Noisy breathing or snoring in children is turbulent airflow through a partially obstructed upper airway during sleep, most commonly caused by adenotonsillar hypertrophy, and may indicate obstructive sleep-disordered breathing requiring further evaluation.

Noisy Breathing / Snoring in Children

"Noisy breathing" is an umbrella term for any audible sound produced during respiration in a child. It is one of the most common presenting complaints in paediatrics — and the key clinical skill is to localise the level of obstruction from the sound character alone, because the sound tells you where the problem is.

Let's break down the key terms:

Sound	Meaning	Level of Obstruction	Phase	Pathophysiology
Stertor (snoring)	Low-pitched inspiratory sound indicating turbulent flow above the larynx, usually due to tongue occluding the pharynx ^[1]	Nose / nasopharynx / oropharynx (supraglottic)	Predominantly inspiratory	Turbulent airflow through a narrowed but floppy supraglottic passage
Stridor	High-pitched monophonic sound heard during breathing indicating obstruction of large airways ^[1]	Larynx / extrathoracic trachea (glottic/subglottic) or intrathoracic large airways	Inspiratory (extrathoracic), expiratory (intrathoracic), or biphasic (fixed/glottic)	Bernoulli effect — negative intraluminal pressure during inspiration collapses a floppy or narrowed extrathoracic airway
Wheeze	High-pitched expiratory monophonic or polyphonic sound indicating obstruction of small airways ^[1]	Intrathoracic small airways (bronchi/bronchioles)	Predominantly expiratory	Positive intrathoracic pressure during expiration narrows already-obstructed intrathoracic airways
Gurgling	Fluid in mouth/upper airway ^[1]	Oropharynx	Variable	Liquid secretions vibrating with airflow
Rattling	Secretions in airway ^[1]	Larger airways	Variable	Mucus or secretions oscillating in medium-sized airways
Crowing	Laryngospasm ^[1]	Glottic	Inspiratory	Involuntary vocal cord adduction

Why does the phase of the respiratory cycle matter? During inspiration, intraluminal pressure in the extrathoracic airway becomes negative (to draw air in), so a floppy or narrowed extrathoracic airway collapses → inspiratory noise. During expiration, intrathoracic pressure rises, compressing intrathoracic airways → expiratory noise. A fixed obstruction (e.g. subglottic stenosis, vascular ring) does not change with the respiratory cycle → biphasic noise.

Key Concept: Sound = Level

The character and phase of noisy breathing is your free localisation tool. Stertor = above larynx. Inspiratory stridor = larynx/extrathoracic trachea. Expiratory stridor or wheeze = intrathoracic. Biphasic = fixed lesion at/near the glottis. Always listen before you scope.

Epidemiology

Anatomy and Function

Understanding noisy breathing requires a solid grasp of paediatric upper airway anatomy and how it differs from adults. This is the foundation for everything that follows.

Feature	Infant/Young Child	Adult	Clinical Implication
Head	Large occiput, short neck	Proportional	Neck flexion in supine position → airway obstruction; use a shoulder roll
Nasal breathing	Obligate nasal breathers up to ~4–6 months	Oro-nasal	Nasal obstruction (e.g. choanal atresia, rhinitis) in neonates → respiratory distress
Tongue	Relatively large for oral cavity	Proportional	Greater tendency to fall back and obstruct oropharynx
Epiglottis	Omega-shaped (Ω), floppy, angled at 45°	Flat, firm	More prone to prolapse over the glottis (laryngomalacia)
Larynx position	High (C3–C4)	Lower (C5–C6)	More anterior larynx; harder to intubate; more susceptible to supraglottic obstruction
Subglottis	Narrowest point (cricoid ring is complete, rigid ring)	Narrowest at glottis (vocal cords)	1mm of oedema in a 4mm infant subglottis → 75% reduction in cross-sectional area (Poiseuille's law: resistance ∝ 1/r⁴); this is why croup is devastating in infants
Airway cartilage	Soft, compliant	Rigid	Greater tendency to dynamic collapse (tracheomalacia, laryngomalacia)
Tonsils/adenoids	Grow from age ~2, peak at 5–7 years	Involuted	Peak obstruction coincides with smallest relative airway size

Poiseuille's Law — Why Paediatric Airways Are Vulnerable

Resistance to airflow ∝ 1/radius⁴. An infant's subglottis is ~4mm in diameter. Just 1mm of circumferential mucosal oedema reduces the radius from 2mm to 1mm → a 16-fold increase in resistance (and ~75% reduction in cross-sectional area). This is why croup, which causes subglottic oedema, produces dramatic stridor in infants but is rarely a problem in adults.

Think of the airway in layers from outside to inside, and from above to below:

Nose/Nasopharynx → Oropharynx → Hypopharynx → Supraglottis → Glottis → Subglottis → Trachea → Bronchi

Nose and Nasopharynx — Nasal passages, adenoids, choanae. Obstruction here → stertor, mouth breathing, nasal voice.
Oropharynx — Palatine tonsils, tongue base, soft palate. Obstruction here → stertor/snoring, muffled "hot potato" voice.
Supraglottis — Epiglottis, aryepiglottic folds, arytenoids. Obstruction here → inspiratory stridor (floppy tissues prolapse inward on inspiration).
Glottis — Vocal cords. Obstruction here → biphasic stridor (or hoarse voice if cords are thickened/inflamed).
Subglottis — Cricoid cartilage (the narrowest point in children). Obstruction here → biphasic stridor with barking cough (croup).
Intrathoracic trachea and bronchi — Obstruction here → expiratory stridor or wheeze.

Aetiology (Focus on Hong Kong)

The causes of noisy breathing in children can be organised anatomically (by level) and by onset (acute vs chronic, congenital vs acquired).

Anatomical Classification

Condition	Congenital/Acquired	Notes
Choanal atresia/stenosis	Congenital	Bony or membranous plate blocking posterior nares; bilateral → neonatal emergency (obligate nasal breathers); unilateral → presents later with unilateral discharge
Nasal septal deviation	Congenital or acquired (trauma)	Common; mild forms often asymptomatic
Allergic rhinitis	Acquired	Very common in HK (~40% school-age children); mucosal oedema → nasal obstruction → mouth breathing → snoring
Adenoidal hypertrophy	Acquired (physiological lymphoid growth)	Most common cause of snoring/OSA in children 2–8 years; lymphoid tissue peaks at 5–7 years
Nasal polyps	Acquired	Think of cystic fibrosis if polyps in a child; also seen in allergic rhinitis
Pyriform aperture stenosis	Congenital	Rare; bony narrowing of anterior nasal opening
Nasopharyngeal tumour	Acquired	NPC (nasopharyngeal carcinoma) is endemic in Southern Chinese/HK population; rare in young children but adolescents can be affected

Condition	Congenital/Acquired	Notes
Tonsillar hypertrophy	Acquired	Often coexists with adenoidal hypertrophy; together they are the dominant cause of paediatric OSA
Peritonsillar abscess (quinsy)	Acquired (infection)	Listed as mural cause of upper airway obstruction ^[1]; acute onset, "hot potato" voice, trismus
Retropharyngeal abscess	Acquired (infection)	Listed as mural cause of upper airway obstruction ^[1]; neck stiffness, drooling, stridor; more common in children < 6 years (retropharyngeal lymph nodes involute after this age)
Macroglossia	Congenital	Down syndrome, Beckwith-Wiedemann syndrome, hypothyroidism, mucopolysaccharidoses
Pierre Robin sequence	Congenital	Micrognathia + glossoptosis + cleft palate → severe supraglottic obstruction in neonates
Lingual thyroid / thyroglossal cyst	Congenital	Midline tongue base mass; rare but important

Condition	Congenital/Acquired	Notes
Laryngomalacia	Congenital	Most common cause of stridor in infants (60–75%); floppy supraglottic structures (epiglottis, aryepiglottic folds) prolapse into airway on inspiration → inspiratory stridor. Typically onset at 2 weeks, peaks at 4–8 months, resolves by 12–18 months. Worsened by feeding, crying, supine position.
Epiglottitis	Acquired (infection)	Listed as mural cause of upper airway obstruction ^[1]; acute, severe, toxic child; historically H. influenzae type b (now rare due to Hib vaccine in HK since 1997); currently Staph aureus, group A Strep, or non-typeable H. influenzae
Croup (laryngotracheobronchitis)	Acquired (infection)	Listed as infection causing upper airway obstruction ^[1]; parainfluenza virus most common; subglottic oedema → barking cough + inspiratory stridor + hoarse voice; peak age 6 months – 3 years
Vocal cord paralysis	Congenital or acquired	2nd most common cause of congenital stridor; unilateral → weak cry, mild stridor; bilateral → severe stridor, may need tracheostomy. Causes: birth trauma, Arnold-Chiari malformation (bilateral), idiopathic, iatrogenic (cardiac surgery → recurrent laryngeal nerve injury)
Subglottic stenosis	Congenital or acquired	Acquired form: most common acquired cause of stridor in neonates/infants due to prolonged intubation (pressure necrosis → fibrosis); congenital form: narrowed cricoid ring
Laryngeal web/atresia	Congenital	Web across glottis → weak/absent cry at birth + stridor; atresia = lethal if complete
Subglottic haemangioma	Congenital	Infantile haemangioma of subglottis; presents at 1–3 months, worsens as haemangioma grows (proliferative phase peaks ~5 months); may have cutaneous haemangiomas. Look for "beard distribution" cutaneous haemangiomas (chin, lip, mandible) — 50% association with airway haemangiomas
Laryngeal papillomatosis	Acquired (vertical HPV transmission)	Recurrent; HPV 6 and 11; hoarse voice/cry + stridor; can be recalcitrant
Laryngospasm	Acquired	Produces crowing sound ^[1]; GORD, post-extubation, hypocalcaemia

Condition	Congenital/Acquired	Notes
Tracheomalacia	Congenital or acquired	Softened tracheal cartilage → dynamic expiratory collapse → expiratory stridor/wheeze; may be primary or secondary to vascular ring, TOF repair
Vascular ring	Congenital	Anomalous aortic arch/vessels encircle and compress trachea/oesophagus → biphasic stridor + dysphagia (dysphagia lusoria); e.g. double aortic arch, right aortic arch with aberrant left subclavian
Foreign body aspiration	Acquired	Listed as intraluminal cause of upper airway obstruction ^[1]; peak 1–3 years (oral exploration phase); peanuts/small toys; right main bronchus more common (wider, more vertical); may present with unilateral wheeze, hyperinflation on CXR, or ball-valve effect
Extrinsic compression — mediastinal mass, lymphadenopathy	Acquired	Lymphoma, TB lymphadenopathy (important in HK)

Condition	Congenital/Acquired	Notes
Cystic hygroma (lymphatic malformation)	Congenital	Large neck mass compressing airway
Penetrating neck injury	Acquired	Listed as extramural cause ^[1]
Oesophageal foreign body	Acquired	Listed as extramural cause of upper airway obstruction ^[1]; posterior compression of trachea

This is clinically very useful because it changes your differential and urgency:

Acute Onset	Chronic / Recurrent
Croup	Laryngomalacia
Epiglottitis	Adenotonsillar hypertrophy / OSA
Foreign body aspiration	Vocal cord paralysis
Anaphylaxis / angioedema	Subglottic stenosis
Retropharyngeal / peritonsillar abscess	Vascular ring
Bacterial tracheitis	Tracheomalacia
Laryngospasm	Laryngeal papillomatosis
Post-extubation stridor	Subglottic haemangioma
Thermal / caustic injury	Allergic rhinitis

Acute vs Chronic: The Exam Pearl

If the question says "acute onset stridor in a 2-year-old with preceding URTI" → think croup. If "acute onset choking episode in a toddler while eating peanuts" → think foreign body. If "progressive stridor since birth, worsens with feeding" → think laryngomalacia. If "habitual snoring with mouth breathing in a 5-year-old" → think adenotonsillar hypertrophy.

Pathophysiology

Classification

Severity	Adult AHI	Paediatric AHI
Normal	< 5	≤1
Mild	5–15	1–5
Moderate	15–30	5–10
Severe	> 30	> 10

Clinical Features

A. Symptoms (with pathophysiological basis)

B. Signs (with pathophysiological basis)

Features of respiratory distress ^[1]:
- Use of accessory muscles of respiration — sternocleidomastoid, intercostal, subcostal retractions; the child recruits additional muscles because the diaphragm alone cannot generate sufficient negative pressure to overcome the increased airway resistance.
- See-saw respirations (paradoxical chest and abdominal movements with chest collapsing when abdomen is bulging out) ^[1] — in upper airway obstruction, the diaphragm contracts (abdomen rises) but air cannot enter the chest → chest wall is sucked inward.
- Central cyanosis (late feature) ^[1] — when SpO₂ drops below ~85% (needs > 5g/dL deoxyHb), indicating severely compromised gas exchange. This is a pre-arrest sign in acute airway obstruction.
- Tracheal tug — visible descent of the trachea during inspiration, indicating increased inspiratory effort.
- Nasal flaring — dilation of the nares during inspiration to reduce nasal airway resistance; a sign of respiratory distress particularly prominent in infants.
- Head bobbing — rhythmic extension of the neck with each breath; a sign of severe respiratory distress in infants (the sternocleidomastoid pulls the head forward as an accessory muscle of respiration).
Growth parameters — Plot height, weight, and BMI. Obese children → risk factor for OSA. Failure to thrive → suggests severe airway obstruction with feeding difficulties or increased metabolic demand.
"Adenoid facies" — The classic appearance of a child with chronic upper airway obstruction from adenotonsillar hypertrophy:
- Long face (dolichocephalic)
- Open mouth posture
- High-arched palate (because the tongue sits low instead of moulding the palate)
- Dental malocclusion, crowded teeth
- "Gummy" smile
- Dark periorbital circles ("allergic shiners" — venous congestion from nasal obstruction)
- Pathophysiology: Chronic mouth breathing during the critical years of facial growth (age 2–10) → the tongue does not rest against the palate → palate narrows and heightens → mandible drops → elongated facial growth pattern.
Pectus excavatum / Harrison's sulcus — In chronic severe obstruction, repeated forceful diaphragmatic contractions against the obstruction → inward deformation of the lower chest wall at the diaphragmatic insertion. This is more common in young children with compliant chest walls.

Special Considerations by Age Group

High Yield Summary

Noisy Breathing / Snoring in Children — Key Points:

Sound localises the level: Stertor = supraglottic (nose/pharynx); inspiratory stridor = extrathoracic larynx; expiratory stridor/wheeze = intrathoracic; biphasic = fixed lesion. Silence = complete obstruction = emergency ^[1].
Paediatric airway is uniquely vulnerable: Obligate nasal breathing (neonates), narrowest at subglottis (cricoid ring), soft compliant cartilage, relatively large tongue and tonsils. Poiseuille's law: 1mm oedema → 16× resistance increase in a 4mm airway.
Most common causes by age: Neonates = laryngomalacia (stridor), choanal atresia; Toddlers = croup, foreign body; School-age = adenotonsillar hypertrophy/OSA (snoring).
Paediatric OSA differs from adult OSA: Adenotonsillar hypertrophy is the #1 cause (not obesity). AHI > 1 = abnormal in children ^[2]. Daytime features are behavioural (hyperactivity, poor concentration), not classic sleepiness.
Pathophysiology of OSA: Anatomical narrowing (adenoids/tonsils/obesity) + loss of neuromuscular tone during sleep → pharyngeal collapse → snoring (partial) or apnoea (complete) → arousal cycle → sleep fragmentation and intermittent hypoxia.
Red flags in noisy breathing: Biphasic stridor (fixed obstruction), stridor at birth (congenital anomaly), feeding difficulties/FTT, cyanosis, apnoeic episodes, failure to thrive, abnormal cry.
ABCDE approach for acute airway obstruction ^[1]: Establish airway → look for see-saw respirations, accessory muscle use, cyanosis → listen for stertor/stridor/wheeze/silence → feel for expired air.
Chronic consequences: Cor pulmonale (severe OSA), adenoid facies, neurocognitive impairment, secondary enuresis, growth failure, pulmonary hypertension.

Active Recall - Noisy Breathing / Snoring in Children

Differential Diagnosis of Noisy Breathing / Snoring in Children

The differential diagnosis of noisy breathing in a child is best approached systematically — first by characterising the sound (which localises the level), then by considering the tempo (acute vs chronic), and finally by the child's age. This section builds on the anatomy, pathophysiology, and clinical features discussed previously.

Differential by Presentation: Acute Noisy Breathing / Stridor

When a child presents acutely with new-onset noisy breathing, the priorities are (1) assess severity and stabilise, (2) distinguish life-threatening from benign causes. Below are the key differentials, each with the distinguishing features that let you tell them apart:

Definition: Acute bacterial infection of the supraglottic structures (epiglottis and aryepiglottic folds).
Aetiology: Historically Haemophilus influenzae type b (now rare in HK since Hib vaccination introduced in 1997); currently Staphylococcus aureus, Group A Streptococcus, non-typeable H. influenzae.
Pathophysiology: Bacterial cellulitis of the epiglottis → rapid, severe supraglottic swelling → the swollen "cherry-red" epiglottis balloons over the laryngeal inlet → can cause complete airway obstruction within hours.
Clinical features:
- Toxic-looking child — high fever, ill-appearing
- 4 D's: Drooling (cannot swallow saliva due to pain/obstruction), Dysphagia, Dysphonia (muffled "hot potato" voice — NOT hoarse, because the vocal cords themselves are not inflamed), Distress
- Tripod position (sitting forward, chin extended, mouth open — to maximise airway diameter)
- Soft inspiratory stridor (because the obstruction is supraglottic, not subglottic)
- ABSENCE of barking cough (the subglottis is not involved)
Key distinguishing features from croup:

Feature	Croup	Epiglottitis
Onset	Gradual (days)	Rapid (hours)
Preceding URTI	Yes	No
Fever	Low-grade	High
Appearance	Non-toxic	Toxic
Cough	Barking cough	No barking cough
Voice	Hoarse	Muffled
Drooling	No	Yes
Position	Any	Tripod / sitting forward
Age peak	6mo–3yr	2–6yr (now any age)

Never Examine the Throat in Suspected Epiglottitis

Attempting to visualise the epiglottis with a tongue depressor in a child with suspected epiglottitis can precipitate complete airway obstruction and cardiac arrest due to laryngospasm. Keep the child calm, in the position of comfort (usually sitting in parent's lap), and call for senior anaesthetic/ENT help for controlled airway examination in theatre.

Differential by Presentation: Chronic Noisy Breathing / Snoring

When the history is of persistent or habitual noisy breathing, the differential shifts toward structural, congenital, and hypertrophic causes:

Sound	Neonate	Infant	Toddler/Preschool	School-age/Adolescent
Stertor	Choanal atresia, Pierre Robin, macroglossia	Adenoidal hypertrophy beginning	Adenotonsillar hypertrophy/OSA, allergic rhinitis	Adenotonsillar hypertrophy, obesity-related OSA, allergic rhinitis, NPC (rare)
Inspiratory stridor	Laryngomalacia, vocal cord paralysis	Laryngomalacia (peak), subglottic haemangioma	Croup, FB aspiration, epiglottitis	Epiglottitis, peritonsillar abscess, anaphylaxis
Biphasic stridor	Subglottic stenosis (congenital), vascular ring, laryngeal web	Subglottic stenosis (acquired — post-intubation), vascular ring	Subglottic stenosis, FB	FB, subglottic stenosis
Expiratory noise/wheeze	Tracheomalacia	Bronchiolitis, tracheomalacia	Asthma, FB (bronchial)	Asthma

The 'Recurrent Croup' Red Flag

A child who presents with "recurrent croup" (≥3 episodes, or croup in an atypical age group like a neonate, or croup requiring intubation) must be investigated for an underlying structural abnormality — subglottic stenosis, subglottic haemangioma, or vascular ring. These children need flexible laryngoscopy/bronchoscopy, not just repeated courses of dexamethasone.

Red Flag	Why It Matters	Think Of
Silence after stridor	Complete obstruction — no air moving ^[1]	Imminent arrest; any cause of acute obstruction
Stridor at birth	Unlikely to be acquired → congenital structural	Vocal cord paralysis, laryngeal web/atresia, subglottic stenosis
Biphasic stridor	Fixed lesion	Subglottic stenosis, vascular ring, laryngeal web
Feeding difficulties / FTT	Severe enough to compromise nutrition	Severe laryngomalacia, vascular ring, Pierre Robin
Abnormal cry	Vocal cord pathology	Vocal cord paralysis, laryngeal web, papillomatosis
Cutaneous haemangiomas in beard distribution	50% risk of airway haemangioma	Subglottic haemangioma
Failure to thrive, finger clubbing, chest deformity	Suggests chronic respiratory disease	To be further investigated ^[5] — CF, chronic aspiration, structural anomaly
Sudden onset with choking, no prodrome	Foreign body until proven otherwise	FB aspiration
Toxic appearance + drooling	Epiglottitis or deep neck space infection	Epiglottitis, retropharyngeal abscess

The history alone will narrow the differential to 1–2 possibilities in most cases. Key questions:

Age of onset? Birth → congenital; 6mo–3yr → croup/FB; 2–8yr → adenotonsillar hypertrophy
Acute or chronic? Hours/days → infectious/FB/anaphylaxis; Weeks/months → structural
Preceding URTI? Yes → croup, bronchiolitis; No with sudden onset → FB; No with high fever → epiglottitis
Character of sound? Stertor (supraglottic) vs stridor (laryngeal) vs wheeze (lower airway)
Positional variation? Worse supine → laryngomalacia, OSA (gravity); Better sitting forward → epiglottitis
Relationship to feeding? Worse → laryngomalacia, vascular ring (oesophageal compression)
Quality of cry/voice? Hoarse → vocal cord/subglottic; Muffled → supraglottic; Weak → vocal cord paralysis
Response to treatment? Responds to nebulised adrenaline → croup; Doesn't respond → bacterial tracheitis, FB, structural
Recurrent episodes? Think subglottic stenosis, spasmodic croup, or allergic/reactive aetiology
Syndromic features? Down, Pierre Robin, Beckwith-Wiedemann, CHARGE

High Yield Summary — Differential Diagnosis

Characterise the sound first: Stertor (supraglottic), inspiratory stridor (extrathoracic larynx), biphasic stridor (fixed lesion), expiratory stridor/wheeze (intrathoracic).
Most common causes by age: Neonate = laryngomalacia/vocal cord paralysis/choanal atresia; Toddler = croup/FB; School-age = adenotonsillar hypertrophy/OSA.
Croup vs Epiglottitis: Croup = gradual onset, barking cough, hoarse voice, URTI prodrome, non-toxic. Epiglottitis = rapid onset, NO barking cough, muffled voice, drooling, toxic, DO NOT examine throat.
Foreign body: Sudden onset, no prodrome, no fever. May be missed if choking episode not witnessed. Unilateral wheeze/hyperinflation on CXR.
Recurrent croup = red flag for structural abnormality (subglottic stenosis, haemangioma, vascular ring).
OSA in children: Adenotonsillar hypertrophy is the #1 cause. AHI > 1 is abnormal. Presents with behavioural disturbance, not classic sleepiness.
Silence is worse than noise — loss of stridor in a deteriorating child = complete obstruction = pre-arrest.

Active Recall - Differential Diagnosis of Noisy Breathing / Snoring

References

^[1] Senior notes: Ryan Ho Critical Care.pdf (Section 1.1 Primary Survey, Section 1.2 Acute SOB and Airway Management) ^[2] Senior notes: Ryan Ho Respiratory.pdf (Section 3.8 Sleep-Associated Disorders, including 3.8.1 Approach to Daytime Sleepiness and 3.8.2 Sleep Apnoea/Hypopnoea Syndrome) ^[3] Senior notes: Adrian Lui Pediatrics.pdf (Pages 155, 161 — Causes of stridor, Croup, Spasmodic croup) ^[4] Senior notes: Ryan Ho Endocrine.pdf (Section 5.2.3 Acromegaly — OSA association) ^[5] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf (Page 15 — Approach to acute cough)

Diagnostic Criteria, Algorithm, and Investigations for Noisy Breathing / Snoring in Children

Diagnostic Criteria

Noisy breathing itself is a symptom, not a single diagnosis — so there is no single set of diagnostic criteria for "noisy breathing." Instead, diagnostic criteria exist for the specific conditions that cause it. The two most important sets of criteria in paediatric practice are for Obstructive Sleep Apnoea (OSA) and Croup severity scoring, because these directly change management.

This is the validated scoring system for acute croup that directly guides management:

Parameter	Score 0	Score 1	Score 2	Score 3	Score 4	Score 5
Level of consciousness	Normal incl sleep	—	—	—	—	Disoriented
Cyanosis	None	—	—	—	With agitation	At rest
Stridor	None	With agitation	At rest	—	—	—
Air entry	Normal	Decreased	Markedly decreased	—	—	—
Retraction	None	Mild	Moderate	Severe	—	—

Severity interpretation ^[3]:

≤2 points → Mild: home treatment with symptomatic care ± PO dexamethasone
3–7 points → Moderate: outpatient treatment with PO dexamethasone + nebulised adrenaline
8–11 points → Severe: hospitalisation with same treatment
≥12 points → Critical: ICU admission with IM/IV dexamethasone ± repeated nebulised adrenaline

The Westley score is elegant because it uses objective physiological parameters: consciousness (reflecting cerebral oxygenation), cyanosis (reflecting SpO₂), stridor timing (reflecting degree of obstruction — at rest is worse than only on agitation because the child is generating more negative pressure during agitation anyway, so stridor at rest means even calm breathing is obstructed), air entry (reflecting actual airflow through the obstruction), and chest wall retractions (reflecting the work of breathing needed to overcome the obstruction).

Diagnostic Algorithm

The approach differs depending on whether the noisy breathing is acute (emergency stabilisation first) or chronic (systematic workup).

Investigation Modalities — Detailed

What it is: An overnight sleep study that simultaneously records multiple physiological parameters during sleep.

What it measures (the name tells you: "poly" = many, "somno" = sleep, "graphy" = recording):

EEG (electroencephalogram) — brain waves → determines sleep stage and arousals
EOG (electro-oculogram) — eye movements → distinguishes REM from NREM sleep
EMG (electromyogram) — chin and limb muscle tone → detects REM atonia, limb movements
Nasal airflow (thermistor and nasal pressure transducer) → detects apnoeas and hypopnoeas
Thoracic and abdominal respiratory effort (impedance bands) → distinguishes obstructive (effort present but no flow) from central (no effort, no flow) apnoea
Pulse oximetry (SpO₂) → detects desaturations
ECG — heart rate and rhythm
End-tidal or transcutaneous CO₂ (capnography) — particularly important in children because they may show obstructive hypoventilation without discrete apnoeic events
Body position — supine vs lateral
Video — records movements, abnormal breathing patterns
Sound/microphone — records snoring

Key findings and interpretation in paediatric OSA:

Parameter	Normal	Abnormal in OSA
AHI	≤1 event/hour	> 1 = OSA; Mild 1–5; Moderate 5–10; Severe > 10 ^[2]
Obstructive Apnoea Index (OAI)	≤1	> 1 supports diagnosis
SpO₂ nadir	> 92%	< 92% = significant desaturation; < 85% = severe
Time with SpO₂ < 90%	Minimal	> 2% of TST = significant
End-tidal CO₂ > 50 mmHg	< 25% of TST	> 25% of TST = obstructive hypoventilation
Arousal index	< 10/hr	Elevated in OSA (but children may have fewer arousals than adults for same severity — higher arousal threshold)

Why is PSG the gold standard? Because clinical assessment alone (history + exam) has poor sensitivity and specificity for paediatric OSA — studies show that even experienced clinicians correctly predict PSG findings only ~50–60% of the time. Tonsil size does NOT reliably correlate with AHI (a child with grade 2 tonsils can have severe OSA if they have a narrow airway or hypotonia).

When to Order PSG in Children

American Academy of Pediatrics (AAP) 2012/2024 guidelines recommend PSG for children with snoring + any of the following before adenotonsillectomy:

Age < 2 years
Obesity
Down syndrome or craniofacial abnormalities
Neuromuscular disorders
Sickle cell disease
Mucopolysaccharidoses
Discordance between tonsil size and symptom severity
When the family prefers watchful waiting and needs objective data
After adenotonsillectomy if symptoms persist (to assess for residual OSA)

In practice, in HK, PSG availability is limited, and many children with straightforward adenotonsillar hypertrophy and classical OSA symptoms proceed to adenotonsillectomy without PSG. However, PSG is strongly recommended for the high-risk groups above.

What it is: A thin flexible fibre-optic endoscope passed through the nose to directly visualise the nasal passages, nasopharynx, oropharynx, supraglottis, glottis, and subglottis.

When to use it: This is the first-line investigation for stridor — both acute (once stabilised) and chronic.

Key findings by condition:

Condition	FNL Findings
Laryngomalacia	Omega-shaped epiglottis, short aryepiglottic folds, redundant arytenoid mucosa prolapsing into the airway on inspiration
Vocal cord paralysis	Unilateral: one cord immobile in paramedian position; Bilateral: both cords adducted, narrow glottic aperture
Subglottic stenosis	Narrowed subglottic lumen (may need to assess with rigid bronchoscopy for grading)
Subglottic haemangioma	Smooth, compressible, submucosal mass in the subglottis (usually posterolateral, left > right)
Laryngeal papillomatosis	Warty, exophytic, grape-like masses on vocal cords ± subglottis
Epiglottitis	Cherry-red, swollen epiglottis (only visualised in a controlled setting!)
Adenoidal hypertrophy	Degree of adenoidal obstruction of the nasopharynx (graded as % obstruction of choanae)

Practical pearl: In children, FNL can be performed awake (with topical lignocaine spray) in cooperative children, or with light sedation. It is generally well-tolerated even in infants when done by experienced hands.

5. Imaging Studies

What it shows and key findings:

Finding	Condition	Interpretation
Steeple (hourglass) sign	Croup ^[3]	Symmetrical narrowing of the subglottic region on AP view — the normal "shouldering" (lateral subglottic walls) is lost because mucosal oedema narrows the airway into a steeple shape
Thumb sign	Epiglottitis	Swollen epiglottis on lateral view resembles a thumb (normal epiglottis is thin like a little finger)
Widened prevertebral soft tissues	Retropharyngeal abscess	Retropharyngeal space > 7mm at C2, or > 14mm at C6 in children (rule of thumb: > ½ AP diameter of adjacent vertebral body). In young children, this can be falsely positive during expiration/crying — ideally taken during inspiration with neck in extension
Adenoidal enlargement	Adenoidal hypertrophy	Lateral view shows soft tissue mass in the nasopharynx narrowing the nasopharyngeal airway. Ratio of adenoid to nasopharyngeal space can be estimated (Fujioka adenoidal-nasopharyngeal ratio > 0.8 = significant)

Imaging for croup: NOT indicated if clinically suggestive ^[3]. Only obtain if diagnosis is unclear or atypical features are present (e.g. no response to treatment, concern for foreign body or retropharyngeal abscess).

When: Suspected foreign body, lower airway pathology, cardiac assessment.

Key findings:

Finding	Condition	Interpretation
Unilateral hyperinflation	Foreign body (bronchial)	Ball-valve effect: air enters past the FB on inspiration but cannot escape on expiration → air trapping → hyperinflated hemithorax with mediastinal shift to the contralateral side. Best seen on expiratory film or lateral decubitus film (the affected side does not deflate)
Radio-opaque FB	Foreign body	Only ~10% of aspirated FBs are radio-opaque (e.g. coins, metallic objects). Organic material (peanuts, food) is radiolucent
Cardiomegaly	Cor pulmonale from chronic severe OSA	Right heart enlargement from pulmonary hypertension
Pulmonary infiltrates	Pneumonia, post-obstructive atelectasis	Consolidation, atelectasis distal to an obstructing lesion

Indication	What it shows
CT neck with contrast	Deep neck space infections (retropharyngeal abscess — ring-enhancing collection), extent of neck masses (cystic hygroma, tumour)
CT chest	Mediastinal masses, vascular anomalies (CT angiography for vascular ring — best non-invasive modality to delineate the vascular anatomy)
CT airway (virtual bronchoscopy)	Can reconstruct 3D airway images — useful for subglottic stenosis grading, tracheal compression assessment

6. Other Investigations

Test	When	Why
FBC, CRP	Acute infections (epiglottitis, retropharyngeal abscess, bacterial tracheitis)	Elevated WCC and CRP support bacterial infection; helps distinguish viral croup (mild elevation) from bacterial superinfection
Blood gas (ABG/CBG)	Severe respiratory distress, altered consciousness	Hypoxia (↓PaO₂), hypercapnia (↑PaCO₂) indicates respiratory failure; respiratory acidosis suggests decompensation
TFTs	Chronic snoring with other hypothyroid features	Hypothyroidism causes submucosal infiltration and narrowing of URT ^[2], macroglossia, and hypotonia — all contributing to airway obstruction
Calcium	Laryngospasm (crowing)	Hypocalcaemia causes laryngospasm — check ionised calcium. In neonates, consider DiGeorge syndrome
Iron studies	Restless sleep, limb movements	Iron deficiency → restless leg syndrome → sleep fragmentation that may mimic or coexist with OSA

Clinical Scenario	First-Line Investigation	Additional / Second-Line
Acute stridor with barking cough — classic croup	Clinical diagnosis; imaging NOT indicated ^[3]	Neck XR only if atypical
Acute stridor, toxic child, drooling	DO NOT examine throat; lateral neck XR if safe → thumb sign	Blood cultures after airway secured; MLB in theatre
Acute choking episode in toddler	CXR (inspiratory + expiratory views)	Rigid bronchoscopy (diagnostic + therapeutic)
Chronic inspiratory stridor since infancy	Flexible nasolaryngoscopy	± MLB if subglottic pathology suspected
Habitual snoring, suspected OSA	Overnight pulse oximetry (screening)	PSG (gold standard) for definitive diagnosis; lateral neck XR for adenoid size
Recurrent croup	Flexible nasolaryngoscopy + MLB	CT/MRI to assess for subglottic stenosis, haemangioma, vascular ring
Biphasic stridor since birth	Flexible nasolaryngoscopy → MLB	CT angiography if vascular ring suspected; MRI if haemangioma suspected
Stridor + dysphagia	Barium swallow	CT angiography for vascular ring; MLB
Bilateral vocal cord paralysis	FNL → confirm immobile cords	MRI brain/posterior fossa (Arnold-Chiari malformation)

Common Interpretation Pitfalls

Lateral neck XR — false positive prevertebral widening: In young children, crying or neck flexion causes the retropharyngeal tissues to appear thickened. Always ensure the film is taken during inspiration with the neck in extension — otherwise you may overcall a retropharyngeal abscess.
Normal CXR does NOT exclude foreign body: Up to 30% of bronchial foreign bodies show a normal CXR. If clinical suspicion is high (witnessed choking episode), proceed to rigid bronchoscopy regardless.
Nocturnal oximetry: positive is useful, negative is NOT reassuring: A positive oximetry (sawtooth desaturations) has high PPV for OSA, but a negative result has poor sensitivity — it does not exclude mild-moderate OSA. PSG is needed if clinical suspicion remains.
Tonsil size does not predict OSA severity: A child with grade 2 tonsils but a narrow craniofacial framework or hypotonia may have worse OSA than a child with grade 4 tonsils. PSG is needed for objective severity assessment.
Imaging for croup is NOT indicated if clinically suggestive ^[3]: Do not delay treatment to obtain imaging. The steeple sign is only ~50% sensitive — a normal XR does not exclude croup.

High Yield Summary — Diagnosis and Investigations

PSG is the gold standard for paediatric OSA diagnosis. AHI > 1 = abnormal in children ^[2]. Record EEG, EOG, EMG, airflow, respiratory effort, SpO₂, CO₂, ECG, video, sound.
Nocturnal oximetry is a useful screening tool: positive result (McGill criteria) has high PPV; negative does NOT rule out OSA.
Croup is a clinical diagnosis — imaging NOT indicated if clinically suggestive ^[3]. Westley score guides management severity ^[3].
Flexible nasolaryngoscopy (FNL) is the first-line investigation for chronic stridor — it directly visualises the airway from nose to glottis.
Rigid MLB under GA is needed for subglottic assessment, FB removal, and grading of stenosis.
Lateral neck XR: Steeple sign (croup), thumb sign (epiglottitis), prevertebral widening (retropharyngeal abscess), adenoidal size.
CXR for foreign body: Look for unilateral hyperinflation on expiratory film. Normal CXR does not exclude FB — proceed to bronchoscopy if clinical suspicion is high.
CT angiography is the investigation of choice for vascular ring.
MRI posterior fossa if bilateral vocal cord paralysis → rule out Arnold-Chiari malformation.
Always check TFTs (hypothyroidism), calcium (hypocalcaemia → laryngospasm), and iron studies (iron deficiency → restless legs) as part of the workup for chronic noisy breathing/sleep disturbance.

Active Recall - Diagnosis and Investigations for Noisy Breathing / Snoring

References

^[1] Senior notes: Ryan Ho Critical Care.pdf (Section 1.1 Primary Survey) ^[2] Senior notes: Ryan Ho Respiratory.pdf (Section 3.8 Sleep-Associated Disorders, including 3.8.2 Sleep Apnoea/Hypopnoea Syndrome) ^[3] Senior notes: Adrian Lui Pediatrics.pdf (Pages 155, 161 — Causes of stridor, Croup, severity assessment) ^[6] Senior notes: Ryan Ho Psychiatry.pdf (Section 9.2 Sleep Disorders — evaluation approach, polysomnography, sleep diary)

Management Algorithm and Treatment Modalities for Noisy Breathing / Snoring in Children

The management of noisy breathing in children is entirely dependent on two things: (1) the tempo — acute or chronic, and (2) the underlying cause. This section walks through the approach systematically.

Part A: Management of ACUTE Noisy Breathing / Airway Obstruction

Step 2: Condition-Specific Acute Management

Management is guided by the Westley Croup Severity Score ^[3]:

Severity	Westley Score	Management
Mild	≤2 points	Home treatment with symptomatic care ± PO dexamethasone ^[3]
Moderate	3–7 points	Outpatient treatment with PO dexamethasone + nebulised adrenaline ^[3]
Severe	8–11 points	Hospitalisation with same treatment as above ^[3]
Critical	≥12 points	ICU admission with IM/IV dexamethasone ± repeated nebulised adrenaline ^[3]

Medications:

Dexamethasone 0.6 mg/kg ^[3] (single dose, oral preferred):
- Why dexamethasone? It is a long-acting glucocorticoid (half-life ~36–54 hours) with potent anti-inflammatory effect. It reduces subglottic mucosal oedema by suppressing the inflammatory cascade (↓prostaglandins, ↓leukotrienes, ↓cytokines, ↓capillary permeability). A single dose is usually sufficient because the long half-life covers the typical duration of croup (2–3 days).
- Route: Oral is preferred (well absorbed, palatability can be improved by mixing with syrup). IM if the child is vomiting or refusing oral. IV if already cannulated.
- Onset: Clinical effect begins within 2–3 hours (anti-oedema) but full effect takes 6 hours.
- Alternative: Prednisolone 1–2 mg/kg/day for 3 days (shorter acting, so requires multiple doses — less convenient). Nebulised budesonide 2 mg is an alternative in the vomiting child but is more expensive and no more effective than oral dexamethasone.
Nebulised adrenaline: 1:1000, 0.5 mL/kg (max 5 mL) ^[3]:
- Why adrenaline? It acts on α₁-adrenergic receptors on the subglottic mucosal vasculature → vasoconstriction → rapid reduction in mucosal oedema. This provides immediate but temporary relief (onset ~10 minutes, duration ~2 hours).
- The "rebound" effect: After 2 hours, the vasoconstriction wears off and oedema may return (sometimes even worse because the underlying inflammation is still active). This is why any child who receives nebulised adrenaline must be observed for at least 2–4 hours before discharge — to ensure they don't deteriorate when the adrenaline wears off.
- Seldom given because of possible paradoxical response ^[3] — though in practice, it is used frequently in moderate-severe croup. The "paradoxical response" refers to rare cases of worsening agitation, which itself can worsen stridor in an already distressed child.
- Can be repeated every 15–20 minutes in severe cases, but if multiple doses are needed, the child needs ICU care.
Supportive care:
- Minimal handling — keep the child calm (in caregiver's arms). Agitation worsens stridor because increased respiratory effort generates more negative intraluminal pressure → more dynamic collapse.
- Humidified air/mist therapy — historically used (cold steam), but evidence shows no benefit and it is no longer routinely recommended.
- Monitoring: SpO₂, respiratory rate, work of breathing.

Croup: The 3 Key Points

(1) Dexamethasone for ALL children with croup (even mild) — a single dose reduces return to ED and need for further treatment. (2) Nebulised adrenaline for moderate-severe — buys you 2 hours while steroids take effect. (3) Observe after adrenaline for rebound.

Consult ENT for recurrent or slow-to-resolve croup: may be associated with underlying subglottic stenosis ^[3].

Management of acute epiglottitis ^[8]:

This is a true airway emergency. The management principle is: secure the airway first, treat infection second.

Do NOT examine the throat — this can precipitate laryngospasm and complete obstruction.
Keep the child calm in the position of comfort (sitting upright in caregiver's lap).
Call for senior anaesthetist + ENT — the airway should be secured under controlled conditions in the operating theatre via gas induction and direct laryngoscopy/intubation.
Intubation: Usually with a tube 0.5–1 size smaller than expected (because the swollen supraglottic structures narrow the glottic aperture).
Supportive care post-intubation ^[8]:
- Fluid and hydration
- Treatment of post-obstructive pulmonary oedema — this occurs because severe airway obstruction generates massively negative intrathoracic pressure → increased venous return + increased LV afterload → transudation of fluid into alveoli. Usually resolves within 24–48 hours with supportive care (supplemental O₂, CPAP/PEEP if needed).
- Sedation and avoid accidental extubation
- Care of ET tube
- Adequate humidification
IV antibiotics: 3rd generation cephalosporin (ceftriaxone 80 mg/kg/day or cefotaxime) — covers H. influenzae (even if Hib is rare post-vaccination, empirical cover is still given), S. aureus, Group A Streptococcus. Add anti-staphylococcal cover (flucloxacillin or vancomycin) if MRSA is suspected.
Extubation criteria ^[8]:
- General condition improving
- Fever subsiding
- Presence of air leak — this is a key sign that the swelling has decreased sufficiently. An air leak around the ETT (heard when the child breathes) indicates that the supraglottic oedema has reduced enough for air to pass around the tube → the airway is now patent enough to sustain unassisted breathing.
- Usually done at 18–24 hours ^[8]

Air Leak Test Before Extubation

Why check for an air leak? The ETT was placed through a swollen supraglottis. If the swelling is still severe, removing the tube may leave the child with an inadequate airway. An air leak means the gap between the tube and the laryngeal wall has increased (swelling reduced) — it is safe to extubate.

Adenotonsillar Hypertrophy and Paediatric OSA

This is the single most common scenario you will encounter. The management pathway is:

1. General Measures and Conservative Management

Sleep hygiene: Regular sleep schedule, adequate sleep duration for age (11–14 hours for toddlers, 9–12 hours for school-age, 8–10 hours for adolescents), avoid screens before bed.
Manage predisposing factors: rhinitis ^[2] — intranasal corticosteroids (e.g. mometasone, fluticasone) reduce adenoidal and nasal mucosal inflammation. Montelukast (leukotriene receptor antagonist) can also reduce adenoidal tissue. Intranasal steroids + montelukast may be trialled for 6–12 weeks in mild OSA as an alternative to surgery, particularly in children < 2 years where surgical risk is higher.
Weight reduction if overweight ^[2] — critical in obese children; even modest weight loss can significantly reduce AHI. In adolescents, the same lifestyle measures apply; in severe adolescent obesity (BMI ≥ 35 with comorbidities), bariatric surgery may be considered ^[4].
Avoid alcohol and sedatives ^[2] — relevant in adolescents; medications with sedating properties (antihistamines, benzodiazepines) should be reviewed and minimised.
Positional therapy: Sleeping on the side rather than supine reduces gravitational collapse of the tongue base and soft palate — less evidence in children than adults but still useful.
Sleep posture: lying laterally ^[2].

2. Adenotonsillectomy (AT) — First-Line Definitive Treatment for Paediatric OSA

Removal of hypertrophic tonsils/adenoids in children ^[2] — this is the definitive treatment for the majority of paediatric OSA.

Why is AT first-line in children but NOT in adults? Because in children, the dominant mechanism of OSA is adenotonsillar hypertrophy (a discrete, removable anatomical obstruction), whereas in adults, the problem is multifactorial (obesity, pharyngeal collapsibility, neuromuscular factors) — so removing one structure doesn't fix the problem.

Indications for adenotonsillectomy in children:

Indication	Explanation
Moderate-severe OSA (AHI > 5 or significant desaturations)	Definitive treatment
Mild OSA (AHI 1–5) with significant symptoms	Behavioural problems, growth failure, enuresis, poor QoL
Recurrent tonsillitis (Paradise criteria)	≥7 episodes in 1 year, ≥5/year for 2 years, ≥3/year for 3 years
Peritonsillar abscess	Risk of recurrence
Suspected malignancy	Asymmetric tonsillar enlargement

Contraindications / Cautions:

Contraindication	Reason
Bleeding diathesis (uncontrolled)	Tonsillectomy is in a highly vascular field; post-tonsillectomy haemorrhage is the most feared complication
Velopharyngeal insufficiency (e.g. submucous cleft palate)	Removing the adenoids may worsen VPI → hypernasal speech. Check for bifid uvula, short palate before adenoidectomy
Active infection	Increased bleeding risk; defer to 2–4 weeks after resolution
Age < 2 years	Higher perioperative risk (especially respiratory complications); these children need PSG confirmation of OSA before surgery and should be managed in a centre with paediatric anaesthesia expertise

Surgical techniques:

Tonsillectomy: Total (extracapsular) vs intracapsular/partial (leaves the capsule intact — less pain, faster recovery, but risk of tonsillar regrowth). Cold steel dissection, electrocautery, coblation, or microdebrider.
Adenoidectomy: Suction diathermy, curette, or microdebrider. Performed under direct vision with a mirror or endoscope.

Expected outcomes:

AT is curative in ~80% of otherwise healthy children with OSA due to adenotonsillar hypertrophy.
Residual OSA post-AT occurs in ~20% — risk factors: obesity, craniofacial anomalies, Down syndrome, neuromuscular disease, severe pre-operative OSA (AHI > 20). These children need post-operative PSG at 6–8 weeks to reassess.

Post-operative complications:

Primary haemorrhage ( < 24 hours): ~0.5–2% — usually from the tonsillar fossa; return to theatre for haemostasis.
Secondary haemorrhage (5–10 days): ~2–4% — due to sloughing of the eschar (the "scab" over the tonsil bed). Infection can precipitate this. Presents with fresh blood in the mouth ± haematemesis (swallowed blood).
Pain: Peaks at day 3–5; adequate analgesia with paracetamol ± ibuprofen (note: some centres avoid NSAIDs in the first 2 weeks due to theoretical bleeding risk, though recent evidence suggests ibuprofen is safe and beneficial). Avoid codeine in children — CYP2D6 ultra-rapid metabolisers can develop fatal respiratory depression (FDA black box warning post-tonsillectomy).
Velopharyngeal insufficiency — hypernasal speech post-adenoidectomy (usually transient).
Dehydration — from poor oral intake due to pain; encourage cold fluids and soft diet.

Codeine After Tonsillectomy — A Deadly Mistake

NEVER prescribe codeine to children post-tonsillectomy. Codeine is a prodrug metabolised by CYP2D6 to morphine. CYP2D6 ultra-rapid metabolisers (prevalence varies by ethnicity: ~1–2% in East Asian populations, up to 10% in some populations) convert codeine to morphine at dangerously high rates → fatal respiratory depression, especially in the post-tonsillectomy child who already has a vulnerable airway. Use paracetamol ± ibuprofen instead.

3. Continuous Positive Airway Pressure (CPAP) / Bilevel Positive Airway Pressure (BiPAP)

Nasal CPAP: application of positive pressure through nasal mask during sleep — most consistently effective treatment of OSA ^[2].

How does CPAP work? It acts as a pneumatic splint — the positive pressure keeps the pharyngeal airway open by exceeding the critical closing pressure (Pcrit). Essentially, it counteracts the negative intraluminal pressure generated during inspiration that would normally collapse the floppy pharynx.

Indications in children:

Residual OSA after adenotonsillectomy
OSA in children who are NOT surgical candidates (e.g. craniofacial anomalies where AT alone won't be curative)
Bridge therapy while awaiting surgery
Central sleep apnoea (BiPAP with backup rate)
Obesity-related OSA where weight loss has not yet been achieved

Practical considerations in paediatric CPAP:

Interface: Nasal mask is preferred over full-face mask in children (lower risk of aspiration, more comfortable). Must be properly fitted — paediatric masks come in multiple sizes.
Pressure titration: Done during a PSG (titration study) — the pressure is gradually increased until apnoeas/hypopnoeas are abolished. Typical pressures in children: 4–10 cmH₂O.
Compliance: This is the Achilles heel of CPAP in children. Compliance rates are ~50–65%. Strategies to improve compliance: behavioural desensitisation (gradual introduction), positive reinforcement, involving the child in choosing mask design, starting at low pressures and titrating up.
Mid-face hypoplasia risk: Prolonged CPAP use in young children (especially < 6 years) with a poorly fitting mask can cause mid-face retrusion over time due to pressure on the developing facial skeleton. Regular craniofacial monitoring is needed.

Mandibular advancement device ^[2]:

Device worn during sleep to advance mandible to enlarge upper respiratory tract and modify muscle collapsibility ^[2].
Variable efficacy, usually cannot completely control severe OSA ^[2].
In paediatrics, rapid maxillary expansion (RME) appliances are more commonly used — these widen the palate and nasal floor, increasing the nasal and oropharyngeal airway. Best results in children aged 4–8 years with high-arched palate and dental malocclusion.

4. Medical Management of Chronic Snoring / Mild OSA

Treatment	Mechanism	Indication	Dose	Evidence
Intranasal corticosteroid (mometasone, fluticasone)	↓Nasal and adenoidal mucosal inflammation, ↓lymphoid tissue volume	Mild OSA, allergic rhinitis coexisting with snoring, pre-/post-AT residual symptoms	Mometasone: 1 spray (50 mcg) each nostril daily (age ≥ 3y); Fluticasone: same	Moderate evidence; RCTs show ↓AHI by 25–50% in mild OSA
Montelukast	Leukotriene receptor antagonist → ↓adenoidal lymphoid hyperplasia	Mild OSA (especially with coexisting allergic rhinitis/asthma)	4 mg (2–5y), 5 mg (6–14y) once daily at bedtime	Some evidence for ↓AHI; may be tried for 6–12 weeks before considering surgery
Combination (intranasal steroid + montelukast)	Synergistic anti-inflammatory effect	Mild OSA, or residual mild OSA post-AT	As above	Better than either alone in small studies

5. Other Surgical and Interventional Treatments

Treatment	Indication	Mechanism / Details
Uvulopalatopharyngoplasty (UPPP)	Variable efficacy, not favoured ^[2] — rarely used in children	Removal/remodelling of uvula, soft palate, and pharynx ^[2]. Risk of VPI in children makes this largely inappropriate.
Supraglottoplasty	Severe laryngomalacia (FTT, significant desaturations, severe stridor causing feeding difficulty)	Endoscopic trimming of redundant aryepiglottic folds, arytenoid mucosa, or omega-shaped epiglottis. ~95% success rate for symptom improvement.
Tongue base reduction (various techniques)	Tongue base collapse causing residual OSA (identified on DISE)	Radiofrequency ablation, midline glossectomy, or lingual tonsillectomy (if lingual tonsils are hypertrophied).
Faciomaxillary/mandibular surgery	Significant maxillofacial anomalies ^[2]	Mandibular distraction osteogenesis (e.g. Pierre Robin sequence) — gradually lengthens the mandible by creating a bony cut and slowly widening the gap with a distraction device.
Tracheostomy	Severe, life-threatening OSA refractory to all other measures; bilateral vocal cord paralysis with severe obstruction	Bypasses upper airway obstruction ^[7]. Most definitive airway but associated with significant morbidity (stomal care, communication difficulties, psychosocial impact). Reserved as last resort.
Propranolol	Subglottic haemangioma	Non-selective β-blocker → inhibits haemangioma growth (↓VEGF, induces apoptosis, vasoconstriction). Dose: 1–3 mg/kg/day in 2–3 divided doses. Treatment typically continued until age 12–18 months (past the proliferative phase). Monitor for bradycardia, hypotension, hypoglycaemia (especially in infants — must be given with feeds).
Vascular ring division	Symptomatic vascular ring	Surgical division of the non-dominant arch or ligamentum arteriosum → relieves tracheal/oesophageal compression. Usually performed via left thoracotomy or thoracoscopically.

6. Management of Secondary Enuresis (in context of OSA)

Treat underlying cause first ^[3] — resolving the OSA (typically by adenotonsillectomy) often resolves the enuresis.

If enuresis persists after OSA treatment:

General measures: education and reassurance, behavioural modification (void before bed, fluid/salt restriction 2h before sleep, star chart) ^[3]
Enuresis alarm: 1st line, most effective long-term therapy ^[3]
- MoA: sensor placed in undergarment or on bed pad → activated and alert when detect moisture ^[3]
- Efficacy: 30–60% success rate but associated with significant relapse rate ^[3]
Medical treatment: desmopressin ± anticholinergics (if component of detrusor overactivity) ^[3]
- Usual use for short-term, e.g. school camps ^[3]
- Note: intranasal formulation is associated with increased risk of seizures and is no longer indicated for treatment of enuresis ^[3] — use oral desmopressin melt/tablet instead (120–240 mcg oral lyophilisate at bedtime)

Condition	Management	Details
Laryngomalacia (mild)	Conservative / watchful waiting	~90% resolve spontaneously by 12–18 months as cartilage matures. Reassure parents. GOR treatment (omeprazole/ranitidine) may help as acid reflux worsens laryngomalacia. Positional advice (prone positioning during supervised awake time).
Laryngomalacia (severe)	Supraglottoplasty	Indications: failure to thrive, significant desaturations on sleep study, severe feeding difficulties, cor pulmonale.
Vocal cord paralysis (unilateral)	Observe + speech therapy	Most unilateral palsies recover spontaneously within 6–12 months. Monitor for aspiration risk. Thickened feeds if aspiration is a concern.
Vocal cord paralysis (bilateral)	Tracheostomy ± later lateralisation procedure	Bilateral paralysis with severe obstruction often requires tracheostomy for airway safety. Later procedures (posterior cordotomy, arytenoidectomy) can widen the glottis but may worsen voice quality. Treat underlying cause (e.g. neurosurgical decompression for Arnold-Chiari).
Subglottic stenosis	Endoscopic dilation ± laryngotracheal reconstruction (LTR)	Grade I–II: may respond to endoscopic balloon dilation ± topical mitomycin C (inhibits fibroblast proliferation). Grade III–IV: open LTR with cartilage grafting (anterior/posterior costal cartilage graft to widen the cricoid).
Subglottic haemangioma	Oral propranolol (1st line)	As above. If refractory: CO₂ laser ablation, intralesional steroid injection, or open excision.
Choanal atresia (bilateral)	Emergent airway → surgical repair	Neonatal emergency: Insert oral airway (McGovern nipple or simply a cut dummy/pacifier taped in place). Definitive: Transnasal endoscopic repair (drill through the bony plate, place stents).
Pierre Robin sequence	Positioning → tongue-lip adhesion → mandibular distraction → tracheostomy (stepwise)	Start with prone positioning; if insufficient, tongue-lip adhesion (suture tongue to inner lip → prevents glossoptosis); if still obstructed, mandibular distraction osteogenesis; tracheostomy as last resort.
Laryngeal papillomatosis	Repeated microlaryngeal surgery + adjuvant therapy	Surgical debulking (CO₂ laser or microdebrider) — recurrence is the rule; adjuvant cidofovir (intralesional antiviral) or bevacizumab (anti-VEGF) for recalcitrant disease. HPV vaccination may reduce recurrence.
Tracheomalacia (mild)	Conservative / watchful waiting	Most improve by age 2 as cartilage matures.
Tracheomalacia (severe)	Aortopexy ± tracheal stenting	Aortopexy: the ascending aorta is sutured to the posterior sternum → pulls the anterior tracheal wall forward → opens the airway. For refractory cases: biodegradable or metallic tracheal stents.
Vascular ring	Surgical division	Division of the ring (usually the smaller/non-dominant arch or ligamentum arteriosum) via thoracotomy or thoracoscopy.

Post-adenotonsillectomy: Reassess symptoms at 6–8 weeks. If symptoms persist → repeat PSG to assess for residual OSA → consider CPAP, weight management, or further investigation (DISE).
Children on CPAP: Regular follow-up every 3–6 months — mask fit, compliance data download, growth monitoring (mid-face development), repeat PSG annually to assess if CPAP pressure needs adjustment.
Children with congenital airway lesions: Long-term ENT follow-up with serial flexible nasolaryngoscopy to monitor airway growth and lesion regression.
Neurodevelopmental monitoring: Children with a history of significant OSA should be monitored for neurodevelopmental and behavioural outcomes — referral to developmental paediatrics or educational psychology if concerns arise.

High Yield Summary — Management

Acute croup: Dexamethasone 0.6 mg/kg PO (single dose) for ALL ^[3] + nebulised adrenaline for moderate-severe ^[3]. Observe after adrenaline for rebound.
Acute epiglottitis: Do NOT examine throat. Secure airway in theatre ^[8]. IV antibiotics. Extubate when fever subsiding + air leak present, usually at 18–24 hours ^[8].
Foreign body: Back blows/chest thrusts for complete obstruction ^[1]. Rigid bronchoscopy for partial obstruction or delayed presentation. Never use abdominal thrusts in infants < 1 year.
Paediatric OSA: Adenotonsillectomy is first-line ^[2] (curative in ~80%). CPAP for residual/non-surgical OSA ^[2]. Intranasal steroids + montelukast for mild OSA as medical trial.
Severe laryngomalacia: Supraglottoplasty. Mild laryngomalacia: conservative (self-resolves by 12–18 months).
Subglottic haemangioma: Oral propranolol.
Never prescribe codeine post-tonsillectomy in children — fatal respiratory depression risk in CYP2D6 ultra-rapid metabolisers.
Enuresis secondary to OSA: Treat OSA first. If persists → enuresis alarm (1st line) ± oral desmopressin ^[3].

Active Recall - Management of Noisy Breathing / Snoring in Children

References

^[1] Senior notes: Ryan Ho Critical Care.pdf (Section 1.1 Primary Survey, Section 1.2.2 Upper Airway Obstruction and Airway Management) ^[2] Senior notes: Ryan Ho Respiratory.pdf (Section 3.8.2 Sleep Apnoea/Hypopnoea Syndrome — Treatment) ^[3] Senior notes: Adrian Lui Pediatrics.pdf (Pages 161, 339 — Croup management, Enuresis management) ^[4] Senior notes: Ryan Ho Endocrine.pdf (Section on Surgical Therapy for Obesity — bariatric surgery indications) ^[7] Senior notes: felixlai.md (Tracheostomy — indications and contraindications) ^[8] Lecture slides: GC 145. A critically ill child childhood medical emergencies.pdf (Pages 28, 38 — Laryngeal mask, Management of acute epiglottitis)

Complications of Noisy Breathing / Snoring in Children

Complications arise from two distinct situations: (1) complications of the untreated underlying condition (particularly chronic upper airway obstruction/OSA), and (2) complications of treatments (particularly adenotonsillectomy). Both are clinically important and examinable. Let's work through each systematically, always explaining why from first principles.

A. Complications of Untreated Chronic Upper Airway Obstruction / OSA

Untreated OSA is associated with a variety of consequences and confers extra mortality! ^[2]

The key pathophysiological mechanisms driving complications are:

Intermittent hypoxia (cyclical desaturation-reoxygenation)
Sleep fragmentation (repeated arousals disrupting sleep architecture)
Intrathoracic pressure swings (exaggerated negative pressure during obstructed inspiration)
Sympathetic nervous system activation (triggered by hypoxia and arousals)
Chronic mouth breathing (bypassing the nasal airway long-term)

Each mechanism produces a distinct set of downstream complications.

Sleep fragmentation → sleepiness → neurocognitive impairments ^[2]

This is arguably the most clinically significant complication in children because of the impact on the developing brain.

Complication	Pathophysiology	Clinical Manifestation
Behavioural disturbance	Sleep fragmentation disrupts restorative slow-wave sleep → impaired prefrontal cortex function → poor executive function, emotional dysregulation	Hyperactivity, impulsivity, aggression, oppositional behaviour — can mimic ADHD. Studies show that up to 25% of children diagnosed with ADHD may actually have underlying OSA.
Poor academic performance	Intermittent hypoxia + sleep fragmentation → impaired hippocampal function → reduced memory consolidation (which occurs during slow-wave and REM sleep)	Declining school grades, difficulty with learning, poor attention in class
Poor concentration and memory ^[6]	Same mechanism as above	Teachers and parents report inattention, forgetfulness
Excessive daytime sleepiness	More prominent in adolescents and severe OSA; in younger children, the paradoxical hyperactivity is more common (see ADHD-like behaviour above)	Falling asleep in class, increased napping — characteristically feel that has been asleep all night but wakes up unrefreshed ^[2]
Morning headache ^[6]	Due to desaturations, CO₂ retention ^[6] — CO₂ is a potent cerebral vasodilator → vasodilation of cerebral arteries during sleep → headache upon waking	Frontal/global headache on waking, resolving within 1–2 hours as CO₂ normalises with wakefulness

OSA and ADHD — The Diagnostic Trap

Before labelling a child with ADHD, always ask about snoring and sleep quality. Up to 25% of children with ADHD symptoms may have underlying OSA. Treating the OSA (typically with adenotonsillectomy) may dramatically improve or completely resolve the behavioural symptoms — saving the child from unnecessary stimulant medication.

Why is the developing brain particularly vulnerable? During childhood, the brain undergoes critical periods of synaptogenesis, myelination, and synaptic pruning — all of which are heavily dependent on adequate sleep. Slow-wave sleep drives growth hormone release (which peaks during the first third of the night in deep NREM sleep) and memory consolidation. Disruption of these processes during the critical developmental window can have lasting consequences.

Complication	Pathophysiology	Clinical Manifestation
Failure to thrive / Growth failure	(a) Growth hormone (GH) is predominantly secreted during deep NREM (slow-wave) sleep — sleep fragmentation ↓GH secretion → impaired linear growth. (b) Increased work of breathing → elevated metabolic expenditure (the child burns more calories breathing than a normal child). (c) Feeding difficulties (dysphagia from large tonsils, anorexia from chronic inflammation, mouth breathing making eating difficult).	Weight and/or height falling across centiles on the growth chart. In severe cases, frank short stature.
Nocturnal enuresis	(a) Nocturia due to arousal and ↑abdominal pressure ^[6] — exaggerated negative intrathoracic pressure during obstructed breathing → increased venous return → atrial stretch → ↑atrial natriuretic peptide (ANP) → ↑urine production. (b) Disrupted ADH circadian rhythm — normally ADH peaks at night to reduce urine production, but sleep fragmentation disrupts this rhythm. (c) Deep arousal threshold — children may fail to wake to the sensation of a full bladder.	Enuresis ^[2] — secondary enuresis (child was previously dry at night) is particularly suggestive of OSA. Resolves in ~50% of children after adenotonsillectomy.

Sympathetic activation → ↑BP → secondary hypertension ^[2] Oxidative stress + release of mediators (hormones, cytokines, adipokines) → ↑atherosclerosis + metabolic disturbances → cardiovascular diseases, eg. CAD, HF, arrhythmia, stroke ^[2] Chronic hypoxaemia → chronic respiratory failure → cor pulmonale ^[2]

These complications are well-described in adults and increasingly recognised in children:

Complication	Pathophysiology	Paediatric Relevance
Systemic hypertension	Intermittent hypoxia → activation of peripheral chemoreceptors (carotid body) → sympathetic activation → ↑BP ^[2]. Repeated sympathetic surges → resetting of the baroreflex → sustained hypertension even during wakefulness. Oxidative stress → endothelial dysfunction → impaired nitric oxide-mediated vasodilation.	Elevated BP on ambulatory monitoring, particularly non-dipping pattern (absence of the normal nocturnal BP decrease). Children with moderate-severe OSA have a 3–4× increased risk of hypertension.
Pulmonary hypertension	Chronic/intermittent alveolar hypoxia → hypoxic pulmonary vasoconstriction (Euler-Liljestrand reflex — pulmonary arterioles constrict in response to low alveolar PO₂ to redirect blood flow away from under-ventilated areas). When this occurs globally and chronically → ↑pulmonary vascular resistance → pulmonary hypertension.	Echocardiography may show elevated PASP, RV hypertrophy. More common in children with severe OSA, especially those with coexisting conditions (Down syndrome, obesity, neuromuscular disease).
Cor pulmonale	Chronic hypoxaemia → chronic respiratory failure → cor pulmonale ^[2]. Sustained pulmonary hypertension → right ventricle must pump against increased afterload → RV hypertrophy → eventually RV dilation and failure.	Late and severe complication. Signs: loud P2, RV heave, hepatomegaly (hepatic congestion from ↑RA pressure), peripheral oedema, raised JVP (though JVP is difficult to assess in young children). Rare in otherwise healthy children but important in high-risk groups.
Cardiac arrhythmias	Intermittent hypoxia + intrathoracic pressure swings + sympathetic/parasympathetic surges → autonomic instability → arrhythmias. Severe desaturations can trigger sinus bradycardia (vagal), followed by tachycardia upon arousal (sympathetic).	Holter monitoring may show cyclical bradycardia-tachycardia pattern correlating with apnoeas.
Left ventricular dysfunction	Exaggerated negative intrathoracic pressure during obstructed inspiration → increased LV transmural pressure → increased LV afterload → LV diastolic dysfunction over time. Also, chronic sympathetic activation → elevated SVR → LV remodelling.	Subtle diastolic dysfunction may be detectable on echocardiography in children with severe OSA.

Why is cor pulmonale rare in children? Because children generally have a higher arousal threshold (they sleep deeply) but also a more compliant cardiovascular system with greater reserve. Cor pulmonale requires prolonged, severe hypoxaemia — most children are diagnosed and treated (adenotonsillectomy) before reaching this stage. It is more common in children with additional risk factors: Down syndrome, obesity hypoventilation, neuromuscular disease, or unrecognised severe OSA.

Oxidative stress + release of mediators → metabolic disturbances ^[2] Complications: HTN, DM, metabolic syndrome ^[2]

Complication	Pathophysiology	Paediatric Evidence
Insulin resistance / Metabolic syndrome	Intermittent hypoxia → sympathetic activation → ↑cortisol, ↑catecholamines → ↑hepatic gluconeogenesis + ↓peripheral glucose uptake. Oxidative stress → ↑TNF-α, IL-6 → chronic low-grade inflammation → insulin resistance. Sleep fragmentation independently impairs glucose metabolism.	Children with moderate-severe OSA have higher fasting insulin levels and HOMA-IR compared to matched controls, independent of BMI. This means OSA itself is a metabolic risk factor, not just obesity.
Dyslipidaemia	Similar inflammatory and sympathetic mechanisms → altered lipid metabolism	Modest associations seen in paediatric studies
Non-alcoholic fatty liver disease	Intermittent hypoxia → hepatic oxidative stress → steatohepatitis	Emerging evidence in obese children with severe OSA

Complication	Pathophysiology	Clinical Manifestation
Adenoid facies	Chronic mouth breathing during the critical years of facial growth (age 2–10) → the tongue rests low instead of against the palate → palate narrows and heightens (high-arched palate) → mandible drops → elongated facial growth pattern. Loss of normal nasal resistance also alters facial bone growth vectors.	Long face (dolichocephalic), narrow maxilla, high-arched palate, dental malocclusion (crowding, open bite, cross bite), gummy smile, open mouth posture
Dental malocclusion	Same mechanism — altered tongue posture and mouth breathing change the balance of forces on the growing maxilla and mandible	May require orthodontic correction even after airway obstruction is resolved
Pectus excavatum / Harrison's sulcus	Chronic severe upper airway obstruction → exaggerated negative intrathoracic pressure during inspiration → repeated forceful diaphragmatic contractions against obstruction → inward deformation of the compliant paediatric chest wall at the diaphragmatic insertions	Visible chest wall deformity. More likely in young children ( < 5 years) with very compliant chest walls.

Adenoid Facies — When the Airway Shapes the Face

The classic "adenoid facies" is not just a cosmetic issue — it represents years of abnormal facial growth driven by chronic mouth breathing. The window for orthodontic correction is during childhood growth. If you recognise adenoid facies, investigate for OSA and treat it early — not only to resolve the OSA but to allow normal facial development to resume. Rapid maxillary expansion can help reverse some of these changes if applied early enough (age 4–8 years).

These are complications of the acute conditions that cause noisy breathing (croup, epiglottitis, FB aspiration), rather than chronic OSA:

Complication	Condition	Pathophysiology
Respiratory failure / Arrest	Any severe acute obstruction	Silence for complete obstruction or apnoea ^[1] → no gas exchange → hypoxia → cardiac arrest. The progression is: partial obstruction → complete obstruction → respiratory failure → bradycardia (hypoxia-driven in children, unlike adults who tend to get tachycardia first) → cardiac arrest. In children, cardiac arrest is almost always secondary to respiratory failure, not primary cardiac.
Post-obstructive pulmonary oedema	Epiglottitis, severe croup, FB aspiration — any condition causing severe negative intrathoracic pressure	During severe obstruction, the child generates massively negative intrathoracic pressure (sometimes -40 to -100 cmH₂O) trying to breathe → ↑LV afterload (increased transmural pressure) + ↑venous return to the RV → ↑pulmonary capillary hydrostatic pressure → transudation of fluid into alveoli → pulmonary oedema. This typically manifests immediately after relief of the obstruction (hence "post-obstructive") and resolves within 24–48 hours with supportive care (O₂, PEEP/CPAP).
Hypoxic brain injury	Prolonged complete obstruction (especially FB aspiration)	Cerebral hypoxia → neuronal death. Children are particularly vulnerable because their higher metabolic rate depletes oxygen reserves faster. Even a few minutes of complete obstruction can cause irreversible brain damage.
Post-obstructive atelectasis	FB aspiration (bronchial)	FB acts as a ball valve OR completely occludes a bronchus → air distal to the FB is absorbed → segmental/lobar atelectasis → secondary infection (post-obstructive pneumonia).
Bacterial superinfection	Croup → bacterial tracheitis	Viral mucosal injury disrupts the epithelial barrier → secondary bacterial invasion → thick purulent pseudomembranes → worsening obstruction. Clinical clue: child with croup who suddenly deteriorates with high fever and poor response to nebulised adrenaline/dexamethasone.

Why do children arrest from respiratory causes rather than cardiac causes? In adults, the most common cause of cardiac arrest is ventricular fibrillation from coronary artery disease. In children, the heart is healthy — the problem is the airway. Hypoxia → brainstem depression → bradycardia → pulseless electrical activity (PEA) / asystole. This is why managing the airway is the absolute #1 priority in paediatric emergencies.

B. Complications of Treatment

Complication	Incidence	Pathophysiology	Management
Primary haemorrhage ( < 24h)	0.5–2%	Surgical bleeding from the tonsillar fossa (branches of the external carotid artery — ascending palatine, tonsillar branch of facial artery, dorsal lingual). Occurs intraoperatively or shortly after.	Return to theatre for haemostasis (cautery, suturing, packing). Ensure IV access, crossmatch blood, fluid resuscitation.
Secondary haemorrhage (5–10 days)	2–4%	Sloughing of the fibrinous eschar (the "scab") over the tonsil bed, sometimes precipitated by infection → exposes underlying vessels. The eschar separates as granulation tissue forms underneath.	Examine in A&E, IV access, crossmatch. If mild bleeding: observe + hydrogen peroxide gargles. If significant: return to theatre. Always assume the child has swallowed blood → may vomit/appear pale disproportionately.
Pain	Universal	Exposed pharyngeal muscles and nerve endings post-excision; inflammation and muscle spasm. Peaks day 3–5 (as the initial surgical oedema resolves and the raw surface is maximally exposed).	Paracetamol 15 mg/kg QDS ± ibuprofen 5–10 mg/kg TDS. NEVER codeine (CYP2D6 ultra-rapid metaboliser risk → fatal respiratory depression). Encourage oral intake (cold fluids, soft diet).
Dehydration	Common	Poor oral intake due to odynophagia → reduced fluid intake → dehydration.	Encourage fluids, IV fluids if unable to maintain hydration.
Velopharyngeal insufficiency (VPI)	~1–2%, usually transient	Adenoidectomy removes the tissue that normally contacts the soft palate during swallowing and speech → the soft palate cannot fully close against the posterior pharyngeal wall → nasal air escape during speech (hypernasal voice) and nasal regurgitation of liquids.	Usually resolves within 2–4 weeks as compensatory palatal movement develops. Persistent VPI → speech therapy ± pharyngoplasty. Screen for submucous cleft palate pre-operatively (bifid uvula, zona pellucida).
Residual OSA	~20%	Persistent obstruction from other levels (tongue base, lateral pharyngeal walls, obesity). More common in obese children, Down syndrome, craniofacial anomalies, severe pre-op OSA.	Post-operative PSG at 6–8 weeks. Consider CPAP, weight management, DISE to identify residual obstruction level, further surgery if indicated.
Nasopharyngeal stenosis	Rare ( < 1%)	Excessive scarring of the nasopharynx post-adenoidectomy → cicatricial narrowing.	Endoscopic assessment, may require surgical revision.

Complication	Pathophysiology	Prevention/Management
Skin pressure injury / Mask discomfort	Pressure from the mask interface on the nasal bridge, forehead, or cheeks → pressure necrosis in severe cases	Proper mask fitting, rotate mask types, use protective dressings (e.g. DuoDERM) on pressure points
Mid-face hypoplasia	Chronic pressure from the nasal mask on the growing mid-face skeleton during childhood → remodelling and flattening of the mid-face. More significant in young children ( < 6 years) with very malleable facial bones.	Regular craniofacial monitoring, avoid excessively tight mask fitting, consider nasal pillows or custom-fitted interfaces. Particularly concerning in children with Down syndrome (who already have mid-face hypoplasia).
Aerophagia	Positive pressure → air enters the oesophagus as well as the airway → gastric distension	Reduce pressure if possible, avoid full-face mask (more aerophagia than nasal mask), treat any coexistent GOR
Nasal dryness / Congestion	High-velocity airflow through the nasal passages → desiccation of nasal mucosa	Heated humidifier (standard with modern CPAP machines), saline nasal spray
Poor compliance	Discomfort, claustrophobia, social embarrassment (especially adolescents), parental fatigue	Behavioural desensitisation, positive reinforcement, involve child in mask choice, regular follow-up with sleep team

Tracheostomy is a last-resort intervention but carries significant complications in the paediatric population:

Complication	Timing	Pathophysiology
Accidental decannulation	Any time	The short paediatric neck and increased activity level → tube displacement. Can be life-threatening if the stoma has not matured (first 5–7 days).
Tube blockage	Any time	Thick secretions, dried crusts → occlude the tube lumen → acute obstruction. Children produce more secretions relative to tube size.
Stomal infection / Granulation	Weeks to months	Chronic inflammation at the stoma → granulation tissue formation → may narrow the stoma or airway.
Tracheal stenosis	Months to years	Chronic pressure from the tube on the tracheal wall → ischaemia → fibrosis → tracheal stenosis at the stoma site or at the tip of the tube. More common with cuffed tubes or oversized tubes.
Speech and language delay	Chronic	The tracheostomy diverts airflow away from the larynx → inability to phonate → delayed speech development. Speaking valves (Passy-Muir) can allow phonation by redirecting exhaled air through the larynx.
Psychosocial impact	Chronic	Body image concerns, social isolation, parental anxiety, impact on schooling, increased care burden. Family-centred care is essential — train parents in tracheostomy care, emergency management, and suction technique.
Swallowing dysfunction	Chronic	Tracheal tube tethers the larynx → impairs normal laryngeal elevation during swallowing → ↑aspiration risk.

Condition	Specific Complication	Pathophysiology
Laryngomalacia (severe)	Failure to thrive, cor pulmonale, GORD-related aspiration	Severe obstruction → ↑work of breathing → ↑metabolic demand + feeding difficulty → FTT. Exaggerated negative intrathoracic pressure → pulls gastric contents into the oesophagus → worsens GORD → laryngeal oedema → worsens laryngomalacia (vicious cycle).
Bilateral vocal cord paralysis	Aspiration pneumonia, need for tracheostomy	Paralysed cords in the paramedian position → adequate phonation but poor abduction → aspiration during swallowing (especially liquids).
Foreign body (retained)	Post-obstructive pneumonia, bronchiectasis, lung abscess	Retained FB → distal atelectasis + bacterial colonisation → recurrent/persistent pneumonia → chronic infection → bronchiectasis (permanent airway dilatation from destruction of bronchial wall).
Subglottic stenosis	Recurrent croup, need for repeated surgeries, tracheostomy dependence	Narrow fixed subglottis → even mild viral-induced oedema that a normal child would tolerate causes clinically significant obstruction → recurrent croup presentations.

High Yield Summary — Complications

Untreated OSA causes: sleep fragmentation → neurocognitive impairment, sympathetic activation → hypertension, oxidative stress → metabolic disturbance and cardiovascular disease, chronic hypoxaemia → cor pulmonale ^[2].
In children, the most important complication of OSA is neurobehavioural: hyperactivity, inattention, poor school performance (can mimic ADHD). Always screen for OSA before diagnosing ADHD.
Growth failure in OSA: ↓GH secretion (disrupted slow-wave sleep) + ↑metabolic expenditure + feeding difficulties.
Adenoid facies: Chronic mouth breathing during critical facial growth years → long face, high-arched palate, dental malocclusion. Early treatment allows catch-up of facial development.
Post-obstructive pulmonary oedema: Occurs after relief of severe acute obstruction due to massive negative intrathoracic pressure → ↑LV afterload + ↑pulmonary capillary pressure. Resolves with supportive care.
Post-adenotonsillectomy: Primary haemorrhage ( < 24h), secondary haemorrhage (day 5–10 from eschar separation), VPI, residual OSA (~20%), dehydration. Never use codeine post-operatively.
CPAP complications in children: Mid-face hypoplasia from chronic mask pressure on growing facial skeleton — monitor regularly.
In paediatrics, cardiac arrest is almost always secondary to respiratory failure — this is why airway management is the #1 priority.

Active Recall - Complications of Noisy Breathing / Snoring in Children

References

^[1] Senior notes: Ryan Ho Critical Care.pdf (Section 1.1 Primary Survey) ^[2] Senior notes: Ryan Ho Respiratory.pdf (Section 3.8.2 Sleep Apnoea/Hypopnoea Syndrome — complications and treatment) ^[6] Senior notes: Ryan Ho Psychiatry.pdf (Section 9.2.6 Other Sleep Disorders — symptoms of OSA)

Noisy Breathing / Snoring

Definition and Terminology

Epidemiology

General

Hong Kong Context

Risk Factors

Anatomy and Function

Paediatric Airway vs Adult Airway

Functional Anatomy — Levels of the Airway

Upper Airway Dilator Muscles

Aetiology (Focus on Hong Kong)

Anatomical Classification

A. Nose and Nasopharynx

B. Oropharynx

C. Larynx (Supraglottic, Glottic, Subglottic)

D. Trachea and Bronchi

E. Extrathoracic Causes

Temporal Classification — Acute vs Chronic

Pathophysiology

Why Does Noisy Breathing Occur? — First Principles

Dynamic vs Fixed Obstruction

Pathophysiology of Snoring / OSA in Children

Classification

By Character of Sound

By Duration

By Timing in Respiratory Cycle

By Severity (for OSA specifically)

By Aetiology of Upper Airway Obstruction [1]

Clinical Features

A. Symptoms (with pathophysiological basis)

1. Snoring / Stertor

2. Mouth Breathing

3. Witnessed Apnoeas

4. Nocturnal Choking

5. Restless Sleep / Abnormal Sleep Positions

6. Excessive Daytime Sleepiness / Behavioural Problems

7. Unrefreshing Sleep / Morning Headache

8. Enuresis (Bedwetting)

9. Stridor

10. Barking Cough

11. Voice / Cry Changes

12. Feeding Difficulties / Failure to Thrive

13. Dry Mouth

14. Nasal Symptoms

B. Signs (with pathophysiological basis)

On General Inspection

On Head and Neck Examination

On Chest Examination

Other Signs

Special Considerations by Age Group

Neonates (0–28 days)

Infants (1–12 months)

Toddlers (1–3 years)

Preschool and School Age (3–12 years)

Adolescents (12–18 years)

Approach to Noisy Breathing — Clinical Framework

Active Recall - Noisy Breathing / Snoring in Children

References

Organising Framework: Sound Character → Level → Differential

Differential by Presentation: Acute Noisy Breathing / Stridor

1. Viral Laryngotracheobronchitis (Croup) — The Most Common Cause of Acute Stridor

2. Spasmodic Croup — The Non-Infective Variant

3. Epiglottitis — A Paediatric Emergency

4. Foreign Body Aspiration

5. Retropharyngeal Abscess

6. Peritonsillar Abscess (Quinsy)

7. Bacterial Tracheitis (Pseudomembranous Croup)

8. Anaphylaxis / Angioedema

9. Other Acquired Causes of Acute Stridor [3]

Differential by Presentation: Chronic Noisy Breathing / Snoring

1. Adenotonsillar Hypertrophy — The Most Common Cause of Chronic Snoring/OSA

2. Obstructive Sleep Apnoea (OSA) — The Syndrome

3. Laryngomalacia — The Most Common Cause of Congenital Stridor

4. Vocal Cord Paralysis — 2nd Most Common Cause of Congenital Stridor

5. Subglottic Stenosis

6. Subglottic Haemangioma

7. Vascular Ring

8. Tracheomalacia / Bronchomalacia

9. Allergic Rhinitis

10. Choanal Atresia/Stenosis