a suitable inhalation agent such as sevoflurane in 100%
oxygen. Induction may be slow if the airway is obstructed and patience to achieve a deep plane of anaesthesia is
required. Standard anaesthetic monitors should be applied. The child may become apnoeic during induction; try to keep
the upper airway patent using chin lift; keep the facemask applied and wait for the child to resume spontaneous
ventilation. Airway obstruction may worsen due to loss of airway tone as anaesthesia deepens, but careful positioning,
gentle application of jaw thrust, and application of 5-10cm of continuous positive airway pressure (CPAP) will generally
maintain airway patency18.

Once a suitable depth of anaesthesia has been achieved, intravenous access should be obtained if this has not been
done already, prior to instrumentation of the airway. Pupils should be small and central, there should be a settled
respiratory pattern, and no response following application of a firm jaw thrust.

Where the supraglottic tissue is inflamed (for instance epiglottitis), it may be very difficult to visualise the glottic opening
at laryngoscopy. The presence of bubbles may indicate the position of the larynx; if the child is adequately
anaesthetised, a sharp manual chest compression may be useful to open the expiratory path momentarily to produce a
few bubbles of expired gas.

MANAGEMENT FOLLOWING INTUBATION

Once the airway obstruction is bypassed, most children will be easy to ventilate. Exceptions might include bacterial
tracheitis if pulmonary involvement is present, inhalational injuries complicated by ARDS or anaphylaxis where
bronchoconstriction can occur. Following intubation, the tracheal tube should only be changed if there is a clear clinical
reason that justifies the risk.

Following intubation:
 Tape the tracheal tube securely at the correct depth
 Sedate and paralyse the child to ensure the continued safety of the airway/tracheal tube, in the absence of an
in-house guideline see CATS website for drug calculator / sedation regime19
 Take a chest X-ray to confirm the tracheal tube position and exclude any other airway pathology

Other interventions will be dictated by the underlying cause of the airway obstruction. Blood cultures should be taken if
infection is suspected, and adjunctive treatments started such as ceftriaxone (80 mg/kg IV) in case of epiglottitis or
tracheitis or dexamethasone (0.15 mg/kg IV QDS) in the case of croup. Patients with bacterial tracheitis may develop
septic shock and require further resuscitation. For burns replace fluids according to burn protocols.

The anaesthetist should remain with the child until transfer to a suitable intensive care, ideally via a dedicated transport
team. The child should be fully monitored and clear communication and records maintained at all times. See CATS
guideline on ‘waiting for the retrieval team’ for interventions / management whilst awaiting retrieval 20. Table 4
summarises the clinical presentation and management of the different causes of UAO discussed in this tutorial.

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 Diagnosis Clinical presentation / Physical examination Treatment
Viral croup Usually seen in children under 2 years of age. Mainstay of treatment are glucocorticoids
Barking seal-like cough, harsh inspiratory stridor, with or without nebulised adrenaline
and hoarse voice / cry, (often starting at night) -
commonly preceded by symptoms of a cold with a Lack of response or deterioration of the
low-grade fever patient may be an indication for intubation

May be signs of increased work of breathing, such

as recession, tachypnoea and tachycardia

Post intubation Stridor or other signs of airway compromise post Usually responds well to dexamethasone
croup extubation and nebulised adrenaline.

Bacterial tracheitis Sick / septic looking child with respiratory distress. 80% require intubation – assemble an
Hoarse voice, stridor and productive cough and experienced team early
copious secretions
No or little response to nebulised
Preceding 2-3 day history of upper respiratory adrenaline
tract infection, followed by rapid deterioration to
presenting state Management of the septic child including
IV antibiotics

Abscess Neck pain and swelling Cultures and IV antibiotics

May cause dysphagia, stridor, trismus and signs May require surgical drainage
of systemic sepsis

Epiglottis Acute, severe, airway obstruction Assemble an experienced

multidisciplinary team early – intubation
Sick looking septic child with soft inspiratory will usually be required and may be
stridor and rapidly increasing respiratory difficulty difficult

Child will usually sit immobile with mouth open IV cultures and antibiotics
and tongue protruding, drooling / unable to
swallow

Foreign body Peak incidence 1-2 years old Cough should be encouraged
aspiration
Sudden onset of respiratory compromise without Surgical removal of FB by ENT surgeon
any preceding illness or fever may be required

Anaphylaxis Respiratory &/or cardiovascular compromise ABCDE management

following exposure to an antigen trigger IM adrenaline

Hereditary Acute, localised, non-pitting, non-pruritic, non- Steps should be taken to secure the
angioedema erythematous angioedema - commonly affecting airway as necessary
eyelids, lips & tongue
Agents commonly used to treat allergic
Airway oedema tends to occur at the level of or angioedema, such as adrenaline, steroids
above the larynx - symptoms include stridor, voice and anti-histamines will not be effective
changes and dysphagia
Treatment requires infusion of C1
esterase inhibitor

Inhalational injury Acute airway compromise / oedema following Early preparation for intubation by an
thermal injury experienced team

Table 4: Diagnosis, presentation and management of the different causes of UAO in children

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 SUMMARY
 Acute upper airway obstruction in a child is an emergency situation requiring timely multidisciplinary
management to prevent deterioration of the clinical situation.
 When assessing or attempting to treat the condition, steps should be taken not to upset the child and further
compromise the airway.
 Inform senior clinicians at an early stage as it may take time to assemble a suitably experienced team if the
child is severely compromised.
 Paediatric intensive care transport services can be a valuable source of telephone advice when managing
compromised children, also from guidance on their websites

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REFERENCES AND FURTHER READING

1. Bryant, H. Batuwitage, B. Whittle, N. (2016) Management of the obstructed airway. Anaesthesia tutorial of the
week. ATOTW 336
2. Macfarlane, K. (2005) Paediatric anatomy and physiology and the basics of paediatric anaesthesia. ATOTW 7
3. Advanced Paediatric Life Support: a practical approach to emergencies, 6 th ed. (2016) ALSG. Wiley-Blackwell
4. Johnson, D.W. (2014) Croup. BMJ Clin Evid. Sep 29
5. Pfleger A, Eber E. (2013) Management of acute severe upper airway obstruction in children. Paediatr Respir
Rev. Jun;14(2): 70-7
6. Children’s Acute Transport Service [online] Available at http://site.cats.nhs.uk/ [Accessed 08 September 2016]
7. Maloney, E. Meakin, G.H. (2007) Acute stridor in children. Continuing education in Anaesthesia, Critical Care &
Pain. Vol 7 No.6
8. Chigaru, L. (2013) Clinical guidelines: Upper airway obstruction (UAO) [online] Children’s Acute Transport
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