Laryngomalacia, tracheomalacia and vocal-cord dysfunction: Viva

Branch 1: Recognising the pattern that is not asthma

The candidate should immediately question the asthma label. A barking, seal-like cough with an expiratory wheeze that does not respond to a bronchodilator, and that may worsen after the reliever, is the classic picture of tracheomalacia rather than asthma. The history of repaired oesophageal atresia and tracheo-oesophageal fistula is the crucial clue, because these children have a structurally soft trachea from the shared foregut origin of the trachea and oesophagus. The recurrent chest infections fit a trachea that clears secretions poorly. [3]

The candidate should explain the localising principle: this is expiratory, intrathoracic noise, which points to the trachea, whereas asthma is small-airway disease that responds to bronchodilator. The mechanism of the salbutamol trap is that the drug relaxes airway smooth muscle and reduces the residual tone splinting the soft trachea open, so it can worsen the collapse. [1]

Branch 2: Confirming tracheomalacia

The examiner will ask how the diagnosis is confirmed. The strong candidate states that the reference standard is a dynamic bronchoscopy performed in a spontaneously breathing child, which captures the expiratory collapse of the trachea. The key teaching point is that positive-pressure ventilation or deep anaesthesia splints the airway open and hides the collapse, so a bronchoscopy done the wrong way can falsely reassure. [2]

The candidate should add that airway fluoroscopy and expiratory cross-sectional imaging can support the diagnosis, and that when an external compression such as a vascular ring is suspected, contrast-enhanced CT or MRI with angiography and a contrast swallow are indicated. In this child a full airway assessment and evaluation of the reflux and the anastomosis are appropriate given the oesophageal-atresia background. [1]

Branch 3: Management of tracheomalacia

The examiner will probe management. The candidate should explain that most tracheomalacia is managed supportively: treatment of contributing reflux and infection, chest physiotherapy, and time, because the tracheal cartilage stiffens as the child grows and most children improve by the preschool years. Continuous positive airway pressure pneumatically splints the collapsing intrathoracic trachea and is useful for symptomatic children. [2]

The examiner will then ask when surgery is indicated. Severe disease with recurrent dying spells, persistent respiratory failure or an inability to wean from support is treated surgically by aortopexy, posterior tracheopexy or, less often, airway stenting. The candidate should recognise the dying spell — a sudden cyanotic collapse from a vagally mediated reflex apnoea during a feed or illness — as a life-threatening event that mandates admission and consideration of definitive treatment. [1]

Branch 4: The adolescent variant

The examiner changes the scenario to a 15-year-old netball player with sudden exertional breathlessness, a noisy inspiration localised to the throat and a sensation of throat tightness, treated for two years as exercise-induced asthma without benefit. The candidate should recognise vocal-cord dysfunction, now termed inducible laryngeal obstruction, in which a hyper-responsive larynx closes the vocal folds paradoxically during inspiration. The discriminators from asthma are the inspiratory timing at peak exercise, the rapid offset on stopping, the localisation to the neck, and the absence of a bronchodilator response. [4]

The candidate should describe confirmation by laryngoscopy during provocation, ideally continuous laryngoscopy during a graded exercise test, and first-line treatment with speech-language therapy that teaches breathing retraining and laryngeal control, alongside treatment of contributing reflux, rhinitis, asthma and anxiety. Escalating steroids for misdiagnosed asthma is the trap to avoid. [4]

Branch 5: Pulling the topic together

The examiner asks the candidate to summarise the unifying principle. The strong answer is that laryngomalacia, tracheomalacia and vocal-cord dysfunction are all dynamic collapse of an airway when transmural pressure exceeds wall stiffness; the phase of the noise localises the lesion, the age and trigger identify which disorder it is, and the severity decides whether the child needs only reassurance or an intervention. The two great traps are treating tracheomalacia as asthma with escalating bronchodilators and treating vocal-cord dysfunction as refractory asthma with rising steroids. [2]