Respiratory: Respiratory Emergencies (Complete)

• Overview: At a Glance | The Acutely Breathless Patient | Respiratory Failure and Blood Gases | Oxygen Therapy | NIV, CPAP and High-flow Oxygen
• Airways: Acute Asthma | COPD Exacerbation | Upper Airway Obstruction and Stridor | Anaphylaxis | Angioedema without Urticaria | Tracheostomy and Laryngectomy Emergencies
• Infection: Community-acquired Pneumonia | Hospital-acquired and Aspiration Pneumonia | Acute Chest Syndrome in Sickle Cell Disease
• Pleura: Tension Pneumothorax | Spontaneous Pneumothorax | Pleural Infection and Large Effusions
• Blood vessels and bleeding: Pulmonary Embolism | Massive Haemoptysis | Diffuse Alveolar Haemorrhage
• Other emergencies: Acute Pulmonary Oedema | ARDS | Neuromuscular Respiratory Failure | Opioids, Carbon Monoxide and Smoke
• Revision: Drug Reference Table | Spot the Emergency | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🫁 Respiratory emergencies are among the commonest reasons for urgent review on the ward and in the emergency department. Breathing problems can kill within minutes (a blocked airway, tension pneumothorax, anaphylaxis) or over hours (exhaustion in asthma, rising CO2 in COPD). This chapter is a practical guide to recognising them and acting in the first hour.
Your four questions for every patient: Is the airway safe? Is the patient tiring, or is the CO2 rising? What oxygen target is right for this person? What is the cause - and what is the ceiling of treatment?

At a Glance

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The Acutely Breathless Patient

ABCDE first. Look at the patient before the numbers:

• Airway: Can they speak? Stridor, gurgling, drooling or a hoarse voice suggest upper airway trouble.
• Breathing:
  • Respiratory rate - the most sensitive early sign of deterioration.
  • Work of breathing: accessory muscles, tripod position, inability to finish sentences.
  • SpO2, chest expansion, percussion, auscultation (wheeze, crackles, silent chest, absent breath sounds).
• Circulation: Heart rate, BP, perfusion, JVP, leg swelling.
• Disability: Drowsiness or confusion may mean hypoxia or rising CO2. Check pupils (opioids) and glucose.
• Exposure: Rash (anaphylaxis, meningococcal), calves (DVT), temperature.

Early tests:

• Arterial blood gas if SpO2 is low, the patient is drowsy, or CO2 retention is possible.
• Chest X-ray; ECG.
• Bloods: FBC, CRP, U&E, lactate; troponin and NT-proBNP if cardiac causes are possible; D-dimer only when PE is clinically unlikely.
• Peak flow in asthma (if the patient is able).
• Point-of-care ultrasound if trained: B-lines (pulmonary oedema), effusion, absent lung sliding (pneumothorax), dilated RV (PE).

Use NEWS2 to track deterioration. Use the SpO2 Scale 2 only for patients with confirmed hypercapnic respiratory failure and a prescribed target of 88–92%.

💡 Clinical Pearl: A normal SpO2 on high-flow oxygen does not mean the patient is safe. A patient who is drowsy, exhausted or "settling" with a rising CO2 may be about to arrest - check a blood gas and call for help.

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Respiratory Failure and Blood Gases

Respiratory failure means the lungs cannot keep blood oxygen up or CO2 down.

• Type 1 (hypoxaemic): PaO2 below 8 kPa with normal or low PaCO2. The problem is gas exchange - pneumonia, pulmonary oedema, PE, ARDS, asthma (early), pneumothorax.
• Type 2 (hypercapnic): PaCO2 above about 6.0–6.5 kPa (usually with low PaO2). The problem is not enough ventilation - COPD, exhaustion in severe asthma, obesity hypoventilation, neuromuscular disease, chest wall deformity, opioids and sedatives.

Reading a blood gas - four steps:

• 1. Oxygenation: Is the PaO2 low? Compare it with the inspired oxygen - roughly, the PaO2 in kPa should be about 10 less than the inspired oxygen percentage. A PaO2 of 12 kPa on 60% oxygen is a big gas exchange problem.
• 2. pH: Acidaemia (below 7.35) or alkalaemia (above 7.45)?
• 3. PaCO2 (normal 4.7–6.0 kPa): High CO2 with low pH is respiratory acidosis.
• 4. Bicarbonate (normal 22–26 mmol/L):
  • Acute type 2 failure: pH low, bicarbonate normal.
  • Chronic type 2 failure: pH near normal, bicarbonate high (the kidneys have compensated).
  • Acute-on-chronic: pH low despite a raised bicarbonate - the typical COPD exacerbation.

Also look at: Lactate, glucose, potassium, haemoglobin and carboxyhaemoglobin on the gas analyser.

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Oxygen Therapy

Oxygen is a drug. It must be prescribed with a target saturation range (BTS emergency oxygen guideline).

• Most acutely ill patients: Target 94–98%.
• At risk of hypercapnic respiratory failure: Target 88–92% until a blood gas is available. This includes:
  • COPD.
  • Severe obesity (obesity hypoventilation).
  • Neuromuscular disease and chest wall deformity.
  • Cystic fibrosis and bronchiectasis with previous CO2 retention.
• Critically ill (cardiac arrest, shock, sepsis, major trauma, anaphylaxis, CO poisoning): Start with 15 L/minute via a reservoir (non-rebreathe) mask, then titrate once stable.
• No oxygen needed if saturations are already in the target range - including uncomplicated MI and stroke.

Devices:

⚠️ Safety Pearl: Pulse oximeters can overestimate oxygen saturation in people with darker skin, and read falsely normal in carbon monoxide poisoning. If the clinical picture does not fit, check an arterial blood gas.

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NIV, CPAP and High-flow Oxygen

Non-invasive ventilation (NIV, "BiPAP") - two pressures through a tight mask: a higher inspiratory pressure (IPAP) that blows off CO2, and a lower expiratory pressure (EPAP) that keeps airways open.

• Main indication: Acute hypercapnic respiratory failure - pH below 7.35 and PaCO2 above 6.5 kPa that persist despite optimal medical treatment (BTS/ICS). Typically COPD, obesity hypoventilation, neuromuscular disease, chest wall deformity.
• Before starting: Agree and document the ceiling of treatment - is the patient for intubation if NIV fails?
• Typical settings: Start with IPAP about 15 cmH2O and EPAP 3–5 cmH2O. Increase IPAP to 20–30 cmH2O over 10–30 minutes as tolerated. Entrain oxygen to 88–92%.
• Monitoring: Blood gas at 1 hour and at 4 hours. No improvement in pH and PaCO2 means NIV is failing - escalate (or move to palliative care if that is the agreed ceiling).
• Contraindications and cautions:
  • Undrained pneumothorax.
  • Inability to protect the airway, vomiting, copious secretions.
  • Facial trauma or burns.
  • Recent upper GI surgery.
  • Severe shock.
• Not routinely used in asthma - intubation is safer if a patient with asthma is tiring.

CPAP (a single continuous pressure, usually 5–10 cmH2O): Keeps alveoli open and improves oxygenation. Used for type 1 failure - especially cardiogenic pulmonary oedema and some pneumonias. It does not directly remove CO2.

High-flow nasal oxygen (HFNO): Warmed, humidified oxygen at up to 60 L/minute.

• Delivers precise oxygen with a small amount of positive pressure.
• Comfortable - the patient can eat and talk.
• Useful in type 1 failure and after extubation.
• It can hide deterioration - set clear escalation criteria and review regularly.

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Acute Asthma

Mechanism: Airway inflammation, bronchospasm and mucus plugging narrow the airways. Air is trapped, the work of breathing soars, and the patient eventually tires. A rising or "normal" CO2 in acute asthma means exhaustion - a sign of life-threatening disease.

Severity (BTS/NICE/SIGN):

• Moderate: Increasing symptoms; PEF above 50–75% of best or predicted; no features of acute severe asthma.
• Acute severe - any one of:
  • PEF 33–50% of best or predicted.
  • Respiratory rate 25 or more.
  • Heart rate 110 or more.
  • Unable to complete sentences in one breath.
• Life-threatening - any one of:
  • PEF below 33%.
  • SpO2 below 92%, PaO2 below 8 kPa.
  • "Normal" PaCO2 (4.6–6.0 kPa).
  • Silent chest, cyanosis, poor respiratory effort.
  • Arrhythmia, hypotension.
  • Exhaustion, altered consciousness.
• Near-fatal: Raised PaCO2 and/or needing mechanical ventilation.

Management in hospital:

• Oxygen to SpO2 94–98%.
• Salbutamol 5 mg nebulised (oxygen-driven). Repeat every 15–30 minutes, or give continuously (5–10 mg/hour) if not improving.
• Ipratropium bromide 0.5 mg nebulised 4–6-hourly in acute severe or life-threatening asthma.
• Steroids: Prednisolone 40–50 mg orally (or hydrocortisone 100 mg IV 6-hourly if unable to swallow). Continue for at least 5 days.
• Magnesium sulfate 1.2–2 g IV over 20 minutes for life-threatening asthma, or acute severe asthma not responding to initial treatment.
• Senior decision only: IV aminophylline (omit the loading dose if already on oral theophylline; monitor levels) or IV salbutamol.
• No sedatives. Chest X-ray if pneumothorax or consolidation is suspected, or if ventilation is needed.
• Antibiotics: Not routinely - most exacerbations are viral.

ICU referral - transfer with a doctor able to intubate if there is:

• Deteriorating PEF.
• Persistent or worsening hypoxia, or hypercapnia.
• Exhaustion, drowsiness or confusion.
• Poor respiratory effort or respiratory arrest.

Discharge:

• PEF above 75% of best, with low diurnal variability.
• Stable on discharge medication for 12–24 hours; inhaler technique checked.
• Prednisolone to complete at least 5 days, plus inhaled steroid.
• Written asthma action plan.
• GP review within 2 working days; respiratory clinic within 4 weeks.

⚠️ Safety Pearl: A quiet chest in severe asthma is not improvement - it means almost no air is moving. Drowsiness, a silent chest or a normal CO2 in a breathless asthmatic needs ICU now.

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COPD Exacerbation

Mechanism: A sustained worsening of breathlessness, cough or sputum, usually triggered by a viral or bacterial infection or pollution. Worsening airflow obstruction and air trapping increase the work of breathing. Tired breathing muscles let CO2 rise.

Assessment:

• Exclude pneumonia, pneumothorax, PE, heart failure and arrhythmia.
• ABG on arrival and after any oxygen change.
• Chest X-ray, ECG, FBC, U&E, CRP.
• Sputum culture if purulent.

Management:

• Controlled oxygen - target 88–92% via a 24% or 28% Venturi mask. Repeat the blood gas within 30–60 minutes.
• Nebulised bronchodilators: Salbutamol 2.5–5 mg and ipratropium 0.5 mg. If hypercapnic, drive the nebuliser with air, with nasal oxygen alongside.
• Prednisolone 30 mg daily for 5 days (NICE NG115).
• Antibiotics if sputum is purulent or there are signs of pneumonia (NICE NG114): e.g. amoxicillin, doxycycline or clarithromycin orally for 5 days; IV options if severe.
• NIV if pH below 7.35 and PaCO2 above 6.5 kPa persist despite these measures.
• Escalation plan: Decide early - and with the patient where possible - whether intubation and ICU are appropriate if NIV fails.
• Recovery:
  • Check inhaler technique.
  • Smoking cessation.
  • Pulmonary rehabilitation referral.
  • Review maintenance treatment.
  • Follow-up within 2 weeks.
  • Consider palliative care input in advanced disease.

💡 Clinical Pearl: In a COPD patient, high-flow oxygen can push the CO2 up and the pH down, causing drowsiness and respiratory arrest. But never withhold oxygen from a hypoxic patient - titrate to 88–92% and check the gas.

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Upper Airway Obstruction and Stridor

Stridor is a harsh, high-pitched noise from turbulent airflow through a narrowed upper airway. Inspiratory stridor suggests an obstruction at or above the larynx. It is a sign of severe narrowing - the airway may close completely without warning.

Causes:

• Anaphylaxis and angioedema.
• Infection: Supraglottitis (epiglottitis), deep neck space infection (quinsy, retropharyngeal abscess, Ludwig's angina), bacterial tracheitis.
• Foreign body - choking.
• Tumour - laryngeal, thyroid, mediastinal.
• Bleeding - neck haematoma after thyroid or carotid surgery.
• Burns and inhalation injury - soot, singed nasal hair, hoarse voice.
• Trauma; bilateral vocal cord palsy; laryngospasm.

Clinical pattern: Stridor, hoarse or muffled ("hot potato") voice, drooling, difficulty swallowing, tripod posture, anxiety, rising breathing effort.

Management:

• Call anaesthetics and ENT immediately - this is a potential difficult airway.
• Keep the patient sitting up, in the position they find most comfortable. Do not lie them flat or send them away for scans unaccompanied.
• High-flow oxygen.
• Nebulised adrenaline (e.g. 1 mg/mL, up to 5 mL nebulised) for temporary relief of airway swelling.
• Dexamethasone IV (e.g. 6.6–8 mg) for inflammatory swelling.
• Treat the cause:
  • IM adrenaline for anaphylaxis.
  • IV antibiotics (e.g. ceftriaxone) for supraglottitis.
  • Drainage for abscesses.
• Heliox (helium-oxygen) can reduce turbulent flow as a temporary bridge.
• Definitive airway in theatre if needed (awake fibreoptic intubation, or a surgical airway).

Choking (RCUK):

• Encourage coughing.
• If the cough becomes ineffective: up to 5 back blows, then up to 5 abdominal thrusts; repeat.
• If the patient becomes unconscious: start CPR.

Neck haematoma after thyroid surgery (DAS guidance) - remember "SCOOP":

• Skin exposure.
• Cut sutures.
• Open skin.
• Open muscles.
• Pack the wound.

This releases pressure on the airway at the bedside - do it immediately if the patient has stridor.

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Anaphylaxis

Mechanism: A severe, life-threatening, generalised hypersensitivity reaction. Mast cells release histamine and other mediators, causing airway swelling, bronchospasm, vasodilatation and capillary leak.

Common triggers:

• Drugs - antibiotics, NSAIDs, neuromuscular blockers, contrast.
• Foods - peanuts, tree nuts, shellfish.
• Insect stings.
• Latex.

Recognition (RCUK): Sudden onset and rapid progression of:

• Airway problems - swelling, hoarseness, stridor; and/or
• Breathing problems - wheeze, breathlessness, hypoxia; and/or
• Circulation problems - hypotension, collapse, tachycardia.

Skin or mucosal changes (urticaria, flushing, angioedema) are usually present, but are absent in up to 1 in 5.

Management (RCUK 2021):

• Remove the trigger (stop the infusion); call for help; lie flat with legs raised - or sit up if breathing is difficult.
• Adrenaline 500 micrograms IM (0.5 mL of 1 mg/mL, 1:1,000) into the anterolateral thigh. Repeat after 5 minutes if not improving.
• High-flow oxygen.
• IV fluid bolus (e.g. 500–1,000 mL crystalloid) for hypotension.
• Refractory anaphylaxis (no improvement after 2 IM doses): Start a low-dose IV adrenaline infusion with expert (critical care) help. Do not give IV adrenaline boluses unless experienced.
• Antihistamines and steroids are not first-line emergency treatment. A non-sedating oral antihistamine can help skin symptoms once stable.
• Mast cell tryptase: Take samples as soon as possible after treatment, at 1–2 hours, and at 24 hours or more (baseline).

After the event:

• Observation - duration depends on severity and response (RCUK). Longer if two or more doses of adrenaline were needed or if there is a risk of a biphasic reaction.
• Prescribe two adrenaline auto-injectors and train the patient to use them.
• Refer to an allergy clinic (NICE CG134).
• Report suspected drug reactions (Yellow Card).

⚠️ Safety Pearl: IM adrenaline is the treatment for anaphylaxis - give it early and repeat it. Delaying adrenaline to give chlorphenamine and hydrocortisone is a common and dangerous mistake.

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Angioedema without Urticaria

Mechanism: Swelling of the lips, tongue, face, throat or gut caused by bradykinin rather than histamine. Because it is not histamine-driven, it responds poorly to adrenaline, antihistamines and steroids, and comes on more slowly (hours). There is no urticaria or itch.

Causes:

• ACE inhibitors - the commonest. It can start years after starting the drug.
• Hereditary angioedema - C1-esterase inhibitor deficiency or dysfunction; family history, recurrent episodes, abdominal attacks; low C4.
• Acquired C1-inhibitor deficiency - lymphoma, autoimmune disease.
• Other drugs - gliptins, sacubitril/valsartan, tPA (alteplase).

Management:

• Airway assessment - tongue and floor-of-mouth swelling can obstruct the airway. Involve anaesthetics and ENT early.
• Stop the ACE inhibitor permanently - record it as an adverse reaction.
• Adrenaline can be tried, especially if anaphylaxis cannot be excluded.
• Specific treatment (specialist): C1-esterase inhibitor concentrate or icatibant (bradykinin receptor blocker) for hereditary angioedema. These are sometimes used off-label for severe ACE inhibitor angioedema. Fresh frozen plasma if neither is available.
• Check C4 and C1-inhibitor levels if hereditary or acquired angioedema is suspected.

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Tracheostomy and Laryngectomy Emergencies

Know which you are dealing with - check the bedhead sign:

• Tracheostomy: The upper airway is still connected to the lungs. You may be able to oxygenate via the mouth and nose as well as the stoma.
• Laryngectomy: The trachea has been brought out to the neck, and there is no connection between the mouth and the lungs. Oxygenate and ventilate via the stoma only.

Blocked or displaced tracheostomy (National Tracheostomy Safety Project):

• Call for help - anaesthetics and ENT.
• Apply high-flow oxygen to both the face and the stoma (unless laryngectomy).
• Use waveform capnography to check airflow.
• Check patency:
  • Remove any speaking valve or cap.
  • Remove the inner tube - many blockages are in the inner tube.
  • Try to pass a suction catheter.
• If the catheter will not pass: deflate the cuff.
• If still not breathing or no improvement: remove the tracheostomy tube. Then oxygenate via the face or the stoma. If not breathing, start CPR and ventilate via the mouth (covering the stoma) or via the stoma.
• Secondary steps (experienced staff): Oral intubation, or intubation via the stoma.

Bleeding from a tracheostomy: Minor bleeding is common. Major bleeding a few days to weeks after insertion may be a tracheo-innominate artery fistula - over-inflate the cuff, apply pressure, and call surgeons immediately.

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Community-acquired Pneumonia

Mechanism: Infection of the alveoli, which fill with pus and fluid. The usual organisms are:

• Streptococcus pneumoniae - the commonest.
• Haemophilus influenzae.
• Atypical organisms: Mycoplasma, Legionella, Chlamydophila.
• Staphylococcus aureus - especially after influenza.
• Viruses: Influenza, SARS-CoV-2, RSV.

Clinical pattern: Cough, fever, breathlessness, pleuritic pain; crackles or bronchial breathing. Older people may present with confusion or falls only.

Severity (NICE NG250) - CURB-65, one point each:

• Confusion (new).
• Urea above 7 mmol/L.
• Respiratory rate 30 or more.
• Blood pressure: systolic below 90 or diastolic 60 or less.
• Age 65 or over.

Score 0–1 is low risk (below 3% mortality); 2 is intermediate (3–15%); 3–5 is high (above 15%). Use clinical judgement too - very low saturations, pleural complications or frailty raise the risk whatever the score.

Timing: Confirm the diagnosis (including chest X-ray) and start antibiotics within 4 hours of presentation - sooner (within 1 hour) if the patient has sepsis.

Investigations (moderate or high severity):

• Blood cultures if sepsis is suspected.
• Sputum culture.
• Pneumococcal urinary antigen.
• Legionella urinary antigen if there are risk factors (travel, hotels, air conditioning, outbreaks).
• Viral PCR in season.
• CRP baseline.

Antibiotics (NICE NG250, adults; usually a 5-day course):

• Use erythromycin instead of clarithromycin in pregnancy.
• Review IV antibiotics by 48 hours and switch to oral when possible.
• Severe pneumonia: NICE NG250 suggests considering corticosteroids (IV hydrocortisone first). Note the MHRA warning about combining fluoroquinolones with steroids (tendon rupture).
• Influenza in season: Antivirals (e.g. oseltamivir) for hospitalised patients.

Do not discharge if, in the past 24 hours, there are two or more of:

• Temperature above 37.5°C.
• Respiratory rate 24 or more.
• Heart rate above 100.
• Systolic BP 90 or below.
• SpO2 below 90% on air.
• Abnormal mental state.
• Unable to eat without help.

Complications:

• Sepsis and AKI.
• Respiratory failure and ARDS.
• Parapneumonic effusion and empyema - suspect with persistent fever or a non-falling CRP.
• Lung abscess.
• AF.

Follow-up: A repeat chest X-ray at about 6 weeks for people at risk of lung cancer (e.g. smokers over 50) or with persisting symptoms.

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Hospital-acquired and Aspiration Pneumonia

Hospital-acquired pneumonia (HAP): Onset 48 hours or more after admission. Gram-negative organisms (Pseudomonas, Klebsiella, E. coli) and MRSA are more likely.

• Send a microbiology sample before antibiotics, and start antibiotics within 4 hours of suspicion.
• Non-severe, low resistance risk: e.g. co-amoxiclav orally (NICE NG250); alternatives include doxycycline or co-trimoxazole.
• Severe or higher risk of resistance (e.g. recent antibiotics, ICU, known resistant organisms): IV piperacillin-tazobactam, a cephalosporin or meropenem, guided by local microbiology.
• MRSA suspected: Add vancomycin or teicoplanin.
• Review at 5 days and stop if stable.

Aspiration:

• Aspiration pneumonitis: Chemical injury from stomach contents. Abrupt breathlessness and hypoxia within hours of vomiting or a seizure. Often does not need antibiotics at first - supportive care.
• Aspiration pneumonia: Infection from inhaled mouth organisms - in people with swallowing problems, reduced consciousness, alcohol excess, stroke or dementia. Typically affects the right lower lobe (or the posterior segments if lying down). Treat as CAP or HAP according to setting; routine extra anaerobic cover is not usually needed.
• Prevention:
  • Swallow assessment (speech and language therapy).
  • Sit upright for meals.
  • Oral care.
  • Review sedating drugs.
• Recurrent aspiration in frailty or dementia: Discuss goals of care and "eating and drinking with acknowledged risks".

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Acute Chest Syndrome in Sickle Cell Disease

Definition: A new infiltrate on chest X-ray in a person with sickle cell disease, plus one or more of:

• Chest pain.
• Fever.
• Tachypnoea or wheeze.
• Cough.
• Hypoxia.

It is a leading cause of death in sickle cell disease. It often develops during a painful crisis.

Triggers: Infection (including atypical organisms), fat embolism from bone marrow infarction, and hypoventilation from rib pain or opioids.

Management:

• Urgent haematology involvement; HDU or ICU if deteriorating.
• Oxygen to keep SpO2 at 95% or more (or at the patient's baseline).
• Analgesia - enough to allow deep breathing, but watch for opioid-induced hypoventilation.
• Incentive spirometry.
• Careful IV fluids (avoid overload).
• Antibiotics covering typical and atypical organisms (e.g. a cephalosporin plus a macrolide).
• Blood transfusion: Top-up or exchange transfusion for severe or worsening disease (falling saturations, multilobar involvement).

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Tension Pneumothorax

Mechanism: Air enters the pleural space with each breath but cannot escape (a one-way valve). Pressure builds, the lung collapses, the mediastinum is pushed across, and venous return to the heart falls - causing shock and cardiac arrest.

Who: Trauma; ventilated patients (including NIV); after central line insertion or other procedures; occasionally spontaneous.

Clinical pattern:

• Severe, rapidly worsening breathlessness and hypoxia.
• Tachycardia and hypotension; raised JVP.
• Absent breath sounds and hyper-resonance on the affected side.
• Tracheal deviation away from the affected side - a late sign.
• Ventilated patients: Rising airway pressures, falling saturations, hypotension.

Management - a clinical diagnosis; do not wait for an X-ray:

• High-flow oxygen.
• Needle decompression with a large cannula (14G):
  • In the 4th or 5th intercostal space just anterior to the mid-axillary line (preferred in adults - the chest wall is thinner), or
  • The 2nd intercostal space in the mid-clavicular line.
• Finger thoracostomy (in trauma or ventilated patients, by trained staff) is more reliable.
• Then insert a chest drain - needle decompression is only temporary, and cannulas can kink or dislodge.

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Spontaneous Pneumothorax

• Primary spontaneous pneumothorax (PSP): No known lung disease. Typically tall, thin young men; smoking (including cannabis) greatly increases the risk.
• Secondary spontaneous pneumothorax (SSP): Underlying lung disease - COPD, asthma, cystic fibrosis, interstitial lung disease, TB, Pneumocystis pneumonia, cancer. Patients are less able to tolerate it, so it is more dangerous.

Clinical pattern: Sudden pleuritic chest pain and breathlessness. There may be reduced breath sounds and hyper-resonance, but small pneumothoraces can be silent. Confirm with chest X-ray (or CT or ultrasound).

BTS 2023 approach: Management is now guided by symptoms and patient priorities, not just size.

• Look for high-risk features:
  • Haemodynamic instability.
  • Significant hypoxia.
  • Bilateral pneumothorax.
  • Underlying lung disease.
  • Age 50 or over with a significant smoking history.
  • Haemothorax.
  These patients usually need a chest drain and admission.
• PSP with minimal symptoms and no high-risk features: Conservative management can be considered whatever the size, with clear safety-netting and follow-up.
• PSP with symptoms: After discussion with the patient:
  • Needle aspiration.
  • An ambulatory device (allows outpatient care).
  • A chest drain.
• SSP: Usually admission and a chest drain. Needle aspiration or an ambulatory device may be suitable for selected patients.
• Chest drain technique:
  • Small-bore (Seldinger), inserted in the "triangle of safety" - the lateral edge of pectoralis major, the anterior edge of latissimus dorsi, and the 5th intercostal space.
  • Use ultrasound guidance where fluid is present.
  • Do not clamp a bubbling drain.
• Persistent air leak or recurrence: Refer to thoracic surgery (pleurodesis or bullectomy). Surgery is also offered after a first pneumothorax in high-risk occupations (e.g. pilots, divers).

Discharge advice:

• Stop smoking - this greatly reduces recurrence.
• Do not fly until the pneumothorax has fully resolved on imaging (and usually for 1–2 weeks after).
• Avoid diving permanently, unless definitive surgery has been done.
• Return immediately if breathlessness worsens.

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Pleural Infection and Large Effusions

Pleural infection (complicated parapneumonic effusion or empyema): Infection spreads from pneumonia into the pleural fluid, which may become loculated and full of pus.

• Suspect it when pneumonia does not settle - persistent fever, rising or non-falling CRP, new effusion.
• Ultrasound-guided pleural aspiration for:
  • Appearance (pus?).
  • pH (use a blood gas analyser).
  • Glucose, LDH, protein.
  • Gram stain and culture.
• Drain it (small-bore chest drain) if there is:
  • Frank pus.
  • Organisms on Gram stain or culture.
  • Pleural fluid pH below 7.2 in a suspected infected effusion.
• Antibiotics: Cover the pneumonia organisms plus anaerobes (e.g. co-amoxiclav, or per local guidance). Courses are typically several weeks.
• If the collection persists: Intrapleural tPA plus DNase (MIST2). Thoracic surgery (VATS) if this fails.
• Prognosis: The RAPID score (Renal, Age, Purulence, Infection source, Dietary factors) helps predict outcome.

Large effusion causing breathlessness:

• Therapeutic aspiration relieves symptoms. Remove no more than about 1.5 L at once, and stop if the patient develops chest tightness or coughing (re-expansion pulmonary oedema).
• A massive effusion with mediastinal shift can compromise breathing and circulation - urgent drainage.
• Recurrent malignant effusions: Indwelling pleural catheter or talc pleurodesis.
• Haemothorax (after trauma or procedures): Large-bore drain and surgical review.

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Pulmonary Embolism

Mechanism: A blood clot, usually from the leg or pelvic veins, lodges in the pulmonary arteries. Small clots cause pleuritic pain and breathlessness. Large clots strain the right ventricle and cause shock.

Risk factors:

• Recent surgery or immobility.
• Cancer.
• Previous VTE.
• Pregnancy and the postpartum period.
• Oestrogen (COCP, HRT).
• Thrombophilia.
• Long-haul travel.
• Obesity.

Clinical pattern: Breathlessness, pleuritic pain, haemoptysis, syncope; tachycardia, tachypnoea, hypoxia, signs of DVT. It can be subtle - the chest X-ray is often normal.

Diagnosis (NICE NG158):

• Calculate the two-level Wells score.
• PE likely (Wells above 4): CTPA immediately. If it is delayed, start interim anticoagulation.
• PE unlikely (Wells 4 or less): D-dimer. If positive, CTPA; if negative, PE is excluded.
• PERC rule: Can be used to avoid testing in low-risk patients. All criteria must be met:
  • Age under 50.
  • Heart rate below 100.
  • SpO2 95% or more.
  • No haemoptysis.
  • No oestrogen use.
  • No previous VTE.
  • No unilateral leg swelling.
  • No recent surgery or trauma.
• Renal impairment or contrast allergy: V/Q scan.
• Pregnancy: Leg ultrasound first if there are leg symptoms; then V/Q or CTPA after discussion. Treat with LMWH while waiting.

Treatment:

• Anticoagulation: Usually a DOAC:
  • Apixaban 10 mg twice daily for 7 days, then 5 mg twice daily.
  • Rivaroxaban 15 mg twice daily for 21 days, then 20 mg once daily.
• Exceptions:
  • LMWH for pregnancy.
  • Warfarin for antiphospholipid syndrome.
  • Severe renal impairment - LMWH, unfractionated heparin or warfarin.
• Outpatient treatment for low-risk patients (e.g. PESI class I–II, or Hestia criteria) with good follow-up.
• High-risk (shocked) PE: Thrombolysis - see the Cardiac Emergencies chapter.
• Duration: At least 3 months. Longer for unprovoked PE or ongoing risk factors, balancing bleeding risk.
• Unprovoked PE: History, examination and basic tests for cancer. Do not routinely do extensive cancer screening or thrombophilia testing.