Respiratory Medicine — Short Cases

13 Respiratory Medicine— Short Cases David Chi-Leung Lam, James Chung-Man Ho, and Mary Sau-Man Ip Overview The goals of clinical examination for the respiratory system, in the format of short case examination, are: 1. To identify the abnormal physical signs. 2. To arrive at the pathophysiologic diagnosis underlying the physical signs and suggest the most likely disease diagnosis or differential diagnoses. 3. To propose, based on the working diagnosis, relevant clinical investigations and briefly discuss salient management issues. General examination In the context of short case examination, this means periph- eral examination for physical signs that are relevant to diseases affecting the respiratory system. Observe the overall patient status, facial expression, posture, breathing pattern; also check for the presence of medical acces- sories on the patient or at the bedside. For example: 1. Ventilators could be portable ones that patient may be using at certain times of the day or at night and thus not dependent on when you examine. 2. Oxygen supplementation vianasal cannula or face mask (Venturi mask). Note the oxygen flow rate or oxygen concentration.

Respiratory Medicine 179 3, Medical drainage systems or intravenous drips. 4. Inhaler devices that patient could be using. 5. Sputum mug for collection of sputum. 6. Any bedside “alert signage” being put up. Get an overall impression whether patient has cachexia/morbid obesity, tachypnea or respiratory distress, such as excessive use of accessory muscles of breathing or paradoxical breathing. Look for pallor, central cyanosis, finger clubbing, ankle or leg swelling, cervical and supraclavicular lymphadenopathy, skin rash, facial/upper limb swelling with dilated veins over chest due to superior vena cava obstruction syndrome, unilateral ptosis sug- gesting possible Horner’s syndrome. Do not restrict your focus on the signs being mentioned above while ignoring gross abnormalities that the patient may show, e.g., rheumatoid hands which support pulmonary fibrosis. Chest examination of the respiratory system Important to note: As you approach the patient from either the front or the back, do not miss the lung apices and the axillary regions, where scars or chest drain sites could be hidden. For the chest, compare the symmetry of findings on the two sides, while taking note of presence of liver and heart. * Inspection: Look at the whole precordium including the base of the neck (supraclavicular areas) and also the axillary region on both sides. Observe, preferably from the end of the bed, any chest wall deformity, thoracotomy scars, use of accessory muscles in breathing, breathing pattern, and chest wall movement. (Note: mid-sternotomy scars generally indicate previous cardiac surgery or thymectomy). Count the respiratory rate: though you may not be required to do so for short case examination with very limited time—you must have an observation of whether the patient is breathing too rapidly or too slowly.

180 Problem-Based Medical Case Management Case 13.1 Palpation: Assess chest wall expansion; the position of the trachea and the apex beat; vocal fremitus (optional if vocal resonance will be performed later; also suggest to put this test till the end if used for confirmation). Percussion: To decide whether percussion note is resonant or dull Auscultation: Assess breath sounds (vesicular, bronchial; prolonged expira- tion), detect added sounds (crackles or crepitations [fine or coarse], thonchi or wheeze, pleural rubs), and assess vocal resonance. 13.1 Bronchiectasis Classical signs . Sputum container filled with purulent or blood stained sputum at the bedside Finger clubbing Reduced chest wall movement Normal percussion ) Bilateral or focal coarse inspiratory crackles that may disappear or are altered in quality after coughing. (Note: crackles may also be persistent). In some patients, rhonchi are also present. Severe cases may be associated with features of cor pulmonale and respiratory distress. Very severe cases are often associated with cachexia. Causes Idiopathic (majority of diffuse bronchiectasis) Post-tuberculosis Post-pneumonic Childhood measles (severe, complicated by pneumonia) or pertussis

Case 13.1 Respiratory Medicine 181 Rheumatological disorders (rheumatoid arthritis, systemic lupus erythematosis, systemic sclerosis, etc.) Gastro-oesophageal reflux Traction bronchiectasis from fibrotic lung diseases (such as pulmonary fibrosis or radiation pneumonitis) Kartagener’s syndrome Hypogammaglobulinaemia Allergic bronchopulmonary aspergillosis (ABPA) Important differential diagnoses For the physical finding of bilateral lung crackles, the major dDx is pulmonary fibrosis. However, the crackles in bronchiec- tasis are usually coarse and may occur through both inspiratory and expiratory phases, while that in pulmonary fibrosis are fine and mainly late inspiratory. Bronchiectasis may have rhonchi/ wheeze, and may show some hyperinflation while pulmonary fibrosis results typically in reduced lung volumes (i.e., restric- tive). Both can have finger clubbing. Chronic obstructive pulmonary disease (COPD) with heavy component of chronic bronchitis may present with similar symptoms of cough and sputum in a smoker. Studies have actu- ally shown a high prevalence of bronchiectasis among patients diagnosed to have COPD. COPD usually have more hyperinfla- tion and less coarse crackles. Asthma presents with dyspnoea, cough, sputum production, and recurrent exacerbations. Asthma affects up to 10% of patients with bronchiectasis and therefore asthmatic patients with copious sputum production should also undergo high resolution computed tomography (HRCT) examination of the chest. Physical examination may show both wheeze/rhonchi in addition to crackles in patients with only bronchiectasis or with both bronchiectasis and asthma. Post-tuberculosis lung destruction with a mixture of bronchiec- tasis, fibrosis, and cavitations. Usually causes focal/unilateral . bronchiectasis.

182 Problem-Based Medical Case Management Case 13.1 Tnvestigations: e CXR and HRCT thorax for definitive diagnosis » Spirometry (may be obstructive or mixed obstructive-restrictive) e Sputum microscopy, Gram’s stain and bacterial and fungal culture, smear and culture for acid-fast bacilli « Sa0, (on room air) or arterial blood gases determination « X-ray sinuses ¢ Other tests as necessary (e.g., aspergillus serology) Discussion « Aectiology of bronchiectasis: — In Hong Kong and the West, bronchiectasis is largely an idiopathic disease. However, TB, pneumonia, and immuno- deficiency also account for a significant proportion. — Cystic fibrosis is extremely rare in Chinese. «+ Differential diagnoses and key distinguishing investigations (see Chapter 14) + Management in acute exacerbations or in severe cases Pitfalls and tips « Failure to recognize nasal tone of chronic nasal obstruction (or other signs of chronic sinusitis) « Failure to detect (i) mediastinal shift in severe bronchiectasis; resulting from associated lobar collapse, or (ii) Situs inversus in particular dextrocardia in Kartagener’s syndrome + Omitting examination of bedside sputum pot Patients with idiopathic pulmonary fibrosis may have “traction bronchiectasis” resulting in mixed features of pulmonary fibro- sis and bronchiectasis.

Case 13.2 Respiratory Medicine 183 13.2 Chronic obstructive pulmonary disease (COPD) Classical signs Central cyanosis (may be masked by use of supplemental oxygen) Bilateral pitting ankle oedema and other features of right heart failure Tachypnea Reduced distance between suprasternal notch and cricoid carti- lage (normal distance depends on individual body build, about 2-3 fingers’ breadth) and increased anteroposterior diameter of the chest (barrel chest) with reduced chest expansion bilater- ally, due to hyperinflation of the lungs Normal or hyper-resonant percussion (obliteration of cardiac and liver dullness) Decreased breath sounds (with prolonged expiratory phase, end expiratory rhonchi or inspiratory crackles depending on the severity of the airflow obstruction and the amount of sputum present) Normal to decreased vocal resonance Risk factors Cigarette smoking: the single most important risk factor Heavy exposure to indoor air pollution, e.g., use of biomass fuels in some rural areas Alpha-1 antitrypsin deficiency: rare in Chinese; this condition should be suspected in young persons (< 50 years old) with COPD who never smoked or were light smokers. Occupational exposures to dusts or fumes Important differential diagnoses * Chronic asthma: both chronic asthma and COPD show airflow obstruction but the former exhibits greater variation in symptoms

184 Problem-Based Medical Case Management Case 13.2 and reversibility of airflow obstruction on spirometry. Asthma usually affects non-smokers with a history of wheezing since childhood. « A group of patients (usually smokers) may have overlapping features of asthma and COPD (ACOS). ¢ Bronchiectasis: both bronchiectasis and COPD may present with chronic cough and sputum (chronic bronchitis component of COPD), and have lung crackles and rhonchi on physical examination. However, patients with bronchiectasis usually are non-smokers, show symptoms dating back to childhood or youth, and produce copious purulent sputum. Bronchiectasis and COPD may also coexist. Important investigations + Chest X-ray: typical COPD features include hyperinflation and bullae; typical complications include infections, pneumotho- rax, cardiomegaly (due to cor pulmonale), prominent pulmo- nary trunks (pulmonary hypertension), and lesions suspicious of lung cancer (another complication of chronic smoking, the main cause of COPD). « Pulse oximetry (assesses Sa0,) or arterial blood gases (assesses pH, PaO, and PaCO,): to confirm/explore severity and type (1 or 2) of respiratory failure « Lung function tests: — Spirometry with bronchodilator reversibility test to confirm and assess severity of airflow obstruction (typically FEV1/ FVC < 70%, FEV1 < 80% of predicted) — Lung volume measurement to assess severity of hyperinfla- tion (RV and RV/TLC) - Diffusing capacity of carbon monoxide (DLco) to assess alveolar destruction due to emphysema » Complete blood count: raised haematocrit indicates erythrocy- tosis secondary to chronic hypoxaemia; high leucocyte count may indicate acute bacterial infection and exacerbation or use of systemic steroids.

Case 13.3 Respiratory Medicine 185 Sputum examination: for patients with infective exacerbations. Note: Sputum culture is not routinely required, as the com- monest isolates are known to be Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. Antibiotics to cover these pathogens are prescribed whenever there is a clinical diagnosis of an infective exacerbation. Nasopharyngeal aspirate for virus. ECG and echocardiogram: to assess right heart strain and cor pulmonale. Pitfalls and tips Look out for sputum container and contents, and presence of inhaler devices or non-invasive ventilators by the bedside. Note whether patient is receiving oxygen usually via nasal cannula (most are), and the rate of supplemental oxygen. Note whether patient is in respiratory distress (rapid and shallow breathing, using accessory respiratory muscles at the neck, intercostal retraction) or drowsy (sign of CO, retention or exhaustion). Note “pursed lip breathing” if present. Note “barrel chest” if present. In patients with severe airflow obstruction (including in asthma), the expiratory phase is prolonged. Expiratory rhonchi/ wheeze may not be apparent unless the patient is requested to carry out a forced full expiration. Note physical signs of cor pulmonale. 13.3 Collapsed lung Classical signs Tachypnea, especially in case of major collapse Decreased chest movement on affected side Tracheal deviation and shifting of apex beat to ipsilateral side. Tracheal deviation occurs in whole lung collapse or upper lobe

186 Problem-Based Medical Case Management Case 13.3 collapse, but not obvious in lower lobe collapse; while apex beat is affected more by lower lobe or whole lung collapse. Dull to percussion (not “stony”) over affected area Decreased breath sounds over affected area Causes Endobronchial obstruction or extrinsic compression by neo- plasms, e.g., lung cancer, rarely bronchial adenoma. Foreign body aspiration Infections, e.g., endobronchial tuberculosis (may present as sequelae of previous tuberculosis) Impacted, thick tenacious sputum, usually in weak and ill patients Important investigations . Chest X-ray: confirms lung collapse radiologically. Then look for mass lesion compressing airway; some foreign bodies are radio-opaque. CT thorax can reveal collapse and mass lesion compressing airway and associated mediastinal lymphadenopathy. Sputum: cytology for malignant cells and smear and culture for acid-fast bacilli Bronchoscopy: to localize obstruction and obtain specimens for diagnosis Discussion Treatment depends on the aetiology. Lung cancer causing bron- chial obstruction: requires surgery (if resectable), radiotherapy and/or medical therapy, bronchoscopic stenting; foreign body requires bronchoscopic removal; active endobronchial tuber- culosis mandates prompt anti-tuberculosis chemotherapy to minimize fibrosis and airway stenosis (use of systemic corti- costeroids is controversial).

Case 13.4 Respiratory Medicine 187 Pitfalls and tips Overlooking cervical lymphadenopathy, especially for sus- pected malignancy Tracheal deviation and shifted cardiac apex related to upper and lower lung collapse, respectively Pleural effusion and lower lobe collapse have similar physical signs except for the degree of dullness, and pleural effusion may be associated with underlying lung collapse giving rise to stony dullness. The directions of mediastinal shift, if present, will be ipsilateral to the side of disease in collapse but to the contralateral side if due to pleural effusion. Signs of lower lobe collapse and lobectomy may be similar, though lobectomy should be accompanied by thoracotomy scar or a few small scars of VATS. In consolidation-collapse, features of consolidation such as localized crackles or even bronchial breathing may be present. Endobronchial tuberculosis (alone or as part of pulmonary parenchymal tuberculosis) is an important benign cause of obstruction, still not uncommon in less developed places. It may be mistaken for tumour on gross bronchoscopic examination. Some patients present with lung collapse as late sequelae of previous tuberculosis. 13.4 Pleural effusion Classical signs Tachypnea Decreased chest movement or expansion on the affected side Tracheal deviation to the contralateral side (if massive) Stony dull percussion note on the affected side Decreased/absence of breath sounds on the affected side; there may be bronchial breath sounds at the upper margin of effusion (egophony) Decreased vocal resonance

188 Problem-Based Medical Case Management Case 13.4 Common predisposing scenarios/causes . Young person with pleurisy due to tuberculosis or lupus Patients with diabetes or on systemic corticosteroids are liable to effusions from bacterial, tuberculous or fungal pleurisy Elderly male chronic smoker (malignant effusion, tuberculous pleurisy) Chronic smoker and alcoholic (malignant effusion, tuberculous pleurisy, suppurative aspiration pneumonia with empyema) Occupational exposure to asbestos (mesothelioma) If bilateral, consider: heart failure and kidney disease (transu- dates). Hepatic hydrothorax (cirrhosis), though transudative, is mostly right-sided. Important investigations Chest X-ray (may include decubitus view for small effusion): to confirm unilateral effusion and detect parenchymal shadows suspicious of tuberculosis or malignancy, mediastinal lymphad- enopathy; rib erosions suggest a malignant process. Ultrasound is useful for further delineation of pleural effusion to guide thoracocentesis. Sputum examination for: cytology, smear and culture for bacte- ria, acid-fast bacilli and fungi as indicated Diagnostic thoracocentesis for: — Inspection of the fluid is important. Turbid fluid should raise concerns of empyema, chylothorax or pseudochylothorax. - Bloody effusion may be a haemorrhagic effusion from malignancy or due to a haemothorax. Presence of food parti- cles indicates oesophageal rupture. , — Biochemistry, including serum/fluid protein and LDH to ascertain exudative or transudative nature — Fluid white cell count and differential (neutrophil predomi- nance — acute inflammation, e.g., bacterial infection; lym- phocyte predominance — tuberculous or vasculitic pleurisy

Case 13.4 Respiratory Medicine 189 such as in lupus). Malignant effusions can be lymphocytic or neutrophilic. — Culture for bacteria/mycobacteria/fungi (note that smear of pleural fluid for acid-fast bacilli is negative as a rule, even in tuberculous pleurisy (except in HIV-infected subjects). TB-PCR is not recommended due to interference from inhibitors in the fluid with poor sensitivity and specificity). — Cytology for malignant cells — Adenosine deaminase level (higher than reference range) suggests tuberculous effusions although ADA can be ele- vated in most effusions of bacterial infection, and some of those from rheumatological causes and cancers. Note: Such aspiration procedures are often followed by a pleural biopsy if effusion is exudative (to look for granuloma- tous tuberculosis or a malignant pathology). In difficult diag- nostic cases, pleuroscopy/VATS may be needed. * CT thorax for better delineation of lung parenchyma and effu- sion as indicated. If clinically indicated, CT pulmonary angio- gram may be needed as some patients with pulmonary emboli will have a (usually small) pleural effusion. * Flexible bronchoscopy if indicated * Search for autoimmune disease markers as indicated. Pitfalls and tips * Presence of an aspiration needle mark (usually posteriorly) pro- vides an additional clue to the presence of an effusion. Mediastinal shift (tracheal deviation) may not be present with small to moderate sized pleural effusions. Mediastinal shift is also modified by presence of both lung collapse and pleural effusion which may occur together. In very weak, bed-bound patients, percussion dullness is detected more in the lateral (dependent) parts of the chest.

190 Problem-Based Medical Case Management Case 13.5 13.5 Upper lobe/apical fibrosis Classical signs « Post-radiotherapy skin changes around the neck or upper chest area ¢ Flattened chest on the affected side (increased supraclavicular fossa hollowing) e Decreased chest movement on the affected side (area) ¢ Tracheal deviation to the affected side « Dull percussion note, particularly over the clavicle » Decreased breath sounds on the affected side with localized fine crackles. Occasionally bronchial breath sounds are present. Common causes ¢ Old pulmonary tuberculosis « Ankylosing spondylitis ¢ Post-radiation pulmonary fibrosis (e.g., for nasopharyngeal car- cinoma or lung cancer) Important investigations * Chest X-ray (may include apico-lordotic view): confirms fibro- sis in lung apex, calcified apical foci suggest old pulmonary tuberculosis, spine may have features of ankylosing spondylitis. » Computed tomography (CT) of thorax: delineates parenchymal lung lesions better [ « Sputum smear and culture for acid-fast bacilli: assess activity of pulmonary tuberculosis Pitfalls and tips ¢ Chest wall expansion may be only mildly diminished, and signs - rather subtle if fibrosis only involves apical area. The only detected sign may be percussion dullness over the clavicle with or without deviation of trachea to affected side. ‘

Examination case Respiratory Medicine 191 «+ Do not forget percussion over the clavicles. + PFeatures of upper lobe collapse or collapse-consolidation due to endobronchial obstruction, e.g., by tumour, may give rise to similar features of tracheal deviation, dull percussion, and decreased breath sounds (or bronchial breath sounds when extensive consolidation is present). + Uncommonly, similar signs are due to Pancoast tumour. Associated Horner’s syndrome may provide the hint. Discussion + Previous pulmonary tuberculosis is a common cause of apical or upper lobe fibrosis in Asians. * There is a need to ascertain any previous investigation and man- agement for pulmonary tuberculosis, including the treatment regime and whether directly observed therapy or “DOT” was adopted (as practised in Hong Kong). Examination case scenarios i. Examine this lady’s lungs. She complained of progressive shortness of breath for a year. Important signs » Tachypneic and using oxygen at 2 litres/minute. * Mild finger clubbing. * Palpation and percussion of chest normal. » Fine end inspiratory crackles in lower zones bilaterally in the posterior and lateral aspects. Diagnosis Idiopathic pulmonary fibrosis

192 Problem-Based Medical Case Management Examination case Questions 1. What other diseases commonly give rise to clubbing together with inspiratory crackles? ¢ Bronchiectasis. ¢ If localized coarse crackles—may also be obstructive pneumonia due to lung cancer. 2. What other features would you look for systemically in case of pulmonary fibrosis? ¢ Features of autoimmune disease such as rheumatoid arthritis. 3. What investigation would be most useful to confirm the diagnosis? * High resolution CT thorax. 4. What would you see on lung function test? * Restrictive pattern with decrease diffusing capacity for carbon monoxide. Pitfalls and tips Remember to auscultate for added lung sounds at the lateral aspects. » Traction bronchiectasis may be present in advanced pulmonary fibrosis. « Typically, features of lung restriction are present in advanced pulmonary fibrosis. « Look for features of autoimmune disease and also occupational exposure/drug history. » Coarse crackles and production of purulent sputum suggest bronchiectasis as dDx or added component.

Examination case Respiratory Medicine 193 ii. Examine this gentleman’s chest. He has dyspnoea and weight loss of 5 kg in the recent 2 months. Important signs . . Cachexic Tachypnea (24/min) Trachea central Decreased chest movement on the right side Very dull percussion note over the lower half on the right side of chest Markedly decreased breath sounds over the right lower zone Vocal resonance decreased over the lower zone Diagnosis Right sided pleural effusion, moderate size Questions 1. What other physical signs should be sought? 2 Clubbing and lymphadenopathy. If present, suggest lung malignancy giving rise to the pleural effusion. Concurrent signs of left ventricular failure or ascites may raise suggestions of heart failure effusion and hepatic hydrothorax respectively. What differential diagnoses can be offered? RLL collapse/consolidation. Raised hemidiaphragm. Large lung mass.

194 Problem-Based Medical Case Management Examination case iii. Examine this woman’s chest. She had no known respiratory disease but was admitted two days ago with hypercapnic respiratory failure. Important signs ~ + Obese (BMI = 35 kg/m”) * Waist circumference: 103cm » Central cyanosis < Bilateral pitting ankle oedema « Symmetrically decreased chest expansion, but no wheeze or crackles ¢ Blood pressure 150/100 mmHg ¢ Left parasternal heave ¢ Increased pulmonic second sound Diagnosis Obesity hypoventilation syndrome (OHS) Questions 1. What are the likely underlying respiratory abnormalities? * Obesity hypoventilation syndrome (presence of hypercapnia and cor pulmonale). « Obstructive sleep apnoea often co-existent in OHS. 2. What is the treatment of choice in the acute admission and in the long term? » Non-invasive ventilation would control the hypercapnic respiratory failure. Long term—use either bi-level or continuous positive airway pressure (CPAP) during sleep. » Supplemental oxygen is often needed for hypoxemia in cases of OHS. ¢ Weight reduction. » Treat right heart failure.