On-Call Guide to Stridor

Definitions

Stertor is a noisy, low-pitched, snoring or gurgling respiratory sound caused by partial obstruction of the airway above the level of the larynx (nasopharynx or oropharynx). It resembles snoring and is commonly heard in unconscious patients or those with large tonsils and adenoids.

Stridor is a high-pitched, harsh respiratory sound caused by turbulent airflow through a partially obstructed airway at or just below the level of the larynx (larynx, subglottis, or extrathoracic trachea). It is a symptom of significant airway compromise and must be taken seriously.

Wheeze is a high-pitched, musical respiratory sound originating from partial obstruction of the small intrathoracic airways (bronchi and bronchioles), as seen in asthma and COPD. It is predominantly expiratory.

In practice, these three can be difficult to differentiate clinically, particularly in young children. Do not fixate on the distinction at the expense of patient management — treat the patient, not the label.

Anatomical Classification and Phase of Stridor

The phase of stridor (inspiratory, expiratory, or biphasic) gives important clues about the anatomical level of obstruction:

• Stertor / noisy inspiratory breathing: Supraglottic obstruction (above the vocal cords) — typically nasopharyngeal or oropharyngeal, with a gurgly or snoring quality.
• Inspiratory stridor (high-pitched): Supraglottic obstruction at the level of the epiglottis, aryepiglottic folds, or vocal cords. Classic in epiglottitis.
• Biphasic stridor (both inspiratory and expiratory): Glottic or subglottic/extrathoracic tracheal obstruction. The airway is narrowed enough to cause turbulence in both phases of breathing. Seen in croup (subglottic oedema).
• Expiratory stridor/wheeze: Intrathoracic airway obstruction. During expiration, positive intrathoracic pressure compresses small airways; during inspiration, negative thoracic pressure holds them open. Seen in bronchial foreign bodies and asthma.

Causes of Stridor

Naso-Oropharyngeal Causes

Congenital

• Oral synechiae and persistent buccopharyngeal membrane
• Choanal atresia or stenosis (unilateral or bilateral — bilateral presents as respiratory distress at birth, as neonates are obligate nasal breathers)
• Oral masses: ranula (mucous retention cyst under the tongue, with or without infection), dermoid, thyroglossal cyst
• Craniofacial syndromes: Pierre Robin sequence (micrognathia with posterior tongue displacement), Treacher Collins syndrome

Inflammatory / Infective

• Adenotonsillar hypertrophy (causes stertor and obstructive sleep apnoea)
• Quinsy (peritonsillar abscess)
• Deep neck space infections: Ludwig's angina (a rapidly spreading bilateral submandibular cellulitis which can compromise the airway), retropharyngeal abscess, parapharyngeal abscess
• Nasal polyps
• Diphtheria (Corynebacterium diphtheriae — now rare in vaccinated populations but important to recognise)
• Allergic rhinitis and anaphylaxis

Neoplastic

• Sinonasal malignancy
• Oropharyngeal malignancy (SCC — increasingly HPV-related)
• Nasopharyngeal angiofibroma (young males, typically causing unilateral nasal obstruction and epistaxis)

Traumatic

• Foreign body (especially children — presents with sudden onset stridor or choking)
• Septal haematoma
• Burns (inhalational — rapidly progressive airway oedema; intubate early)
• Post-operative oedema
• Facial fractures with pharyngeal haematoma

Laryngeal Causes

Congenital

• Laryngomalacia: The most common cause of stridor in infancy. The supraglottic structures (aryepiglottic folds, epiglottis) are floppy and collapse inward during inspiration. Characteristically an intermittent, positional inspiratory stridor worsening when the infant is supine or crying, and improving in the prone position. Usually self-limiting by 18 to 24 months.
• Vocal cord palsy (unilateral or bilateral) — bilateral causes biphasic stridor and may require tracheostomy
• Glottic or subglottic webs
• Cystic hygroma (lymphatic malformation of the neck)
• Vascular slings and rings (aberrant vessels compressing the trachea)
• Laryngeal cysts

Inflammatory / Infective

• Anaphylaxis: Causes supraglottic and glottic oedema rapidly. Give IM adrenaline (epinephrine) 0.5 mg (1:1000) immediately and follow ALS anaphylaxis protocol.
• Epiglottitis: Acute bacterial infection of the epiglottis and supraglottic structures, classically caused by Haemophilus influenzae type B (Hib) — now rare in vaccinated children but still occurs in unvaccinated individuals and adults (Streptococcus and Staphylococcus are increasingly implicated in adults). The patient sits bolt upright, drooling, with a high fever and a characteristic "tripod" position. Do NOT examine the throat with a tongue depressor, do NOT attempt cannulation or cause distress — the airway can occlude completely. Arrange urgent secure airway in theatre with ENT and anaesthetics simultaneously present.
• Laryngotracheobronchitis (croup): Subglottic inflammation caused by viral infection (most commonly parainfluenza virus), producing a characteristic "barking" seal-like cough and biphasic stridor. Peaks between 6 months and 3 years. Severity is graded by the Westley croup score (0 to 17). Management: oral dexamethasone 0.15 mg/kg (a single dose is effective), nebulised adrenaline (5 ml of 1:1000) for moderate to severe croup.
• Laryngitis
• Neck space infections including tuberculous lymphadenopathy

Neoplastic

• Laryngeal SCC — progressive hoarseness preceding stridor; higher risk in smokers and heavy alcohol users
• Recurrent respiratory papillomatosis (RRP) — caused by HPV types 6 and 11; causes wart-like growths on the larynx, particularly in young children
• Haemangioma
• Lymphoma
• External compression by thyroid tumour or goitre

Traumatic

• Foreign body inhalation — the most common cause of acute stridor in young children
• Post-intubation subglottic stenosis (tracheal stenosis from prolonged intubation or high cuff pressures)
• Vocal cord paralysis after thyroid, parathyroid, or cardiac surgery (damage to the recurrent laryngeal nerve — the left RLN is particularly vulnerable due to its course around the aortic arch)
• Inhalation burn injuries
• Laryngeal fracture

Management

Localising the Obstruction

Whilst assessing and resuscitating the patient, attempt to determine where the obstruction is. This guides management:

• Stertor — suggests supraglottic obstruction (nasopharynx/oropharynx); gurgling or snoring quality
• High-pitched inspiratory stridor — supraglottic to glottic (consider epiglottitis)
• Biphasic stridor — subglottic and extrathoracic tracheal obstruction (consider croup)
• Expiratory stridor — intrathoracic; foreign body or small airway disease

A targeted history provides valuable diagnostic clues:

• Sudden onset — foreign body, anaphylaxis, trauma
• Preceding sore throat and high fever — epiglottitis, tonsillitis with peritonsillar/parapharyngeal abscess
• Barking cough in a child — croup
• Recent intubation or surgery — post-intubation subglottic stenosis, RLN palsy
• Progressive hoarseness — laryngeal tumour
• Congenital or neonatal — laryngomalacia, subglottic stenosis
• Systemic symptoms (weight loss, night sweats) — malignancy, lymphoma

Treatment — Stepwise Approach

1. Oxygen: High-flow oxygen via facemask. Some units use humidified oxygen, though evidence for its superiority over standard oxygen is limited. Position the patient as they find most comfortable — do not force them to lie down.
2. Nebulised adrenaline (epinephrine): 5 ml of 1:1000 adrenaline (5 mg) via nebuliser. This causes mucosal vasoconstriction and reduction in oedema. Effect is rapid (within minutes) but temporary (30 to 60 minutes). Used in croup, post-extubation stridor, and other inflammatory causes. Note: nebulised adrenaline in croup can cause rebound oedema — patients who receive it should be observed for at least 2 hours.
3. Steroids:
   • Dexamethasone 0.6 mg/kg up to 8 mg IV or IM — the most effective and rapid-onset option for inflammatory airway oedema
   • Alternatively, if the situation is less acute, oral prednisolone 1 mg/kg (up to 40 mg)
   • Alternatively, nebulised budesonide 2 mg — slower onset than systemic steroids but useful if IV access is not available
   • Combinations can be given
4. Antibiotics: Administer IV if an infective cause (epiglottitis, neck abscess) is suspected. Choice depends on suspected organism — in epiglottitis, IV co-amoxiclav or cefuroxime. Seek microbiological advice. Antibiotics are not beneficial in viral croup.
5. Heliox: A mixture of 21% oxygen and 79% helium (or 30% oxygen and 70% helium). Helium is less dense than nitrogen, so the mixture produces less turbulent flow through a narrowed airway and is easier to breathe. Heliox buys time while definitive management is arranged, but it does not treat the underlying cause. It is contraindicated if oxygen requirements are high (high FiO2 needed), as increasing the oxygen concentration reduces the helium fraction and negates its physical benefit.
6. Intubation: Call the anaesthetist. In epiglottitis, this must be performed in a controlled setting (operating theatre) with ENT immediately available to perform emergency tracheostomy if intubation fails. An inhalational induction with sevoflurane is usually preferred to maintain spontaneous ventilation.
7. Needle cricothyroidotomy: If intubation fails and the airway is lost, perform a needle cricothyroidotomy as an emergency rescue procedure. Insert a 12 G (brown) IV cannula through the cricothyroid membrane — the space between the inferior border of the thyroid cartilage and the superior border of the cricoid cartilage — at 45 degrees in a caudal direction. Confirm position by aspiration of air. Connect to a jet insufflation system. This technique provides temporary oxygenation only — CO2 accumulation means you have approximately 30 to 45 minutes maximum before a definitive airway is mandatory.
8. Surgical tracheostomy: If a definitive airway cannot be secured by any other route, emergency tracheostomy is performed. This should ideally be performed by an ENT surgeon in theatre, but in extremis may need to be performed at the bedside. For patients with tracheostomies already in situ who develop stridor, the most likely cause is a blocked tube — thoroughly suction the inner tube, remove and clean it, or replace it before escalating.