Upper airways obstruction

At resting levels of ventilation, the main airway can be reduced to a diameter of 3 mm or so before respiratory distress and stridor occur. Little more narrowing is required to precipitate complete asphyxia, hence when upper airways obstruction is suspected, assessment of severity, diagnosis, and treatment is a medical emergency.

Clinical features and diagnosis—recognizing the presence of upper airways obstruction requires a high degree of clinical suspicion: stridor or noisy breathing will initially only be heard on exercise, but will gradually appear at lower and lower levels of activity; a patient’s complaint that the problem is ‘somewhere in the neck’ should be taken seriously.

Investigation—peak expiratory flow rate is reduced disproportionately to the forced expiratory volume in 1 s (FEV₁), but the best functional evidence of upper airways obstruction is obtained with a flow–volume loop, which shows a squared appearance.

Acute upper airway obstruction—this can be caused by aspiration, oedema (allergic, hereditary, and acquired angio-oedema, smoke inhalation), and infection (more commonly in children). The emergency treatment for aspiration is the Heimlich manoeuvre (abdominal thrust); allergic causes require intramuscular adrenaline (0.5 ml of 1:1000, and see Chapter 17.2 for details of the management of anaphylaxis). Intubation or emergency cricothyroidotomy (in rare cases) may be required.

Nonacute upper airway obstruction—this can be caused by tumours, tracheal stenosis (usually after intubation or tracheostomy), tracheal compression, various tracheal abnormalities, and laryngeal dysfunction. Spread of a primary bronchial carcinoma into the base of the trachea is probably the commonest cause. This unfortunately becomes a terminal event in many cases, when adequate sedation must be given to make the patient unaware that they are asphyxiating and choking to death.