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Respiratory symptoms and physical signs 

Respiratory symptoms and physical signs
Chapter:
Respiratory symptoms and physical signs
Author(s):

Huw Llewelyn

, Hock Aun Ang

, Keir Lewis

, and Anees Al-Abdullah

DOI:
10.1093/med/9780199679867.003.0006
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Chest pain—sharp and aggravated by breathing or movement

This is a common symptom that is experienced in mild or transient forms by many in the population and resolves with no cause being discovered. It frightens a patient into seeking advice when it is severe or accompanied by other symptoms such as breathlessness. Initial investigations (other tests in bold below): FBC, U&E, ECG, troponin 12h after onset of the pain.

Main differential diagnoses and typical outline evidence, etc.

Musculoskeletal injury or inflammation

  • Suggested by: associated focal tenderness ± history of trauma or lying awkwardly.

  • Confirmed by: normal (or no changes in) troponins, ECG, and CXR. Good response to simple analgesia.

  • Finalized by the predictable outcome of management, e.g. simple analgesia (e.g. NSAIDs) and avoidance of strenuous activity until pain improves.

  • Chest wall pain

  • e.g. Tietze’s syndrome

  • Suggested by: chest pain and tenderness of chest wall on twisting of neck or thoracic cage.

  • Confirmed by: normal (or no changes in) troponins, ECG, and CXR. Good response to simple analgesia.

  • Finalized by the predictable outcome of management, e.g. simple analgesia (e.g. NSAIDs) and avoidance of strenuous activity until pain improves.

Pneumonia with pleurisy

  • Suggested by: onset over hours or days, rusty brown sputum ± blood. Sharp pain worse on inspiration, fever, cough, crackles, dullness to percussion, bronchial breathing, WCC: ↑neutrophils, ↑CRP.

  • Confirmed by: patchy shadowing on CXR and organisms grown in sputum/blood culture.

  • Finalized by the predictable outcome of management, e.g. analgesia and provisional antibiotic, e.g. amoxicillin/clarithromycin PO for 5d. If >2 features of Confusion, Resp. rate >30/min, BP <90/60, age >65y), then antibiotic IV, e.g. amoxicillin/co-amoxiclav or cefuroxime + controlled O2 and fluids. If suspected aspiration, then anti-anaerobics, e.g. cefuroxime/metronidazole IV. If hospital/nursing home acquired, cefuroxime or piperacillin with tazobactam IV.

Pulmonary embolus/ infarction arising from deep veins or in left atrium

  • Suggested by: sudden breathlessness, pleural rub, cyanosis, tachycardia, loud P2, associated DVT or risk factors such as recent surgery, immobility, previous emboli, malignancy, etc.

  • Confirmed by: CT pulmonary angiogram showing clot in pulmonary artery.

  • Finalized by the predictable outcome of management, e.g. LMW heparin (treatment dose), then warfarin. Thrombolysis if ↓BP, large bilateral clots, or acutely dilated right ventricular on echocardiogram.

Pneumothorax (‘tension’, moderate, or mild)

  • Suggested by: pain in centre or side of chest with abrupt breathlessness, diminished breath sounds, and hyper-resonance to percussion.

  • Confirmed by: above findings, tracheal deviation, and distress suggesting tension pneumothorax, or expiration CXR showing loss of lung markings outside sharp line (‘moderate’ if >5cm gap from lung edge to chest wall; ‘mild’ if <5cm).

  • Finalized by the predictable outcome of management, e.g. if tension pneumothorax, insertion of large Venflon into 2nd intercostal (IC) space, midclavicular line. Giving O2 if breathless. Analgesia. Aspiration if moderate; if unsatisfactory or prior lung disease, insertion of IC drain into ‘triangle of safety’. If ‘mild’ (<5cm gap) and not breathless, observation.

  • Pericarditis

  • caused by myocardial infarction, infection (especially viral), malignancy, uraemia, connective tissue diseases

  • Suggested by: sharp pain worse lying flat, but relieved by leaning forward. Pericardial rub.

  • Confirmed by: ECG: concave ↑ST, ‘bright’ pericardial signal on echocardiogram. CXR showing cardiomegaly and globular heart shadow if significant pericardial effusion.

  • Finalized by the predictable outcome of management, e.g. close cardiac monitoring, NSAIDs and treating cause (e.g. viral—typically self-limiting; if uraemic, treating renal failure; steroids if autoimmune).

Referred cervical root pain

  • Suggested by: previous minor episodes of exacerbation of chest pain by neck movement (producing closure of nerve root foramina related to area of pain).

  • Confirmed by: clinical features and MRI scan.

  • Finalized by the predictable outcome of management, e.g. analgesia, trial of neck collar, and physiotherapy.

Shingles

  • Suggested by: pain (often burning in nature) in a dermatomal distribution, recent exposure to chicken pox, or previous shingles attacks.

  • Confirmed by: vesicles appearing within days in the same dermatome.

  • Finalized by the predictable outcome of management, e.g. NSAIDs ± co-analgesics, e.g. cabamazepine/gabapentin. Aciclovir if severe/immunosuppressed.

Sudden breathlessness, onset over seconds

This situation may be life-threatening. Initial investigations (other tests in bold below): FBC, U&E, CXR, ECG, D-dimer.

Main differential diagnoses and typical outline evidence, etc.

  • Pulmonary embolus/ infarction

  • arising from deep veins or in left atrium

  • Suggested by: sudden breathlessness, pleural rub, cyanosis, tachycardia, loud P2, associated DVT, or risk factors such as recent surgery, immobility, previous emboli, malignancy, etc.

  • Confirmed by: CT pulmonary angiogram showing clot in pulmonary artery.

  • Finalized by the predictable outcome of management, e.g. LMW heparin (treatment dose), then warfarin. Thrombolysis if ↓BP, large bilateral clots or acutely dilated right ventricular on echocardiogram.

Pneumothorax (‘tension’, moderate, or mild)

  • Suggested by: pain in centre or side of chest with abrupt breathlessness, diminished breath sounds and hyper-resonance to percussion.

  • Confirmed by: tracheal deviation and distress suggesting tension pneumothorax, or expiration CXR showing loss of lung markings outside sharp line (‘moderate’ if >5cm gap from lung edge to chest wall; ‘mild’ if <5cm).

  • Finalized by the predictable outcome of management, e.g. if tension pneumothorax, insertion of large Venflon into 2nd intercostal (IC) space, mid-clavicular line. Giving O2 if breathless and analgesia. Aspiration if moderate; if this is unsatisfactory or prior lung disease, insertion of IC drain into ‘triangle of safety’. If ‘mild’ (<5cm gap) and not breathless, observation.

Anaphylaxis

  • Suggested by: onset over minutes, history of recent allergen exposure, feeling of dread, flushing, sweating, facial oedema, urticaria, warm clammy extremities, dyspnoea and tachypnoea, wheeze. Tachycardia and ↓BP.

  • Confirmed by: clinical presentation and response to adrenaline (epinephrine) IM. Results of controlled allergen exposure.

  • Finalized by the predictable outcome of management, e.g. removal of antigen (e.g. bee sting, medication). Adrenaline IM 1 in 1,000. Securing of airway early if stridor. High flow O2, fast fluids IV, steroids IV and antihistamines IV. Transferring to HDU/ITU.

Inhalation of foreign body

  • Suggested by: history of putting an object in mouth, e.g. peanut. Sudden stridor, severe cough, low-pitched, monophonic wheeze, and reduced breath sounds, typically on the right.

  • Confirmed by: if not in extremis, CXR/CT thorax or bronchoscopy to show foreign body.

  • Finalized by the predictable outcome of management, e.g. if in extremis, slap back between the shoulder blades with patient leaning forward. If fails, perform Heimlich manoeuvre.

Cardiac arrhythmia

  • Suggested by: palpitations, chest pain, dizziness, pallor, hypotension, tachycardia or ± ↓BP.

  • Confirmed by: ECG (pulse typically >140 or <40) and improvement in symptoms/signs as pulse rate improves.

  • Finalized by the predictable outcome of management, e.g. controlled O2. If pulse >140, vasovagal manoeuvres or rate-lowering medication or electric cardioversion. If pulse <40, atropine IV or pacing (external, temporary internal), transferring to CCU.

Acute breathlessness, wheeze ± cough

This symptom suggests airway narrowing. The commonest cause is bronchospasm (constriction of the smooth muscle in the distal bronchioles); less common causes are wheeze due to inhalation of a foreign body or hydrostatic pulmonary oedema, i.e. ‘cardiac wheeze.’ Initial investigations (other tests in bold below): FBC, U&E, CRP, ABG, ECG, CXR.

Main differential diagnoses and typical outline evidence, etc.

Exacerbation of asthma

  • Suggested by: widespread polyphonic wheeze with exacerbations over hours. Silent chest if severe. Anxiety, tachypnoea, tachycardia, and use of accessory muscles.

  • Confirmed by: reduced peak flows. FEV1 that improves by >15% with treatment.

  • Finalized by the predictable outcome of management, e.g. high flow O2, prednisolone PO or hydrocortisone IV. Nebulized salbutamol and ipratropium ± magnesium IV and aminophylline IV. NB. Keeping hydrated, and monitor ABG and serum K+. HDU if drowsy, ↑CO2.

Exacerbation of COPD

  • Suggested by: long history of cough ± sputum, many pack years of smoking, recurrent ‘exacerbations’. CXR: radiolucent lungs.

  • Confirmed by: spirometry: FEV1<80% predicted and FEV/FVC ratio <0.7. <15% reversibility. Emphysema on CT chest ± reduced α1-antitrypsin levels.

  • Finalized by the predictable outcome of management, e.g. controlled O2, prednisolone 7–10d, and nebulized bronchodilators. Antibiotics if worsening breathlessness, cough, and mucopurulent sputum. Stopping smoking. Trials of bronchodilators prn, then regular long-acting bronchodilators. Regular inhaled steroids if FEV<50% predicted and three COPD exacerbations per year.

Acute viral or bacterial bronchitis

  • Suggested by: onset of wheeze over days. No dramatic progression. Fever, mucopurulent sputum, dyspnoea.

  • Confirmed by: sputum culture and sensitivities. No consolidation on CXR.

  • Finalized by the predictable outcome of management, e.g. simple analgesia and antibiotics if continued purulent sputum.

Acute left ventricular failure due to ?cardiac event, valvular disease, electrolyte imbalance, arrhythmia

  • Suggested by: onset minutes to hours. Breathless, distressed and clammy, displaced tapping apex beat, 3rd heart sound, bilateral basal late fine inspiratory crackles. Often also signs of right ventricular failure (↑JVP, swollen legs).

  • Confirmed by: CXR: fluffy opacification (greatest around the hila), horizontal linear opacities peripherally, bilateral effusions, large heart. Impaired left ventricular function on echocardiogram.

  • Finalized by the predictable outcome of management, e.g. sitting patient up, controlled O2, diuretics IV. Nitrates IV if very breathless and systolic BP >90. Identifying and treating potential causes. Chronic: thiazide or loop diuretic, ACE inhibitor (or angiotensin receptor blocker). β-blocker and spironolactone (monitor K+).

Anaphylaxis ?precipitant

  • Suggested by: dramatic onset over minutes, recent allergen exposure. Flushing, sweating facial oedema, urticaria, and warm but clammy extremities, tachypnoea, bronchospasm, and wheeze. Tachycardia and hypotension.

  • Confirmed by: precipitant identification and response to adrenaline (epinephrine) IM.

  • Finalized by the predictable outcome of management, e.g. removal of antigen (e.g. bee sting, medication). Adrenaline IM 1 in 1,000. High flow O2, fast fluids IV, steroids IV, and antihistamines IV. If stridor, securing of airway early as laryngeal oedema may progress, and HDU/ITU care.

Chronic breathlessness

Initial investigations (other tests in bold below): FBC, U&E, ECG, CXR, serial peak expiratory flow rates (PEFRs).

Main differential diagnoses and typical outline evidence, etc.

Obesity and muscle deconditioning

  • Suggested by: more breathlessness on exertion. No cough or other symptoms. High BMI, but no other abnormality on examination, and normal baseline tests.

  • Confirmed by: normal or mild restrictive defect on spirometry, CXR, and ECG. Improvement with weight loss and graduated aerobic exercise programme.

  • Finalized by the predictable outcome of management, e.g. weight loss and reconditioning.

Asthma precipitated by allergens, e.g. pollen, house mites, etc.

  • Suggested by: wheeze, chronic cough worse at night/early morning, specific triggers. Family history or childhood history of asthma or atopy.

  • Confirmed by: spirometry: reduced peak flow. FEV1 that improves by >15% with treatment.

  • Finalized by the predictable outcome of management, e.g. high flow O2, prednisolone PO or hydrocortisone IV. Nebulized salbutamol and ipratropium ± magnesium IV and aminophylline IV. Long-term care: identifying precipitants. Stopping smoking. Trial of bronchodilator prn and inhaled steroids, long-acting β-agonist/steroid combinations, leukotriene inhibitors/antihistamines.

COPD caused by smoking, smoke pollution, α1-antitrypsin deficiency

  • Suggested by: long history of cough ± sputum, many pack years of smoking, recurrent ‘exacerbations’. CXR: radiolucent lungs.

  • Confirmed by: spirometry: FEV1<80% predicted and FEV/FVC ratio <0.7. <15% reversibility. Emphysema on CT chest ± ↓α1-antitrypsin levels.

  • Finalized by the predictable outcome of management, e.g. stopping smoking. Trials of bronchodilators prn, then regular long-acting bronchodilators. Regular inhaled steroids if FEV <50% predicted and three COPD exacerbations per year. If cough and breathless persists, prednisolone PO. If respiratory failure, home O2.

Left ventricular dysfunction caused or made worse by atrial fibrillation, ischaemic heart disease, mitral stenosis, or regurgitation, hypertension. Anaemia, thyrotoxicosis, chest infections

  • Suggested by: fatigue, orthopnoea, and reduced exercise capability. Resting tachycardia with S3 and displaced apex, bibasal crackles. Evidence of causes.

  • Confirmed by: reduced left ventricular function on echocardiogram. CXR: large cardiac shadow, upper lobe vein dilatation, loss of costophrenic angle, hilar shadows.

  • Finalized by the predictable outcome of management, e.g. thiazide or loop diuretics, ACE inhibitors (or angiotensin receptor blockers). β-blockers, spironolactone to improve prognosis. Treating causes.

  • Pulmonary fibrosis/interstitial lung disease

  • NB majority of cases have no cause identified

  • Suggested by: chronic dry cough, occupational exposure or evidence of underlying connective tissue disease. Clubbing, cyanosis, reduced chest expansion, coarse late inspiratory bibasal crackles.

  • Confirmed by: ↓lung volumes and reticular nodular shadowing on CXR. Interstitial shadowing and/or subpleural fibrosis on high resolution CT chest.

  • Finalized by the predictable outcome of management, e.g. home O2 if saturations <93%. Specialist opinion for detailed lung function, lung biopsy, immunosupression, antifibrotics, palliation.

Neuromuscular disease complicated by respiratory failure

  • Suggested by: muscle weakness, orthopnoea, daytime sleepiness and/or early morning headaches (due to nocturnal hypoventilation). Muscle wasting, fasciculation, calf hypertrophy, etc. Abnormal ABG.

  • Confirmed by: clinical presentation and muscle biopsy. Restrictive defect on spirometry + FVC, and fall in FVC by ≥20% on lying flat. Small volume lungs on CXR.

  • Finalized by the predictable outcome of management, e.g. non-invasive ventilation if ABGs show respiratory failure. Follow-up by neurologist and multidisciplinary team.

  • Pulmonary hypertension

  • (1° pulmonary hypertension in 20%; in 80%, 2° to previous pulmonary emboli, vasculitis, chronic lung disease)

  • Suggested by: features of underlying cause. Loud P2. Desaturation in pulse oximetry on walking and low transferring factor.

  • Confirmed by: ↑pulmonary pressures and/or right ventricular dysfunction on echocardiogram.

  • Finalized by the predictable outcome of management, e.g. treat underlying cause (anticoagulate with heparin and warfarin if severe pulmonary hypertension—even if no proven pulmonary emboli). O2 to maintain saturations >93%. Managed in chest clinic.

Psychogenic

  • Suggested by: no other associated features of pulmonary or cardiac disease. Underlying anxiety (e.g. high Nijmegan score), triggered by stressful situations.

  • Confirmed by: no appearance of organic cause over time

  • Finalized by the predictable outcome of management, e.g. relaxation, control breathing exercises. Explanation and reassurance.

Chronic thrombo-emboli with or without pulmonary hypertension

  • Suggested by: underlying risk factors, borderline hypoxia (e.g. saturations of 92–95%), resting tachycardia. No loud P2.

  • Confirmed by: echocardiogram showing no signs of pulmonary hypertension. CT-PA showing occluded vessels or V/Q scans (showing ventilation/perfusion mismatch (better at detecting peripheral smaller clots below 4th division of pulmonary arteries).

  • Finalized by the predictable outcome of management, e.g. warfarin for at least 3mo, treating risk factors.

Frank haemoptysis (or sputum streaked with blood)

Haemoptysis rarely causes hypovolaemia from blood loss, but if there is hypotension or tachycardia, consider their causes (see Respiratory symptoms and physical signs Blood pressure very low, p.[link]; Respiratory symptoms and physical signs Tachycardia (e.g. pulse rate >120bpm), p.[link]). If tuberculosis (TB) is suspected, patient should be isolated whilst tests are carried out. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Acute viral or bacterial bronchitis

  • Suggested by: days of fever, mucopurulent sputum, dyspnoea. Typically only streaky haemoptysis and self-limiting.

  • Confirmed by: sputum culture and sensitivities, response to appropriate antibiotics.

  • Finalized by the predictable outcome of management, e.g. analgesia and antibiotics.

Pulmonary embolus/ infarction arising from deep veins

  • Suggested by: sudden breathlessness, pleural rub, cyanosis, tachycardia, loud P2, associated DVT, or predisposing risk factors such as recent surgery, immobility, malignancy, etc.

  • Confirmed by: CT pulmonary angiogram showing clot in pulmonary artery.

  • Finalized by the predictable outcome of management, e.g. LMW heparin (treatment dose), then warfarin. Thrombolysis if ↓BP, large bilateral clots, or acutely dilated right ventricle on echocardiogram.

Carcinoma of lung

  • Suggested by: weeks or months of weight loss, chest pain, typically smoking history, associated with new or worsening cough. Opacity on CXR and/or CT.

  • Confirmed by: tumour cells on sputum cytology or on endobronchial/CT guided biopsy.

  • Finalized by the predictable outcome of management, e.g. O2 if dyspnoea or hypoxic. Analgesia, including diamorphine if distressed. Nebulized adrenaline and tranexamic acid PO before an urgent bronchoscopy.

Pulmonary TB

  • Suggested by: weeks or months of fever, malaise, weight loss, and a contact history/high-risk groups.

  • Confirmed by: CXR: opacification, especially in apical segments but can be anywhere. Acid-fast bacilli (AFB) on smear sputum, culture and/or response to treatment (when cultures negative and no other explanation for symptoms).

  • Finalized by the predictable outcome of management, e.g. isolating patient until smear test known and preferably at least 2 weeks treatment. Initially 4 drug regime of rifampicin, isoniazid, pyrazinamide, ethambutol, and if malnourished, adding pyridoxine. Specialist management and contact tracing.

Upper respiratory tract infection (URTI), abnormalities, and bleeding, e.g. nasal polyps, laryngeal carcinoma, pharyngeal tumours

  • Suggested by: days of purulent rhinorrhoea (blood from URTI swallowed or inhaled and coughed back up).

  • Confirmed by: nasendoscopy, CT/MRI, head and neck and surgery/biopsy.

  • Finalized by the predictable outcome of management, e.g. packing, cautery of (Little’s) bleeding area, removal of lesion.

Lung abscess

  • Suggested by: days or weeks of copious and foul-smelling sputum, fevers, chest pain. Typically preceded by a prior significant respiratory infection (e.g. pneumonia).

  • Confirmed by: CXR: circular opacity with fluid level, sputum culture/culture of CT guided aspirate.

  • Finalized by the predictable outcome of management, e.g. analgesia, high dose broad-spectrum antibiotics IV for Gram +ve and Gram –ve bacteria, e.g. co-amoxiclav + flucloxacillin + metronidazole for 14d ± CT guided drainage (send for TB and fungal cultures) or surgical removal.

Bronchiectasis

  • Suggested by: progression over months or years. Cupful(s) of pus-like sputum per day. Clubbing, typically bilateral consolidation, and bilateral coarse late inspiratory crackles. Typically obstructive deficit on spirometry.

  • Confirmed by: CXR: cystic shadowing; high resolution CT chest: honeycombing and thickened dilated bronchi.

  • Finalized by the predictable outcome of management, e.g. chest physiotherapy (including postural drainage and cough clearance), sputum cultures. Mucolytics, bronchodilators, regular exercise, winter vaccinations. When unwell, treatment with 10–14d antibiotics IV according to last sputum cultures. NB. Anti-pseudomonas treatment (aminoglycoside cover). Monitoring for weight loss and managing secondary causes.

Wegener’s granulomatosis

  • Suggested by: months of cough, breathless ± microscopic haematuria (i.e. triad of upper/lower respiratory tract and renal abnormalities). Arthritis, myalgia, skin rashes, and nasal bridge collapse. Renal impairment.

  • Confirmed by: CXR showing cavitating shadows. ↑cANCA antibody titre, and microscopic arteritis on biopsy.

  • Finalized by the predictable outcome of management, e.g. immunosuppression with steroids, azathioprine, and cyclophosphamide jointly by renal, respiratory physicians, etc.

Pneumonia

  • Suggested by: onset over hours or days. Rusty brown sputum (i.e. purulent sputum tinged with blood). Sharp chest pains worse on inspiration, fever, cough, signs of consolidation, etc.

  • Confirmed by: patchy shadowing on CXR and sputum/blood culture.

  • Finalized by the predictable outcome of management, e.g. 5d course of oral amoxicillin/clarithromycin PO unless more features of CRB-65 (Confusion, Respiratory rate >30/min, Blood pressure <90/60 mmHg and age >65y). If so, amoxicillin/co-amoxiclav IV or cefuroxime with controlled O2 and fluids. If reduced consciousness/aspiration, then cefuroxime/metronidazole IV. If hospital/nursing home acquired, cefuroxime or piperacillin with tazobactam IV.

Pulmonary arterio-venous malformation

  • Suggested by: haemoptysis alone. No other symptoms. CXR normal or showing coin-shaped lesion with feeding blood vessel.

  • Confirmed by: vascular red-blue lesion on bronchoscopy (if endobronchial) or enhancing lesion on a CT chest with (delayed) contrast, pulmonary arteriogram shows feeding vessels.

  • Finalized by the predictable outcome of management, e.g. embolization if bleeding is recurrent or a large quantity. Lobectomy if this fails.

Also

Opportunistic mycobacteria, Goodpasture’s syndrome, aspergilloma, mitral valve stenosis (if on warfarin), other endobronchial tumours (including benign lesions), hereditary haemorrhagic telangiectasia, endobronchial amyloid, any cause of systemic clotting abnormality.

Cough with sputum

Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

COPD caused by smoking, smoke pollution, α-antitrypsin deficiency

  • Suggested by: long history of cough ± sputum, many pack years of smoking, recurrent ‘exacerbations’. CXR: radiolucent lungs.

  • Confirmed by: spirometry: FEV <80% predicted and FEV/ FVC ratio <0.7. <5% reversibility. Emphysema on CT chest ± dα-antitrypsin levels.

  • Finalized by the predictable outcome of management, e.g. stopping smoking. Trials of bronchodilators prn, then regular long-acting bronchodilators. Inhaled steroids if FEV <50% predicted and three COPD exacerbations per year. If cough and breathlessness persists, prednisolone PO. If respiratory failure, home O2.

Acute viral bronchitis

  • Suggested by: onset over hours or days. Fever, myalgia, fatigue, and white/yellow sputum.

  • Confirmed by: no focal chest signs, no consolidation on CXR, resolution within 5d.

  • Finalized by the predictable outcome of management, e.g. rest and simple analgesia such as paracetamol.

Acute bacterial bronchitis

  • Suggested by: onset over hours or days. Fever, mucopurulent sputum, dyspnoea.

  • Confirmed by: no focal chest signs, FBC: ↑neutrophils, no consolidation on CXR, pathogens in sputum culture, and rapid response to appropriate antibiotics.

  • Finalized by the predictable outcome of management, e.g. simple analgesia, amoxicillin/clarithromycin PO for 5–7d.

Pneumonia

  • Suggested by: onset over hours or days. Rusty brown sputum. Sharp chest pain (worse on inspiration), fever, cough, signs of consolidation.

  • Confirmed by: patchy shadowing on CXR and sputum/blood culture.

  • Finalized by the predictable outcome of management, e.g. 5d course of amoxicillin/clarithromycin PO unless 2 or more features of CRB-65 (Confusion, Respiratory rate >30min, Blood pressure <90/60mmHg and age >65y). If so, amoxicillin/co-amoxiclav IV or cefuroxime with controlled O2 and fluids. If reduced consciousness/aspiration, then cefuroxime/metronidazole IV. If hospital/nursing home acquired, cefuroxime or piperacillin with tazobactam IV.

Lung abscess

  • Suggested by: days or weeks of copious and foul-smelling sputum, fever, chest pain. Typically preceded by a prior significant respiratory infection (e.g. pneumonia).

  • Confirmed by: CXR: circular opacity with fluid level, sputum culture/culture of CT guided aspirate.

  • Finalized by the predictable outcome of management, e.g. analgesia, high dose broad-spectrum antibiotics IV for Gram +ve and Gram –ve bacteria, e.g. co-amoxiclav + flucloxacillin + metronidazole for 14d ± CT guided drainage (send for TB and fungal cultures) or surgical removal.

Also

Broncho-alveolar cell carcinoma, pulmonary alveolar proteinosis, bronchiectasis associated with immunodeficiency states/primary ciliary dyskinesia, etc.

Persistent dry cough with no sputum

The duration of symptoms, severity, and progression will help determine the causes of a dry cough. No cause is found in up to 15% patients. As this symptom is non-life-threatening, initial management can be delayed until the exact cause is found. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Smoking

  • Suggested by: smoking history.

  • Confirmed by: stopping smoking, cough often worsens initially as ciliary motility is restored, but improves within 3mo.

  • Finalized by the predictable outcome of management, e.g. giving generic advice and adjunct pharmacotherapy. Referring to smoking cessation specialist, if available, and patient is keen to stop.

Chronic asthma

  • Suggested by: chronic cough, worse at night and early morning. Seasonal variation and other specific triggers (e.g. aerosol sprays, cold air, perfumes, smoke, infections exercise, etc.). Family history or childhood history of asthma or atopy.

  • Confirmed by: reduced or variable peak flow (classical dipping early morning/late evening) and FEV1 that improve by >15% with treatment.

  • Finalized by the predictable outcome of management, e.g. identifying precipitants, stopping smoking, trial of bronchodilator prn, regular inhaled steroids, long-acting β-agonist/steroid combinations, leukotriene inhibitors/antihistamines. Managed in chest clinic.

Gastro- oesophageal reflux

  • Suggested by: cough worse lying flat and after heavy meals. Heart burn/indigestion. Absent stomach bubble on CXR (of hiatus hernia).

  • Confirmed by: 24h oseophageal pH monitoring or improvement in cough on raising head of bed and with acid suppression (often need very high doses of more than one antacid, combined with promotility drugs).

  • Finalized by the predictable outcome of management, e.g. proton pump inhibitor (PPI) bd combined with H2 antagonist (e.g. ranitidine 150mg bd) and metoclopramide tds, domperidone 20mg tds, and even baclofen bd, in a stepwise fashion.

Post-nasal drip

  • Suggested by: feeling of catarrh and drip in back of throat, worse at night, nasal polyps.

  • Confirmed by: improvement with nasal decongestion.

  • Finalized by the predictable outcome of management, e.g. nasal steroids and or nasal ipratropium sprays. Antihistamines. ENT specialist if fails.

Viral infection with slow recovery

  • Suggested by: original onset over days, fever, sore throat, generalized aches.

  • Confirmed by: spontaneous (slow) improvement.

  • Finalized by the predictable outcome of management, e.g. observation.

ACE inhibitors

  • Suggested by: drug history. (NB Symptoms can start after taking ACE inhibitors for a long time.)

  • Confirmed by: cough improves when ACE inhibitor stopped, may take several months.

  • Finalized by the predictable outcome of management, e.g. substitute with angiotensin receptor blocker for ACE inhibitor.

COPD caused by smoking, smoke pollution, α1-antitrypsin deficiency

  • Suggested by: long history of cough ± sputum, many pack years of smoking, recurrent ‘exacerbations’. CXR: radiolucent lungs.

  • Confirmed by: spirometry: FEV1 <80% predicted and FEV/FVC ratio <0.7. <15% reversibility. Emphysema on CT chest ± ↓α 1-antitrypsin levels.

  • Finalized by the predictable outcome of management, e.g. stopping smoking. Trials of bronchodilators prn, then regular long-acting bronchodilators. Inhaled steroids if FEV <50% predicted and three COPD exacerbations per year. If cough and breathless persists, prednisolone PO. If respiratory failure, home O2.

Carcinoma of lung

  • Suggested by: weeks or months of weight loss, chest pain, typically smoking history, associated with new or worsening cough. Opacity on CXR and/or CT.

  • Confirmed by: tumour cells on sputum cytology or on endobronchial/CT guided biopsy.

  • Finalized by the predictable outcome of management, e.g. O2 if dyspnoea or hypoxic. Surgery, chemoradiotherapy, and supportive care.

Pulmonary TB

  • Suggested by: weeks or months of fever, malaise, weight loss, and a contact history/high-risk groups.

  • Confirmed by: CXR: opacification, especially in apical segments, but can be anywhere. AFB on smear sputum, culture, and/or response to treatment (when cultures negative and no other explanation for symptoms).

  • Finalized by the predictable outcome of management, e.g. isolating patient until smear test known and preferably at least 2 weeks treatment. Initially 4 drug regime of rifampicin, isoniazid, pyrazinamide, ethambutol, and if malnourished, adding pyridoxine. Specialist management and contract tracing.

Interstitial lung disease

  • Suggested by: chronic dry cough, occupational exposure, or evidence of underlying connective tissue disease. NB Majority of cases have no cause identified. Clubbing, cyanosis, reduced chest expansion, coarse late inspiratory bibasal crackles.

  • Confirmed by: reduced lung volumes and reticular nodular shadowing on CXR. Interstitial shadowing and/or subpleural fibrosis on high resolution CT chest.

  • Finalized by the predictable outcome of management, e.g. O2 if saturations <93%. Specialist opinion for detailed lung function, lung biopsy, immunosuppression, antifibrotics, palliation.

Also

Inhaled foreign body, benign endobronchial lesions (e.g. hamartomas), psychogenic.

Hoarseness

Hoarseness of some weeks’ or months’ duration may have some sinister causes that need urgent attention. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Inhaled steroids

  • Suggested by: drug history.

  • Confirmed by: improvement on stopping steroids.

  • Finalized by the predictable outcome of management, e.g. improve inhaler technique (especially using spacer) and rinsing mouth after inhalers.

Chronic laryngitis

  • Suggested by: onset over months or years. History of recurrent acute laryngitis.

  • Confirmed by: inflamed cords at laryngoscopy and no other pathology.

  • Finalized by the predictable outcome of management, e.g. stopping smoking and reduce alcohol.

Singer’s nodes

  • Suggested by: onset over months. Long history, often occupational, in teachers or singers due to voice strain, singing, alcohol, fumes, etc.

  • Confirmed by: nodules on cord at laryngoscopy. Initial management: speech therapy, surgical removal.

Laryngeal carcinoma (glottic, supra-glottic, or subglottic tumour)

  • Suggested by: progressive hoarseness over weeks to months. Smoker, including cannabis. Dysphagia, haemoptysis, ear pain.

  • Confirmed by: laryngoscopy, biopsy, staging.

  • Finalized by the predictable outcome of management, e.g. surgical removal.

Vocal cord paresis due to vagal nerve trauma, cancer (thyroid, oesophagus, pharynx, bronchus) or tuberculosis, multiple sclerosis, polio, syringomyelia, (no cause identified in 15%)

  • Suggested by: onset after surgery or otherwise over weeks and months. Bovine cough. Symptoms of cause. Abnormal CXR, barium swallow, MRI.

  • Confirmed by: paresis or abnormal movement of cords on laryngoscopy.

  • Finalized by the predictable outcome of management, e.g. urgent ENT referral. May be considered for vocal cord prosthesis/implant after treatment of cause.

Functional hoarseness

  • Suggested by: recurrence at times of stress. Variable symptoms, able to cough normally.

  • Confirmed by: no abnormality laryngoscopy.

  • Finalized by the predictable outcome of management, e.g. counselling and behavioural therapy.

Myxoedema

  • Suggested by: onset over months or years. Fatigue, puffy face, obesity, cold intolerance, bradycardia, slow relaxing reflexes.

  • Confirmed by: swollen vocal cords at laryngoscopy.TSH,FT4.

  • Finalized by the predictable outcome of management, e.g. thyroxine replacement.

Acromegaly

  • Suggested by: swollen vocal cords at laryngoscopy. Large, wide face, embossed forehead, jutting jaw (prognathism), widely spaced teeth, and large tongue.

  • Confirmed by:IGF, failure to suppress growth hormone to <2mU/L with oral GTT. Skull X-ray confirming bony abnormalities. Hand X-ray showing typical tufts on terminal phalanges. MRI or CT scan showing enlarged pituitary fossa.

  • Finalized by the predictable outcome of management, e.g. hormone replacement and pituitary surgery/radiotherapy.

Sicca syndrome due to old age, Sjögren’s syndrome, rheumatoid, sarcoid, etc.

  • Suggested by: onset over months to years. Dry mouth and eyes.

  • Confirmed by: clinical presentation and inflamed cords at laryngoscopy and no other pathology.

  • Finalized by the predictable outcome of management, e.g. lubricant lozenges ± artificial tears, address related conditions.

Granulomas due to syphilis, TB, sarcoid, Wegener’s

  • Suggested by: onset over months with symptoms and signs in other systems. Abnormal CXR or other system involvement.

  • Confirmed by: granulomata on cords at laryngoscopy. Biopsy. Culture and sensitivity.

  • Finalized by the predictable outcome of management, e.g. if TB cultured, 6mo of triple/quadruple therapy. If Wegener’s granulomatosis/sarcoid, immunosuppression with systemic steroids + azathioprine + cyclophosphamide. Surgical intervention for possible vocal cord prosthesis.

Some thoughts when examining the respiratory system

The findings are described here in the sequence of inspection, palpation, percussion, and then auscultation. While inspecting, think of blood gas status, and when palpating, think of the mechanisms of ventilation. When percussing, think of the pleural surfaces, contents of the pleural cavity, and lung tissue. When auscultating, think of the state of the lung and overlying tissue as well as the airways.

Appearance suggestive of blood gas disturbance

Look at hands for cyanosis, feel for warmth, ask patient to hold arms out and extended at the wrists to see if there is a coarse tremor and/or muscle twitching in the arms. Look at the fingers for peripheral cyanosis and more importantly here, the tongue and lips for central cyanosis. Initial investigations (other tests in bold below): FBC, U&E, CXR, ABG.

Main differential diagnoses and typical outline evidence, etc.

Hypoxic

  • Suggested by: blue fingernails (peripheral) and tongue (central cyanosis), restless, confused, drowsy, or unconscious.

  • Confirmed by: PaO2 <8kPa on blood gas analysis (or pulse oximetry of <92% (mild) or <85% (severe).

  • Finalized by the predictable outcome of management, e.g. controlled O2 via Venturi and continuous clinical/physiological monitoring whilst addressing underlying cause.

CO2 retention

  • Suggested by: warm hands, bounding pulse, dilated veins on hands and face, twitching of facial muscles, headaches, confusion, and drowsy.

  • Confirmed by: PaCO2 >6.5kPa on blood gas analysis. Typically >8.0 kPa to be symptomatic.

  • Finalized by the predictable outcome of management, e.g. control O2 delivery <28% (with Venturi mask to keeping O2 saturation 88–92%). Address underlying cause of respiratory depression if respiratory rate <10 breaths per min.

Hypocapnia

  • Suggested by: dizzy, anxious, paraesthesiae around lips or fingers, tachypnoea.

  • Confirmed by: PaCO2 <4.0kPa on blood gas analysis.

  • Finalized by the predictable outcome of management, e.g. address underlying illness; giving supplemental O2. If CO2 low, then slow breathing by getting patient to relax; can try rebreathing with a paper bag.

Respiratory rate low (<10/min)

Count the number of respirations for a whole minute if rate appears low. Initial management is to check patient is conscious and securing of airway as per Basic Life Support. Removal of any obvious cause (e.g. high flow O2 if saturations are >88%, needlesticks, etc). These patients typically have reduced consciousness and, therefore, are at risk of losing their airway patency (e.g. aspiration), so they must be treated in a high-dependency area. Initial investigations (other tests in bold below): FBC, U&E, CXR, ABGs.

Main differential diagnoses and typical outline evidence, etc.

CO2 narcosis (very high blood CO2) due to excess O2 administration

  • Suggested by: warm hands, bounding pulse, dilated veins on hands and face, twitching of facial muscles, drowsy. High flow O2 being given.

  • Confirmed by: PaCO2 >6.5kPa on blood gas analysis.

  • Finalized by the predictable outcome of management, e.g. reduce inhaled O2 to keeping saturation 88–92%. Address underlying cause of respiratory depression if respiratory rate is <10 breaths per min.

Drugs, e.g. opiates, alcohol, benzodiazepines, muscle relaxants

  • Suggested by: pinpoint pupils (needle track marks). History of ingestion, empty medication bottle.

  • Confirmed by: response to drug withdrawal or antidotes, e.g. naloxone IV/IM, flumazenil IV. Drug levels on toxicology screen.

  • Finalized by the predictable outcome of management, e.g. if saturations >90% and no other airway or cardiovascular compromise, observation only until the sedative wears off. Securing of airway and trial of antidote; needs high dependency setting with anaesthetist support.

Raised intracranial pressure

  • Suggested by: papilloedema, focal neurology, severe headaches, and vomiting.

  • Confirmed by: CT brain (loss of normal sulci, cerebral oedema).

  • Finalized by the predictable outcome of management, e.g. securing of airway, breathing, and circulation. Monitor neuro-observations. Nurse with head up at 45°. Dexamethasone IV, mannitol IV, and phenytoin IV if fits. Neurology referral.

Head injury (without raised intracranial pressure) or cervical cord trauma

  • Suggested by: history and signs of assault/trauma. Other abnormal neurology (upper or lower motor neurone signs).

  • Confirmed by: CT brain (loss of normal sulci, cerebral oedema).

  • Finalized by the predictable outcome of management, e.g. ATLS (Advanced Trauma Life Support) algorithm. NB Care stabilizing cervical spine.

Acute (-on-chronic) neuromuscular disease, e.g. Guillain-Barré syndrome

  • Suggested by: known neurological disease, recent viral illness, autonomic dysfunction, ascending weakness, etc. ± other lower motor neurone signs.

  • Confirmed by: muscle weakness and ↓PaO2, ↑PaCO2 on blood gas analysis.

  • Finalized by the predictable outcome of management, e.g. ventilatory support (if appropriate), supplemental O2. Specific measures depending on cause.

Severe hypothermia

  • Suggested by: exposure, immobility, reduced GCS, bradycardia.

  • Confirmed by: core temp <33°C.

  • Finalized by the predictable outcome of management, e.g. gentle rewarming (space blankets, fluids IV, bladder irrigation, etc.)

Chest wall abnormalities

Inspect the chest shape and then its change on movement for asymmetry. Initial investigations (other tests in bold below): FBC, U&E, CXR, ABGs.

Main differential diagnoses and typical outline evidence, etc.

Pectus carinatum (developmental or associated with emphysema)

  • Suggested by: prominent sternum, often associated with indrawing of the ribs (Harrison’s sulci) above the costal margins.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. manage emphysema.

Pectus excavatum (developmental defect)

  • Suggested by: depression of the lower end or whole sternum.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. explanation.

Kyphosis (congenital or due to anterior collapse of spinal vertebrae, e.g. severe osteoporosis, spinal TB)

  • Suggested by: spine curved forward.

  • Confirmed by: CXR, spinal X-ray.

  • Finalized by the predictable outcome of management, e.g. assess partly using blood gases, need for (nocturnal) Non-Invasive Ventilatory support (NIV) if symptoms of ventilatory failure and/or PaO2 <8kPa with PaCO2 >6.5kPa.

Scoliosis (congenital, neuromuscular disease, surgery, spinal TB)

  • Suggested by: spine curved laterally.

  • Confirmed by: CXR, spinal X-ray.

  • Finalized by the predictable outcome of management, e.g. assess partly using blood gases, need for (nocturnal) Non-Invasive Ventilatory support (NIV) if symptoms of ventilatory failure and/or ↓PaO2 <8kPa with ↑PaCO2 >6.5kPa.

Absence of part of chest wall bone structure (congenital—Poland’s syndrome—or post-surgery, e.g. thoracoplasty for TB, cancer)

  • Suggested by: absence of ribs, pectoralis muscle, clavicle, etc.

  • Confirmed by: history, scars, CXR, spinal X-ray.

  • Finalized by the predictable outcome of management, e.g. assess partly using blood gases, need for (nocturnal) NIV support if symptoms of ventilatory failure and/or PaO2 <8kPa with PaCO2 >6.5kPa.

Bilateral poor chest expansion

Consider all the causes of a low respiratory rate (see Respiratory symptoms and physical signs Respiratory rate low (<10/min), p.[link]) and also the following that typically do not cause a low respiratory rate. Initial investigations (other tests in bold below): FBC, U&E, CXR, ABG.

Main differential diagnoses and typical outline evidence, etc.

Obesity possibly causing obesity hypoventilation syndrome

  • Suggested by: insidious onset of breathlessness in obese individual.

  • Confirmed by: examination (BMI often needs to be >40kg/m2 to cause chest wall compromise).

  • Finalized by the predictable outcome of management, e.g. weight loss, including dietitian referral and weight-lowering medications. Assess partly using blood gases, need for (nocturnal) NIV support if symptoms of ventilatory failure and PaO2 <8kPa with PaCO2 >6.5kPa (obesity hypoventilation syndrome).

Emphysema (overlaps with COPD) caused by smoking, smoke pollution, α1-antitrypsin deficiency

  • Suggested by: long history of cough ± sputum, many pack years of smoking, recurrent ‘exacerbations’, pursed lip, breathing (a chronic behavioural adaptation), hyperinflation, reduced chest expansion, reduced breath sounds and hyper-resonance. CXR: radiolucent lungs.

  • Confirmed by: spirometry: FEV1 <80% predicted and FEV/FVC ratio <0.7. <15% reversibility. Emphysema on CT chest ±↓α1-antitrypsin levels.

  • Finalized by the predictable outcome of management, e.g. stopping smoking. Trials of bronchodilators prn, regular long-acting bronchodilators. Regular inhaled steroids if FEV <50% predicted and three COPD exacerbations per year. If cough and breathless persists, prednisolone PO. If respiratory failure, home O2.

Pulmonary fibrosis/interstitial lung disease NB Majority of cases have no cause identified

  • Suggested by: chronic dry cough, occupational exposure, or evidence of underlying connective tissue disease. Clubbing, cyanosis, reduced chest expansion, coarse late inspiratory bibasal crackles.

  • Confirmed by: ↓lung volumes and reticular nodular shadowing on CXR. Interstitial shadowing and/or subpleural fibrosis on high resolution CT chest.

  • Finalized by the predictable outcome of management, e.g. home O2 if saturations <93%. Specialist opinion about detailed lung function, lung biopsy, immunosuppression, antifibrotics, palliation.

Muscular dystrophy (other rarer myopathies, e.g. limb-girdle dystrophy, acid maltase deficiency, etc.)

  • Suggested by: early age onset, family history, calf hypertrophy, lower motor neurone signs.

  • Confirmed by: restrictive deficit on spirometry (especially when lying flat). Sparing of transferring factor, globally low volumes, especially reduced residual volumes and mouth (inspiratory) pressures on detailed lung function; muscle biopsy.

  • Finalized by the predictable outcome of management, e.g. assess need for (nocturnal) NIV support if symptoms of ventilatory failure and/or blood gases show PaO2 <8kPa with PaCO2 >6.5kPa. Neurology clinic for long-term care.

Motor neurone disease

  • Suggested by: late-onset mixed upper and lower motor neurone signs, tongue fasciculation, bulbar palsy.

  • Confirmed by: clinical and electromyography (EMG). Restrictive deficit (globally low volumes) on spirometry (especially when lying flat). Sparing of transferring factor, reduced residual volumes and mouth (inspiratory) pressures on detailed lung function.

  • Finalized by the predictable outcome of management, e.g. medications to reduce upper airway secretions. Assess need for (nocturnal) NIV support if symptoms of ventilatory failure and/or blood gases show PaO2 <8kPa with PaCO2 >6.5kPa. Urgent referral to neurologist.

Multiple sclerosis

  • Suggested by: restrictive deficit (globally low volumes) on spirometry (especially when lying flat).

  • Confirmed by: MRI brain, visual evoked responses. Sparing of transferring factor, reduced residual volumes and mouth (inspiratory) pressures on detailed lung function.

  • Finalized by the predictable outcome of management, e.g. assess need for (nocturnal) NIV support if symptoms of ventilatory failure and/or blood gases show PaO2 <8kPa with PaCO2 >6.5kPa. Neurology clinic for long-term care.

Guillain–Barré syndrome

  • Suggested by: ascending weakness, autonomic disturbances, and recent infection. Restrictive deficit on lung function (especially when lying flat).

  • Confirmed by: rapid deterioration on lung function (FVC). Sparing of corrected transferring factor. Progress of illness worsening over days to weeks, then improvement.

  • Finalized by the predictable outcome of management, e.g. ventilatory support if PaO2 falling and/or PaCO2 rising, steroids, and plasmapheresis/immunoglobulin infusions.

Also

Myasthenia gravis, Eaton–Lambert syndrome, muscle relaxant drugs, e.g. suxamethonium, neurotoxins (including organophosphates), severe electrolyte abnormalities (↓↑K+, ↓Ca2+).

Unilateral poor chest expansion

If the patient has become ill rapidly, then this sign has a short differential diagnosis: tension pneumothorax (which needs to be treated without doing ‘initial tests’), flail segment, or severe pneumonia, and needs rapid diagnosis and urgent treatment. Less urgent causes are more common; the more dangerous are giving in precedent here. Initial investigations (other tests in bold below): FBC, U&E, CXR, ABG.

Main differential diagnoses and typical outline evidence, etc.

Pneumothorax (‘tension’, moderate, or mild)

  • Suggested by: pain in centre or side of chest with abrupt breathlessness, diminished breath sounds, and hyper-resonance to percussion.

  • Confirmed by: tracheal deviation and distress suggesting tension pneumothorax, or expiration CXR showing loss of lung markings outside sharp line (‘moderate’ if >5cm gap from lung edge to chest wall, ‘mild’ if <5cm.)

  • Initial management: if tension pneumothorax, insertion of large Venflon into 2nd intercostal (IC) space, mid-clavicular line. Giving O2 if breathless. Analgesia. Aspiration if moderate; if this is unsatisfactory or prior lung disease, insertion of IC drain into ‘triangle of safety’. If ‘mild’ (<5cm gap) and not breathless, observation.

Flail segment following trauma

  • Suggested by: paradoxical movement of part of chest wall.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. apply direct pressure and ‘splint’ the segment. Apply ATLS algorithm.

Extensive consolidation due to bacterial infection, but possibly autoimmune disease, malignancy, or drugs

  • Suggested by: reduced breath sounds, bronchial breathing, increased tactile vocal fremitus, reduced percussion note.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. if not very ill, but fever and ↑neutrophil count, analgesia, and an empiric 5d course of amoxicillin/clarithromycin PO. If ≥2 features of CRB-65, then amoxicillin/co-amoxiclav IV or cefuroxime with controlled O2 and fluids. If history of reduced consciousness/aspiration, then cefuroxime/metronidazole IV. If hospital/nursing home acquired infection, cefuroxime or piperacillin with tazobactam IV. If no fever or WCC normal, investigate non-infective possibilities.

Fractured ribs possibly complicated by pneumothorax, haemothorax

  • Suggested by: history of trauma, focal tenderness.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. analgesia and rest. Admit to hospital for observation if breathless or worsening pain.

Pleural effusion

  • Suggested by: reduced breath sounds, reduced tactile vocal fremitus, stony dull percussion note.

  • Confirmed by: homogeneous opacification with meniscus level on CXR and fluid on US scan/CT chest.

  • Finalized by the predictable outcome of management, e.g. if breathless at rest, aspiration of 500mL (therapeutic) and send fluid for tests, not draining to dryness if cause unknown as thoracoscopy/pleural biopsy required. If known malignancy, also insertion of IC drain directly and pleurodesis.

Musculoskeletal e.g. previous thoracoplasty

  • Suggested by: history, scar.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. assess need for (nocturnal) NIV support if symptoms of ventilatory failure and/or blood gases show PaO2 <8kPa with PaCO2 >6.5kPa. Neurology clinic for long-term care.

Trachea displaced

First assess the patient—if clinically compromised, suspect tension pneumothorax. Although this is a rare cause of displaced trachea, it must be managed immediately both in primary and secondary care. Palpate with middle finger and with the index and ring finger on either side of trachea. Localize apex beat to see if lower mediastinum is also displaced. Initial investigations (after treating ing any tension pneumothorax based on clinical diagnosis—other tests in bold below): FBC, U&E, CXR, ABG.

Main differential diagnoses and typical outline evidence, etc.

Pushed by contralateral tension pneumothorax

  • Suggested by: in extremis with high pulse rate and hypotension, reduced/absent breath sounds, reduced tactile vocal fremitus, hyper-resonant percussion note.

  • Confirmed by: escape of air after insertion of a Venflon into 2nd IC space, opposite side of tracheal deviation.

  • Finalized by the predictable outcome of management, e.g. insertion of a Venflon as above; expertly secured emergency IC drain insertion of ion. O2 and analgesia.

Pulled by ipsilateral pneumothorax (‘tension’, moderate, or mild)

  • Suggested by: pain in centre or side of chest with abrupt breathlessness, diminished breath sounds, and hyper-resonance to percussion.

  • Confirmed by: tracheal deviation and distress suggesting tension pneumothorax, or expiration CXR showing loss of lung markings outside sharp line (‘moderate’ if >5cm gap from lung edge to chest wall, ‘mild’ if <5cm).

  • Initial management: O2 if breathless. Analgesia. Aspiration if moderate; if this is unsatisfactory or prior lung disease, insertion of IC drain into ‘triangle of safety’. If ‘mild’ (<5cm gap) and not breathless, observation.

Pulled by ipsilateral upper lobe fibrosis, collapse, or removal

  • Suggested by: TB (chronic), radiation fibrosis (skin changes, tattoo marks), surgery (scar), ankylosing spondylitis, chronic sarcoidosis. If smoker and focal lobar collapse, endobronchial tumour. Reduced upper chest wall expansion.

  • Confirmed by: CXR showing diminished abnormal chest anatomy ‘pulling’ on mediastinum with trachea deviated towards the same side.

  • Finalized by the predictable outcome of management, e.g. review old CXR; for CT chest and bronchoscopy if new upper lobe collapse. Assess need for (nocturnal) NIV support if symptoms of ventilatory failure and/or blood gases show PaO2 <8kPa with PaCO2 >6.5kPa.

Pushed by contralateral pleural effusion

  • Suggested by: reduced breath sounds, reduced tactile vocal fremitus, stony dull percussion note.

  • Confirmed by: CXR showing large homogeneous white opacification ‘pushing’ on mediastinum.

  • Finalized by the predictable outcome of management, e.g. if breathless at rest, aspiration of 500mL (therapeutic) and send fluid for tests. Do not drain to dryness if cause unknown, thoracoscopy/pleural biopsy is required. If known cause (e.g. malignancy), aspiration of 500mL or insertion of IC drain directly and pleurodesis.

Scoliosis

  • Suggested by: chest wall deformity and curved spine.

  • Confirmed by: spinal X-ray, CXR.

  • Finalized by the predictable outcome of management, e.g. analgesia, physiotherapy, calcium supplements. Assess need for (nocturnal) NIV support if symptoms of ventilatory failure and/or blood gases show PaO2 <8kPa with PaCO2 >6.5kPa.

Reduced tactile vocal fremitus

If in extremis, treat as tension pneumothorax. If not, Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Pleural effusion

  • Suggested by: reduced breath sounds, reduced tactile vocal fremitus, stony dullness to percussion.

  • Confirmed by: homogeneous opacification with meniscus level on CXR and fluid on US scan/CT chest.

  • Initial management: if breathless at rest, aspiration of 500mL (therapeutic) and send fluid for tests. Do not drain to dryness if cause unknown, thoracoscopy/pleural biopsy is required. If known cause (e.g. malignancy), aspiration of 500mL or insertion of IC drain directly and pleurodesis.

Pneumothorax (‘tension’, moderate or mild)

  • Suggested by: pain in centre or side of chest with abrupt breathlessness, diminished breath sounds, and hyper-resonance to percussion.

  • Confirmed by: above findings, tracheal deviation, and distress suggesting tension pneumothorax, or expiration CXR showing loss of lung markings outside sharp line (‘moderate’ if >5cm gap from lung edge to chest wall, ‘mild’ if <5cm.)

  • Initial management: if tension pneumothorax, insertion of large Venflon into 2nd IC space, mid-clavicular line. Giving O2 if breathless. Analgesia. Aspiration if moderate; if this unsatisfactory or prior lung disease, insert IC drain into ‘triangle of safety’. If ‘mild’ (<5cm gap) + not breathless, observation.

Collapsed lobe with no consolidation

  • Suggested by: reduced breath sounds, reduced expansion, normal percussion note.

  • Confirmed by: CXR (collapse of different lobes will have different patterns radiologically, e.g. showing fan-shaped shadow arising from mediastinum, mediastinal shift, raised hemidiaphragm, displaced horizontal fissure or ‘sail sign’). CT thorax confirms lobar collapse.

  • Finalized by the predictable outcome of management, e.g. bronchoscopy to removal of any foreign body or debris, or to biopsy obstructive growth.

Increased tactile vocal fremitus

Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Extensive consolidation due to bacterial infection, but possibly autoimmune disease, malignancy, or drugs

  • Suggested by: reduced breath sounds, bronchial breathing, increased tactile vocal fremitus, reduced percussion note.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. if not very ill, but fever and ↑neutrophil count on FBC, analgesia and an empiric 5d course of amoxicillin/clarithromycin PO. If ≥2 features of CRB-65, then amoxicillin/co-amoxiclav IV or cefuroxime with controlled O2 and fluids. If history of reduced consciousness/aspiration, then cefuroxime/metronidazole IV. If hospital/nursing home acquired infection, cefuroxime or piperacillin with tazobactam IV. If no fever or WCC normal, investigate non-infective possibilities.

Stony dull percussion

This implies pleural effusion. The causes of pleural effusion are traditionally divided into transudates and exudates. Initial investigations (other tests in bold below): FBC, U&E, CXR, diagnostic pleural aspiration.

Main differential diagnoses and typical outline evidence, etc.

Transudates

  • Suggested by: bilateral effusions, underlying clinical cause.

  • Confirmed by: protein in pleural effusion <30g/L or <0.5 ratio to serum protein (except can be higher in treated heart failure).

Left heart failure (LVF), superior vena cava (SVC) obstruction, pericarditis, peritoneal dialysis

  • Suggested by: peripheral oedema, ↑JVP, basal crackles, 3rd heart sound, if LVF. Headache, swollen/plethoric face, and dilated superficial venules across anterior chest if SVC obstruction.

  • Confirmed by: CXR, echocardiogram, CT thorax (if considering SVC obstruction).

  • Initial treatment: diuretics and ACE inhibitors if LVF. Steroids and anticoagulation if SVC obstruction. NSAIDs and treating cause if pericardial effusion.

Low albumin states, e.g. liver cirrhosis, nephrotic syndrome

  • Suggested by: malnutrition, generalized oedema. Evidence of other disease.

  • Confirmed by:serum albumin.

  • Initial treatment: try to correct serum albumin with appropriate diet.

Rare causes

Hypothyroidism, Meig’s syndrome.

Exudates

  • Suggested by: typically unilateral effusion (but may be bilateral). Signs and symptoms of underlying disease.

  • Confirmed by: protein in effusion >30g/dL or >0.5 ratio to serum protein.

Infective: bacterial/empyema, TB, viral, etc.

  • Suggested by: history, fever, ↓pH, ↓glucose in pleural fluid.

  • Confirmed by: pleural aspiration of pus with organisms on Gram stain or culture in bacterial pneumonia. ↑lymphocytes suggest TB (confirmed by +ve cultures or Ziehl–Neelsen (ZN) stain on fluid or pleural biopsy or of caseating granuloma).

  • Finalized by the predictable outcome of management, e.g. appropriate antibiotic treatment and IC drain to remove fluid or pus, or surgery.

Neoplastic: lung 1° or 2°, breast, ovarian, reticuloses, Kaposi’s, local chest wall tumours, mesothelioma

  • Suggested by: history, especially weight loss. Signs of local or distal spread.

  • Confirmed by: pleural aspiration (cytology), pleural biopsy or other tissue histology.

  • Finalized by the predictable outcome of management, e.g. once cancer confirmed, typically needs IC drain, and drain to dryness followed by pleurodesis. Oncology opinion for active treatment or palliative care.

Rheumatoid, systemic lupus erythematosus, etc.

  • Suggested by: history, other organ specific involvement, e.g. joints, +ve rheumatoid factor in fluid, very low fluid glucose.

  • Confirmed by: +ve autoantibodies and clinical criteria, response to immunosuppression.

  • Finalized by the predictable outcome of management, e.g. steroids/azathioprine/cyclophosphamide.

Pulmonary infarction/ embolus

  • Suggested by: sudden/acute worsening of breathlessness, pleural rub, cyanosis, tachycardia, loud P2, associated DVT, or risk factors such as recent surgery, immobility, previous emboli, malignancy, etc. Other tests typically show raised D-dimers, tachycardia or right heart strain, and rarely S1Q3T3 on ECG.

  • Confirmed by: CT pulmonary angiogram showing clot in pulmonary artery. Echocardiogram (right heart strain) is useful for risk stratification if pulmonary embolus confirmed.

  • Finalized by the predictable outcome of management, e.g. LMW heparin (treatment dose not prophylactic dose) and 3mo anticoagulation with warfarin (longer if ongoing risk factors). Thrombolysis if ↓BP, large and bilateral clots, no response to anticoagulation or acutely dilated right ventricle on echocardiogram.

Dull to percussion but not stony dull

Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Consolidation due to bacterial infection, but possibly autoimmune disease, malignancy, or drugs.

  • Suggested by: reduced breath sounds, bronchial breathing, increased tactile vocal fremitus, reduced percussion note.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. if not very ill, but fever and ↑neutrophil count on FBC, analgesia and an empiric 5d course of amoxicillin/clarithromycin PO. If ≥2 features of CRB-65, then amoxicillin/co-amoxiclav IV or cefuroxime with controlled O2 and fluids. If history of reduced consciousness/aspiration, then cefuroxime/metronidazole IV. If hospital/nursing home acquired infection, cefuroxime or piperacillin with tazobactam IV. If no fever or WCC normal, investigate non-infective possibilities.

Pulmonary oedema due to acute left ventricular failure or chronic (congestive) cardiac failure due to ischaemic heart disease, mitral stenosis

  • Suggested by: background fatigue and exertional breathless, cardiac risk factors. Displaced apex beat, 3rd heart sound, bilateral basal fine crackles. ↑JVP and leg swelling.

  • Confirmed by: CXR: fluffy opacification, especially near hila. Loss of costophrenic angle. Impaired left ventricular function on echocardiogram.

  • Finalized by the predictable outcome of management, e.g. sitting patient up, controlled O2, diuretics IV. Nitrates IV if very breathless and systolic BP> 90.

  • In the long term: thiazide or loop diuretic, ACE inhibitor (or angiotensin receptor blocker). β-blocker and spironolactone (monitor K+).

Elevated hemidiaphragm

  • Suggested by: typically asymptomatic, reduced/absent breath sounds, no other abnormalities unless from underlying cause, e.g. pulmonary embolus, tumour, phrenic nerve scar, etc. (often no cause found).

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. anticoagulate if pulmonary embolus, seek old CXR to see if longstanding.

Severe fibrosis/collapse

  • Suggested by: clubbing and signs of underlying cause, reduced chest expansion, tracheal deviation. Reduced breath sounds, course crackles.

  • Confirmed by: CXR, high resolution CT thorax.

  • Finalized by the predictable outcome of management, e.g. bronchoscopy if new lobar collapse to remove foreign body.

Severe pleural thickening, e.g. due to pleural secondaries or mesothelioma

  • Suggested by: chest pain, weight loss, history of asbestos exposure, clubbing, reduced breath sounds.

  • Confirmed by: CT thorax and pleural biopsy.

  • Finalized by the predictable outcome of management, e.g. analgesia (e.g. opiates) and controlled O2. Oncologist/chest physician for specialist treatment.

Hyper-resonant percussion

If in extremis, the rare, but immediately life-threatening, cause of tension pneumothorax. Initial investigations (other tests in bold below): FBC, U&E, CXR, ABG.

Main differential diagnoses and typical outline evidence, etc.

Emphysema (overlaps with COPD) caused by smoking, smoke pollution, α-1 antitrypsin deficiency

  • Suggested by: long history of cough ± sputum, many pack years of smoking, recurrent ‘exacerbations’, pursed lip, breathing (a chronic behavioural adaptation), hyperinflation, reduced chest expansion, reduced breath sounds, and hyper-resonance. CXR: radiolucent lungs.

  • Confirmed by: spirometry: FEV1 <80% predicted and FEV/FVC ratio <0.7. <15% reversibility. Emphysema on CT chest ± ↓α1-antitrypsin levels.

  • Finalized by the predictable outcome of management, e.g. stopping smoking. Trials of bronchodilators prn, regular long-acting bronchodilators. Regular inhaled steroids if FEV <50% predicted and three COPD exacerbations per year. If cough and breathlessness persists, prednisolone PO. If respiratory failure, home O2.

Large bullae

  • Suggested by: other signs of emphysema but can be isolated finding, and often congenital in otherwise normal lungs.

  • Confirmed by: CT thorax.

  • Finalized by the predictable outcome of management, e.g. observation. Can mimic partial pneumothorax (NO insertion of intercostal drain!). Cardiothoracic surgical referral for bullectomy or endobrachial valve if symptomatic and no widespread emphysema.

Pneumothorax (‘tension’, moderate, or mild)

  • Suggested by: pain in centre or side of chest with abrupt breathlessness, diminished breath sounds, and hyper-resonance to percussion.

  • Confirmed by: above findings, tracheal deviation, and distress suggesting tension pneumothorax, or expiration CXR showing loss of lung markings outside sharp line (‘moderate’ if >5cm gap from lung edge to chest wall, ‘mild’ if <5cm).

  • Initial management: if tension pneumothorax, insert large Venflon into 2nd IC space, mid-clavicular line. Give O2 if breathless. Analgesia. Aspiration if moderate; if this is unsatisfactory or prior lung disease, insert IC drain into ‘triangle of safety’. If ‘mild’ (<5cm gap) and not breathless, observation.

Reduced breath sounds

When auscultating the lungs, think of the underlying lung parenchyma and overlying tissues. Ensure patient breathes with mouth open, regularly and deeply, and does not vocalize (e.g. groaning). Reduced breath sounds may be because:

  • air is not entering/leaving the lung(s);

  • excess air, fat, or fluid between lung and your stethoscope;

  • good air entry but abnormal lung parenchyma.

Initial investigations (other tests in bold below): FBC, U&E, CXR, ABG.

Air is not entering/leaving the lung(s): Main differential diagnoses and typical outline evidence, etc.

Poor respiratory effort

  • Suggested by: reduced consciousness/cooperation, any cause of poor chest wall expansion (see Respiratory symptoms and physical signs Bilateral poor chest expansion, p.[link]).

  • Confirmed by: ABG (type 2 failure).

  • Finalized by the predictable outcome of management, e.g. treating cause (e.g. removal of high flow O2, respiratory sedative) and non-invasive ventilation.

Endobronchial obstruction, e.g. tumour, retained secretions, inhaled foreign body

  • Suggested by: cough, stridor, unilateral signs of dullness to percussion, crackles, and unilateral reduced breath sounds (unless pathology is above the carina).

  • Confirmed by: CT thorax, bronchoscopy.

  • Finalized by the predictable outcome of management, e.g. bronchoscopy and removal obstruction, if possible.

Severe asthma or anaphylaxis (bronchoconstriction)

  • Suggested by: history, sudden onset, often precipitating factor. Patient in extremis, reduced consciousness.

  • Confirmed by: peak flow rate undetectable. ABG shows type 2 respiratory failure.

  • Finalized by the predictable outcome of management, e.g. high flow O2, high dose bronchodilators (β2-agonists and anticholinergics) via nebulizer. Hydrocortisone IV 200mg. magnesium IV, antihistamines IV, and aminophylline IV can be considered. NB Keeping hydrated and monitor ABG and serum K+. HDU if drowsy, ↑CO2 (as this is an ominous sign in asthma).

Excess air, fat, or fluid between lung and your stethoscope: Main differential diagnoses and typical outline evidence, etc.

Obesity (leading to ventilatory failure = obesity hypoventilation syndrome)

  • Suggested by: insidious onset of breathlessness with rising weight.

  • Confirmed by: examination (BMI typically >40kg/m2 to cause chest wall compromise).

  • Finalized by the predictable outcome of management, e.g. weight loss, including dietitian referral and weight-lowering medications. Assess need for (nocturnal) NIV support (i.e. if symptoms of ventilatory failure and PaO2 <8kPa with PaCO2 >6.5kPa).

Pneumothorax (‘tension’, moderate, or mild)

  • Suggested by: pain in centre or side of chest with abrupt breathlessness, diminished breath sounds, and hyper-resonance to percussion.

  • Confirmed by: above findings, tracheal deviation, and distress suggesting tension pneumothorax, or expiration CXR showing loss of lung markings outside sharp line (‘moderate’ if >5cm gap from lung edge to chest wall, ‘mild’ if <5cm).

  • Initial management: if tension pneumothorax, insertion of large Venflon into 2nd IC space, mid-clavicular line. O2 if breathless. Analgesia. Aspiration if moderate; if this is unsatisfactory or prior lung disease, insertion of IC drain into ‘triangle of safety’. If ‘mild’ (<5cm gap) and not breathless, observation.

Pleural effusion

  • Suggested by: reduced breath sounds, reduced tactile vocal fremitus, stony dull percussion note.

  • Confirmed by: homogeneous opacification with meniscus level on CXR and fluid on US scan/CT chest.

  • Finalized by the predictable outcome of management, e.g. if breathless at rest, aspiration of 500mL (therapeutic) and send fluid for tests, not draining to dryness if cause unknown, as thoracoscopy/pleural biopsy required. If known malignancy, also insertion of IC drain directly and pleurodesis.

Severe pleural thickening, e.g. due to pleural secondaries or mesothelioma

  • Suggested by: chest pain, weight loss, history of asbestos exposure, clubbing, reduced breath sounds.

  • Confirmed by: CT thorax and pleural biopsy.

  • Finalized by the predictable outcome of management, e.g. analgesia (e.g. opiates) and controlled O2. Oncologist/chest physician for specialist treatment.

Good air entry but abnormal lung parenchyma: Main differential diagnoses and typical outline evidence, etc.

Emphysema (overlaps with COPD) caused by smoking, smoke pollution, α1-antitrypsin deficiency

  • Suggested by: long history of cough ± sputum, many pack years of smoking, recurrent ‘exacerbations’, pursed lip, breathing (a chronic behavioural adaptation), hyperinflation, reduced chest expansion, reduced breath sounds, and hyper-resonance. CXR: radiolucent lungs.

  • Confirmed by: spirometry: FEV1 <80% predicted and FEV/FVC ratio <0.7. <15% reversibility. Emphysema on CT chest ± ↓α1-antitrypsin levels.

  • Finalized by the predictable outcome of management, e.g. stopping smoking. Trials of bronchodilators prn, regular long-acting bronchodilators. Regular inhaled steroids if FEV <50% predicted and three COPD exacerbations per year. If cough and breathlessness persists, prednisolone PO. If respiratory failure, home O2.

Large bullae

  • Suggested by: other signs of emphysema but can be isolated finding, and often congenital in otherwise normal lungs.

  • Confirmed by: CT thorax.

  • Initial treatment: observation. Can mimic partial pneumothorax, but do NOT insert IC drain. Refer to cardiothoracics for bullectomy or endobrachial valve if symptomatic and not widespread emphysema.

Consolidation due to bacterial infection, but possibly autoimmune disease, malignancy, or drugs

  • Suggested by: reduced breath sounds, bronchial breathing, increased tactile vocal fremitus, reduced percussion note.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. if not very ill, but fever and ↑neutrophil count, analgesia, an empiric 5d course of amoxicillin/clarithromycin PO. If ≥2 features of CRB-65, then amoxicillin/co-amoxiclav IV or cefuroxime with controlled O2 and fluids. If history of reduced consciousness/aspiration, then cefuroxime/metronidazole IV. If hospital/nursing home acquired infection, cefuroxime or piperacillin with tazobactam IV. If no fever or WCC normal, investigation for non-infective possibilities.

Bronchial breathing

Prolonged expiration phase with a definite silence between inspiration and expiration (same as sound heard with stethoscope bell over trachea). Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Consolidation due to bacterial infection, but possibly autoimmune disease, malignancy, or drugs

  • Suggested by: reduced breath sounds, bronchial breathing, increased tactile vocal fremitus, reduced percussion note.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. if not very ill, but fever and ↑neutrophil count on FBC, analgesia, and an empiric 5d course of amoxicillin/clarithromycin PO. If ≥2 features of CRB-65, then amoxicillin/co-amoxiclav IV or cefuroxime with controlled O2 and fluids. If history of reduced consciousness/aspiration, then cefuroxime/metronidazole IV. If hospital/nursing home acquired infection, cefuroxime or piperacillin with tazobactam IV. If no fever or WCC normal, investigation for non-infective possibilities.

Lung cavity

  • Suggested by: localized bronchial breathing, otherwise normal examination.

  • Confirmed by: CXR, CT thorax (should have greater than 2mm wall thickness to differentiate from a lung cyst).

  • Finalized by the predictable outcome of management, e.g. compare with old CXR. Consider TB and lung cancer. Chest clinic follow-up.

Pulmonary fibrosis/interstitial lung disease NB Majority of cases have no cause identified

  • Suggested by: chronic dry cough, occupational exposure or evidence of underlying connective tissue disease. Clubbing, cyanosis, reduced chest expansion, coarse late inspiratory bibasal crackles.

  • Confirmed by: ↓lung volumes and reticular nodular shadowing on CXR. Interstitial shadowing and/or subpleural fibrosis on high resolution CT chest.

  • Finalized by the predictable outcome of management, e.g. home O2 if saturations <93%. Specialist opinion about detailed lung function, lung biopsy, immunosuppression, antifibrotics, palliation.

Fine inspiratory crackles

Very fine crackles are like the sound made when hair next to the ear is rolled between finger and thumb, or opening a velcro pad! Initial investigations (other tests in bold below): FBC, U&E, CXR, ABG.

Main differential diagnoses and typical outline evidence, etc.

Incidental due to normal secretions

  • Suggested by: late in inspiration, disappear on coughing.

  • Confirmed by: CXR showing normal lung fields.

Pulmonary oedema due to acute left ventricular failure or chronic (congestive) cardiac failure due to ischaemic heart disease, mitral stenosis

  • Suggested by: background fatigue and exertional breathless, cardiac risk factors. Displaced apex beat, 3rd heart sound, bilateral basal fine crackles. ↑JVP and leg swelling.

  • Confirmed by: CXR: fluffy opacification, especially near hila. Loss of costophrenic angle. Impaired left ventricular function on echocardiogram.

  • Finalized by the predictable outcome of management, e.g. sitting patient up, controlled O2, diuretics IV. Nitrates IV if very breathless and systolic BP >90.

  • Chronic: thiazide or loop diuretic, ACE inhibitor (or angiotensin receptor blocker). β-blocker and spironolactone (monitor K+).

Pulmonary oedema due to acute lung injury/acute respiratory distress syndrome (ARDS)

  • Suggested by: Acutely ill patient with severe hypoxia. History of precipitating cause (e.g. smoke inhalation, aspiration, drug exposure, fat/amniotic fluid emboli, viral infection, disseminated intravascular coagulation (DIC)), no clinical signs of left ventricular failure. CXR: symmetrical, diffuse, poorly defined opacities, which become confluent. Normal heart size.

  • Confirmed by: (1) acute onset, (2) bilateral infiltrates, (3) pulmonary capillary wedge pressure <19mmHg or no congestive cardiac failure, (4) PaO2:FiO2<200 in the presence of good left ventricular function.

  • Finalized by the predictable outcome of management, e.g. intubation; ventilation with small volumes and consider prone ventilation/steroids. Treatment of underlying cause.

Pulmonary fibrosis/interstitial lung disease NB Majority of cases have no cause identified

  • Suggested by: chronic dry cough, occupational exposure or evidence of underlying connective tissue disease. Clubbing, cyanosis, reduced chest expansion, coarse late inspiratory bibasal crackles.

  • Confirmed by: ↓lung volumes and reticular nodular shadowing on CXR. Interstitial shadowing and/or subpleural fibrosis on high resolution CT chest.

  • Finalized by the predictable outcome of management, e.g. home O2 if saturations <93%. Specialist opinion about detailed lung function, lung biopsy, immunosuppression, antifibrotics, palliation.

Chronic bronchitis (overlaps with COPD)

  • Suggested by: long history of cough (productive grey/ white sputum or dry). Typically >10-pack year smoking. Recurrent ‘exacerbations’ of cough lasting days, needing antibiotics.

  • Confirmed by: spirometry shows FEV1 <80% predicted and FEV/FVC ratio <0.7, little reversibility (FEV1 improves <15% with treatment).

  • Finalized by the predictable outcome of management, e.g. stopping smoking. Winter vaccinations. Improvement with inhalers.

Emphysema (overlaps with COPD) caused by smoking, smoke pollution, α1-antitrypsin deficiency

  • Suggested by: long history of cough ± sputum, many pack years of smoking, recurrent ‘exacerbations’, pursed lip, breathing (a chronic behavioural adaptation), hyperinflation, reduced chest expansion, reduced breath sounds, and hyper-resonance. CXR: radiolucent lungs.

  • Confirmed by: spirometry: FEV1 <80% predicted and FEV/FVC ratio <0.7. <15% reversibility. Emphysema on CT chest ± ↓α1-antitrypsin levels.

  • Finalized by the predictable outcome of management, e.g. stopping smoking. Trials of bronchodilators prn, regular long-acting bronchodilators. Regular inhaled steroids if FEV <50% predicted and three COPD exacerbations per year. If cough and breathless persists, prednisolone PO. If respiratory failure, home O2.

Consolidation due to bacterial infection, but possibly autoimmune disease, malignancy, or drugs.

  • Suggested by: reduced breath sounds, bronchial breathing, increased tactile vocal fremitus, reduced percussion note.

  • Confirmed by: CXR.

  • Finalized by the predictable outcome of management, e.g. if not very ill, but fever and ↑neutrophil count on FBC, analgesia, and an empiric 5d course of oral amoxicillin/clarithromycin. If ≥2 features of CRB-65, then amoxicillin/co-amoxiclav IV or cefuroxime with controlled O2 and fluids. If history of reduced consciousness/aspiration, then cefuroxime/metronidazole IV. If hospital/nursing home acquired infection, cefuroxime or piperacillin with tazobactam IV. If no fever or WCC normal, investigate non-infective possibilities.

Coarse crackles

Bubbly crackles, often heard in both inspiration and expiration. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Bronchiectasis

  • Suggested by: progression over months or years. Cupful(s) of pus-like sputum per day. Clubbing, typically bilateral consolidation, and bilateral coarse late inspiratory crackles. Typically obstructive deficit on spirometry.

  • Confirmed by: CXR: cystic shadowing; high resolution CT chest: honeycombing and thickened dilated bronchi.

  • Finalized by the predictable outcome of management, e.g. chest physiotherapy (including postural drainage and cough clearance), sputum cultures. Mucolytics, bronchodilators, regular exercise, winter vaccinations. When unwell, treatment with 10–14d antibiotics IV according to last sputum cultures. NB Anti-pseudomonas treatment (aminoglycoside cover). Monitor for weight loss.

Pulmonary fibrosis/interstitial lung disease NB Majority of cases have no cause identified

  • Suggested by: chronic dry cough, occupational exposure or evidence of underlying connective tissue disease. Clubbing, cyanosis, reduced chest expansion, coarse late inspiratory bibasal crackles.

  • Confirmed by: ↓lung volumes and reticular nodular shadowing on CXR. Interstitial shadowing and/or subpleural fibrosis on high resolution CT chest.

  • Finalized by the predictable outcome of management, e.g. home O2 if saturations <93%. Specialist opinion about detailed lung function, lung biopsy, immunosuppression, antifibrotics, palliation.

Pleural rub

This sound can be reproduced by placing one finger over your ear and scratching the nail bed with your opposite index finger (or crunching through snow). Pleural rub is caused by inflammation of the pleura. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Pneumonia with pleurisy

  • Suggested by: onset over hours or days, rusty brown sputum ± blood. Sharp pains worse on inspiration, fever, cough, crackles, dullness to percussion, bronchial breathing, WCC: ↑neutrophils, ↑CRP.

  • Confirmed by: patchy shadowing on CXR and sputum/blood culture.

  • Initial management: analgesia and provisional antibiotic e.g. amoxicillin/clarithromycin PO for 5d. If >2 features of Confusion, Resp. rate >30/min, BP <90/60, age >65y), then antibiotic IV, e.g. amoxicillin/co-amoxiclav or cefuroxime, and controlled O2 and fluids. If suspected aspiration, then anti-anaerobics, e.g. cefuroxime/metronidazole IV. If hospital/nursing home acquired, cefuroxime or piperacillin with tazobactam IV.

Pulmonary embolus/infarction arising from deep veins or in left atrium

  • Suggested by: sudden breathlessness, pleural rub, cyanosis, tachycardia, loud P2, associated DVT, or risk factors such as recent surgery, immobility, previous emboli, malignancy, etc.

  • Confirmed by: CT pulmonary angiogram showing clot in pulmonary artery.

  • Finalized by the predictable outcome of management, e.g. LMW heparin (treatment dose), then warfarin. Thrombolysis if ↓BP, large bilateral clots or acutely dilated right ventricle on echocardiogram.

Severe pleural thickening, e.g. due to pleural secondaries or mesothelioma

  • Suggested by: chest pain, weight loss, history of asbestos exposure, clubbing, reduced breath sounds.

  • Confirmed by: CT thorax and pleural biopsy.

  • Finalized by the predictable outcome of management, e.g. analgesia (e.g. opiates) and controlled O2. Oncologist/chest physician for specialist treatment.

Stridor ± inspiratory wheeze

This suggests obstruction in or near the larynx. This represents a medical emergency. Attempts to examine the upper airway outside of a specialist setting may make matters worse. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Epiglottitis

  • Suggested by: fever, URTI coryzal symptoms (the 4 Ds = drooling, drawn facies, dysphonia, dysphagia).

  • Confirmed by: indirect laryngoscopy under controlled (anaesthetic) conditions.

  • Finalized by the predictable outcome of management, e.g. penicillin IV, and refer for emergency treatment with ENT and anaesthetic opinion.

Croup

  • Suggested by: high-pitched cough in infants.

  • Confirmed by: above presentation and findings.

  • Finalized by the predictable outcome of management, e.g. paediatric support if respiratory compromise.

Inhaled foreign body

  • Suggested by: history of inhaled peanut, bead, etc. typically right-sided chest signs.

  • Confirmed by: CXR, CT thorax, bronchoscopy.

  • Finalized by the predictable outcome of management, e.g. slap between shoulder blades/Heimlich manoeuvre if acutely ill. CT and bronchoscopy if not acutely ill.

Rapidly progressive laryngomalacia

  • Suggested by: change in voice over months to years.

  • Confirmed by: indirect laryngoscopy, CT thorax.

  • Finalized by the predictable outcome of management, e.g. ENT surgical intervention.

Laryngeal papillomas

  • Suggested by: change in voice over weeks to months.

  • Confirmed by: indirect laryngoscopy.

  • Finalized by the predictable outcome of management, e.g. ENT surgical intervention.

Anaphylaxis causing laryngeal oedema

  • Suggested by: onset over minutes, history of recent allergen exposure, feeling of dread, flushing, sweating, facial oedema, urticaria, warm clammy extremities, dyspnoea and tachypnoea, wheeze. Tachycardia and ↓BP.

  • Confirmed by: clinical presentation and response to adrenaline (epinephrine) IM. Results of controlled allergen exposure.

  • Finalized by the predictable outcome of management, e.g. removal of antigen (e.g. bee sting, medication). Adrenaline IM 1 in 1,000. Securing of airway early if stridor. High flow O2, fast fluids IV, steroids IV, and antihistamines IV. HDU/ITU care.

Inspiratory monophonic wheeze

This suggests large airway obstruction, often very proximal. A lesion just above the carina can be immediately life-threatening as neither lung can be ventilated, and tracheostomy will also not get below the obstruction. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Acute bilateral vocal cord paralysis

  • Suggested by: change in voice, bilateral reduced breath sounds, and wheeze.

  • Confirmed by: laryngoscopy.

  • Finalized by the predictable outcome of management, e.g. ENT surgical intervention.

Inhalation of foreign body

  • Suggested by: history of putting an object in mouth, e.g. peanut. Sudden stridor, severe cough, low-pitched, monophonic wheeze, and reduced breath sounds, typically on the right.

  • Confirmed by: if not in extremis, CXR/CT thorax or bronchoscopy to show foreign body.

  • Finalized by the predictable outcome of management, e.g. if in extremis, slap back between the shoulder blades with patient leaning forward; if fails, perform Heimlich manoeuvre.

Tracheal tumours or stenosis after ventilation

  • Suggested by: stridor, over weeks to months, bilateral reduced breath sounds, and bilateral wheeze.

  • Confirmed by: CXR, CT thorax and neck, bronchoscopy.

  • Initial treatment: controlled O2, and/or steroids IV.

Extrinsic compression of large airways by mediastinal masses

  • Suggested by: neck/chest discomfort ± swelling over weeks to months. Look for signs of SVC obstruction. Can be focal (unilateral) or bilateral wheeze, depending on site of obstruction.

  • Confirmed by: CT thorax and neck.

  • Finalized by the predictable outcome of management, e.g. steroids and palliative chemo-radiotherapy.

Extrinsic compression by oesophageal tumours

  • Suggested by: dysphagia, weight loss over weeks to months.

  • Confirmed by: CT thorax and neck.

  • Finalized by the predictable outcome of management, e.g. soft pureed diet. Barium swallow if high dysphagia or oesophagogastroduodenoscopy (OGD) if low dysphagia.

Tracheal blunt trauma

  • Suggested by: history, pain and swelling, change in voice over minutes or hours after trauma.

  • Confirmed by: laryngoscopy, bronchoscopy.

  • Finalized by the predictable outcome of management, e.g. early intubation and steroids.

Expiratory monophonic wheeze

This suggests obstruction of a large airway. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Endobronchial carcinoma (benign lesions very rare)

  • Suggested by: smoker, weight loss, cough, chest pain, and haemoptysis, clubbed. Unilateral wheeze (typically occur below the carina) and unilateral reduced breath sounds. Often signs of consolidation distal to obstruction. CXR can be normal.

  • Confirmed by: sputum cytology, CT chest, bronchoscopy and biopsy.

  • Finalized by the predictable outcome of management, e.g. possible radiotherapy, tracheal stenting, cryotherapy, laser therapy, brachytherapy (radioactive source put close to tumour).

Acute bilateral vocal cord paralysis

  • Suggested by: change in voice, bilateral reduced breath sounds, and wheeze.

  • Confirmed by: laryngoscopy.

  • Finalized by the predictable outcome of management, e.g. ENT surgical intervention for possible intubation and tracheostomy.

Inhalation of foreign body

  • Suggested by: history of putting an object in mouth, e.g. peanut. Sudden stridor, severe cough, low-pitched, monophonic wheeze, and reduced breath sounds, typically on the right.

  • Confirmed by: if not in extremis, CXR/CT thorax or bronchoscopy to show foreign body.

  • Finalized by the predictable outcome of management, e.g. if in extremis, slap back between the shoulder blades with patient leaning forward; if fails, perform Heimlich manoeuvre. CT and bronchoscopy if not acutely ill.

Tracheal tumours

  • Suggested by: stridor over weeks to months, bilateral reduced breath sounds, and bilateral wheeze.

  • Confirmed by: CXR, CT thorax and neck, bronchoscopy.

  • Initial treatment: controlled O2, and/or steroids IV.

Extrinsic compression by mediastinal masses

  • Suggested by: neck/chest discomfort ± swelling over weeks to months. Look for signs of SVC obstruction. Can be focal (unilateral) or bilateral wheeze, depending on site of obstruction.

  • Confirmed by: CT thorax and neck.

  • Finalized by the predictable outcome of management, e.g. steroids and palliative chemo-radiotherapy.

Extrinsic compression by oesophageal tumours

  • Suggested by: dysphagia, weight loss over weeks to months.

  • Confirmed by: CT thorax and neck.

  • Finalized by the predictable outcome of management, e.g. soft pureed diet. Barium swallow if high dysphagia or OGD if low dysphagia.

Tracheal blunt trauma

  • Suggested by: history, pain and swelling, change in voice over minutes or hours after trauma.

  • Confirmed by: laryngoscopy, bronchoscopy.

  • Finalized by the predictable outcome of management, e.g. steroids and ENT intervention for possible intubation and tracheostomy.

Expiratory polyphonic, high-pitched wheeze

This suggests small airways obstruction. Initial investigations (other tests in bold below): FBC, U&E, CXR.

Main differential diagnoses and typical outline evidence, etc.

Exacerbation of asthma

  • Suggested by: widespread polyphonic wheeze with exacerbations over hours. Silent chest if severe. Anxiety, tachypnoea, tachycardia, and use of accessory muscles.

  • Confirmed by: reduced peak flows. FEV1 that improves by >15% with treatment.

  • Finalized by the predictable outcome of management, e.g. high flow O2, prednisolone PO or hydrocortisone IV. Nebulized salbutamol and ipratropium ± magnesium IV and aminophylline IV. NB. Keeping hydrated, and monitor ABG and serum K+. HDU care if drowsy, ↑CO2 or silent chest.

‘Wheezy bronchitis’

  • Suggested by: wheeze association with infective episodes of bronchitis alone.

  • Confirmed by: FEV1 response to bronchodilators and antibiotics.

  • Finalized by the predictable outcome of management, e.g. antibiotics if high fever, mucopurulent sputum.

Viral wheeze

  • Suggested by: wheeze associated URTI viral illness, poor response to bronchodilators.

  • Confirmed by: resolving spontaneously.

  • Finalized by the predictable outcome of management, e.g. analgesic and antipyretic, e.g. paracetamol.

Anaphylaxis

  • Suggested by: onset over minutes, history of recent allergen exposure, feeling of dread, flushing, sweating, facial oedema, urticaria, warm clammy extremities, dyspnoea and tachypnoea, wheeze. Tachycardia and ↓BP.

  • Confirmed by: clinical presentation and response to adrenaline (epinephrine) IM. Results of controlled allergen exposure.

  • Finalized by the predictable outcome of management, e.g. removal of antigen (e.g. bee sting, medication). Adrenaline IM 1 in 1,000. Securing of airway early if stridor. High flow O2, fast fluids IV, steroids IV, and antihistamines IV. HDU/ITU care.

Pulmonary oedema due to acute left ventricular failure or chronic (congestive) cardiac failure due to ischaemic heart disease, mitral stenosis

  • Suggested by: background fatigue and exertional breathless, cardiac risk factors. Displaced apex beat, 3rd heart sound, bilateral basal fine crackles. ↑JVP and leg swelling.

  • Confirmed by: CXR: fluffy opacification, especially near hila. Loss of costophrenic angle. Impaired left ventricular function on echocardiogram.

  • Finalized by the predictable outcome of management, e.g. sitting patient up, controlled O2, diuretics IV. Nitrates IV if very breathless and systolic BP >90.

  • Chronic: thiazide or loop diuretic, ACE inhibitor (or angiotensin receptor blocker). β-blocker and spironolactone (monitor K+).