• Classically cough (productive or non-productive), fever, breathlessness, chest pain, abnormal CXR. There may be prodromal symptoms of coryza, headache, and muscle aches.
• The aetiological agent cannot be predicted from the clinical features (see Box 2.1).
• Immunocompromised patients may present with agitation, fever, tachypnoea, and routine oximetry readings. CXR abnormalities may be subtle.
• Patients with right-sided endocarditis (e.g. IV drug users) may present with haemoptysis, fever, and patchy consolidation ± cavitation.
• Severity assessment is the key to deciding the site of care (i.e. home, medical ward, or critical care ward) and guiding general management and antibiotic treatment.
• CURB-65 score ≥3: high risk of mortality; should be admitted and managed as having severe pneumonia.
• CURB-65 score of 2: risk of mortality, need short-stay inpatient treatment or hospital-supervised outpatient treatment.
• CURB-65 score of 0–1: low risk of mortality, may be suitable for home treatment.
Reproduced from Thorax, 'Defining community acquired pneumonia severity on presenation to hospital: an international derivation and validation study', Lim WS, et al. 58: 377-82, copyright 2003, with permission from BMJ Publishing Group Ltd.
General resuscitation and investigations
• Check ‘ABC’ (airway, breathing, and circulation). Arrange for urgent CXR.
• Secure venous access: if there are signs of dehydration, start IV crystalloids; examine regularly for signs of fluid overload.
• Send bloods: FBC, U&Es, LFTs, CRP.
• Check ABG: correct hypoxia (PaO2 ≤10kPa) with O2, at least 35%. If hypoxia fails to correct, despite maximum inspired O2, or there is hypercapnia (PaCO2 ≥6kPa), the patient is likely to require ventilation. Patients in type 2 respiratory will require controlled O2 therapy. Involve ITU early to plan the patient’s care.
• Culture blood and sputum.
• Pain relief: paracetamol or an NSAID usually suffice. Morphine may be required; respiratory depression is unlikely to be a problem if PaCO2 is low or normal and it may be reversed with naloxone.
Indications for intensive care
• Patients with >2 components of CURB (Confusion, raised Urea, raised Respiratory rate, low BP; see Box 2.2) who do not respond rapidly.
• Persisting hypoxia with PaO2 <8kPa despite maximal O2 administration.
• Progressive hypercapnia (PaCO2 ≥6kPa), progressive exhaustion.
• Severe acidosis (pH <7.26).
• Shock, depressed consciousness.
• Involve ITU early—this may help avoid ventilation as an emergency.
British Thoracic Society, Community Acquired Pneumonia in Adults Guideline Group. Guidelines for the management of community acquired pneumonia in adults: update 2009. https://www.brit-thoracic.org.uk/document-library/clinical-information/pneumonia/adult-pneumonia/bts-guidelines-for-the-management-of-community-acquired-pneumonia-in-adults-2009-update/
All patients should have:
• ABGs (on air and O2).
• FBC, U&Es, LFTS, ESR, CRP.
• CXR (see Fig. 2.1).
• Blood cultures.
• Sputum culture, Gram stain, ZN stain (if suspicious of TB), cytology.
• Pleural fluid aspiration (if present) for microscopy, culture, and sensitivity (MC&S), protein, and pH.
• Pneumococcal antigen: urine, sputum, or blood.
• Serology (acute and convalescent).
• Cold agglutinins (Mycoplasma days 7–14).
• Urine for Legionella antigen, sputum for Legionella culture, and direct immunofluorescence.
Where appropriate, consider:
• Bronchoscopy [± bronchoalveolar lavage (BAL)] (if immunocompromised, or if fails to respond to first-line antibiotics and no organism identified).
• CTPA (to exclude infected pulmonary infarct).
• Transbronchial or open lung biopsy.
• Aspiration of pleural fluid for MC&S.
• Viral titres.
• For management key points, see Box 2.4.
• ‘Blind’ treatment should be started as soon as appropriate cultures have been sent (see Table 2.1). Modify therapy in light of subsequent investigations or positive cultures.
• Start on IV therapy (for at least 48h in patients with high CURB scores); adjust according to clinical condition and response (see Table 2.1).
• All patients should receive appropriate O2 therapy (aim SpO2 94–98%; 88–92% if known COPD/risk of hypercapnic respiratory failure).
• In patients with COPD or asthma, consider treatment with salbutamol (2.5–5mg nebulized q4–6h) to relieve bronchospasm. This may also ‘loosen secretions’ and improve mucociliary action.
• Continue IV fluids, as necessary, to keep the patient well hydrated.
• Prophylaxis for venous thromboembolism (VTE) with LMWH should be considered for all patients who are not fully mobile.
• Monitor response to therapy with:
• FBC, CRP.
• Pulse oximetry or ABGs.
• CXR at days 3–5 (sooner if deteriorating).
• Total duration of therapy usually 5–7 days (in low-risk patients), up to 10 days (in high-risk patients).
• Follow-up CXR 4–6 weeks after discharge mandatory to exclude an underlying endobronchial lesion.
• Patients should not be discharged if they have >1 of the following features of instability: temperature >37.8°C; pulse rate >100 bpm; RR >24/min; SBP <90mmHg; O2 saturation <90%; abnormal mental status; and inability to maintain oral intake.
Table 2.1 Empirical therapy for pneumonia
Community-acquired pneumonia (CAP)
Mild (CURB-65: 0–1)
Amoxicillin 500mg tds PO
or doxycycline 200mg loading dose, then 100mg daily
or clarithromycin 500mg bd
Moderate (CURB-65: 2)
Amoxicillin 500mg–1g tds plus clarithromycin or doxycycline*
Severe (CURB-65: 3–5)
Co-amoxiclav 1.2g tds plus clarithromycin 500mg bd IV
or cefuroxime/cefotaxime plus clarithromycin 500mg bd IV
Cefotaxime (or ceftazidime) ± metronidazole
Post-influenza pneumonia (S. aureus possible)
Cefuroxime (or amoxicillin + clarithromycin + flucloxacillin)
If MRSA isolated or suspected
Switch flucloxacillin to vancomycin
Cefuroxime + metronidazole or benzylpenicillin + gentamicin + metronidazole
Patient with risk factors for HIV and suspicion of PCP
As for CAP + high-dose IV co-trimoxazole
If intolerant of β-lactam or macrolide, use a fluoroquinolone with activity against S. pneumoniae (e.g. levofloxacin) or doxycycline (200mg, then 100mg od).
Choice of antibiotics
In severely ill patients, the history may point to a likely pathogen:
• COPD: S. pneumoniae, H. influenzae, M. catarrhalis.
• Alcoholism: S. pneumoniae, S. aureus, H. influenzae, Klebsiella, TB, anaerobes, Gram –ve bacteria.
• Recent ‘flu’: S. aureus, S. pneumoniae, H. influenzae.
• Risk of aspiration: anaerobes, Gram –ve bacteria.
• Contact with birds: Chlamydia psittaci.
• Haemoptysis: streptococci, S. aureus, lung abscess, necrotizing Gram –ve bacteria, invasive aspergillosis.
• Diarrhoea, abdominal pain: Legionella.
• Pharyngitis/otitis media: Mycoplasma, anaemia/cold agglutinins.
• Risk factors for HIV: S. pneumoniae, H. influenzae, CMV, Pneumocystis jiroveci (carinii) pneumonia (PCP), Cryptococcus.
• Hospital-acquired: Gram –ve bacteria, S. aureus.
• Neutropenia: Pseudomonas aeruginosa, Gram –ve bacteria, Aspergillus.
• Drug addicts: S. aureus, Candida.
• Nursing home patients: higher risk of aspiration—anaerobes, Gram –ve bacteria.
• Most patients can be adequately treated with oral antibiotics.
• Consider IV antibiotics if adverse prognostic features present ( Acute pneumonia: assessment, p. [link]).
In patients with a good history of penicillin allergy (anaphylaxis, urticaria). alternatives include erythromycin, clarithromycin, levofloxacin, and moxifloxacin (NB Ciprofloxacin is not very active against S. pneumoniae). Alternatives for flucloxacillin include vancomycin, teicoplanin, or rifampicin [consult the British National Formulary (BNF) for dosages].
Acute pneumonia: specific situations
• Either amoxicillin or cefuroxime plus clarithromycin to cover atypicals plus flucloxacillin if S. aureus is suspected.
• Penicillin allergy: cephalosporins are usually safe where there is a history of rashes with penicillin. If there is a history of anaphylaxis, consider clarithromycin as sole therapy, or if unwell, seek respiratory/microbiological advice.
• Risk factors include: seizures, reduced conscious level, stroke, dysphagia, periodontal disease, alcohol dependence, general anaesthesia, and nursing home residents. Always admit.
• Anaerobic bacteria and Gram –ve enteric bacilli may be more common.
• Clinical features include: wheeze and frothy non-purulent sputum (as soon as 2–4h after aspiration), tachypnoea, cyanosis, and respiratory distress.
• Gastric acid destroys alveoli, resulting in capillary permeability and pulmonary oedema. Haemorrhage is common. Severe necrotizing pneumonia may result.
• Treatment: cefuroxime + metronidazole or amoxicillin + metronidazole + gentamicin.
• Most likely organisms are enteric Gram –ve bacteria ± anaerobes.
• Patients with diabetes are more susceptible to bacteraemic pneumococcal pneumonia.
• Treatment: broad-spectrum cephalosporin (e.g. cefotaxime 2g tds IV) and metronidazole (500mg IV tds). If intubated for ≥48h, use anti-pseudomonal antibiotic (e.g. ceftazidime 2g tds; modify dose in renal failure).
Pneumonia in the immunocompromised
• All ‘routine’ pathogens are possible; other infections depend on the nature of immunosuppression. TB and atypical mycobacteria are more common.
• Since the introduction of combination antiretroviral treatment, opportunistic infections are less common and pulmonary Kaposi’s sarcoma or lymphoma are rarely seen. However, pulmonary opportunistic infection may be the first manifestation of HIV before it is diagnosed, the most common being Pneumocystis carinii. Fungal and viral (CMV) pneumonitis may also occur. Desaturation on exercise in the presence of a normal CXR or one with diffuse interstitial shadowing is highly suggestive of PCP.
• Recipients of organ transplants have depressed cell-mediated immunity due to anti-rejection immunosuppressive therapy. Additional pathogens to which they are susceptible include PCP, viruses [e.g. CMV, respiratory syncytial virus (RSV), influenza and parainfluenza, adenovirus], and fungi (Aspergillus and Candida spp.). CXR abnormalities tend not to be specific for the pathogen, and treatment should cover all possible pathogens.
• In general, early bronchoscopy and BAL are indicated for diagnosis; management should be discussed early with the respiratory/ID/microbiology team.
Community-acquired pneumonia that fails to respond
• Review the diagnosis (? PE, pulmonary oedema, pulmonary vasculitis, alveolar haemorrhage, cavitation, organizing pneumonia, eosinophilic pneumonia, bronchiectasis).
• Repeat CXR, and arrange for CT chest to look for cavitation or empyema. Refer to the respiratory team. Repeat culture of relevant specimens (e.g. sputum, blood). Consider possible resistant organism or underlying disease, e.g. bronchial carcinoma.
• Consider bronchoscopy to exclude TB, PCP, or an obstructing lesion.
• Review antibiotic dosages, and intensify (e.g. inadequate oral clarithromycin for Mycoplasma pneumonia).
Parapneumonic pleural effusion or empyema
• Parapneumonic pleural effusions develop in up to 50% of patients with bacterial pneumonia admitted to hospital.
• Image-guided diagnostic tap should be performed on all parapneumonic effusions to exclude an empyema. Send pleural fluid for MC&S, urgent Gram stain, and pH analysis.
• Empyema (visibly cloudy fluid, pus, or organisms on Gram stain) or a complicated parapneumonic effusion (visibly clear fluid with pH <7.2) should be removed with pleural space drainage under US guidance. Discuss with respiratory physicians.
• US may help look at the level of the effusion and demonstrate loculation with an empyema.
• If an empyema fails to resolve with pleural space drainage, arrange chest CT and discuss with cardiothoracic surgeons ( Indications for specialist referral, p. [link]).
Cavitation or abscess
Any severe pneumonia may cavitate, but particularly S. aureus, Klebsiella spp., TB, aspiration pneumonia, bronchial obstruction (foreign body, tumour), or PEs (thrombus or septic emboli, e.g. from DVT with superadded infection or tricuspid endocarditis; Right-sided endocarditis, p. [link]).
• Seek advice from the respiratory team. Most respond to appropriate antibiotics but may require a more prolonged course. Surgical drainage or CT-guided percutaneous aspiration may be necessary.
• ‘Blind’ treatment: cefuroxime 1.5g tds IV (or cefotaxime 2g tds IV) + flucloxacillin 1–2g qds IV + gentamicin loading dose (100–120mg IV), then 6–7mg/kg od (according to renal function and levels) ± metronidazole 500mg IV tds.
• Long-term antibiotics (4–6 weeks) likely to be required.
• Disease of young adults. Low-grade fever, dry cough, headache, and myalgia. Erythema multiforme may be seen in ~25%; ~5% have meningoencephalitis.
• Epidemics occur every 4 years in the UK.
• WCC is often normal; ESR is high; specific immunoglobulin M (IgM) is seen early, then levels decline. ~50% develop cold agglutinins (also seen in measles, EBV) which may cause haemolysis. CXR may show reticulonodular shadowing (lower lobe > upper lobe), which may take over 6 weeks to resolve (unlike bacterial pneumonia).
• Treatment is with erythromycin 500mg qds PO/IV, clarithromycin 500mg bd PO/IV, or tetracycline 500mg qds PO/IV.
• Illness of middle-aged men; more severe in smokers. Incubation 2–10 days, followed by high fever, rigors, headache, myalgia, dry cough, progressive respiratory distress, and confusion. Abdominal pain, diarrhoea, nausea and vomiting, and palpable hepatomegaly are seen in ~30%. Complications include pericarditis (± effusion), encephalopathy [cerebrospinal fluid (CSF) is usually normal], and rarely renal failure.
• Moderate leucocytosis (≤20 × 109/L, neutrophilia, lymphopenia), hyponatraemia, deranged LFTs, proteinuria, haematuria, and myoglobinuria. Diagnosis: rise in specific IgM and immunoglobulin G (IgG) titres (urine, blood, sputum).
• Worth sending urine for urinary Legionella antigen.
• CXR may show anything from diffuse patchy infiltrates to lobar or segmental changes and usually deteriorates in spite of treatment. Pleural effusions are seen in ~50%.
• Treatment is with clarithromycin 500mg bd PO/IV. Continue therapy for 14–21 days. Add rifampicin (600mg bd PO/IV) if symptoms do not settle within 72h.
• Pontiac fever is a self-limiting (2–5 days), acute, non-pneumonic Legionella infection with high fever, rigors, myalgia, headache, and tracheobronchitis.
Clinical features resemble Mycoplasma pneumonia ( Mycoplasma pneumonia, p. [link]). Diagnosis is by a 4-fold increase in specific antibody titres.
Most common viral infection in AIDS and following solid organ or bone marrow transplantation (BMT), presenting as fever, dry cough, and progressive respiratory distress with hypoxia and bilateral crackles. CXR shows diffuse infiltrates; a miliary pattern is associated with rapid progression and poor outcome, whereas an interstitial pattern has a better prognosis (see Fig. 2.1). Treat with ganciclovir 5mg/kg IV q12h for 2–3 weeks.
Coxsackie and echovirus
Titres often rise in ‘epidemic pleurodynia’ (Bornholm’s disease), a self-limiting illness with chest pain, exacerbated by coughing and deep breathing, myalgia, and muscle tenderness. Treatment: analgesia (paracetamol, NSAIDs).
• C. pneumoniae presents in older adults with headaches and longer duration of symptoms before hospital admission. Extra-pulmonary manifestations may include meningoencephalitis, Guillain–Barré syndrome (GBS), arthritis, and myocarditis.
• Treatment: erythromycin 500mg qds PO/IV, clarithromycin 500mg bd PO/IV, or tetracycline 500mg qds PO/IV.
• C. psittaci produces fever, cough, myalgia, and, in severe cases, delirium (psittacosis). Complications include pericarditis, myocarditis, and hepatosplenomegaly. Diagnosis is by serology.
• Acquired from birds and animals (so may be a clue in the history), but human-to-human spread may occur.
• Treat with tetracycline 500mg PO qds for 2–3 weeks.
In summary, the likely aetiological agent causing CAP cannot be accurately predicted from the clinical features. However, some patient groups/signs and symptoms tend to be more commonly associated with certain pathogens:
• S. pneumoniae: increasing age, comorbidity, high fever, pleuritic chest pain.
• Bacteraemic S. pneumoniae: ♀, excess alcohol, diabetes mellitus (DM), COPD, dry cough.
• Legionella: younger patient, smoker, absence of comorbidity, diarrhoea, neurological symptoms, multisystem involvement.
• Mycoplasma: younger patient, prior antibiotics, less multisystem involvement.
• C. pneumoniae: longer duration of symptoms prehospital admission and headache.
• Coxiella burnetti: ♂, dry cough, high fever.
Hypersensitivity pneumonitis (extrinsic allergic alveolitis)
May mimic viral pneumonia and present as breathlessness, dry cough, myalgia, and fever, with neutrophilia (eosinophils usually normal acutely) and patchy radiographic changes. There is usually a history of exposure to the allergen, and serum precipitins are detectable. BAL shows predominance of mast cells and lymphocytes. Treatment is with steroids.
This is a heterogenous group of disorders characterized by eosinophilic pulmonary infiltrates, producing respiratory symptoms, CXR shadowing, and blood and sputum eosinophilia. The cause may be unknown, as in cryptogenic eosinophilic pneumonia, or it may be due to drugs (e.g. nitrofurantoin, phenytoin, and ampicillin), helminth infections (e.g. Ascaris lumbricoides, hookworms, Strongyloides stercoralis), tropical pulmonary eosinophilia (lymphatic filarial infection), or small-vessel systemic vasculitis (Churg–Strauss).
Allergic bronchopulmonary aspergillosis
This is a hypersensitivity reaction of airways colonized by Aspergillus spp. producing pulmonary eosinophilia. It typically occurs in asthmatics with repeated episodes of bronchial obstruction, inflammation, and mucus impaction, resulting in bronchiectasis and upper lobe fibrosis. Such patients are usually Aspergillus skin-prick test [immunoglobulin E (IgE)] and serum precipitins (IgG) positive. Treatment depends on the underlying condition.
Cryptogenic organizing pneumonia
May present with fever, malaise, cough, breathlessness, and pulmonary shadows on CXR. Characteristically, infiltrates in different lobes over different time courses, or pneumonia unresponsive to antibiotics. Excessive proliferation of granulation tissue within small airways and alveoli, cryptogenic organizing pneumonia (COP) is the idiopathic form of bronchiolitis obliterans organizing pneumonia (BOOP). Organizing pneumonia can also be associated with collagen vascular diseases (RA, lupus, dermatomyositis), chronic infection (Legionella, CMV, Mycoplasma), and drugs (amiodarone, bleomycin). Treatment is with steroids.
Intrapulmonary haemorrhage may present with cough, fever, and breathlessness. Haemoptysis may be absent in 30%. The CXR may show diffuse alveolar opacities. BAL shows predominantly RBCs. Causes include systemic vasculitis (e.g. Wegener’s granulomatosis, microscopic polyangiitis), collagen vascular diseases (e.g. SLE), Goodpasture’s syndrome, ARDS, and idiopathic pulmonary haemosiderosis. Treatment depends on the cause.
• The classical triad is wheeze ± chest tightness, breathlessness, and cough. Symptoms are often worse at night and first thing in the morning. Acute attacks may build up over minutes, hours, or days, and the patients may deteriorate very rapidly and present as respiratory or cardiorespiratory arrest.
• Factors increasing the risk of severe life-threatening asthma include: previous ventilation, hospital admission for asthma in the last year, heavy rescue medication use, >3 classes of asthma medication, repeated attendances at A&E for asthma care, and brittle asthma.
• No clear precipitating cause can be identified in over 30% of patients.
• Exposure to known allergen or irritant (e.g. pollens, animals, dusts, cigarette smoke).
• Upper respiratory tract infection (URTI) (commonly viral).
• Lower respiratory tract infection (LRTI)—viral or bacterial.
• Neglect or poor compliance with regular inhaled or oral steroids.
• Emotional stress.
• Cold air or exercise-induced asthma.
Markers of severity
• For assessment of the severity of asthma, see Box 2.5.
• The severity of an attack may be easily underestimated. Assess:
• The degree of airflow obstruction.
• The effect of work of breathing on the patient.
• The extent of V/Q mismatch.
• For any evidence of ventilatory failure.
Source: data from SIGN 153: British guideline on the management of asthma (2016). https://www.brit-thoracic.org.uk/standards-of-care/guidelines/btssign-british-guideline-on-the-management-of-asthma
[Patients with marked ‘morning dips’ in the peak expiratory flow (PEF) are at risk of sudden severe attacks.]
• ABG: patients with SpO2 <92% on air or with other features of severe asthma require ABG measurement. Hypoxaemia on room air is almost invariable. In attempting to maintain alveolar ventilation initially, there is hypocapnia and respiratory alkalosis. PaCO2 suggests incipient respiratory failure due to exhaustion; contact ITU immediately. Poorly controlled asthma over several days may be recognized by a mild ‘non-anion gap’ acidosis (serum bicarbonate 20–24mmol/L). Lactic acidosis is seen with severe asthma.
• Pulse oximetry: continuous oximetry is essential; aim for 94–98%.
• CXR: to exclude pneumothorax and diagnose any parenchymal infection.
• ECG: usually normal; in severe asthmatics, signs of right heart strain may be present.
• FBC, U&Es, CRP: assess for signs of infection and eosinophilia; K+ may be lowered by high doses of β-agonists.
1. Treat hypoxia.
2. Treat bronchospasm and inflammation.
3. Assess the need for intensive care.
4. Treat any underlying cause, if present (e.g. infection, pneumothorax).
• Patients may deteriorate rapidly and should not be left unattended.
• Remain calm: reassurance is important in reducing the patient’s anxiety which may further increase the respiratory effort (see Box 2.6).
Severe or life-threatening attack
(See Box 2.7.)
1. Initial treatment
• Sit the patient up in bed.
• O2: the highest percentage available, ideally at least 60% or 15L/min with a high-flow mask. CO2 retention is not a problem in asthmatic patients. Maintain O2 saturations >92%.
• Nebulized bronchodilators: give nebulized salbutamol 2.5mg or terbutaline 10mg, administered via O2, and repeat up to every 15–30min if required. Consider continuous nebulization of salbutamol 5–10mg/h if inadequate response to initial treatment.
• Add ipratropium bromide 0.5mg 4- to 6-hourly if initial response to β2 agonists is poor.
• Obtain IV access.
• Start steroids: if able to take tablets, prednisolone 40mg PO; if not, 200mg of hydrocortisone IV (steroids should still be used in pregnant women, as the risk of fetal anoxia from asthma is high). Continue prednisolone 40mg od PO.
• Antibiotics should be given if there is evidence of chest infection (purulent sputum, abnormal CXR, raised WCC, fever). Yellow sputum may just be due to eosinophils, and a raised WCC may be due to steroids. See Acute pneumonia: management, pp. [link]–[link] for choice of antibiotics. Routine prescription of antibiotics is not recommended for patients with acute asthma if no evidence of an infective precipitant.
• Adequate hydration is essential and may help prevent mucus plugging. Ensure an intake (IV or PO) of 2–3L/day, taking care to avoid overload. Supplement K+, as required.
2. Monitoring progress
• Pre- and post-nebulizer peak flows.
• Repeated ABGs 1- to 2-hourly or according to response, especially if SpO2 <93%. Remember ABGs are painful—the British Thoracic Society (BTS) guidelines state that a local anaesthetic should be used. Alternatively, consider an arterial line if frequent sampling.
3. If response to treatment not brisk or if the patient’s condition is deteriorating
• Continue O2 and nebulized β2 agonist every 15min.
• Give a single dose of IV magnesium sulfate (see Box 2.8).
• Summon anaesthetic help.
• Consider starting an IV aminophylline infusion (see Box 2.8).
• Consider starting an IV salbutamol infusion (see Box 2.8).
• Cautious CPAP may help reduce the work of breathing in patients with respiratory muscle fatigue but may not increase the functional residual capacity further. Involve ITU early, so as not to delay invasive ventilation.
• Ketamine (a dissociative anaesthetic agent) may be useful in ventilated patients (1–3mg/min), probably by increasing circulating catecholamines by blocking uptake into adrenergic nerve endings.
• Inhalational anaesthetic agents (e.g. halothane, enflurane, isoflurane) have been reported to improve bronchospasm and may be useful when initiating ventilation.
• Mechanical ventilation may be lifesaving but has a high risk of complications and an overall mortality of ~13%. Barotrauma is seen in ~14% (e.g. pneumothorax, pneumomediastinum, or subcutaneous emphysema), and hypotension in ~38% (usually a combination of intrathoracic pressure, intravascular fluid depletion due to dehydration, and dilating effect of anaesthetic agents). Seek expert advice from your intensive care physician for the practical management of ventilation of the asthmatic patient.
• Adequate humidification and warming of inspired gases.
• Low-frequency ventilation (6–10 breaths/min).
• Low tidal volumes (6–10mL/kg).
• Long expiratory phase of the cycle (I:E ratio 1:3 or longer).
• Minimize airway pressures (aim for <50cmH2O, normal <25cmH2O).
• Maintain PaO2 >8.0 kPa; allow PaCO2 to rise, provided pH >7.2.
• Adequate sedation and paralysis to overcome respiratory drive.
• Avoid opiates and atracurium (may release histamine).
• Consider benzodiazepine, ketamine, vecuronium, isoflurane, etc.
• Once improvement established, continue nebulized β2-agonist, reducing this to 4-hourly and PRN after 24–48h.
• PEFR should be measured before and after each nebulizer.
• Maintain O2 saturations 94–98%.
• Continue nebulized ipratropium bromide 6-hourly until the condition is improving.
• Continue steroids, 40mg od prednisolone PO, for 10–14 days.
• Monitor IV aminophylline levels every 24h.
• Monitor serum K+ daily while unwell, and supplement as necessary.
• Checking inhaler technique predischarge is essential.
• Discharge criteria (see Box 2.9).
Mild asthmatic attack
No severe features, PEF ≥75% of predicted (or of best when well).
• Administer the patient’s usual bronchodilator (e.g. two puffs of salbutamol by metered-dose inhaler).
• Observe for 60min. If PEF remains ≥75% of predicted value, then discharge.
• Ensure the patient is on at least 1000 micrograms of inhaled beclometasone or equivalent per day.
• Advise the patient to get early GP follow-up, monitor PEF, and return to hospital early if the asthma deteriorates.
Moderate asthmatic attack
No acute severe features, PEF 51–75% of predicted (or of best when well).
• Administer nebulized β-agonist (salbutamol 5mg or terbutaline 10mg) and oral prednisolone 30–60mg.
• Reassess after 30min. If worse or PEF ≤50% of predicted, then admit and assess as for severe asthma.
• If PEF 51–75% predicted, then repeat nebulizer and observe for a further 60min.
• The patient may be discharged from A&E if stable after 1–2 nebulizers and PEFR ≥75%.
• Discharge on:
• Oral prednisolone (usual dose 30–40mg od for at least 5 days).
• Inhaled corticosteroid (≥1000 micrograms/day of inhaled beclometasone).
• Inhaled β-agonist.
• Advise the patient to seek GP follow-up within 48h and to return early to A&E if there is any deterioration.
• Consider referral to chest clinic.
Sending people home from A&E
• Mild to moderate exacerbations may be fit to be discharged from A&E.
• If there are any features of acute severe asthma (see Box 2.4), then admission is mandatory.
• A history of brittle asthma or previous attacks requiring mechanical ventilation is always a requirement for admission.
• Deterioration of pre-existing symptoms of exertional breathlessness, cough (sometimes with daily sputum production), and wheeze (unrelieved or only partially relieved by inhaled bronchodilators).
• Respiratory failure ( Respiratory failure: assessment, pp. [link]–[link]): may be type 1 (normal PaCO2, low PaO2) or type 2 (high PaCO2, low PaO2, reflecting severe bronchospasm and/or alveolar hypoventilation).
• Positive smoking history (if not, then late-onset asthma is likely or the rarer diagnosis of α1-antitrypsin deficiency should be considered).
• Confusion/impaired consciousness (exhaustion, CO2 retention).
• Infective exacerbation (no new CXR changes): typically H. influenzae, S. pneumoniae, Moraxella catarrhalis. Commonly viral.
• CAP (new CXR changes) (see Fig. 2.1).
• Exposure to known allergen: COPD may coexist with allergic asthma.
• Expansion of large bullae.
• Sputum retention with lobar or segmental collapse (atelectasis): pneumonia, excessive sedation or opioid analgesia (trauma, post-surgery), impaired consciousness.
• Confounding or contributing factors: myocardial ischaemia, pulmonary oedema, cor pulmonale, PE.
All patients should have:
• U&Es: look for dehydration and renal failure. Monitor K+.
• FBC: look for leucocytosis or anaemia (chronic respiratory failure may produce secondary polycythaemia).
• Pulse oximetry and ABGs: to assess the degree of respiratory failure and pH, and to guide appropriate O2 treatment.
• Septic screen: sputum should be sent for culture. Blood cultures if febrile or CXR changes suggest pneumonia.
• CXR: focal changes suggest pneumonia ( Acute pneumonia: investigations, p. [link]).
• ECG: myocardial ischaemia or arrhythmia.
Assessment of severity
• History: assess the severity of COPD when stable, and compare with current exacerbation. Ask about symptoms and functional capacity when well (distance walked on flat, stairs climbed, frequency of exacerbations, previous admissions, ? ever ventilated). Assess the level of usual treatment (regular nebulized bronchodilators or oral steroids, home O2) and concurrent illnesses (IHD, renal impairment). Any previous documentation [pulmonary function tests (PFTs), ABGs].
• Examination: assess for severity of respiratory distress (RR >25/min, use of accessory muscles, or paradoxical chest wall movements), hypoxia (cyanosis), hypercapnia (CO2 retention flap, confusion), and cor pulmonale (peripheral oedema) (see Box 2.10).
(See Box 2.11.)
Treat hypoxia and respiratory failure
• The distinction between ‘pink puffers’ (breathless to maintain PaO2 and so keep PaCO2 down) and ‘blue bloaters’ (lose breathless drive to maintain PaO2 and so PaCO2 rises) is unhelpful, as most patients have features of both.
• Commence O2 therapy: uncontrolled O2 therapy may worsen CO2 retention in some patients. While awaiting ABGs, give controlled 24–28% O2 via a Venturi mask. Nasal cannulae give unreliable inspired O2 concentration and may be dangerous. Once ABG results available, adjust FiO2 accordingly.
• If the patient is not retaining CO2 (PaCO2 <6kPa) and is hypoxic (PaO2 <10kPa), then give O2 28–40%. Repeat ABGs 30min later (sooner if conscious level deteriorates) to ensure correction of hypoxia and exclude rising PaCO2. Aim to maintain O2 saturations 88–92%.
• If CO2 retention is present, then use 24–28% O2 and consider ventilatory support. Non-invasive ventilation (NIV) is the first-line treatment of choice for COPD exacerbations with type 2 respiratory failure in patients who fail to respond to initial therapy. It allows the administration of higher O2 concentrations without an uncontrolled rise in PaCO2. NIV reduces the need for intubation, decreases mortality and hospital stay, and should be considered in all patients with COPD exacerbations with PaCO2 ≥6.0kPa and pH ≤7.35 who have failed to respond to initial bronchodilator therapy.
• Mechanical ventilation: this should be considered in patients unlikely or unable to tolerate NIV ( Mechanical ventilation, p. [link]).
• Respiratory stimulants: these have generally been superseded by NIV. However, where NIV is not available or has not been successful and mechanical ventilation is not considered appropriate, a trial of doxapram may be worthwhile. It is not beneficial in type 2 respiratory failure due to poor respiratory effort.
Treat bronchospasm and obstruction
• Nebulized β-agonists (salbutamol 2.5mg or terbutaline 10mg q4h and PRN) via O2 or air if CO2 retention. (If the patient is very hypoxic, give 2L/min O2 via nasal cannulae while nebulizer in progress.)
• Patients with COPD may have relatively fixed bronchospasm, but where the patient is very unwell, then consider IV aminophylline and/or IV β-agonists, as for severe asthma (see Box 2.5).
• Include nebulized ipratropium bromide 500 micrograms 6-hourly. This tends to be more effective in patients with COPD than in those with asthma.
• Give steroids: 30mg prednisolone PO for 7–10 days; there is no advantage in prolonging therapy.
• Urgent physiotherapy may help clear bronchial secretions.
• COPD per se is not a contraindication to ventilation in appropriately selected patients. Ventilation should be considered where respiratory failure is present (PaO2 ≤7.3kPa), regardless of CO2 levels, and in those patients who have failed to respond to first-line treatment (including NIV) or who are very severely unwell and unlikely to respond to any other intervention.
• Discuss with a senior colleague or ITU staff prior to intubation.
In favour of a good outcome from ventilation
• Acute respiratory failure (normal bicarbonate, acute history).
• Relatively young patient.
• Obvious remediable cause (e.g. pneumonia).
• Good recent exercise tolerance and quality of life.
• Not previously known to retain CO2 when well.
Against a good outcome from ventilation
• Other comorbid conditions (e.g. IHD, renal failure).
• Previous difficulty weaning from ventilator.
• On maximal therapy at home (home nebulizer, long-term O2 therapy).
• Poor quality of life or poor exercise tolerance.
Management of gas exchange during ventilation
• Patients who are chronically hypoxic or CO2 retainers will tolerate poor blood gases better than those patients with other causes of respiratory failure.
• When ventilating patients with COPD, achieving a ‘normal’ PaCO2 and PaO2 may not be appropriate. Those who are chronically hypoxic or who chronically retain CO2 (as evidenced by previous abnormal gases or a raised bicarbonate with a normal or near-normal pH) are unlikely to breath spontaneously or wean from the ventilator, unless their blood gases are allowed to mirror what is probably their chronic state. Thus, a patient with chronic type 2 respiratory failure may need a PaCO2 of 6–7.5kPa ± mild hypoxia, even on the ventilator, to achieve successful weaning.
Treat the cause of exacerbation
• Suggested by purulent sputum or an increase in sputum production.
• For lobar consolidation or bronchial pneumonia, follow guidelines described under Acute pneumonia: management, pp. [link]–[link] and Acute pneumonia: specific situations, p. [link]. Otherwise treat with amoxicillin 500mg–1g tds or doxycycline 200mg loading dose, then 100mg daily PO; if unwell or failure to respond, treat with cefuroxime 750mg tds IV for improved cover of resistant Haemophilus spp.
• Follow local protocols.
See Pulmonary embolism (PE): assessment, p. [link].
Respiratory failure is present when gas exchange becomes significantly impaired. Clinically, it is not possible to predict the PaO2 or PaCO2, and so this diagnosis relies on ABG analysis. There are two types:
• Type 1: hypoxia PaO2 ≤8kPa on air or O2 with normal or low PaCO2 (i.e. mainly V/Q mismatch).
• Type 2: hypoxia PaO2 ≤8kPa on air or O2 with raised PaCO2 (>6kPa) (i.e. predominantly alveolar hypoventilation).
In practice, both types may coexist.
(See Box 2.12.)
• Shortness of breath is the most common presentation. Ask about the speed of onset (sudden onset may suggest pneumothorax, PE, or cardiac failure).
• Respiratory failure may present without dyspnoea, particularly exacerbations of COPD with hypoventilation and non-respiratory causes such as GBS ( Guillain–Barré syndrome, pp. [link]–[link]) or drug overdose. Neuromuscular respiratory failure is discussed under Neuromuscular respiratory failure: assessment, pp. [link]–[link].
• Confusion may be the sole presentation in the elderly.
The history may point to the cause of respiratory failure:
• History of asthma/chronic bronchitis and smoking.
• History of other chronic lung disease (e.g. fibrosing alveolitis, sarcoidosis).
• Sputum production and fevers (pneumonia).
• Swollen legs due to the development of cor pulmonale or hypoxic/hypercapnic renal fluid retention in patients with chronic lung disease.
• Haemoptysis (pneumonia, PE).
• Cardiac history, including palpitations and/or chest pain.
• Drug and/or overdose history.
• Neurological symptoms, including painful legs and paraesthesiae (GBS).
Try to assess the functional capacity when well, e.g. distance walked on flat, stairs climbed without stopping, frequency of attacks, previous admissions,? ever ventilated, concurrent illnesses (heart disease, renal impairment, liver impairment), etc.
• Listen to the breathing: stridor (upper airway obstruction), wheeze (localized or generalized airflow limitation secondary to asthma, COPD, pulmonary oedema), coarse crackles (due to consolidation of fluid), fine crackles (due to fibrotic change), bronchial breathing (indicates consolidation or collapse but may also occur with fibrosis or above a pleural effusion).
• Palpate the upper chest and neck for crepitus (pneumothorax or pneumomediastinum).
• ABG: on air immediately, or if very unwell while on O2 (note FiO2).
• CXR (see Fig. 2.1).
• ECG: look for signs of PE (tachycardia, RBBB, anterior T-wave changes, RAD, rarely S1Q3T3; Pulmonary embolism (PE): assessment, p. [link]), tachyarrhythmias, or myocardial ischaemia.
• Blood tests: FBC (anaemia, leucocytosis), U&Es, glucose.
• Inspect sputum: yellow, green, mucoid, streaky, or frank blood.
• FEV1 and FVC: if suspected muscle weakness (e.g. GBS).
• Septic screen: sputum culture, blood cultures if febrile or if CXR suggests infection.
Where indicated, consider
• Aspirin and paracetamol levels.
• Plasma and urine for toxicology.
• Urinalysis for glucose and ketones.
• Examine the CXR systematically for any abnormality.
• Consolidation/alveolar shadowing: may be lobar or patchy. Presence of an air bronchogram suggests pneumonia.
• Pulmonary oedema due to LVF (cardiogenic): typically perihilar (‘bats-wing’), upper lobe venous congestion, Kerley B lines in peripheral lung fields, ± pleural effusions, ± cardiomegaly.
• Non-cardiogenic pulmonary oedema (ARDS/ALI): typically peripheral alveolar shadowing ± air bronchogram, no upper lobe venous congestion, Kerley B lines, pleural effusions, or cardiomegaly.
• Pleural effusions.
• Masses suggesting bronchogenic carcinoma.
• PE: wedge-shaped peripheral opacities, small pleural effusions, localized areas of oligaemia, enlarged PA.
• Pneumothorax (distinguish from large bullae).
• Trauma/rib fractures.
• Interstitial lung disease: small lung fields, interstitial reticulonodular shadowing peripherally and basally.
The severity of respiratory failure depends upon response to O2. Failure of hypoxia to correct on 40–60% O2 or progressive hypercapnia implies that non-invasive or mechanical ventilation may be necessary, depending on the clinical condition and underlying cause.
Poor prognostic signs on presentation include
• Inability to speak due to dyspnoea.
• RR (>40/min).
• PEF ≤33% of predicted in acute asthma.
• Tachycardia (HR ≥100bpm) or bradycardia (HR ≤60bpm).
• Exhaustion or coma (ventilatory support is required urgently).
• Pulse oximetry saturation of <90%.
• Shock (tachycardia + hypotension). May indicate tension pneumothorax ( Tension pneumothorax, p. [link]), severe LVF ( Pulmonary oedema: assessment, pp. [link]–[link]), severe pneumonia (p Acute pneumonia: management, pp. [link]–[link]), or large PE ( Pulmonary embolism (PE): assessment, p. [link]).
Hypercapnia is the end-result of many causes of respiratory failure (including asthma and pneumonia), not just COPD, and indicates a tiring patient. Even if relatively elderly, the patient may respond well to ventilation, with a satisfactory final outcome, depending on the disease and premorbid condition.
General resuscitation (ABC)
• Ensure the airway is patent and the mouth is clear.
• Sit the patient up (unless hypotensive), and administer O2 at 60% unless there is a history of COPD (use 24–28% O2).
• Ensure that respiratory effort is adequate and effective (measure RR and assess the depth of respiration); use pulse oximetry to monitor the PaO2.
• If the patient is exhausted, with a failing respiratory drive, call for anaesthetic assistance and consider urgent transfer to ITU (see Box 2.13).
• In comatose patients with poor respiratory effort, consider drug overdose with opiates (pinpoint pupils) or benzodiazepines. Give naloxone 200–400 micrograms (2–4 micrograms/kg) IV bolus, followed by an infusion, depending on response, and/or IV flumazenil (200 micrograms over 15s, then 100 micrograms at 60s intervals if required—max. total dose 1mg (2mg if on ITU).
• Measure BP and HR; look for signs of cardiac failure (raised JVP, inspiratory crackles, oedema) or signs of PE (raised JVP, tachycardia, hypotension, normal breath sounds ± pleural rub).
See Box 2.14 for management key points.
Adult respiratory distress syndrome 1
ALI and its more severe subset ARDS result from the development of excessive pulmonary inflammation in response to initial injury, such as sepsis, which may be pulmonary or extra-pulmonary in origin. It is characterized by injury to the alveolar epithelial and endothelial barriers of the lung, acute inflammation, and protein-rich pulmonary oedema, leading to acute respiratory failure. Often occurs in the setting of multi-organ failure (MOF).
• Acute onset of respiratory failure with one or more risk factors (see Box 2.15).
• ALI: ratio PaO2 (kPa):FiO2 <40.
• ARDS: ratio PaO2 (kPa):FiO2 <27.
• Bilateral infiltrates on CXR.
• PCWP <19mmHg, with normal colloid oncotic pressure [in patients with hypoalbuminaemia, the critical PCWP is approximately serum albumin (g/L) × 0.57] or clinical exclusion of cardiac failure.
• ABG (consider arterial line as regular samples may be required).
• Take blood for FBC, U&Es, LFTs and albumin, coagulation, cross-match, and CRP.
• Septic screen (culture blood, urine, and sputum).
• Consider drug screen, amylase if history suggestive.
• PA catheter to measure PCWP, cardiac output, and mixed venous O2 saturation and to allow calculation of haemodynamic parameters.
• Other investigations if appropriate:
• CT chest.
• BAL for microbiology and cell count (? eosinophils).
• Carboxyhaemoglobin estimation.
See Box 2.16 for management key points.
• Almost all cases of ALI alone will require HDU/intensive care unit (ICU) care: liaise early.
• The main aim is to identify and treat the underlying cause, while providing support for organ failure:
• Respiratory support to improve gas exchange and correct hypoxia.
• Cardiovascular support to optimize O2 delivery to tissues.
• Reverse or treat the underlying cause.
Many drugs trialled have been aimed at inhibiting the inflammatory cascade and preventing injurious inflammation. More recently, cell-based therapy has focused on redirecting the immune/inflammatory response to a reparative state.
Spontaneously breathing patient
• In very mild ALI, hypoxia can be corrected with inspired O2 concentrations (FiO2 40–60%).
• Patients invariably require higher O2 concentrations (non-rebreather masks with reservoir FiO2 ~60–80%) or CPAP ( Continuous positive airways pressure, p. [link]). Consider transfer to HDU/ICU.
• Indications for mechanical ventilation:
• Inadequate oxygenation (PaO2 <8kPa on FiO2 >0.6).
• Rising or elevated PaCO2 (>6kPa).
• Clinical signs of incipient respiratory/cardiovascular failure.
This is the realm of the ICU physician. The main aim is to improve oxygenation/ventilation, while minimizing the risk of further ventilator-induced lung injury, termed lung-protective ventilation. Lung-protective ventilation should be implemented immediately because of the excellent evidence that low tidal volume and low inspiratory pressure ventilation improve survival rates.
• Controlled mechanical ventilation with sedation [± neuromuscular blockade (NMB)]. By preventing skeletal muscle activity, NMB increases chest compliance, improves patient–ventilator synchrony, and reduces airway pressures, reducing ventilator-associated lung injury (VALI).
• Ventilation with smaller tidal volumes is associated with improved outcome, compared to the traditional approach.
• PEEP improves oxygenation in most patients and allows reduction in FiO2. Usual starting level is 5–10cmH2O, with optimal levels in the range of 10–15cmH2O. Beware of hypotension due to reduction in venous return.
• The use of smaller tidal volumes may impair CO2 clearance, with resulting acidosis despite high ventilatory rates (20–25 breaths/min). Gradual increases in pCO2 (up to ~13kPa) are well tolerated in most patients, and acidosis (pH <7.25) can be treated with IV bicarbonate, the so-called permissive hypercapnia.
• Arterial line is essential for continuous BP measurements. Other invasive monitoring is invariably used [PA catheter, pulse contour cardiac output (PiCCO), oesophageal Doppler], but their individual roles and effects on outcome are unclear.
• Most patients are haemodynamically compromised due to the underlying condition and/or ventilatory management, and benefit from fluid resuscitation. This may risk worsening capillary leak in the lung and compromise oxygenation/ventilation. Aim for a low-normal intravascular volume, while maintaining the cardiac index and MAP.
• Inotrope and/or vasopressor support is commonly required, and the choice of agent is usually decided on a combination of clinical evaluation and invasive haemodynamic monitoring. Agents commonly employed include dobutamine, dopamine, adrenaline, and NA.
• Repeated assessment is essential.
• Look for, and treat, a precipitant (see Box 2.13).
• Fever, neutrophilia, and raised inflammatory markers are common in ALI/ARDS and do not always imply sepsis.
• A trial of empiric antibiotics, guided by possible pathogens and following an appropriate septic screen (consider BAL once intubated and stable), should be considered. Antibiotics should be modified or discontinued in light of microbiological results.
• Indwelling CVP catheters are a common source of sepsis.
• Consider low-dose steroid infusion.
• Renal failure: common and may require renal replacement therapy (RRT) to control fluid balance and blood biochemistry.
• Enteral feeding: helps maintain the integrity of the gut mucosa and is associated with a lower risk of systemic sepsis, when compared to parenteral feeding [total parenteral nutrition (TPN)]. Delayed gastric emptying and reduced gut motility are common in ICU patients and may respond to prokinetic drugs (metoclopramide, erythromycin) or may require nasojejunal feeding. Stress ulcer prophylaxis (H2-blockers) should be considered if mechanical ventilation >48h or MOF.
• Coagulopathy: common and, if mild, does not require therapy. If severe/DIC, expert advice should be sought.
• Steroid therapy:
• Consider corticosteroids for patients with life-threatening hypoxaemia that has failed to respond to previous therapies. If no improvement in PaO2/FiO2, compliance, and PaCO2 within 72h, then discontinue treatment. If there is benefit, treatment can be extended, but optimal duration is currently unknown.
• Emerging therapy:
• Statins, insulin, ACEI, and macrolides all have anti-inflammatory and immunomodulatory ± antithrombotic actions. Conflicting evidence exists with regard to the mortality benefit associated with any individual treatment or indeed combinations of drugs in ALI/ARDS. Macrolides show particular promise in pneumonia-induced ALI, as they have the added benefit of antimicrobial activity.
• Cell-based therapy, particularly use of mesenchymal stem/stromal cells, is an attractive option being extensively investigated.
• Sepsis: evidence suggests that some patients with refractory septic shock (ongoing/increasing vasopressor requirements) may have ‘relative’ or ‘functional’ adrenal insufficiency and may benefit from ‘supraphysiological’ steroid replacement (200–300mg/day of hydrocortisone). Identification of patients likely to benefit is unclear at present, but adrenocorticotrophic hormone (ACTH) stimulation test may help discriminate.
See Box 2.17 for causes of sudden deterioration in ARDS.
• Outcome for ALI/ARDS has improved in recent years, with overall mortality rates of ~40%.
• Patients with ALI/ARDS and sepsis, liver disease, non-pulmonary organ dysfunction, or advanced age have higher mortality rates.
• In survivors, although formal lung function tests are abnormal, respiratory compromise at 1–2 years is unusual.
• There is increasing evidence that survivors suffer considerable neuromuscular and psychological disability. This may reflect the period of prolonged critical illness, rather than be specific for ALI/ARDS.
Diaz JV, Brower R, Calfee CS, Matthay MA. Therapeutic strategies for severe acute lung injury. Crit Care Med. 2010;38:1644–50.Find this resource:
Sweeney RM, Griffiths M, McAuley D. Treatment of acute lung injury: current and emerging pharmacological therapies. Semin Respir Crit Care Med. 2013;34:487–98.Find this resource:
Most individuals presenting to hospital with a spontaneous pneumothorax have no recognized underlying lung disease. The most common presenting symptoms are:
• Breathlessness: usually abrupt in onset (young, fit patients may have very little, but patients with COPD or asthma may present with sudden deterioration). The presence of breathlessness influences the management strategy.
• Chest pain: dull, central, heavy; or there may be a pleuritic element.
• In an inpatient, consider the diagnosis in anyone who is:
• Breathless after an invasive thoracic procedure (e.g. subclavian vein cannulation).
• Increasingly hypoxic or has rising inflation pressures on mechanical ventilation.
• Primary/spontaneous: healthy subjects, no known underlying lung disease. More common in tall, young men who smoke, aged 20–40 years. Probably due to rupture of apical subpleural blebs/bullae.
• Secondary/spontaneous (SSP): pleural rupture due to underlying lung disease: emphysema, fibrosing alveolitis, cystic fibrosis, sarcoidosis. Symptoms tend to be greater in SSP, even if the pneumothorax is relatively small in size.
• Infection: cavitating pneumonia, e.g. staphylococcal, lung abscess, TB, PCP.
• Trauma: particularly chest trauma in road traffic accident (RTA).
• Iatrogenic: after pleural biopsy or aspiration, transbronchial biopsy, percutaneous lung biopsy, subclavian vein cannulation, and mechanical ventilation with high airway pressures.
Investigations: the chest radiograph
• The classical clinical signs may not always be present.
• Standard erect CXR in inspiration is recommended for initial diagnosis.
• In a supine patient, a pneumothorax may not be easy to see. Look for hyperlucency of one lung field or a line parallel to the chest wall (caused by retraction of the right middle lobe). An erect CXR may show blunting of the costophrenic angle on the affected side.
• If a patient has COPD and marked bullous disease, take care that the suspected pneumothorax is not a large, thin-walled bulla. CT scanning is recommended for uncertain or complex cases.
• Tension pneumothorax: midline shift away from the pneumothorax, raised or obstructed JVP, hypotension, tachycardia, shock.
• Size of pneumothorax: percentages of a pneumothorax are hard to estimate and less important than the degree of clinical compromise; classify according to the size of the visible rim between the lung margin and the chest wall at the level of the hilum on the CXR:
• Small pneumothorax: visible rim <2cm.
• Large pneumothorax: visible rim >2cm.
(NB A large pneumothorax approximates to a 50% loss of lung volume.)
• Hypoxia: PaO2 ≤10kPa on air (may simply reflect underlying lung disease).
• Severe dyspnoea.
Who to discharge from A&E
Patients with primary spontaneous pneumothorax (PSP) or SSP and breathlessness associated with any size of pneumothorax should undergo active intervention, as well as supportive treatment (including O2).
• Small PSP, rim of air <2cm on CXR, no significant dyspnoea, and no underlying chronic lung disease.
• Large PSP following successful aspiration (<2cm rim of air on repeat CXR), no significant dyspnoea or underlying lung disease.
• All patients with an SSP should be referred early to a chest physician.
• Follow-up in chest clinic in 10–14 days with a repeat CXR.
• Advise the patient to return to A&E if breathless or increasing chest pain.
• Air travel should be avoided until full resolution.
Who to admit for observation
• All patients with pneumothorax secondary to trauma or with an underlying lung disease, even if aspiration has been successful—discharge after 24h if follow-up CXR shows no recurrence.
• Patients in whom aspiration has failed to re-expand the lung fully.
• Give O2 (>35% unless there is clinical evidence of COPD, in which case start with 24–28% and check ABGs). This accelerates the reabsorption of the pneumothorax up to 4-fold. Most of the pneumothorax is nitrogen (N2) (air), and supplemental O2 decreases the partial pressure of N2 in blood, increasing the gradient for its reabsorption.
Attempt chest aspiration in patients with
• Primary pneumothorax: all large primary pneumothoraces, whether symptomatic or not.
• Secondary pneumothorax: all small secondary pneumothoraces, only if asymptomatic and <50 years. Admit for observation, and if there is minimal or no pneumothorax on CXR after 24h, discharge with follow-up in chest clinic in 10–14 days with CXR.
• Needle aspiration should not be repeated, unless there were technical difficulties.
Proceed to intercostal chest tube drainage in patients with
• Primary pneumothorax: failed aspiration.
• Secondary pneumothorax: small pneumothorax if symptomatic or >50 years; failed aspiration after one attempt.
• If the lung has re-expanded and the drain is not bubbling, wait 24h and repeat CXR to exclude recurrence, and remove the drain.
• A collapsed lung and bubbling drain suggests persistent air leak, and suction may be required.
• A collapsed lung and no bubbling suggests the drain is blocked, displaced, or clamped. If a new drain is required, it should be through a new incision.
• Patients with a persistent air leak should be discussed with a cardiothoracic surgeon at 48h.
• Use of suction:
• Suction should not be routine. Caution is required because of the risk of re-expansion pulmonary oedema.
• High-volume, low-pressure suction systems are recommended.
• Usually seen in patients receiving mechanical ventilation or post-CPR.
• Patient is usually distressed and tachypnoeic, with cyanosis, profuse sweating, and marked tachycardia and hypotension.
• This requires immediate attention.
• Do not leave the patient unattended. Give maximal inspired O2 to reverse hypoxia.
• Insert an 18G (green) cannula (or the largest available), perpendicular to the chest wall, into the second intercostal space in the mid-clavicular line on the side of the pneumothorax on clinical examination (reduced breath sounds and trachea deviated away). Relief should be almost immediate. Leave the cannula in place until the air ceases to rush out.
• Insert a chest drain as soon as possible.
• If no air rushes out when the cannula is inserted, the patient does not have a tension pneumothorax and the cannula should be removed.
• Haemoptysis is coughing up of blood from the lungs or tracheobronchial tree (see Box 2.19).
• Massive haemoptysis is defined as ≥400mL over 3h or ≥600mL over 24h. The common causes of massive haemoptysis are bronchiectasis, bronchial carcinoma, infection (e.g. TB, lung abscess, or aspergilloma), or trauma.
• Often the cause is obvious from the history. Patients with large bleeds may be able to locate the site of bleeding by a ‘gurgling’ within the chest. Ask specifically for smoking and drug history.
• Examine for an underlying cause (see Box 2.19) and to assess the haemodynamic and respiratory effects of the bleed.
• Consider that the blood may be coming from somewhere other than the lungs: upper respiratory tract, GI tract, nasopharynx.
See Box 2.20 for management key points.
Stabilize the patient
• Massive haemoptysis should usually be managed at a hospital with cardiothoracic surgical backup, and urgent transfer should be considered if this is not available.
• Give high inspired O2.
• Place the patient in the recovery position, with the bleeding lung down (if it is known which side the bleeding is from) to try to keep the unaffected lung free of blood.
• If aspiration of blood is threatened, get anaesthetic help urgently; anaesthetize, intubate, and ventilate. A double-lumen ETT may be used to isolate the lungs, but the narrow lumen may make subsequent flexible bronchoscopy difficult.
• Insert a large-bore peripheral cannula, followed by a central line if indicated; the internal jugular route is preferred to minimize the risk of pneumothorax.
• Support the circulation; haemoptyses are rarely severe enough to warrant transfusion. But cross-match 2–4U if bleeding ongoing. Monitor the urine output, pulse, BP, and, if appropriate, CVP.
Diagnose the source of bleeding
• CXR: this should be examined systematically for a mass lesion ± hilar nodes, bronchiectasis (tramline shadows), and old or new cavities which may suggest aspergillomas. Look for causes of minor haemoptysis, if this is the current problem.
• Fibreoptic or rigid bronchoscopy: this should be performed urgently in all cases of massive haemoptysis. This is unlikely to localize the exact source but may help localize the lung or lobe affected, to guide surgeons or radiologists. Bleeding may be arrested by endoscopically administered adrenaline (1mL of 1:10 000) or, in massive haemoptysis, a balloon catheter may be inflated for 24–48h within a segmental or sub-segmental bronchus.
• Selective pulmonary angiography: can identify the bleeding source in 90% of patients and, when combined with embolization, is effective in controlling bleeding in up to 90%. Multiple procedures may be necessary.
• High-resolution CT chest: may help identify parenchymal lesions and peripheral endobronchial lesions.
• Correct coagulopathy: if the haemoptysis is relatively minor, it may be sufficient to correct an excessively elevated INR to a therapeutic range (INR 1.5–2.0) with FFP. In patients with a prosthetic valve and massive haemoptysis, the clotting must be normalized as best as possible. Discuss with your local haematologists or cardiologists. Support platelets if <50 × 109/L.
• Patients with minor haemoptysis should be fully investigated (see Box 2.21). No cause is found in ~10%.
• Patients with massive haemoptysis should undergo urgent fibreoptic bronchoscopy to locate the bleeding source.
• Angiography and embolization should be considered for all patients with massive haemoptysis prior to surgery.
• If angiography is not available, patients who continue to bleed >600mL/day or who have an identifiable lesion (e.g. lung abscess, aspergilloma, trauma) should have definitive surgery.
• Discuss all cases of haemoptysis with the chest team. Patients with massive haemoptysis should be managed in a specialist centre with appropriate cardiothoracic and radiological backup. Transfer the patient (ventilated if unstable) if the patient is fit enough.
• Infection is a common precipitant (e.g. in bronchiectasis). Consider antibiotics (e.g. co-amoxiclav 1g IV q6–8h or cefotaxime 2g IV q8h) after appropriate cultures. TB or lung parasites will require specific antimicrobial therapy.
• Chest discomfort or sensation of heaviness.
• Symptoms of malignancy: loss of appetite, weight, and energy.
• Symptoms of infection: fever, cough, sputum, night sweats.
Severity depends on
• Speed of onset (e.g. traumatic or post-procedural).
• Haemodynamic compromise (hypotension, tachycardia).
• Hypoxia or respiratory failure.
• Presence of underlying disease (e.g. heart failure, COPD).
Transudate (protein <30g/L)
Exudate (protein >30g/L)
See Box 2.22 for management key points.
• If acute, then stabilize the patient and insert a chest drain.
• If effusion is chronic, then reach a diagnosis and treat accordingly.
• Image guidance: a recent CXR should be available prior to performing aspiration/drainage. Thoracic US guidance is strongly recommended for all procedures for pleural fluid. Prior marking of the spot for subsequent remote intervention is not recommended, except for large pleural effusions.
Acute massive effusion
• Give O2.
• IV access: via a wide-bore cannula or an internal jugular central line (being careful not to cause further lung injury).
• Take blood: for FBC, clotting, and urgent cross-match (6U).
• Restore circulating volume: if BP low or tachycardic, then give a plasma expander 500mL stat, according to the size of effusion drained and response.
• Insert a chest drain ( Insertion of a chest drain 1, pp. [link]–[link] and Insertion of a chest drain 2, p. [link]). The drain should be left unclamped and allowed to drain freely, and the amount drained should be recorded.
Indications for specialist referral
• Traumatic haemothorax should be referred to cardiothoracic surgeons.
• Haemothorax secondary to procedures should be referred if the patient is shocked and/or there is ongoing significant blood loss requiring transfusion at a rate ≥1U every 4h (approximately).
• When in doubt, discuss the case with the surgical team.
A unilateral chronic effusion will usually have accumulated over weeks or perhaps even months. The most common cause is malignancy. Empyema, TB, autoimmune diseases (e.g. rheumatoid), and cirrhotic ascites with transdiaphragmatic movement are alternative aetiologies.
• Diagnostic aspiration under US guidance. A sample should then be withdrawn (50mL) and split into three for:
—Protein ≥30g/L implies an exudate.
—Protein <30g/L implies a transudate.
—LDH to assess Light’s criteria (see Box 2.23).
—pH <7.2 suggests a possible empyema.
—Glucose <3.3mmol suggests a possible empyema (also seen in TB and autoimmune-related effusions).
—Amylase if acute pancreatitis suspected.
—Triglycerides if chylothorax suspected.
—Turbid fluid with neutrophils implies an infection.
—Bloodstained fluid implies malignancy but may be a haemothorax (check fluid haematocrit: if >1/2 blood haematocrit, suspect haemothorax).
—ZN staining for acid-fast bacilli (AFB) (+ve in only 20% of pleural TB).
—Culture for TB and routine culture.
• Cytology: for primary and secondary tumours. Positive in 60%, so negative does not exclude malignancy.
• Pleural biopsy should be performed if malignancy or TB is suspected.
• Chest CT with contrast may help differentiate benign from malignant disease, pleural thickening, mesothelioma, or intrapulmonary pathology.
• The main priorities are diagnosis (if unknown) and symptomatic relief.
• Advice should be sought from the respiratory team for symptomatic/malignant effusions.
• The fluid may be drained by aspiration or by insertion of a small-bore intercostal drain (10–14F) ( Insertion of a chest drain 1, pp. [link]–[link] and Insertion of a chest drain 2, p. [link]), which should be clamped and released to drain 1.5L/day (this is the only instance when a chest drain may be clamped).
• Drainage of >1.5L on a single occasion may result in reperfusion pulmonary oedema so is not recommended.
• If the malignant effusion reaccumulates rapidly, consider chemical or surgical pleurodesis, unless lung significantly trapped. Seek advice from the respiratory team.
• In cases of ‘trapped lung’, indwelling catheters offer a better approach to management than recurrent aspiration/drainage.
This is a serious complication of bacterial chest infection ( Acute pneumonia: complications, p. [link]). All effusions associated with sepsis or pneumonia should be tapped and pH assessed if non-purulent and pleural infection suspected.
• To avoid long-term scarring and loculated infection, the empyema requires urgent drainage by US guidance and usually the positioning of an intercostal drain.
• Frequently, drainage fails as the empyema organizes with dense adhesions producing loculations. This can be assessed by US. Surgical drainage may be required.
• Empyema should always be discussed with a respiratory physician or cardiothoracic surgeon.
• There is no indication for routine use of intrapleural fibrinolytics.
• All patients with pleural infection are high risk for the development of VTE and should receive adequate thromboprophylaxis unless contraindicated.
See Box 2.23 for Light’s criteria for pleural fluid analysis.
British Thoracic Society, Pleural Disease Guideline Group (2010). BTS pleural disease guideline 2010. https://www.brit-thoracic.org.uk/document-library/clinical-information/pleural-disease/pleural-disease-guidelines-2010/pleural-disease-guideline
• Stridor: inspiratory noise. Generated by the collapse of the extrathoracic airway during inspiration.
• Inability to swallow secretions (hunched forward, drooling).
Ask colleagues to call a senior anaesthetist and for ENT assistance immediately, while you continue your assessment.
Identify the cause
(See Box 2.24.)
• History: sudden onset, something in the mouth or child playing with unsafe toy (foreign body), fever (epiglottitis, diphtheria, tonsillitis), hoarse voice (epiglottitis), sore throat (infective as listed), travel (Eastern Europe—diphtheria), smoker + longer history + systemic symptoms (? carcinoma), trauma.
• Examination: where an infective cause is suspected, then examination of the oropharynx must be undertaken in an area where the patient may be immediately intubated, with an anaesthetist standing by.
• Fever, drooling, stridor. Bull neck, lymphadenopathy, pseudomembrane over the oropharynx (diphtheria). Swollen throat + epiglottis on direct/indirect laryngoscopy (epiglottitis).
• Investigations: do not delay treatment if the patient is in distress. If the patient is relatively stable, perform a CXR (foreign body) or lateral neck X-ray (swollen epiglottis). FBC, U&Es, ABGs.
Indications for ITU/surgical referral
• Prior to examination of the oropharynx if infective cause suspected.
• Failure to maintain adequate airway or oxygenation.
• Inability to swallow secretions.
• Ventilatory failure (PaO2 ≤10kPa, PaCO2 ≥6kPa).
• Severe dyspnoea.
• If severe, liaise immediately with ITU and ENT or general surgeons (potential for urgent tracheostomy).
• Priorities are:
• Stabilize the patient: ensure adequate airway.
• Identify the cause of obstruction.
• Specific treatment measures.
Stabilize the patient
• Take ABGs, and give high percentage O2 (≥60%).
• If a clear cause of obstruction (foreign body, post-operative thyroid surgery) (see Box 2.24), then take appropriate measures to gain patient airway.
• If the patient is becoming increasingly exhausted or there is acute failure of ventilation, then summon colleagues and be prepared to intubate or perform a tracheostomy.
With total upper airway obstruction, perform the Heimlich manoeuvre (stand behind the patient, grip the wrists across the patient’s upper abdomen, and tug sharply to raise the intrathoracic pressure and expel the foreign body). Otherwise perform a CXR, and liaise with the respiratory/ENT/cardiothoracic teams for retrieval under direct vision.
Usually H. influenzae type b, also S. pneumoniae. Treat with third-generation cephalosporin, e.g. cefotaxime 2g tds (adults). Children more likely to require intubation, but if any concerns over airway, then the patient (adult or child) should be monitored on ITU after anaesthetic assessment.
Uncommon in the UK; occasionally seen in patients returning from abroad. Toxin-mediated problems include myocarditis and neuritis. Treat with diphtheria antitoxin + antibiotic eradication of organism (consult microbiology).
Unlikely to cause life-threatening obstruction without warning symptoms over at least a few days. If significant stridor is present, then administer 200mg of hydrocortisone, and thereafter prednisolone 40mg od PO. If laryngeal origin, liaise with ENT regarding tracheostomy. Lung cancer in the trachea, or extrinsic cancer eroding into the trachea, will require urgent radiotherapy (or occasionally laser or cryotherapy via a bronchoscope).