Acute Stridor = in Children

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Acute Stridor in Children

Emma Maloney; George H. Meakin

Cont Edu Anaesth Crit Care & Pain. = 2007;7(6):183-186.=20 =A92007 Oxford University Press

Posted 12/28/2007

Introduction

Stridor is a harsh, vibratory sound produced when the airway = becomes=20 partially obstructed, resulting in turbulent airflow in the = respiratory=20 passages. It is symptomatic of underlying pathology and may herald = life-threatening airway obstruction. This article reviews the = assessment,=20 common causes, and treatment of a child with a previously normal = airway=20 presenting with acute stridor.

Anatomy and Physiology

Several anatomical and physiological features of the = respiratory system=20 in infants (age <1 yr) and young children render them = susceptible to=20 airway obstruction. The upper and lower airways are small, prone = to=20 occlusion by secretions, and susceptible to oedema and swelling. = As=20 resistance to laminar airflow increases in inverse proportion to = the=20 fourth power of the radius (Poiseuille's law), a small decrease in = the=20 radius of the airway results in a marked increase in resistance to = airflow=20 and the work of breathing.

The support components of the airway are less developed and = more=20 compliant than in the adult. The ribs are cartilaginous and = perpendicular=20 relative to the vertebral column, reducing the effect of the = =91bucket=20 handle=92 movement of the rib cage. In addition, the intercostal = muscles and=20 accessory muscles of ventilation are immature. As a result, = children are=20 more reliant on the diaphragm for inspiration. Increased = respiratory=20 effort causes subcostal and sternal recession, and the mechanical=20 efficiency of the chest wall is reduced. Higher metabolic rate and = increased oxygen demand mean children with airway compromise can=20 deteriorate very quickly. Also, with a smaller functional residual = capacity and fewer fatigue-resistant fibres in the diaphragm, = there is=20 little respiratory reserve at times of = stress.^[1]

Assessment

A stridulous, distressed child should be disturbed as little as = possible as crying and agitation increase respiratory effort and = might=20 precipitate complete airway obstruction. Therefore, the child = should be=20 allowed to adopt the posture in which they are most comfortable = and the=20 parents should be present. Examination of the throat and i.v. = cannulation=20 should not be attempted.

The phase of stridor may indicate the level at which the airway = is=20 compromised ( Table 1 ).^[2] It is important to = appreciate=20 that the volume of stridor does not correlate with the degree of=20 obstruction. For example, a progressive decrease in volume may = signify a=20 decreasing conscious level.

Examination may be limited to inspection for signs of increased = work of=20 breathing ( Table 2 ), although a pulse oximeter probe is = usually=20 well tolerated and gentle examination of the chest may be = possible.=20 Laboratory tests are not helpful in the early assessment of a = child with=20 acute stridor. Radiology may be useful in less acute cases, but it = should=20 only be performed at the bedside with minimal disturbance to the = child.=20 Children with symptoms and signs of severe airway obstruction = require=20 urgent examination of the airway under anaesthesia to determine = the cause=20 and secure the airway. Collaboration with an experienced ENT = surgeon is=20 essential for optimal management of these cases.

Viral Croup

Viral croup (laryngotracheobronchitis) is responsible for more = than 80%=20 of cases of acute stridor in children. It is usually due to = infection with=20 parainfluenza viruses, but it may also be caused by influenza = viruses type=20 A or B, respiratory syncytial virus or rhinovirus. It commonly = affects=20 children age 6 months to 3 yr with a peak incidence at 2 yr. Only = 2% of=20 cases are admitted to hospital each year, of which only 0.5=961.5% = will=20 require intubation.^[2,3] Infection results in = subglottic and=20 tracheal swelling causing stridor and other signs of respiratory=20 obstruction. In the more severe cases, it also affects the small = airways,=20 resulting in bronchial constriction, oedema, and atelectasis.

Croup develops 2=963 days into an upper respiratory tract = infection and=20 is characterized by a barking cough (which gives the condition its = name),=20 low-grade fever, inspiratory stridor, and increased respiratory = effort=20 progressing to fatigue, hypoxia, and hypercarbia. A scoring system = for=20 croup is useful in assessing severity. Ongoing, serial bedside = assessment=20 of a child with croup is key to determining the success of medical = treatment or need for further interventions, such as admission to = a high=20 dependency unit or tracheal intubation ( Table3 ).^[4]

Treatment includes humidification of respiratory gases, oxygen, = steroids, and nebulized epinephrine.^[5] Nebulized = epinephrine=20 is believed to reduce oedema by alpha-adrenergic-mediated = vasoconstriction=20 of the inflamed subglottic mucosa. In North America, racemic = epinephrine=20 containing equal amounts of the L- and D-isomers (L-isomer 30 = times more=20 active) is widely used. In the UK, only L-epinephrine is = available. The=20 usual dose of racemic epinephrine is 0.5 ml of a 2.25% solution = diluted to=20 4 ml with saline or water, repeated hourly, as necessary. This = dose=20 contains approximately 5 mg of active L-epinephrine, equivalent to = 5 ml of=20 (non-racemic) epinephrine 1/1000.^[6] Accordingly, in = many UK=20 hospitals, moderate to severe croup is treated with nebulized = epinephrine=20 1/1000, 0.5 ml kg⁼⁹⁶¹ to a maximum of 5 ml, repeated if = necessary=20 after 30=9660 min. The improvement in the croup score after this = can be=20 dramatic, but the effects are short-lived; repeated administration = is=20 required. Although cardiovascular side-effects are rare, ECG = monitoring is=20 recommended.

Steroids reduce symptoms and improve croup scores 6=9624 h = after initial=20 dosing, thereby reducing the need for intubation or shortening the = time to=20 extubation. Randomized controlled trials have shown that = parenteral=20 dexamethasone 0.6 mg kg⁼⁹⁶¹, oral dexamethasone 0.6 mg=20 kg⁼⁹⁶¹, and nebulized budesonide 2 mg have similar = efficacy in=20 treating croup. As oral administration of dexamethasone is quicker = and=20 causes less distress than nebulization or parenteral = administration, it=20 may be preferable for children admitted to hospital with = moderate=96severe=20 croup.^[5] In the PICU setting, dexamethasone 0.1 mg=20 kg⁼⁹⁶¹ 6 h⁼⁹⁶¹ is = recommended.^[3]

Heliox is a 70:30% helium=96oxygen mixture that is less dense = than air or=20 100% oxygen. The lower gas density facilitates laminar (rather = than=20 turbulent) flow in narrowed airways allowing more efficient = ventilation in=20 a child with a compromised airway. In a randomized controlled = trial,=20 heliox administration resulted in similar improvements in croup = score as=20 administration of nebulized epinephrine.^[5] However, = limiting=20 the percentage of oxygen that can be administered to 30% could be = a=20 disadvantage in children with marked bronchial involvement.

Severe respiratory obstruction, as indicated by a persistently = high=20 croup score, despite ongoing medical treatment (e.g. score ≥ = 7, Table 3 ), is an indication for tracheal = intubation.=20 Once preparations for intubation have been made, the patient = should be=20 escorted to theatre by an anaesthetists or other person capable of = managing the airway. Oxygen should be given by mask if required.=20 Historically, halothane was the agent of choice for induction and=20 maintenance of anaesthesia in upper airway obstruction; however,=20 sevoflurane is safe and effective in this situation and it is = appropriate=20 that anaesthetists use the agent with which they are most=20 familiar.^[7]

The child should be anaesthetized using only the volatile agent = in=20 oxygen. It is not necessary to apply full monitoring before = induction, but=20 an oxygen saturation probe and end-tidal carbon dioxide monitoring = are=20 invaluable. Inhalation induction will take longer than usual in = children=20 with severe upper airway obstruction, since alveolar ventilation = is=20 restricted. Spontaneous ventilation should be maintained and = applying=20 continuous positive airway pressure (CPAP) via a T piece will help = to=20 splint the airway open. I.V. access should be established as soon = as=20 possible after the patient loses consciousness. Once the pupils = are small=20 and central, the level of anaesthesia is usually sufficient to = allow=20 laryngoscopy and tracheal intubation.^[8]

Visualization of the larynx should not be a problem; however, a = smaller=20 tracheal tube than normal for the age is usually required because = of=20 subglottic oedema. Oral intubation is preferred initially as it = allows=20 rapid control of the airway. When the child is fully oxygenated = and=20 clinically stable, the oral tube is replaced with a nasal one of = the same=20 size. I.V. sedation (e.g. midazolam 2=968 =B5g kg⁼⁹⁶¹=20 min⁼⁹⁶¹ and morphine 20=9640 =B5g kg⁼⁹⁶¹ = h⁼⁹⁶¹)=20 should be commenced before discontinuing anaesthesia and continued = in the=20 PICU along with CPAP, humidified air=96oxygen, and i.v. fluid = therapy. Arm=20 splinting should be considered in the awake, sedated child to = prevent=20 self-extubation. In cases with extensive small airway involvement, = intermittent positive pressure ventilation (IPPV) and frequent = suctioning=20 of the tracheal tube will be required. Antibiotics are reserved = for=20 patients with evidence of bacterial infection. Extubation may be = attempted=20 when a leak develops around the tracheal tube. Owing to the = variable=20 nature of the disease, this can take 2=9610 = days.^[5]

Postintubation Croup

Stridor and other signs of respiratory obstruction due to = subglottic=20 oedema may occasionally occur after routine intubation, usually = with an=20 unduly large tracheal tube. Clinical signs generally appear within = 30 min=20 of extubation and respond well to treatment with nebulized = epinephrine and=20 i.v. dexamethasone. Day case patients treated for postintubation = croup=20 should be observed in hospital for at least 2 h before discharge, = as signs=20 of respiratory obstruction may recur. Persistent or recurrent = signs of=20 airway obstruction are an indication for admission to = hospital.

Epiglottitis

Epiglottitis is a life-threatening emergency caused by = bacterial=20 infection of the epiglottis, aryepiglottis, and arytenoids. In = children,=20 it is almost always due to infection with Haemophilus = influenzae=20 type b (Hib), although it can be caused by beta-haemolytic = streptococci,=20 staphylococci, and pneumococci. Since the introduction of Hib = vaccine in=20 1992, childhood epiglottis has become rare. During a recent = resurgence in=20 Hib infections, a corresponding increase in the number of children = with=20 epiglottitis was observed, although numbers were still much = smaller than=20 those reported before Hib vaccination.^[9] In a recent=20 retrospective study, 10% of children presenting with epiglottis = were found=20 to have Hib infection, despite having being = vaccinated.^[10]=20 These findings highlight the importance of considering acute = epiglottitis=20 in the differential diagnosis of a child presenting with upper = airway=20 obstruction. This is particularly relevant since, in future, fewer = doctors=20 will be familiar with the symptoms and signs of the disease.

Epiglottitis is distinguished from croup by its fulminant onset = and the=20 toxic appearance of its victims. It occurs usually in children = aged 2=966=20 yr, with a peak incidence at 3 yr. Clinically, there is an abrupt = onset of=20 high fever, sore throat, dysphagia, stridor, and drooling. Speech = may be=20 muffled or lost and there is an absence of spontaneous cough. = Typically,=20 the child looks ill and may prefer to sit leaning forwards, mouth = open,=20 and with tongue and jaw protruding in order to open the airway. In = contrast to viral croup, the signs of respiratory obstruction in=20 epiglottitis are unlikely to be relieved by administration of = nebulized=20 epinephrine. The disease can be rapidly progressive with the use = of the=20 accessory muscles, cyanosis, and alteration in conscious level = indicating=20 severe respiratory compromise.^[3]

Many hospitals have a protocol for managing epiglottitis; the = key is to=20 secure the airway under inhalation anaesthesia in a manner similar = to that=20 described for severe viral croup. An experienced ENT surgeon = should be=20 standing by in case an immediate bronchoscopy or tracheostomy = becomes=20 necessary. Anaesthesia will normally be induced in the sitting = position=20 and i.v. cannulation is only attempted once the child is = sufficiently=20 obtunded. At laryngoscopy, the epiglottis will be red and swollen = and the=20 arytenoids and other supraglottic tissues inflamed, so that the = glottic=20 opening may be extremely difficult to visualize. In these = circumstances,=20 an abrupt manual chest compression may open the expiratory passage = momentarily or produce a few bubbles of expired gas. A tracheal = tube=20 0.5=961.0 mm (ID) size smaller than normal for the child's age = should be=20 chosen to assist passage through the partially obstructed glottic = opening.=20 Stiffening the tube with a stylet or by refrigeration may also be = helpful.=20 Successful intubation can usually be achieved by directing the tip = of the=20 oral tracheal tube to the spot where the glottic opening was = visualized or=20 the bubbles emerged. When the child is fully oxygenated, the oral = tube is=20 replaced with a nasal one. Laryngeal and blood cultures should be = obtained=20 during anaesthesia, after which antibiotic treatment should be = commenced=20 with an extended spectrum cephalosporin (e.g. ceftriaxone 80 mg=20 kg⁼⁹⁶¹ day⁼⁹⁶¹ max 4 g day⁼⁹⁶¹). = The return of=20 normal body temperature and an increased leak around the tracheal = tube are=20 indicators of recovery, which usually occurs about 48 h after the=20 institution of antibiotic therapy. Direct examination under = anaesthesia=20 with propofol will confirm the presence of a normal epiglottis and = the=20 patient can be extubated when fully awake.^[3]

Bacterial Tracheitis

Bacterial tracheitis is uncommon, but after the introduction of = the Hib=20 vaccine, it may have overtaken epiglottitis as a cause of = life-threatening=20 respiratory obstruction in some paediatric centres.^[11] = The=20 condition may occur at any age. The usual pathogens are = Staphylococcus=20 aureus, Haemophilus influenzae, streptococci, and = Neisseria=20 species.^[3]

The signs and symptoms of bacterial tracheitis are frequently=20 intermediate between those of viral croup and epiglottitis. After = an=20 antecedent upper respiratory tract infection of 2=963 days, the = child=20 becomes rapidly (8=9610 h) and seriously ill with a high fever and = respiratory distress. Coughing produces copious tracheal = secretions and=20 retrosternal pain. The voice may be hoarse and stridor prominent, = but=20 there is no dysphagia or drooling and the patient can usually lie = flat.=20 The larynx, trachea, and bronchi can become acutely obstructed = with=20 purulent debris and inflammation with adherent pseudomembranes = overlying=20 friable tracheal mucosa.

Most patients with bacterial tracheitis will require tracheal=20 intubation and the same protocol used for epiglottitis should be = followed.=20 At laryngoscopy, the epiglottis and supraglottic structures will = appear=20 normal, although slough and pus may be visible beyond the vocal = cords.=20 Bronchoscopy should be performed to remove the purulent debris = from the=20 trachea before intubation. After intubation, any remaining = purulent=20 material may be aspirated via suction catheters. Tracheal = intubation may=20 be required before anaesthesia and bronchoscopy if a child is in = extremis.=20 In these circumstances, initial intubation may result in complete=20 respiratory obstruction due to blockage of the tracheal tube with=20 inspissated pus and an immediate tube change will be required to = clear the=20 airway. Once the airway is secured, samples of blood and tracheal = aspirate=20 should be sent for culture and sensitivity tests. Ceftriaxone is a = reasonable first line antibiotic therapy. Methicillin-resistant=20 Staphylococcus aureus (MRSA) is an important consideration = since=20 treatment with vancomycin (15 mg kg⁼⁹⁶¹ 8 = h⁼⁹⁶¹, max 2 g=20 day⁼⁹⁶¹) may be necessary. Further management in the = PICU will=20 include sedation, IPPV/CPAP, frequent suctioning of the tracheal = tube to=20 prevent occlusion, and fluid resuscitation. The average duration = of=20 tracheal intubation is 6=967 days. Antibiotic therapy and = hospitalization=20 may be required for up to 14 days.^[3] Tracheal stenosis = is a=20 late complication.

Retropharyngeal or Tonsillar Abscess

A retropharyngeal abscess forms in the space between the = posterior=20 pharyngeal wall and the prevertebral fascia by lymphatic spread of = infection from the sinuses, teeth, or middle ear. A tonsillar = abscess=20 forms in the potential space between the superior constrictor = muscles and=20 the tonsil. Staphylococci and streptococci are the usual causal = agents.=20 Subsequent oedema of the pharynx may result in inspiratory = stridor.=20 Children under the age of 6 are affected most commonly, presenting = with=20 neck swelling and pain, fever, drooling, dysphagia, trismus, and = limited=20 neck movement. The diagnosis is made clinically, but a lateral = soft tissue=20 neck film can confirm retropharyngeal thickening. Surgery is = required in=20 most cases and care must be taken during intubation to avoid = abscess=20 rupture and aspiration of pus into the airways.^[7] The = patient=20 will usually be extubated at the end of the procedure. Subsequent=20 treatment consists of i.v. hydration and broad-spectrum=20 antibiotics.^[3]

Foreign Body Aspiration

Aspiration of a foreign body, commonly food, has a peak = incidence at=20 1=962 yr of age. A sudden onset of coughing, gagging, and choking = are=20 suggestive of foreign body aspiration and may necessitate basic = life=20 support manoeuvres for the choking child.^[12] A foreign = body at=20 or above the vocal cords can cause complete obstruction of the = upper=20 airway, stridor, or a change or loss of voice, and the cough and = dyspnoea=20 with which foreign bodies lower down the airway present. Partial=20 obstruction of a lower airway may cause air trapping behind the = foreign=20 body (ball and valve effect) with pneumothorax, surgical = emphysema, and=20 pneumomediastinum a possibility. In this situation, the usual = inspiratory=20 chest X-ray can appear normal; however, an expiratory film may = reveal air=20 trapping. Depending on the cause, location, and duration of airway = blockage, collapse and consolidation of a lobe or an entire lung = with=20 bronchial breathing, inspiratory crackles, and expiratory wheeze = may be=20 found on examination. Without a clear history of choking, the = symptoms can=20 be difficult to differentiate from acute asthma. Indeed, a = presentation of=20 refractory asthma may be explained by a previously missed foreign=20 body.

Rigid bronchoscopy with the patient breathing spontaneously = under deep=20 inhalation anaesthesia supplemented with up to 3 mg = kg⁼⁹⁶¹ of=20 topical lidocaine will confirm the diagnosis and allow for removal = of the=20 foreign body. The severity of symptoms and degree of airway = obstruction=20 will dictate the urgency with which this is performed. = Dexamethasone and=20 nebulized epinephrine will help ameliorate airway oedema after a = lengthy=20 bronchoscopy.^[3,8]

Table 1. Correlation Between Phase of Stridor and = Probable Level=20 of Airway Obstruction

Stridor Level of obstruction

Inspiratory Above the cords (extrathoracic); e.g. croup,=20 epiglottitis

Expiratory Below the cords (intrathoracic); e.g. foreign = body

Biphasic At or below the cords (intra or extrathoracic); e.g. = foreign=20 body, bacterial tracheitis

Table 2. Signs of Increased Work of Breathing

Ventilatory = frequency

   Infant >50 bpm

   Child >30 bpm

Effort

   Infant Head bobbing; nasal flaring

   Child =91See-saw=92 chest and abdomen; recession: subcostal, = sternal,=20 intercostal, tracheal tug; nasal flaring

Posture

   Infant Arching backwards

   Child Tripod position

Noise Infants grunt to generate auto-CPAP; wheezing can occur = with=20 an inhaled foreign body; stridor

Ineffective breathing Hypoxaemia and hypercarbia produce tachycardia, = sweating,=20 restlessness and confusion, agitation and anxiety, pallor, = or=20 mottling

Impending respiratory arrest Decreased conscious level, slowing ventilatory = frequency,=20 episodes of apnoea, silent chest despite vigorous = respiratory=20 effort, bradycardia

Table 3. Table 3 Croup Score.^[4] Mild Croup, = 0-3;=20 Moderate Croup, 4-6 (Transfer to HDU); Severe Croup, 7-10 (Patient = Requires Tracheal Intubation)

Score 0 1 2

Breath sounds Normal Harsh, wheeze Delayed

Stridor None Inspiratory Inspiratory and expiratory

Cough None Hoarse cry Bark

Recession/flaring None Flaring, suprasternal recession Flaring, suprasternal and intercostal=20 recession

Cyanosis None In air In oxygen 40%

References

Morton NS. Large airway obstruction in children. Part = 1:=20 causes and assessment. Royal College of Anaesthetists = Newsletter=20 (1999) 47:159=9662.
Bew S. Acute and chronic airway obstruction. Anaesth = Intensive=20 Care Med (2006) 7:164=968.
Al-Jundi S. Acute upper airway obstruction: croup,=20 epiglottitis, bacterial tracheitis and retropharyngeal = abscess.=20 In: Essentials of Pediatric Intensive Care=97Levin DL, = Morriss FC,=20 eds. (1997) 2nd Edn. New York: Churchill Livingstone Inc. = 121=969.
Downes JJ, Raphaely RC. Pediatric intensive care.=20 Anesthesiology (1975) 43:238=9650.
Johnson D, Croup. Clin Evid (2005) 14:1=964. Availabe = from=20 http://www.clinicalevidence.com/ceweb/about/index.jsp.
Remington S, Meakin G. Nebulised Adrenaline 1:1000 in = the=20 treatment of croup. Anaesthesia (1986) 41:923=966.
Sobolov I, Plunkett N, Barker I. Acute epiglottitis,=20 sevoflurane and HIB vaccine. Anaesthesia (2001) = 56:807=968.
Robinson D. Airway management. In: Paediatr Intensive=20 Care.=97Morton N, ed. (1997) Oxford: Oxford University = Press.=20 81=96108.
McVernon J, Slack MP, Ramsay ME. Changes in the = epidemiology=20 of epiglottitis following introduction of Haemophilus = infuenzae=20 type b (Hib) conjugate vaccines in England: a comparison = of two=20 data sources. Epidemiol Infect (2006) 134:570=962.
McEwan J, Giridharan W, Clarke RW, et al. Pediatric = acute=20 epiglottitis: not a disappearing entity. Int J Pediatr=20 Otorhinolaryngol (2003) 67:317=9621.
Hopkins A, Lahiri T, Salerno R, et al. Changing = epidemiology=20 of life-threatening upper airway infections: the = reemergence of=20 bacterial tracheitis. Pediatrics (2006) 118:1418=9621.
Advanced Life Support Group. Advanced Paediatric Life = Support=20 (2006) 4th Edn. BMJ publishing=20 Group.

Reprint Address

George H. Meakin, MD FRCA, Senior Lecturer in Paediatric = Anaesthesia,=20 Royal Manchester Children's Hospital Pendlebury Manchester M27 4HA = UK Tel:=20 +44 161 992 2291 Fax: +44 161 992 2439 E-mail: http://www.medscape.com/viewarticle/george.meakin@manches= ter.ac.uk

Emma Maloney, BM BCh BA FRCA, Clinical = Fellow in=20 Paediatric Anaesthesia

George H. Meakin, MD FRCA, = Senior=20 Lecturer in Paediatric Anaesthesia