‘All that wheezes is not asthma’—a reminder that the physical examination

An educational goal for our Symptoms to Diagnosis series, edited by Dr. Gregory Rutecki, is to give readers the opportunity to work through a patient’s clinical course along with the treating physicians, sharing some of their diagnostic and therapeutic cognitive branch points. At times, the series highlights missed opportunities in diagnosis and treatment that became evident over time. For those of you who enjoy the experience of working through these “cases,” I suggest that you stop and first read the paper in this issue by Johnson et al¹ about the treatment of a “20-year-old woman with a 9-year history of shortness of breath.”

The young woman in the article had a nearly decade-long history of significant dyspnea on exertion and had recently immigrated to the United States. There are many potential contributors to the delay in her diagnosis, particularly following her arrival in the United States, including language barriers and fears of accessing medical care due to her immigrant status. The impact of social determinants on her medical care likely played a role in the delayed diagnosis and should not be dismissed, but the major teaching points relate to the many opportunities where the physical examination and a reflective review of her medical history could have led to an earlier diagnosis. A marked delay in the diagnosis of upper airway obstruction, which is frequently treated as refractory asthma, is quite common.^2,3

Stridor is an uncommon clinical finding that we should promptly recognize and distinguish from wheezing. Unlike the expiratory wheeze of asthma, which is best appreciated over the lungs, stridor is a high-pitched sound produced by turbulent airflow through a narrowed upper airway. It is heard best from the suprasternal notch upward to over the trachea. It may be loud enough to be heard without a stethoscope. Stridor, unlike the wheezing of bronchospasm, is characteristically more prominent during inspiration than expiration² and may be biphasic. This contrasts sharply with asthma, where expiratory wheezing predominates over the lung fields and only rarely radiates loudly to the trachea. Hearing a prominent inspiratory component is distinctly unusual and should prompt checking for an upper airway obstructive process.

Beyond auscultation, clinicians should assess for associated historical features and physical findings. The presence or history of a saddle-nose deformity, auricular chondritis, or nasal septal perforation suggests the need to consider the diagnosis of granulomatosis with polyangiitis or relapsing polychondritis. These uncommon conditions can also be suggested by a clinical history or unexplained laboratory findings consistent with a systemic inflammatory disease. A history of previous intubation raises the possibility of delayed traumatic airway stenosis.

Vocal cord dysfunction, also termed paradoxical vocal fold motion, deserves special emphasis, as it frequently masquerades as severe asthma and often is unrecognized for years.^3,4 This condition involves inappropriate adduction of the vocal cords during inspiration, creating airflow limitation at the laryngeal level accompanied by stridorous breathing. In a seminal study of 95 patients with vocal cord dysfunction,⁵ 42 were misdiagnosed with asthma for years, with most patients having received high-dose glucocorticoids on multiple occasions. They received an incorrect diagnosis despite the fact that expiratory wheezing over the lung fields is a rare finding in patients with vocal cord dysfunction. These patients averaged 6 hospitalizations yearly, and 28% required intubation. Dyspnea was often worse during exercise, but significant oxygen desaturation was uncommon. Importantly, bronchodilator therapy was rarely effective. The diagnostic test for vocal cord dysfunction is direct visualization of vocal cord adduction during inspiration. Pulmonary function tests (PFTs) may reveal a flattened inspiratory flow loop—a component of PFTs that is often overlooked—and do not demonstrate reversible smaller airway obstruction.

Relapsing polychondritis is a rare autoimmune disorder characterized by recurrent inflammation of cartilaginous structures, including the trachea. Airway involvement occurs in 21% to 70% of patients with relapsing polychondritis and may be the initial manifestation, presenting as some combination of dyspnea, hoarseness, and tracheal tenderness.⁶ Notably, for those with relapsing polychondritis or vocal cord dysfunction, marked anxiety can be a prominent (and understandable, once the diagnosis is confirmed) component of the patient’s history and may lead to a delay in diagnosis.

Granulomatosis with polyangiitis may involve the large airways, and the subglottic area is a common site of airway involvement.⁷ Subglottic stenosis may be the presenting component of the disease, particularly in young patients. Airway symptoms include voice changes, dyspnea, and cough, with the physical finding of stridor present on examination as the narrowing progresses. In patients with granulomatosis with polyangiitis, there may also be significant sinus and lung involvement, which may delay recognition of the upper airway involvement. As subglottic stenosis often does not respond to systemic therapy, it may not be recognized until other components of the disease respond to treatment while dyspnea persists.

Isolated subglottic stenosis can occur following traumatic intubations, but can also be idiopathic or congenital. If relatively mild, congenital stenosis may not be diagnosed until adolescence or adulthood⁸; sometimes there is a genetic predisposition,⁹ as may have been the case in the patient described by Johnson et al.¹

Evaluation of stridor in adults requires integration of the history, physical examination, and objective testing. The patient’s history should assess the timing of symptoms related to exercise, their response to bronchodilators, and the presence of triggers (eg, environmental irritants, gastroesophageal reflux, postnasal drip) and include a thorough review of symptoms. Physical examination should be thorough and include auscultation of the chest and neck and assessment of the upper airway, sinonasal passages, skin, and ears.

As appropriate for most patients with undefined respiratory symptoms, PFTs should be obtained, and these should include a bronchodilator challenge. PFTs may relieve the suspicion for bronchospasm, although subglottic stenosis and distal airway obstruction may rarely coexist.¹⁰ Direct visualization remains the gold standard for definitive diagnosis. Flexible nasolaryngoscopy or laryngoscopy can identify vocal cord dysfunction, subglottic stenosis, and supraglottic pathology. Bronchoscopy permits wider evaluation of the airways and may reveal mucosal inflammation, distal stenoses, or malacia not apparent on imaging.

But it is the physical examination, particularly the location and timing of abnormal breath sounds, that can provide the clues to the diagnosis and direct further testing. Inspiratory stridor heard over the trachea, especially with the associated lack of a physiologic response to bronchodilators, and a fairly normal oxygen saturation measurement during an episode of acute dyspnea suggest upper airway obstruction rather than asthma. Recognizing these findings on physical examination can prevent years of misdiagnosis and possible inappropriate treatment.

This topic was similarly discussed by Bhat and Ashton¹¹ in the Journal 5 years ago.

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