The Respiratory Block

Cases 1–8 · 12,309 words · Download this chapter as PDF

This block covers the respiratory teaching of both internal medicine courses. Bacterial pneumonia is taught in the infectious diseases block but presents as a respiratory case and is placed here for clinical coherence. The second course adds cases 7 and 8.

Pulmonary thromboembolism is taught in the second course and is covered as Seminar 11 in Part Two, where the pre-test probability and imaging decisions can be set out properly. The approach to obstructive airway disease, a second-course seminar, is covered by Cases 2 and 3.

Case numbering is provisional and will be reconciled when the blocks are compiled into a single volume.

System Opener · The Respiratory History and Examination

This page is the framework the cases assume. Learn it once and the cases become variations on it rather than separate lists to memorise.

The history

The six cardinal symptoms

Then the four contexts that change the differential

• Exposures. Smoking in pack-years, including waterpipe and vaping. Occupation over the whole working life — dust, silica, asbestos with its decades of latency, farming, welding. Birds, mould, air conditioning. Travel and tuberculosis contact.

• Drugs. Beta blockers and aspirin provoke bronchospasm; amiodarone, methotrexate, nitrofurantoin and bleomycin cause parenchymal disease; angiotensin-converting enzyme inhibitors cause a dry cough.

• Atopy and family history. Eczema, allergic rhinitis, food allergy, and a family history of asthma, tuberculosis, cystic fibrosis or alpha-1 antitrypsin deficiency. Ask about consanguinity where relevant.

• Disease burden. Number of exacerbations, courses of oral steroids and admissions in the past year; any previous intensive care admission or intubation; home oxygen or non-invasive ventilation; current inhalers, adherence and technique; vaccination status.

The examination

From the end of the bed

• Respiratory rate counted over a full minute, respiratory distress, posture, ability to complete a sentence, cachexia, audible wheeze or stridor, pursed-lip breathing, the oxygen device and its flow rate, and the sputum pot — always look inside it.

• Chest shape: barrel chest of hyperinflation, kyphoscoliosis, pectus deformity, thoracoplasty or lobectomy scars.

Hands, face and neck

• Clubbing. In respiratory disease it means bronchial carcinoma, bronchiectasis, lung abscess or empyema, idiopathic pulmonary fibrosis, cystic fibrosis or mesothelioma. It is not caused by asthma or by chronic obstructive pulmonary disease — if you find it in a patient labelled with either, you have found a second diagnosis.

• Tar staining, fine tremor of beta-agonist overuse, the coarse flapping tremor of carbon dioxide retention, wasting of the small hand muscles in an apical tumour, bounding pulse and warm hands in hypercapnia, pulsus paradoxus in severe asthma.

• Central cyanosis at the tongue, Horner syndrome, jugular venous pressure, supraclavicular and cervical lymph nodes, tracheal position, cricosternal distance (reduced in hyperinflation) and tracheal tug.

The chest, in the order that survives an examiner

• Inspect — symmetry of movement, scars, dilated veins, radiotherapy field markings.

• Palpate — expansion upper and lower, tactile vocal fremitus, apex beat position, chest wall tenderness.

• Percuss — including the clavicles and the axillae, and note the upper level of liver dullness, which is lost in hyperinflation.

• Auscultate — breath sound intensity and character, added sounds, vocal resonance. Always examine the back, where the lower lobes actually are.

• Finish — ankle and sacral oedema, calves, peak expiratory flow, and the observation chart.

Case 1 · Community-Acquired Pneumonia

1. Focused History

Characterise the presenting complaint

• Onset and tempo. Abrupt onset over hours with a rigor suggests bacterial, classically pneumococcal, disease. A gradual prodrome over one to two weeks with headache and myalgia points to an atypical organism.

• Cough and sputum. Ask about volume, colour and blood. Rust-coloured sputum is classically pneumococcal; foul-smelling sputum suggests anaerobic infection or abscess; copious purulent sputum daily for years suggests underlying bronchiectasis.

• Pleuritic chest pain. Localises the affected lobe and tells you the pleura is inflamed. Pain that persists or worsens after 48 hours of antibiotics raises the question of empyema.

• Breathlessness. Quantify against his own baseline — "how far could you walk last week, and how far today?" — not against an abstract scale.

Red flags to exclude at once

• Confusion or drowsiness, syncope, inability to speak in full sentences, cyanosis, haemoptysis, poor oral intake and reduced urine output. Any of these moves the patient to the resuscitation area before the history is finished.

Questions that discriminate between causes

Risk factors and background

• Host factors: age, smoking, chronic obstructive pulmonary disease, diabetes mellitus, chronic kidney or liver disease, heart failure, malnutrition.

• Immunosuppression: corticosteroids, chemotherapy, biologic agents, human immunodeficiency virus (HIV) infection, asplenia, transplant. This changes the organism list and therefore the antibiotic.

• Recent healthcare exposure and antibiotics within 90 days — the strongest single predictor of resistance.

• Vaccination status for pneumococcus and influenza, and drug allergies, especially to penicillin.

• Functional baseline and social circumstances. Whether he lives alone, and who can observe him, decides admission as often as the physiology does.

2. Physical Examination

General inspection and vital signs

• Respiratory distress: accessory muscle use, nasal flaring, inability to complete a sentence, tripod posture.

• A complete set of vital signs including the respiratory rate. The respiratory rate is the earliest and most sensitive marker of deterioration and the one most often left unrecorded. Count it for a full minute.

• Level of consciousness — formally, using an abbreviated mental test or the Glasgow Coma Scale, because "confusion" scores a point on the severity index and must be documented objectively.

• Peripheral perfusion: capillary refill, warm vasodilated peripheries with a bounding pulse in early sepsis, cool and mottled in late shock.

Hands, face and neck

• Tar staining, peripheral and central cyanosis, a carbon dioxide retention flap if there is coexisting chronic obstructive pulmonary disease, herpes labialis around the mouth, dehydrated mucous membranes.

• Tracheal position — central in uncomplicated consolidation. Deviation means collapse (pulled towards) or a large effusion or tension pneumothorax (pushed away).

The chest, in sequence

• Inspect: reduced movement on the affected side, tachypnoea, scars, chest wall deformity.

• Palpate: chest expansion, comparing sides; tactile vocal fremitus is increased over consolidated lung because solid tissue transmits sound better than air.

• Percuss: dull over consolidation. Stony dullness means fluid, not consolidation — this single distinction changes your next step from antibiotics alone to a diagnostic pleural tap.

• Auscultate: bronchial breathing over the consolidated lobe, coarse late inspiratory crackles, increased vocal resonance and whispering pectoriloquy. A pleural rub may be heard where the pain is.

• Then look for complications: an area of stony dullness with absent breath sounds at the base (parapneumonic effusion or empyema), a new murmur (endocarditis as a source), neck stiffness (meningitis from the same pneumococcus).

The bedside distinction you must be able to make. Four processes reduce chest expansion and all four appear in examinations. The table below is the answer to the commonest viva question in respiratory medicine.

3. Differential Diagnosis

4. Investigations

At the bedside

• Pulse oximetry on room air, documented as such — a saturation on oxygen without the flow rate recorded is uninterpretable.

• Arterial blood gas if the saturation is below 94%, if there is shock, or if chronic obstructive pulmonary disease raises the possibility of carbon dioxide retention. Expect type 1 respiratory failure; a rising carbon dioxide in a tiring patient is an ominous sign.

• Electrocardiogram — to detect the atrial fibrillation that sepsis commonly precipitates, and because chest pain in a 68-year-old deserves one.

• Capillary blood glucose — infection destabilises diabetes and may precipitate a hyperglycaemic emergency.

Laboratory

Imaging

• Chest radiograph, posteroanterior. Expect lobar consolidation with an air bronchogram. Use the silhouette sign to localise: loss of the right heart border places the disease in the right middle lobe; loss of a hemidiaphragm places it in a lower lobe. Also inspect for effusion, cavitation and a mass.

• Point-of-care chest ultrasound. More sensitive than the radiograph for pleural fluid and it guides the needle. It has largely replaced the lateral decubitus film.

• Computed tomography of the chest if the pneumonia fails to resolve, if complications are suspected, or if the radiograph is equivocal in a very sick patient.

• Repeat the chest radiograph at six weeks in every smoker and in anyone over 50. Persistent consolidation is a bronchial carcinoma until proved otherwise. This is the single follow-up step most often forgotten.

Pleural fluid, if an effusion is present

Any effusion more than 1 cm deep on ultrasound in a febrile patient should be sampled. Send protein, lactate dehydrogenase, glucose, pH, Gram stain, culture and cytology. A pH below 7.2, glucose below 2.2 mmol/L, or frank pus means a complicated parapneumonic effusion or empyema, and the treatment is a chest drain, not more antibiotics.

5. Management

Immediate — the first hour

• Oxygen titrated to a saturation of 94–98%, or 88–92% if there is a risk of carbon dioxide retention.

• Intravenous access, fluid resuscitation with balanced crystalloid for hypotension, and hourly urine output measurement.

• Antibiotics within one hour if septic, and within four hours in all other cases. Take the cultures on the way, not instead.

• Escalate early. Persistent hypotension after fluid, a rising lactate, or exhaustion means a critical care referral now rather than at the next ward round.

Score the severity — CURB-65

• 0–1: low risk, suitable for treatment at home.

• 2: moderate risk, admit to a general ward.

• 3–5: high risk, consider critical care. Our patient scores 4 (confusion, respiratory rate, blood pressure, age) and requires a high-dependency bed.

The score guides but does not replace judgement. A hypoxic patient with a score of 1, or one who cannot manage at home, is still admitted.

Antibiotic therapy

Switch from intravenous to oral once the patient has been afebrile for 48 hours, is haemodynamically stable and is absorbing enterally. A macrolide is added, not substituted, because atypical organisms are not covered by beta-lactams and cannot be excluded clinically at the front door.

Supportive care

• Venous thromboembolism prophylaxis, analgesia adequate to allow deep breathing and coughing, early mobilisation, chest physiotherapy if sputum retention is a problem, attention to nutrition and to glycaemic control.

• Corticosteroids are not given routinely, but there is now evidence of benefit in severe pneumonia requiring critical care. Follow your local protocol.

Complications to anticipate

• Parapneumonic effusion and empyema, lung abscess, acute respiratory distress syndrome, sepsis with acute kidney injury, new atrial fibrillation, and non-resolving pneumonia.

Discharge and follow-up

• Discharge when the patient is afebrile, saturating adequately on room air, eating and drinking, mentally back to baseline, and has no more than one instability criterion.

• At discharge: smoking cessation advice, pneumococcal and influenza vaccination, a clear safety-net for return, and the six-week chest radiograph booked before he leaves the ward.

6. Teaching Points and Viva Questions

• The respiratory rate is the most useful and most neglected vital sign. A rate of 30 in a quiet-looking patient is a medical emergency.

• Bronchial breathing requires a patent airway leading to solid lung; absent breath sounds with stony dullness means fluid between the lung and your stethoscope.

• The elderly may present with confusion, a fall or simply "off legs", and may be afebrile. Absence of fever does not exclude pneumonia.

• Urea appears in the severity score because it reflects both volume depletion and the catabolic burden of severe infection.

• Chest signs may be entirely normal in the first 24 hours. A normal examination does not exclude the diagnosis.

Questions you should be able to answer:

• Distinguish consolidation from a pleural effusion at the bedside using four signs.

• This patient is not improving on day three. What are your next four steps?

• When do you drain a parapneumonic effusion, and on what result?

• Why is a macrolide added to a beta-lactam rather than used alone?

• Why does a smoker need a repeat chest radiograph after recovery?

Case 2 · Acute Severe Asthma

1. Focused History

Take it in parallel with treatment. Nebulised salbutamol does not wait for the social history.

This attack

• Speed of onset — over hours suggests a viral or allergen trigger; over minutes raises anaphylaxis or an inhaled foreign body.

• The trigger: upper respiratory infection, allergen, exercise, cold air, cigarette or waterpipe smoke, emotion, occupational exposure, or a drug — aspirin, other non-steroidal anti-inflammatory drugs, and beta blockers, including eye drops.

• How much reliever has been used, and whether it is still working. Diminishing response to salbutamol is a severity marker.

Background asthma control

• Night waking, morning dipping, and days per week of symptoms — the practical measure of control.

• Current inhalers, adherence, and technique. Ask her to demonstrate rather than to describe. Poor technique is the commonest reason an apparently adequate regimen fails.

• Number of oral corticosteroid courses in the past twelve months and the number of reliever canisters used per month.

2. Physical Examination

The four bedside measurements that grade the attack

• Can she complete a sentence? Ask her name and address and listen to the phrasing, not the answer.

• Respiratory rate and heart rate, counted, not estimated.

• Oxygen saturation on room air.

• Peak expiratory flow against predicted or her own best. It is the single most useful measurement in asthma and takes fifteen seconds.

Signs of danger

• Accessory muscle use, tracheal tug, tripod posture, inability to lie flat.

• A silent chest. Air must move to make a wheeze. A chest that has gone quiet in a distressed patient means airflow has fallen too low to generate sound, and is a pre-terminal sign.

• Cyanosis, exhaustion, drowsiness or confusion, bradycardia, hypotension, arrhythmia — the peri-arrest picture.

• Pulsus paradoxus, and subcutaneous emphysema or asymmetric signs suggesting pneumothorax or pneumomediastinum.

3. Grading the Attack

4. Differential Diagnosis

5. Investigations

• Peak expiratory flow before and after treatment — the measure of response.

• Pulse oximetry, aiming to keep saturation at 94–98%.

• Arterial blood gas if saturation stays below 92% or there are life-threatening features. Expect a low carbon dioxide from hyperventilation. A normal or rising carbon dioxide means the patient is tiring and requires immediate senior and critical care involvement.

• Chest radiograph only if pneumothorax or consolidation is suspected, if there is no response to treatment, or if ventilation is being considered. It is not routine.

• Potassium — both beta agonists and corticosteroids lower it, and the treatment itself is the commonest cause of hypokalaemia here. Also glucose, complete blood count and C-reactive protein.

No investigation should delay the first nebuliser.

6. Management

Immediate, in this order

• Antibiotics are not routine. Most attacks are triggered by viruses. Give them only for genuine evidence of bacterial infection.

• Never sedate a breathless asthmatic. Agitation is hypoxia, not anxiety.

Monitoring

• Peak flow before and after every nebuliser; continuous oximetry; potassium after repeated doses; repeat blood gas if the first was abnormal or the patient is not improving.

Discharge and follow-up

• Discharge when peak flow exceeds 75% of best or predicted, when she has been off nebulisers for 24 hours, and when saturations are stable on air.

• Before she leaves: inhaler technique observed and corrected, the inhaled corticosteroid restarted or stepped up, the remainder of the prednisolone course dispensed, and a written personalised asthma action plan in her hand.

• Primary care review within 48 hours and a respiratory clinic appointment within four weeks. Every admission is a failure of chronic control and should trigger a review of it.

Complications

• Pneumothorax and pneumomediastinum, hypokalaemia, lactic acidosis from high-dose beta agonists, and respiratory arrest.

7. Teaching Points and Viva Questions

• The silent chest is the most dangerous sign in the room and the easiest to misread as improvement.

• A normal carbon dioxide in a patient who has been hyperventilating for hours is a warning, not a reassurance.

• Peak flow is objective, repeatable and free. Record it before and after every intervention.

• Overuse of reliever inhaler and underuse of preventer is the pattern behind almost every severe attack.

• Clubbing does not occur in asthma. If you see it, look for bronchiectasis or cancer.

Questions you should be able to answer:

• Grade this attack and justify each criterion you use.

• Why is a normal arterial carbon dioxide a life-threatening feature?

• When would you give magnesium, and what is the evidence for it?

• Her potassium is 2.9 mmol/L after four nebulisers. Explain why.

• What must be done before she is allowed home?

Case 3 · Exacerbation of Chronic Obstructive Pulmonary Disease

1. Focused History

Characterise the exacerbation

• The three cardinal symptoms: increased breathlessness, increased sputum volume, and increased sputum purulence. How many are present decides whether antibiotics are indicated.

• Baseline exercise tolerance, described in metres or stairs, and how far it has fallen.

• Fever, pleuritic pain, haemoptysis, unilateral leg swelling, chest pain — each pointing to a different complication or alternative diagnosis.

Establish the baseline disease

• Exacerbations, courses of steroids and admissions in the past year; previous non-invasive ventilation or intubation, and whether it helped; home nebulisers, home oxygen and its prescribed hours.

• Current inhalers, adherence and technique; vaccination status; smoking status now, not only historically.

• Comorbidity that mimics or coexists: ischaemic heart disease, heart failure, atrial fibrillation, anxiety, osteoporosis, malnutrition.

• Alpha-1 antitrypsin deficiency if the disease began young, if he is a light smoker, or if there is liver disease or a family history.

• Function and wishes. How he lives, who helps him, and whether escalation to ventilation has ever been discussed. This conversation is far easier now than at three in the morning.

2. Physical Examination

Signs of the underlying disease

• Pursed-lip breathing, accessory muscle use, tripod posture, barrel-shaped chest, reduced cricosternal distance, tracheal tug, indrawing of the lower ribs on inspiration.

• Hyperinflation: reduced expansion, hyper-resonant percussion with loss of cardiac and liver dullness, and quiet breath sounds throughout. Wheeze may be present or absent.

Signs of carbon dioxide retention

• Drowsiness and confusion, a coarse flapping tremor, bounding pulse, warm peripheries, headache, and in extreme cases papilloedema.

Signs of cor pulmonale

• Raised jugular venous pressure, right ventricular heave, loud pulmonary second sound, tender pulsatile hepatomegaly, ankle and sacral oedema.

Signs that mean something else is going on

• Clubbing — not a feature of chronic obstructive pulmonary disease; look for carcinoma or bronchiectasis. Focal consolidation, stony dullness, unilateral hyper-resonance, or an asymmetric swollen calf.

3. Differential Diagnosis

4. Investigations

• Arterial blood gas on a documented inspired oxygen concentration, repeated 30–60 minutes after any change in oxygen therapy or treatment.

• Chest radiograph — to exclude pneumonia, pneumothorax and a mass, and to look for hyperinflation with flattened hemidiaphragms.

• Electrocardiogram — right axis deviation, P pulmonale, right bundle branch block, atrial fibrillation or multifocal atrial tachycardia, and ischaemia.

• Complete blood count — secondary polycythaemia reflects chronic hypoxaemia; anaemia worsens breathlessness. Urea and electrolytes, C-reactive protein, glucose, and theophylline level if he takes it.

• Sputum culture if purulent or if he has failed previous antibiotics; blood cultures if febrile.

• Natriuretic peptide, troponin, or computed tomographic pulmonary angiography when heart failure, ischaemia or embolism cannot be excluded clinically.

Reading the film

• Hyperinflation is more than six anterior ribs above the diaphragm in the midclavicular line, flattened hemidiaphragms, a narrow vertical heart, and increased retrosternal air on the lateral view. Then look specifically at the apices and the lateral edges for a pneumothorax, which is easily missed against emphysematous lung.

5. Management

Immediate treatment

Non-invasive ventilation — what a student must know

• It is a treatment, not a sign of failure, and it reduces mortality and the need for intubation in this exact situation.

• Contraindications: inability to protect the airway, vomiting, facial trauma or burns, an undrained pneumothorax, haemodynamic instability, and a patient who cannot tolerate the mask.

• Decide the ceiling of care before starting, and document it: is non-invasive ventilation a bridge to intubation, or the ceiling itself? Involve the patient and family while he can still participate.

• Reassess with a blood gas one hour after starting. Failure to improve means escalation or a change of plan, not more of the same.

Before discharge, and for the long term

• Smoking cessation — the only intervention that alters the decline in lung function. Offer pharmacotherapy, not only advice.

• Pulmonary rehabilitation — the intervention with the largest effect on symptoms and quality of life, and the one most often not referred for.

• Inhaler technique reviewed and the regimen rationalised; influenza and pneumococcal vaccination; a rescue pack with a written plan for its use.

• Long-term oxygen therapy assessment when stable, at least 8 weeks after the exacerbation: arterial oxygen at or below 7.3 kPa, or at or below 8 kPa with polycythaemia, peripheral oedema or pulmonary hypertension. It must be used at least 15 hours a day to prolong life, and never with continued smoking.

• Nutritional assessment, anxiety and depression screening, and an honest conversation about the trajectory of the disease.

6. Teaching Points and Viva Questions

• Give oxygen, but give it in a measured concentration with a written target. Withholding it altogether is as much an error as flooding the patient with it.

• The bicarbonate is the historian of the blood gas — it tells you how long this has been going on.

• Smoking cessation and pulmonary rehabilitation change outcomes more than any inhaler.

• A patient with chronic obstructive pulmonary disease who deteriorates suddenly has a pneumothorax or a pulmonary embolism until proved otherwise.

• Ceiling-of-care decisions belong in the notes early, made with the patient, not improvised during a crisis.

Questions you should be able to answer:

• Explain the mechanism by which high-concentration oxygen raised this man’s carbon dioxide.

• What are your criteria for starting non-invasive ventilation, and what would you do if it fails?

• When do you give antibiotics in an exacerbation, and why not always?

• List the criteria for long-term oxygen therapy and explain why it must be worn 15 hours a day.

• He has clubbing. Does that change your thinking?

Case 4 · Suppurative Lung Disease: Bronchiectasis and Lung Abscess

1. Focused History

Characterise the sputum — this is the diagnostic history

• Daily volume, quantified against a household measure. Daily purulent sputum for years is bronchiectasis until proved otherwise, and no other common condition produces it.

• Smell. Foul or putrid sputum means anaerobic organisms, and therefore aspiration, abscess or empyema.

• Haemoptysis, quantified. Bronchiectasis is one of the commonest causes of massive haemoptysis.

• Whether the symptoms have been lifelong, or began after a specific illness.

Find the underlying cause

2. Physical Examination

• Clubbing — present in established suppurative lung disease and a key discriminator from chronic obstructive pulmonary disease.

• Cachexia and reduced muscle bulk, reflecting the metabolic cost of chronic sepsis.

• Inspect the sputum pot. Copious purulent sputum that separates into a frothy upper layer, a clear middle layer and a dense purulent lower layer is characteristic.

• Coarse early inspiratory crackles that change or clear with coughing — secretions moving in large airways. Wheeze is common. Signs may be focal or widespread.

• Look for complications: dullness with absent breath sounds (empyema), focal consolidation, and the raised jugular venous pressure, right ventricular heave and oedema of late cor pulmonale.

• Look for the cause: nasal polyps and sinus tenderness, dextrocardia, the teeth and gums, deforming arthropathy of the hands.

3. Differential Diagnosis

4. Investigations

Establish the diagnosis

• High-resolution computed tomography of the chest is the diagnostic test. Look for a bronchoarterial ratio greater than one — the signet ring sign — failure of the airways to taper towards the periphery, and visible airways within one centimetre of the pleura.

• Chest radiograph — tramline and ring shadows, crowded markings, and in abscess a cavity with an air-fluid level. A normal film does not exclude bronchiectasis.

• The distribution is a clue to the cause: upper lobes in cystic fibrosis, tuberculosis and allergic bronchopulmonary aspergillosis; lower lobes in post-infective and aspiration disease; the right middle lobe and lingula in non-tuberculous mycobacterial infection.

Establish the organism

• Sputum for Gram stain and culture, three specimens for acid-fast bacilli, and fungal culture. Know the colonising organism: Haemophilus influenzae early, and Pseudomonas aeruginosa later, which marks more severe disease and changes every future antibiotic choice.

Establish the underlying cause

• Complete blood count with differential, immunoglobulins G, A and M, and specific antibody responses; human immunodeficiency virus test; total and aspergillus-specific immunoglobulin E and aspergillus precipitins; sweat chloride and cystic fibrosis genotyping where suggestive; rheumatoid factor and anti-cyclic citrullinated peptide antibodies; alpha-1 antitrypsin level.

• Spirometry — usually an obstructive pattern; used to follow progression.

• Bronchoscopy if disease is confined to one lobe, if a foreign body or tumour is possible, or for persistent haemoptysis.

5. Management

Treat the exacerbation

• Send sputum, then start antibiotics guided by previous isolates. Treat for 14 days, considerably longer than for pneumonia.

• If colonised with Pseudomonas: oral ciprofloxacin, or intravenous piperacillin–tazobactam or ceftazidime for severe episodes.

• For a lung abscess: 4–6 weeks of antibiotics with anaerobic cover — co-amoxiclav or clindamycin — with postural drainage. Most resolve medically; percutaneous or surgical drainage is reserved for failure. Arrange dental assessment, since the mouth is usually the source.

The long-term programme — where the real benefit lies

• Daily airway clearance physiotherapy is the cornerstone of treatment. Active cycle of breathing, postural drainage, and oscillating positive expiratory pressure devices. Teach it, and check she is still doing it at every visit.

• Nebulised isotonic or hypertonic saline before physiotherapy to aid clearance.

• Long-term azithromycin three times weekly reduces exacerbation frequency. Exclude non-tuberculous mycobacterial infection and check the corrected QT interval and liver function before starting.

• Treat the underlying cause — immunoglobulin replacement in antibody deficiency, corticosteroids in allergic bronchopulmonary aspergillosis, modulator therapy in cystic fibrosis.

• Bronchodilators if there is demonstrable reversibility, vaccination, nutritional support, pulmonary rehabilitation, and surgical resection for localised disease that remains refractory.

6. Teaching Points and Viva Questions

• Clubbing with crackles is never simple chronic obstructive pulmonary disease. Think suppurative lung disease, fibrosis or cancer.

• The volume of daily sputum is the single most discriminating point in the history.

• High-resolution computed tomography makes the diagnosis; the plain film may be normal.

• Foul-smelling sputum means anaerobes, which means aspiration — so examine the teeth and ask why she aspirated.

• Physiotherapy is not an adjunct to treatment. In bronchiectasis it *is* the treatment, and antibiotics are the adjunct.

Questions you should be able to answer:

• How do you distinguish bronchiectasis from chronic obstructive pulmonary disease at the bedside?

• Name six causes of bronchiectasis and the single question that screens for each.

• Why does the distribution of disease on the computed tomogram matter?

• Why is Pseudomonas colonisation significant?

• She coughs up 400 mL of blood in an hour. What are your first five actions?

Case 5 · Acute-on-Chronic Hypercapnic Respiratory Failure

1. The Framework

Respiratory failure is not a diagnosis. It is a physiological state with two patterns, and the whole of the assessment follows from deciding which one is in front of you.

For type 2 failure, ask three questions in order. They generate the entire differential.

• Will he not breathe? Central depression — opioids, benzodiazepines, alcohol, brainstem stroke, raised intracranial pressure, hypothyroidism.

• Can he not breathe? Pump failure — neuromuscular disease (Guillain–Barré syndrome, myasthenia gravis, motor neurone disease, muscular dystrophy), phrenic nerve palsy, or chest wall restriction from kyphoscoliosis, circumferential burns or obesity hypoventilation.

• Is the load too great? Airway and lung disease — chronic obstructive pulmonary disease, severe asthma late in an attack, bronchiectasis, advanced fibrosis.

2. Focused History

• Speed of onset. Minutes suggests drugs, a neurological event or a pneumothorax; days suggests infection on a chronic background; months suggests progressive neuromuscular or chest wall disease.

• Symptoms of chronic hypoventilation: morning headache, daytime somnolence, poor concentration, disturbed sleep, snoring with witnessed apnoeas, ankle swelling.

• Neuromuscular screening questions: difficulty rising from a chair or climbing stairs, double vision, slurred speech, choking on food, breathlessness on lying flat (a diaphragmatic sign), and recent gastrointestinal or respiratory infection preceding weakness.

• Every sedative, opioid, alcohol and recreational drug taken. Any oxygen given before arrival, and at what rate.

• Previous non-invasive ventilation or continuous positive airway pressure at home, and adherence to it.

3. Physical Examination

• Conscious level, scored and repeated — the most important single observation, and the one that decides whether non-invasive ventilation is safe.

• Respiratory rate and pattern. A high rate that falls as the patient tires is ominous. Paradoxical inward abdominal movement on inspiration indicates diaphragmatic fatigue or paralysis.

• Bedside tests of respiratory muscle strength: ask him to count aloud from one on a single breath, and test neck flexion strength. Both correlate with vital capacity and can be repeated hourly.

• Signs of retention — flapping tremor, bounding pulse, warm peripheries, papilloedema. Central cyanosis. Signs of cor pulmonale.

• Pupils and injection sites if opioids are possible; the chest wall for deformity; a full neurological examination when weakness is suspected.

4. Investigations

• Arterial blood gas is the definitive investigation and must be repeated. Record the inspired oxygen concentration every time or the result is uninterpretable.

• Calculate the alveolar–arterial oxygen gradient. A normal gradient with hypercapnia means pure hypoventilation — the lungs are healthy and the pump has failed. A raised gradient means there is lung disease as well. This single calculation separates the two mechanisms.

• Chest radiograph, electrocardiogram, complete blood count (polycythaemia in chronic hypoxaemia), urea and electrolytes, C-reactive protein, thyroid function, creatine kinase.

• In suspected neuromuscular disease, measure the forced vital capacity serially and act on it. A value below 15–20 mL/kg, or a fall of more than 30% from baseline, indicates the need for ventilatory support. Do not wait for the carbon dioxide to rise — in neuromuscular failure hypercapnia is a late and pre-terminal finding.

• Later, when the acute episode has settled: sleep studies, spirometry with lung volumes, and echocardiography for pulmonary hypertension.

5. Management

The oxygen ladder — and why the device matters

Sequence for this patient

• Controlled oxygen by Venturi mask, targeting a saturation of 88–92%, with a gas repeated in 30 minutes.

• Reverse what is reversible: treat the chest infection, give bronchodilators if there is any airflow obstruction, and give naloxone if opioids are conceivable.

• Non-invasive ventilation for the persisting acidaemia, since the pH is below 7.35 with a carbon dioxide above 6.5 kPa. His drowsiness makes this a decision for a senior clinician in a monitored area, because the same drowsiness raises the risk of aspiration.

• Document the ceiling of care and discuss it with the patient and family before he deteriorates further.

• Repeat the gas at one hour. Improvement in pH is the marker of success. No improvement means intubation or an explicit change of plan.

Complications and longer-term care

• Aspiration, barotrauma and pneumothorax, pressure injury from the mask, hypotension from positive pressure, and oxygen-induced hypercapnia.

• After recovery: sleep-disordered breathing assessment and home nocturnal ventilation, weight management referral, avoidance of sedatives, treatment of cor pulmonale, and long-term oxygen assessment when stable.

6. Teaching Points and Viva Questions

• Hypercapnia is a pump problem. Ask in order: will he not breathe, can he not breathe, or is the load too great?

• The alveolar–arterial gradient separates a failing lung from a failing pump, and costs nothing to calculate.

• In neuromuscular weakness, measure the vital capacity. By the time the carbon dioxide rises, the patient is close to arrest.

• A falling respiratory rate in a previously tachypnoeic patient means exhaustion, not recovery.

• Write the target saturation range on the chart. An unqualified instruction to "give oxygen" is how patients like this one become drowsy.

Questions you should be able to answer:

• Classify this man’s respiratory failure and justify it from the gas.

• His bicarbonate is 33. What does that tell you about the timescale?

• Give four contraindications to non-invasive ventilation.

• Why is a Venturi mask preferred to nasal cannulae here?

• A patient with Guillain–Barré syndrome has a normal blood gas but a vital capacity of 1.1 litres. What do you do?

Case 6 · Pleural Effusion

1. Focused History

The two questions that shape everything

• How quickly did it come on? Days suggests infection, embolism or trauma. Weeks to months suggests malignancy, tuberculosis or heart failure.

• Is it painful? Pleuritic pain means the parietal pleura is inflamed and favours an exudate — infection, infarction, malignant invasion. Painless effusions are more often transudates.

Then screen for each cause directly

2. Physical Examination

Confirm the effusion

• Reduced expansion, stony dullness, absent or greatly reduced breath sounds, reduced vocal resonance and fremitus, with bronchial breathing at the upper border where compressed lung lies beneath.

• Tracheal position: central in a moderate effusion; pushed away by a massive one. If the trachea is pulled towards a white-out, the diagnosis is collapse, not effusion — and the management is entirely different.

Then find the cause

• Cervical and supraclavicular lymph nodes, breast examination, clubbing, chest wall masses or tenderness (mesothelioma), radiotherapy marks or surgical scars.

• Raised jugular venous pressure, third heart sound, bilateral oedema (heart failure); jaundice, spider naevi, ascites (cirrhosis); periorbital oedema (nephrotic syndrome); synovitis and deformity (rheumatoid disease); an abdominal or pelvic mass.

3. Investigations

Imaging — reading the film

• On the posteroanterior radiograph, about 200 mL is needed before the costophrenic angle blunts; on the lateral film as little as 50 mL is visible. Expect a homogeneous opacity with a concave upper border — the meniscus sign.

• A complete white-out: look at the trachea. Pushed away means effusion or a large mass; pulled towards means collapse or pneumonectomy; central suggests consolidation.

• Thoracic ultrasound before every pleural procedure. It confirms fluid, estimates depth, identifies septations, and marks the site. It has substantially reduced the complication rate of pleural aspiration and its use is now the standard of care.

• Contrast-enhanced computed tomography for any undiagnosed exudate, performed before complete drainage so the pleural surfaces can be assessed. Nodular or circumferential pleural thickening, thickening greater than one centimetre, or mediastinal pleural involvement all suggest malignancy.

Diagnostic aspiration

Note the appearance first: straw-coloured, turbid, frank pus, blood-stained, or milky. Then send the fluid for protein, lactate dehydrogenase, glucose, pH, Gram stain and culture, acid-fast staining and culture, adenosine deaminase, cytology, and triglycerides if it looks milky. Send paired serum protein and lactate dehydrogenase at the same time — without them the fluid results cannot be interpreted.

Interpreting the fluid

• Cytology is positive in only about six in ten malignant effusions. A negative result does not exclude cancer. If two aspirates are non-diagnostic and suspicion persists, proceed to local anaesthetic thoracoscopy with pleural biopsy, which has the highest yield in both malignancy and tuberculosis.

• Do not aspirate bilateral effusions in a patient with clear heart failure. Treat the failure and reassess; tap only if the effusions are asymmetric, painful, febrile, or fail to resolve.

4. Management

• Treat the cause. Transudates resolve when the underlying disorder is treated — diuresis for heart failure, albumin and sodium restriction in cirrhosis. Drainage alone achieves nothing lasting.

• Therapeutic drainage for symptomatic relief. Remove no more than 1–1.5 litres at one sitting, and stop immediately for chest tightness, pain or persistent coughing, because of the risk of re-expansion pulmonary oedema.

• Empyema or complicated parapneumonic effusion: prompt chest drain plus antibiotics covering anaerobes, continued for two to six weeks. Intrapleural fibrinolytic therapy for loculated collections, and surgical decortication when drainage fails.

• Malignant effusion: treat the underlying cancer. For recurrent symptomatic effusions, offer either an indwelling pleural catheter for drainage at home or talc pleurodesis; the choice depends on performance status, lung re-expansion and patient preference.

• Tuberculous effusion: standard antituberculous chemotherapy; most resolve without drainage.

• Procedural complications: pneumothorax, bleeding, infection, injury to liver or spleen, and re-expansion oedema. Ultrasound guidance, a properly positioned patient and a limited volume prevent most of them.

5. Teaching Points and Viva Questions

• Stony dullness with absent breath sounds is fluid. Dullness with bronchial breathing is consolidation. This distinction changes the next step from a prescription to a procedure.

• In a complete white-out, the trachea tells you the answer before any test does.

• Never perform a pleural procedure without ultrasound, and never on a patient who is sitting unsupported.

• Light’s criteria misclassify diuretic-treated heart failure. Remember the albumin gradient.

• A lymphocytic exudate with a high adenosine deaminase in a young patient in this region is tuberculosis until proved otherwise.

• An occupational history taken properly can be the single most valuable part of this consultation, and it must cover the whole working life.

Questions you should be able to answer:

• State Light’s criteria and explain the one situation in which they mislead.

• The pleural fluid pH is 7.05 after a pneumonia. What do you do, and why does the pH matter?

• List five causes of a lymphocytic exudative effusion.

• You drain 2.5 litres and the patient becomes acutely breathless. What has happened?

• Cytology is negative twice but you still suspect mesothelioma. What is your next investigation?

Case 7 · Lung Cancer

1. Focused History

Local invasion — each symptom localises the tumour

Metastatic and paraneoplastic disease

• Metastases: bone pain, headache, seizure or focal neurological deficit, jaundice or right upper quadrant pain, skin nodules.

So the biochemistry hints at the histology before the biopsy does. Hyponatraemia points towards small cell disease; hypercalcaemia towards squamous.

Risk and context

• Smoking quantified in pack-years, including waterpipe, and second-hand exposure. Asbestos with its decades of latency, radon, silica, arsenic, chromium, diesel exhaust, and biomass cooking smoke and heavy incense use, which are relevant exposures here.

• Previous thoracic radiotherapy, chronic obstructive pulmonary disease, pulmonary fibrosis, human immunodeficiency virus, and family history.

• Performance status, comorbidity and current lung function — these determine what treatment is possible at least as much as the stage does. And ask, early and gently, what the patient understands and wants to know.

2. Physical Examination

• Cachexia; clubbing and hypertrophic pulmonary osteoarthropathy; tar staining; hoarseness; Horner syndrome and wasting of the thenar and interosseous muscles.

• Cervical and supraclavicular nodes — a palpable supraclavicular node is often the easiest route to tissue and should be sought before anything invasive is planned.

• Tracheal position; signs of collapse, consolidation or effusion; signs of superior vena caval obstruction.

• Liver edge, bone tenderness, skin nodules, and a full neurological examination.

3. Investigations

• Chest radiograph: mass, hilar enlargement, lobar collapse, effusion, bony lesion, elevated hemidiaphragm. Then contrast-enhanced computed tomography of the chest, abdomen and pelvis, which must include the adrenals and liver.

• Positron emission tomography with computed tomography for staging in anyone being considered for treatment with curative intent, and magnetic resonance imaging of the brain where indicated.

• Tissue is essential, and the route depends on the location: bronchoscopy with endobronchial ultrasound and mediastinal nodal sampling for central lesions; computed tomography-guided biopsy for peripheral ones; pleural aspiration and biopsy; or biopsy of that supraclavicular node.

• Bloods: complete blood count, sodium, corrected calcium, liver function with alkaline phosphatase, lactate dehydrogenase, renal function.

• Before surgery: spirometry with gas transfer, and cardiopulmonary exercise assessment where lung function is marginal.

4. The Division That Determines Everything

5. Management

• Every case goes to a multidisciplinary team, and the decision turns on histology, molecular profile, stage, lung function and performance status together.

• Non-small cell: lobectomy for early disease with adequate reserve; stereotactic ablative radiotherapy for the medically inoperable; concurrent chemoradiotherapy for locally advanced disease; and for advanced disease, a targeted inhibitor where a driver mutation is present, or immunotherapy guided by PD-L1, with or without chemotherapy.

• Small cell: chemotherapy with thoracic radiotherapy in limited stage, chemoimmunotherapy in extensive stage.

6. Teaching Points and Viva Questions

• It is the change in the cough, not the cough, that matters.

• A normal chest radiograph does not exclude lung cancer.

• Hoarseness in a smoker with weight loss is nerve involvement, not laryngitis.

• Hyponatraemia suggests small cell; hypercalcaemia suggests squamous.

• Small cell versus non-small cell decides whether surgery is even on the table.

• Take enough tissue for molecular testing, or the patient may be denied the best treatment.

• Palliative care belongs at diagnosis, and it improves survival.

Questions you should be able to answer:

• What does his hoarseness tell you anatomically, and what does it imply about stage?

• His sodium is 122. What is the mechanism and which histology does it suggest?

• Which single physical finding offers the easiest route to a diagnosis, and why does that matter?

• The biopsy confirms adenocarcinoma but there is insufficient tissue for molecular studies. What are the consequences?

• He develops mid-thoracic back pain and difficulty walking. What is your sequence of actions?

Case 8 · Pulmonary Hypertension

1. Think First — Five Groups, and the Group Decides the Treatment

2. Focused History

• Breathlessness on exertion is the earliest and often the only symptom. Then fatigue, exertional chest pain, presyncope and syncope, palpitations, and finally ankle swelling and abdominal distension as the right ventricle fails.

• Hoarseness from compression of the left recurrent laryngeal nerve by a dilated pulmonary artery.

• Screen for each group by history: cardiac symptoms and hypertension; known lung disease, smoking, snoring and daytime somnolence, altitude of residence; previous deep vein thrombosis or pulmonary embolism; Raynaud phenomenon, skin tightening and reflux for systemic sclerosis; liver disease; congenital heart disease and murmurs in childhood; appetite suppressant or stimulant use; freshwater exposure in a schistosomiasis-endemic area; sickle cell disease or thalassaemia.

• Family history — heritable disease is autosomal dominant with incomplete penetrance.

• Pregnancy plans and contraception, which must be discussed at the first consultation for the reason given below.

3. Physical Examination

• Then examine for the cause: sclerodactyly, telangiectasia, calcinosis and Raynaud changes; fine crackles of fibrosis; clubbing; stigmata of chronic liver disease; central cyanosis and shunt murmurs; body habitus and neck circumference.

4. Investigations

• Echocardiography is the screening test — right ventricular size and function, estimated pulmonary artery pressure, tricuspid regurgitation, and exclusion of left heart disease and intracardiac shunts.

• Right heart catheterisation is required to confirm the diagnosis and is mandatory before any targeted therapy is started. Pre-capillary disease is defined by a mean pulmonary artery pressure above 20 mmHg with a raised pulmonary vascular resistance and a normal wedge pressure — the wedge is what separates group 1 from group 2, and it cannot be inferred from an echocardiogram.

• Electrocardiogram — right axis deviation, right ventricular hypertrophy, P pulmonale, right bundle branch block. Chest radiograph — enlarged central pulmonary arteries with pruned peripheral vessels and right ventricular enlargement.

• The rest of the workup: pulmonary function tests with gas transfer; high-resolution computed tomography; overnight oximetry or sleep study; autoimmune screen; human immunodeficiency virus test; liver function and abdominal ultrasound; schistosomiasis serology where exposure is plausible; and genetic testing where the history suggests heritable disease.

• For risk stratification and follow-up: functional class, six-minute walk distance, and N-terminal pro-B-type natriuretic peptide. Risk category, reassessed at every visit, drives escalation of therapy.

5. Management

• Refer to a specialist pulmonary hypertension centre. The diagnosis requires catheterisation and the targeted drugs require specialist prescribing and monitoring; this is not a condition to manage alone.

• Group 4: refer for assessment for pulmonary endarterectomy, which may be curative; lifelong anticoagulation; balloon pulmonary angioplasty and riociguat for inoperable disease.

• Group 1 targeted therapy: endothelin receptor antagonists, phosphodiesterase-5 inhibitors, riociguat and prostacyclin pathway agents. Most patients now start on combination therapy, escalated according to risk. Calcium channel blockers are used only in the small minority shown to be vasoreactive at catheterisation — given empirically they cause harm.

• Supportive care: diuretics for right heart failure, oxygen for hypoxaemia, iron replacement, supervised exercise rehabilitation, vaccination, and caution with anaesthesia — these patients tolerate hypotension and hypoxia very badly, and the anaesthetist must be told.

• Lung transplantation for disease refractory to maximal therapy, referred before the patient becomes too unwell to be a candidate.

6. Teaching Points and Viva Questions

• Progressive breathlessness with a clear chest and a loud pulmonary second sound: request an echocardiogram.

• All the signs are right-sided, which is why the chest sounds normal.

• Exertional syncope means the right ventricle cannot increase output — an ominous sign.

• Catheterisation confirms the diagnosis, and the wedge pressure assigns the group.

• Ventilation–perfusion scan, not computed tomography, to find the curable group.

• Do not give pulmonary vasodilators for left heart disease.

• Raise contraception at the first visit.

Questions you should be able to answer:

• Why is her chest clear, and why does that make the diagnosis rather than exclude it?

• What does the normal wedge pressure tell you, and what would a raised one have meant?

• Which imaging do you use to exclude chronic thromboembolic disease, and why not the other?

• A patient with heart failure and a preserved ejection fraction has pulmonary hypertension on echocardiography. Should you start sildenafil?

• She tells you she is hoping to start a family. What do you say?