Respiratory Examination — Clinical Case

DCE Short Case

Patient brief (provided to trainee)

Patient: Mrs Margaret Wilson, 66 years old, retired factory worker. [1]

Presenting complaint: Six months of progressive exertional dyspnoea (now breathless walking 50 metres on the flat), a dry non-productive cough, and a 6-kilogram weight loss. She has been referred by her general practitioner for a respiratory assessment. [1]

Past history: Hypertension (treated with amlodipine). No previous respiratory disease. She smoked 40 pack-years and stopped 2 years ago. She worked in a textile factory for 25 years. [1]

Examination findings (trainee elicits): [1]

End of bed: The patient is thin (cachectic), breathless walking to the examination couch, with a respiratory rate of 22. She is not using accessory muscles. No oxygen supplementation. No inhaler visible. [1]

Hands: Grade 3 finger clubbing (loss of the nail-fold angle, bulbous fingertip appearance, Schamroth's window absent). No peripheral cyanosis. No fine tremor. No asterixis. No tar staining (she stopped smoking 2 years ago). No stigmata of connective tissue disease. [1]

Face: No plethoric facies. No Horner syndrome. No central cyanosis. No oral candidiasis. Conjunctivae are pale (possible anaemia of chronic disease). [1]

Neck: JVP not elevated. Trachea central. Cricosternal distance normal. No cervical or supraclavicular lymphadenopathy. [1]

Anterior chest: No deformity, no scars, symmetrical movement. Chest expansion reduced bilaterally (approximately 3 cm). Percussion note normal (not hyperresonant, not dull). Auscultation: vesicular breath sounds with bilateral fine, late-inspirational, Velcro-like crackles at the bases, not clearing with coughing. No wheeze. Vocal resonance not increased. [1]

Posterior chest: Reduced expansion bilaterally. Normal percussion note. Bilateral fine, late-inspirational, Velcro-like basal crackles, not clearing with coughing. No sacral oedema. [1]

Legs: No peripheral oedema. No DVT signs. Peripheral pulses present and symmetrical. [1]

Additional observations: The trainee checks the pulse oximetry: SpO2 94 per cent on room air, dropping to 89 per cent on ambulation. [1]

Trainee presentation (model answer)

"Mrs Wilson is a 66-year-old retired textile factory worker who presents with six months of progressive exertional dyspnoea, a dry cough, and weight loss. She is a 40-pack-year ex-smoker who stopped two years ago. [1]

On general inspection, she is cachectic and breathless on minimal exertion, with a respiratory rate of 22. [1]

In the hands, there is grade 3 finger clubbing with the loss of the Schamroth window. There is no peripheral cyanosis, no asterixis, and no tremor. [1]

In the face, there is no Horner syndrome and no central cyanosis. The conjunctivae are pale. [1]

In the neck, the JVP is not elevated and the trachea is central. [1]

On examination of the chest, there is reduced expansion bilaterally. The percussion note is normal. Auscultation reveals bilateral fine, late-inspirational, Velcro-like crackles at the bases that do not clear with coughing. There is no wheeze. These findings are present anteriorly and posteriorly. [1]

The oxygen saturation is 94 per cent on room air, dropping to 89 per cent on ambulation. [1]

In summary, the constellation of progressive dyspnoea, a dry cough, weight loss, grade 3 clubbing, bilateral fine basal Velcro crackles, and exertional desaturation is consistent with interstitial lung disease. My differential diagnosis includes idiopathic pulmonary fibrosis (the most likely, given the clinical picture and the smoking history), asbestosis (given the factory work, though the asbestos exposure history needs to be clarified), connective tissue disease-associated interstitial lung disease (though there are no joint or skin signs), and hypersensitivity pneumonitis. [1]

My plan is a high-resolution CT chest, pulmonary function tests (spirometry, lung volumes, and diffusion capacity), an autoimmune screen (ANA, rheumatoid factor, anti-CCP, extractable nuclear antigens), and a six-minute walk test. If the CT shows a usual interstitial pneumonia pattern, the diagnosis of idiopathic pulmonary fibrosis can be made without a biopsy, according to the 2018 ATS/ERS/JRS/ALAT guideline [3]."

Examiner probing questions and model answers

Q1: "What is the significance of the fine Velcro crackles?" [1]

"The fine, late-inspirational, Velcro-like crackles are the hallmark of interstitial lung disease. They are produced by the sudden opening of small airways and alveoli that have collapsed during expiration in the stiff, fibrotic lung. They differ from coarse crackles, which are mid-inspiratory, low-pitched, bubbling, and may clear with coughing — those indicate secretions in the larger airways from pneumonia, bronchiectasis, or chronic bronchitis. The fine crackles of fibrosis do not clear with coughing because the pathology is in the parenchyma, not the airway. The term Velcro rales comes from the resemblance to the sound of opening a Velcro fastener [1]."

Q2: "Why is clubbing significant in this patient?" [1]

"Clubbing in the context of bilateral fine basal crackles strongly supports interstitial lung disease. The lung causes of clubbing are lung cancer, bronchiectasis, pulmonary fibrosis (especially idiopathic pulmonary fibrosis and asbestosis), mesothelioma, and lung abscess or empyema [2]. In this patient with the clinical picture of ILD, the clubbing is consistent with idiopathic pulmonary fibrosis — in which clubbing is present in up to 50 per cent of patients at diagnosis. The clubbing also makes me consider asbestosis (given the factory work history) and lung cancer (the fibrotic lung is a risk factor for lung adenocarcinoma). I would clarify the occupational exposure history for asbestos."

Q3: "What pulmonary function test pattern do you expect?" [1]

"A restrictive pattern: reduced lung volumes (reduced FVC and TLC with a normal or increased FEV1/FVC ratio), and critically, a reduced diffusion capacity (DLCO), which reflects the impaired gas transfer across the thickened alveolar-capillary membrane. The restrictive pattern differs from the obstructive pattern of COPD (reduced FEV1/FVC ratio with increased lung volumes). The six-minute walk test showing desaturation is an important prognostic marker — a drop of more than 4 per cent (or below 88 per cent) indicates significant impairment." [1]

Q4: "What would you look for on the high-resolution CT?" [1]

"The high-resolution CT is the key diagnostic investigation. For idiopathic pulmonary fibrosis, I would look for a usual interstitial pneumonia (UIP) pattern: basal-predominant, subpleural reticulation with honeycombing and traction bronchiectasis, without significant ground-glass change. According to the 2018 ATS/ERS/JRS/ALAT guideline, a definite UIP pattern on CT is sufficient for a non-invasive diagnosis of IPF in the appropriate clinical context — a surgical lung biopsy is not required [3]. If the pattern is probable UIP (reticulation and traction bronchiectasis without honeycombing), a bronchoalveolar lavage or a cryobiopsy may be needed to exclude alternative diagnoses. I would also look for features of asbestosis (pleural plaques and basal fibrosis) and for any mass lesion that would suggest lung cancer."

Q5: "What is the significance of the occupational history?" [1]

"The textile factory work raises the question of occupational lung disease. Asbestosis produces a similar clinical picture to IPF (progressive dyspnoea, bilateral basal crackles, clubbing, and a restrictive pattern on lung function), but with the addition of pleural plaques on the CT — the hallmark of asbestos exposure. Other occupational exposures I would ask about include silica (silicosis — stonemasonry, mining, sandblasting) and bird feather or mould exposure (hypersensitivity pneumonitis). The occupational history is part of the diagnostic process because the treatment and the compensation implications differ: IPF is treated with antifibrotic therapy (nintedanib or pirfenidone), while occupational lung disease is managed by removal from exposure and supportive care." [1]

Q6: "What is the prognosis and the management plan?" [1]

"The prognosis of idiopathic pulmonary fibrosis is poor — the median survival from diagnosis is 3 to 5 years without treatment. The management has been transformed by antifibrotic therapy: nintedanib (a tyrosine kinase inhibitor) and pirfenidone (an antifibrotic and anti-inflammatory agent) both slow the decline in lung function and are now the standard of care for IPF. I would also address the supportive care: supplemental oxygen for the hypoxaemia, pulmonary rehabilitation, vaccination (influenza, pneumococcal), management of the gastro-oesophageal reflux (a possible contributor to IPF progression), and early referral for lung transplant assessment in the appropriate patient. The palliative care and the advance care planning should be introduced early, because IPF is a progressive and ultimately fatal disease." [1]