Pulmonary · Topic 25 of 28

Upper Airway Obstruction & Angioedema

Pulmonary · threatened airway

Upper Airway Obstruction & Angioedema

Stridor with distress means the airway comes first. Then sort the swelling: itchy hives answer to epinephrine; bradykinin angioedema does not.

Key numbers

ACE-inhibitor angioedema: stop the drugResolves 24–48 h off ACEi

Failed cuff leak: steroids 4 h before extubationSteroids ≥ 4 h before

01 · FirstStridor with distress: secure the airway

Stridor with drooling, tripod posture, hypoxemia, inability to speak or reduced consciousness signals impending airway loss: defer the full exam and secure the airway, in the operating room with ENT when feasible.

02 · Don't confuseNo hives or itch: bradykinin angioedema

Mast cell (histamine) angioedema comes with urticaria and pruritus and develops over minutes to hours; bradykinin angioedema (ACE inhibitor, hereditary or acquired C1-inhibitor deficiency) has no urticaria or itch and evolves over hours to days.

03 · DoACE-inhibitor angioedema: stop the drug

ACE-inhibitor angioedema is bradykinin-mediated: stop the ACE inhibitor permanently; swelling usually resolves 24–48 hours later. Epinephrine, antihistamines and steroids are unproven; for severe or refractory cases try C1-inhibitor concentrate, FFP, icatibant or ecallantide.

Causes & risk factors

Why it happens

ACE inhibitors: about 30% of ED angioedemaACE inhibitors cause angioedema in < 1% of users yet account for about 30% of ED angioedema; onset can be early or years into therapy, favoring the face, tongue and upper airway, sometimes the bowel.

Presentation

What you'll see

Inspiratory stridor = obstruction above the thoraxStridor is turbulent flow through a narrowed large airway: inspiratory with supraglottic or glottic narrowing, expiratory with intrathoracic tracheobronchial obstruction, biphasic with a fixed glottic or subglottic lesion.

Adult epiglottitis: fever, sore throat, droolingEpiglottitis is now more common in adults: abrupt fever, severe sore throat, drooling and distress. Do not instrument the mouth; image only if stable; examine and intubate in the operating room if distressed.

Ventilated: high peak, normal plateau = obstructionOn the ventilator, a peak-to-plateau gap over 10 cm H₂O (high resistive pressure) points to a kinked or secretion-plugged endotracheal tube, an airway mass or bronchospasm — suction and check the tube.

Diagnosis & monitoring

Work-up

Screen hereditary angioedema with a C4 levelSuspect C1-inhibitor deficiency with recurrent angioedema without urticaria, a family history, or attacks after trauma or dental work; check C4, C1-inhibitor level and function (low C4 with low C1-inhibitor level or function confirms it).

Do right now

In this order

First moves

Stridor with distress: secure the airway

→

Have a surgical airway ready

→

Give IM epinephrine unless clearly bradykinin-mediated

→

ACE-inhibitor angioedema: stop the drugResolves 24–48 h off ACEi

Why each step

Stridor with distress: secure the airwayStridor with drooling, tripod posture, hypoxemia, inability to speak or reduced consciousness signals impending airway loss: defer the full exam and secure the airway, in the operating room with ENT when feasible.

Have a surgical airway readyAirway edema makes intubation difficult — prepare for emergency cricothyrotomy or tracheostomy. In angioedema, stridor, drooling or distress means emergent intubation; hoarseness, dysphagia or dyspnea without distress warrants fiberoptic laryngoscopy.

Give IM epinephrine unless clearly bradykinin-mediatedIf angioedema involves the airway and is not obviously bradykinin-mediated, give IM epinephrine as for anaphylaxis, plus an H1 blocker and a systemic glucocorticoid (e.g., methylprednisolone 125 mg IV, diphenhydramine 50 mg IV).

ACE-inhibitor angioedema: stop the drugACE-inhibitor angioedema is bradykinin-mediated: stop the ACE inhibitor permanently; swelling usually resolves 24–48 hours later. Epinephrine, antihistamines and steroids are unproven; for severe or refractory cases try C1-inhibitor concentrate, FFP, icatibant or ecallantide.

Management

Orders

HAE attack: C1-inhibitor or icatibant must knowTreat a hereditary angioedema attack with C1-inhibitor concentrate, icatibant (bradykinin B2 blocker) or a kallikrein inhibitor (ecallantide, sebetralstat); use FFP if none is available. Epinephrine, antihistamines and glucocorticoids are usually ineffective.

Temporize with heliox and racemic epinephrineAs a bridge in severe large-airway obstruction, heliox lowers turbulent flow and work of breathing; nebulized racemic epinephrine and dexamethasone help when edema is the cause (e.g., post-extubation laryngeal edema).

HAE: C1-inhibitor before dental or airway proceduresBefore dental or airway procedures in hereditary angioedema, give C1-inhibitor concentrate about 1 hour beforehand; attenuated androgens (from 5 days before) or 2 units of FFP are alternatives when it is unavailable.

Failed cuff leak: steroids 4 h before extubationPerform a cuff leak test before extubating patients at high risk of post-extubation stridor; if it fails, give systemic corticosteroids at least 4 hours before extubation.

Mucus plugging: clear secretions, then bronchoscopyMucus plugging causes lobar or whole-lung collapse: treat with chest physiotherapy, directed cough, suctioning and nebulized dornase alfa or bronchodilators; perform bronchoscopy if these fail or another obstruction is suspected.

The rules

Know these

Laryngeal edema or intubated: admit to ICUDisposition of ACE-inhibitor angioedema: laryngeal edema or intubation → ICU; tongue, floor-of-mouth or pharyngeal edema, progression, or prior episodes → monitored bed; isolated lip or facial swelling → ED observation.

Mast cell or bradykinin angioedema?

Commonly confused

Urticaria and itching	Usually present
Onset	Minutes to hours
Epinephrine, antihistamine, steroid	Effective
Specific therapy	IM epinephrine, H1 blocker, glucocorticoid
Intubation	Less often needed — swelling falls quickly

More detail

Reference

Show 6 reference facts

Common adult causes of stridor: vocal fold dysfunction, post-extubation laryngeal edema, vocal fold edema or paralysis, laryngeal tumors and allergic reactions.

Vocal fold dysfunction (paradoxical vocal fold motion) causes recurrent episodic stridor that mimics asthma and fails to respond to asthma therapy; laryngoscopy confirms it.

For chronic or intermittent stridor, flow-volume loops show upper airway obstruction; follow with neck and chest CT or laryngoscopy (smoking and alcohol raise suspicion of laryngeal cancer).

Long-term hereditary angioedema prophylaxis: plasma-derived C1-inhibitor, lanadelumab, berotralstat, garadacimab or donidalorsen; attenuated androgens only where these are unavailable.

Ecallantide carries a boxed warning for anaphylaxis and must be given by a clinician in a monitored setting, never self-administered.

Hereditary angioedema type 3 has normal C1-inhibitor and normal C4 (some cases from factor XII or plasminogen mutations) and is more common in women.

Pearl

No hives, no itch, on an ACE inhibitor: think bradykinin — epinephrine will not shrink it, so secure the airway early.

Sources · Merck Manual Professional — Stridor · Merck Manual Professional — Angioedema · Merck Manual Professional — Hereditary and Acquired C1 Inhibitor Deficiency or Dysfunction · AAEM Clinical Practice Statement — ED management of angioedema secondary to an ACE inhibitor (2011) · Girard TD et al. ATS/ACCP Clinical Practice Guideline: Liberation from Mechanical Ventilation in Critically Ill Adults (cuff leak tests). Am J Respir Crit Care Med 2017;195:120–133 · Merck Manual Professional — Atelectasis · Merck Manual Professional — Overview of Mechanical Ventilation · Starter sheet built from the verified AGACNP fact map (facts reviewed 2026-10-15).