Oxford Medical Publications Oxford Handbook for the Foundation Programme

► Airway	Check airway is patent; consider manoeuvres/adjuncts
► Breathing	If no respiratory effort—CALL ARREST TEAM
► Circulation	If no palpable pulse—CALL ARREST TEAM

►► Call for senior help early if patient is deteriorating. Use emergency call bell to summon help quickly—don’t leave the patient.

• Sit patient up

• 15L/min O₂ in all patients if acutely unwell

• Monitor pulse oximeter, BP, defibrillator’s ECG leads if unwell

• Obtain a full set of observations including temp

• Take a brief history if possible/check notes/ask ward staff

• Examine patient: condensed RS, CVS, ±abdo exam

• Establish likely causes and rule out serious causes

• Initiate further treatment, see pp. 277–278

• Venous access, take bloods:

•FBC, U+E, LFT, CRP, bld cultures, D-dimer, cardiac markers

• Arterial blood gas, but don’t leave the patient alone

• ECG to exclude arrhythmias and acute MI

• Request urgent CXR, portable if too unwell

• Call for senior help

• Reassess, starting with A, B, C …

• In COPD/known CO₂ retention, rapidly titrate down O₂ to lowest flow to maintain normal sats for this patient (usually 88–92%). Beware of CO₂ retention and have a low threshold for repeat ABG.

Breathlessness and low sats

► Worrying features RR >30, sats <92%, systolic BP <100mmHg, chest pain, confusion, inability to complete sentences, exhaustion, tachy/bradycardia, silent chest.

Think about ► Life-threatening causes of respiratory failure See Table 8.1; Most likely COPD/asthma, pneumonia, pulmonary oedema (LVF), PE, MI; Others Pneumothorax, pleural effusion, arrhythmia, acute respiratory distress syndrome (ARDS), sepsis, metabolic acidosis, anaemia, pain, panic, foreign body/aspiration; Chronic COPD, lung cancer, bronchiectasis, interstitial lung disease, TB.

Ask about Speed of onset, cough, change in sputum (quantity, colour), haemoptysis, wheeze, chest pain (related to movement, pleuritic), chest trauma, palpitations, dizziness, difficulty lying flat, recent travel, weight loss; PMH Cardiac or respiratory problems, malignancy, old or exposure to TB; DH Inhalers, home nebulizers, home O₂, cardiac medication, allergies; SH Smoking (pack-years), pets, exercise tolerance, previous/current occupation (asbestos exposure). PE risk factors Recent surgery/immobility/fracture/travel/hospitalization, oestrogen (pregnancy, HRT, the pill), malignancy, previous PE/dvt, thrombophilia, varicose veins, obesity, central lines.

Obs Temp, RR (11–20 is normal), BP, HR, sats (should be >94%¹), O₂ requirements (improving or worsening?).

Look for Ability to speak full sentences, confusion, cyanosis, CO₂ flap, tremor, clubbing, rashes, itching, swollen lips/eyes, raised JVP, tracheal shift and tug, use of accessory muscles, abnormal percussion, unequal air entry, crackles, stridor, wheeze, bronchial breathing, swollen/red/hot/tender legs, swelling of ankles, cold peripheries.

Investigations PEFR If asthma suspected (may be too ill); blds FBC, U+E, LFT, CRP, D-dimer (if PE suspected and Wells score <4 p. 284), cardiac markers, blood cultures; Sputum (May need physio or saline nebs to help) inspect and send for M,C+S; AFBs if TB risk; ABG ( pp. 598–599), keep on O₂ if acutely SOB; ECG ( pp. 586–588); CXR ( pp. 596–597); portable if unwell, though image quality may be poor; Spirometry Should be done once the patient has been stabilized to help confirm the diagnosis ( p. 600).

Treatment Sit all patients up and give 15L/min O₂ – this saves lives. This can be reduced later since CO₂ retention in COPD takes a while to develop. Check sats and ECG in all patients:

• Stridor—call an anaesthetist ( p. 291)

• Wheeze—give nebulizer ( p. 279), eg salbutamol 5mg ±ipratropium 500micrograms STAT (drive by oxygen or air as appropriate)

• Unilateral resonance, reduced air entry ±tracheal deviation and shock—consider tension pneumothorax and treat urgently ( p. 285)

• Asymmetrical coarse crackles,↓air entry, bronchial breathing—consider pneumonia ( p. 282)

• Symmetrical fine crackles,↓air entry,↑ JVp—consider LVF ( p. 288)

• Normal exam—consider PE, asthma, cardiac, and systemic causes.

Table 8.1 Common causes of breathlessness

	History	Examination	Investigations
COPD	Usually smoker, change in productive cough, worsening wheeze	±wheeze/crackles, ±cyanosed/pursed-lip breathing, look for infection and pneumothorax	CXR hyperexpanded, flat diaphragms; exclude pneumonia and pneumothorax ABG; sputum
Asthma	Known asthma, recent exposure to cold air, allergens or drugs (NSAIDs, β-blockers), viruses	Wheeze ±crackles, look for signs of infection or pneumothorax	↓PEFR; CXR; exclude pneumonia and pneumothorax ABG; eosinophil count
Pneumonia	Productive cough, green sputum, feels unwell ±pleuritic pain	Febrile, asymmetrical air entry, crackles, bronchial breath sounds ±↓percussion	↑WCC/NØ/CRP, consolidation or blunted angles on CXR ( pp. 596–597); sputum MC and S
Pulmonary embolism	PE risk factors, leg pain, ±pleuritic chest pain and haemoptysis	↑JVP, ↑HR (may be only sign); may have evidence of DVT; can be severely shocked	↓PaCO₂ ±hypoxia on ABGs, ↑D-dimer, CXR often normal
Pulmonary oedema	Known cardiac problems, orthopnoea, swollen legs	↑JVP, symmetrical fine inspiratory crackles, pink frothy sputum, dependent oedema, cold peripheries	Cardiomegaly + fluid overload on CXR ( pp. 596–597), ECG may show ischaemia or previous MI
Pneumo- thorax	Sudden onset pleuritic chest pain ±trauma. Underlying lung disease and previous episodes or tall, thin, male	Unequal air entry and expansion, hyper-resonant ±displaced trachea (late)	Needle decompression of tension pneumothorax; CXR shows pleura separated from ribs
Pleural effusion	Gradual onset breathlessness, ±pleuritic chest pain	Reduced expansion, stony dull base	Effusion on CXR
ARDS	Concurrent severe illness	Hypoxic, very unwell	New bilateral infiltrates on CXR
Anaemia/MI/ARRHYTHMIAS	Chest pain, palpitations, dizziness, tiredness	Irregular or fast pulse, shocked, pale	Abnormal ECG ( pp. 586–588), ↓Hb, ↑cardiac markers
►► Anaphylaxis	Sudden onset, itching, swelling, urticarial rash, new drugs/food	Stridor, ±wheeze, shock, swollen lips and eyes, blanching rash	IM adrenaline, IV steroids ( pp. 484–485); acute and convalescent serum tryptase

Asthma

A common chronic disease characterized by variable airflow obstruction, inflammation, and hyper-responsiveness that results in wheeze, chest tightness, dyspnoea, and cough.

Symptoms Episodic breathlessness, wheeze and chest tightness; family or personal Hx of atopy (hayfever, eczema, asthma).

Signs Wheeze, tachypnoea, silent chest, hyperinflated chest.

Investigations PEFR Reduced in acute setting compared with best or predicted based upon age/height, or diurnal variation on self-monitoring as out- patient; ABG Normal or ↓ PaO₂ with a ↓ PaCO₂ due to hyperventilation. ►► Beware normal/rising CO₂ ?Patient tiring; CXR Hyperexpanded, exclude pneumonia and pneumothorax; Spirometry ↓ FEV₁, ↓ FEV₁:FVC ratio. Acute exacerbation Sit up and give 15L/min O₂. Salbutamol 5mg NEB ±ipratropium 500micrograms NEB and prednisolone 40mg PO (or hydrocortisone 200mg IV). Drive the nebulizer mask from O₂ supply, not air. Repeat salbutamol 2.5mg neb every 10–15min and reassess PEFR and sats frequently. Antibiotics if evidence of infection.

►► Severe Incomplete sentences, PEFR <50% of best, HR >110, RR >25.

►► Life-threatening PEFR <33% of best, silent chest, sats <92%, PaO₂ <8kPa, normal PaCO₂, poor respiratory effort, exhaustion, cyanosis, altered GCS, arrhythmia. ► C all ICU.

►► Near-fatal CO₂ retention. ► C all ICU.

► Beware those with previous ICU admissions.

No improvement Call for senior help. Consider:

• Early ICU input/assessment

• Aminophylline 0.5–0.7mg/kg/h, discontinue any oral theophylline and monitor levels (under senior guidance)

• Mg²⁺sulfate 2g (8mmol) IV over 20min.

Improving Admit those in whom PEFR<75% predicted after 1h therapy; gradually reduce supplemental O₂ and step from nebs to inhalers over several days; always check inhaler technique and ensure patient books follow-up with GP 48h post discharge.

Chronic treatment ( OHCM10 p. 182.) See Table 8.2, aiming for minimum treatment resulting in symptom control; monitor PEFR; always check inhaler technique before escalation; ensure allergen avoidance, smoking cessation and co-morbidities (GORD, nasal polyposis, OSA, breathing pattern disorder) identified and controlled.

Table 8.2 Simplified stepwise management of asthma (2016)

STEP	1	2	3*	4*	5
Salbutamol/terbutaline	✓	✓	✓	✓	✓
Low-dose inhaled corticosteroid (ICS)	✓
Low-dose ICS and LABA (combination)		✓
Medium-dose ICS and LABA (combination)			✓	✓	✓
Additional treatment (high-dose ICS/long-acting muscarinic agonist/leukotriene receptor antagonist/theophylline)				✓	✓
Oral steroids					✓

* If no response to LABA, stop LABA use medium–high-dose ICS alone. BTS guidelines include tables to predict PEFR where unknown. Source: data from https://www.brit-thoracic.org.uk/document-library/clinical-information/asthma/btssign-asthma-guideline-quick-reference-guide-2016

COPD ( OHAM4 p. 186.)²

Predominantly fixed airflow obstruction due to loss of elastic recoil in alveoli (emphysema) and narrowing of airways with excess secretions (bronchitis).

► Worrying signs ↓ GCS, rising CO₂.

Symptoms Breathlessness, cough, ↑sputum, tight chest, confusion, ↓exercise tolerance. NB ↑index of suspicion in (ex-)smoker.

Signs Wheeze, cyanosis, barrel-chested, poor expansion, tachypnoea.

Investigations ABG Often deranged in COPD, with type 2 RF common. Compare with previous samples and pay close attention to FiO₂; repeat after 30min in seriously ill patients; CXR Hyperexpanded, flat diaphragm (look for evidence of infection, pneumothorax, or bullae); Spirometry ( p. 600) ↓ FEV₁, ↓ FEV₁:FVC ratio (<70%).

Acute exacerbation Sit the patient up and give the minimum amount of O₂ to maintain sats ≥88% (aim for PaO₂~8kPa). Give salbutamol 2.5mg ±ipratropium 500micrograms NEB (drive by air, leaving nasal O₂ cannulae on under mask if necessary) and prednisolone 30mg PO (or hydrocortisone 200mg IV). Sputum for M,c+S. Get an ABG and CXR (portable if unwell). Use ABG results and clinical observations to guide further management:

• Normal ABG (for them) Continue current O₂ and give regular nebs

• Worsening hypoxaemia↑FiO₂, repeat ABG <30min, watch for confusion which should prompt a repeat ABG sooner; consider NIV

•↑ CO2 retention or ↓ GCS Request senior help ► urgently; consider:

• ICU input/assessment

• Aminophylline 0.5–0.7mg/kg/h, discontinue any oral theophylline and monitor levels (under senior guidance)

• NIV (Box 8.1).

Antibiotics Consider prescribing antibiotics (eg PO doxycycline or amoxicillin) if the patient has ↑ SOB, fevers, worsening cough, purulent sputum, or focal changes on CXR.

Chronic treatment ( OHCM10 p. 184) Smoking cessation is paramount. Stepwise therapy with inhalers can reduce symptoms, reduce the frequency and severity of exacerbations, and improve health status and exercise tolerance (Table 8.3). If still breathless despite maximal inhaler therapy, give home nebulizers. If PaO₂ consistently ≤7.3kPa (or ≤8kPa with additional risk factors), long-term O₂ therapy aiming for a minimum of 15h/d confers survival advantage. Annual influenza and pneumococcal vaccines decrease incidence of LRTI.³ Consider prescribing rescue packs (abx/steroids) to patients for acute (infective) exacerbation. Pulmonary rehab (see Box 8.2).

Complications Exacerbations, infection, cor pulmonale, pneumothorax, respiratory failure, lung cancer (beware haemoptysis and weight loss).

Box 8.1 Non-invasive ventilation (NIV)

Machines assist ventilation through a tightly fitting mask. Bi-level positive airway pressure (BiPAP) used in COPD patients with a pH ≤7.35 and CO₂ ≥6.0kPa who have failed to respond to initial medical therapy reduces mortality and length of admission. Patients who need NIV usually stay on the respiratory ward or HDU/ICU. Continuous positive airway pressure (CPAP) is not NIV since it does not help with mechanics of ventilation ( p. 288).

Table 8.3 Simplified COPD severity assessment and treatment (GOLD guidelines)

GOLD stage	Yearly exacerbations	Dyspnoea	Treatment	Severity of airflow limitation (FEV₁ % predicted)
A	1 or less	Breathless only on strenuous exercise	SABA or SAMA	≥80—GOLD 1 (Mild)
B	1 or less	Having to stop on walking	LAMA or/ + LABA	50–79—GOLD 2 (Moderate)
C	2 or more (or 1 hospital admission)	Breathless only on strenuous exercise	LAMA + LABA or LABA + ICS	30–49—GOLD 3 (Severe)
D	2 or more (or 1 hospital admission)	Having to stop on walking	ICS + LABA + LAMA (triple therapy)	<30—GOLD 4 (Very severe)

Source: data from Global Initiative for Chronic Obstructive Lung Disease, 2017 report, http://goldcopd.org/wp-content/uploads/2016/12/wms-GOLD-2017-Pocket-Guide.pdf

Table 8.4 Some common inhalers for asthma and COPD

Drug type	Medication	Trade name eg	Colour
Short-acting β agonist	Salbutamol	Ventolin^®	Blue
Short-acting β agonist	Terbutaline	Bricanyl^®	Blue
Inhaled steroids	Beclometasone	Qvar^®	Brown
	Budesonide	Pulmicort^®	Brown
	Fluticasone	Flixotide^®	Orange
	Ciclesonide	Alvesco^®	Red
Inhaled steroids and long-acting β agonist (combination)	Beclomethasone/formoterol	Fostair^®	Pink
	Budesonide/formoterol	Symbicort^®	Red
	Fluticasone/salmeterol	Seretide^®	Purple
	Fluticasone/vilanterol	Relvar^®	Yellow
Long-acting anticholinergic	Tiotropium	Spiriva^®	Grey
	Umeclidinium	Incruse^®	Green
	Glycopyrronium	Seebri^®	Orange
	Aclidinium	Eklira (Genuair)^®	Green
Long-acting β agonist and long-acting anticholinergic (combination)	Vilanterol and umeclidinium	Anoro^®	Red
	Indacaterol and glycopyrronium	Ultibro^®	Yellow
	Oldaterol and tiotropium	Spiolto^®	Green
	Formoterol and aclidinium	Duaklir^®	Orange

Box 8.2 Pulmonary rehabilitation

Patients with chronic lung disease who take part in a structured 8–12wk pulmonary rehabilitation programme with a graduated exercise regimen see increased exercise tolerance and improved well-being,⁴ although this does not reverse pathological processes or improve spirometry. Diet and other lifestyle advice are also covered.

Pneumonia ( OHAM4 p. 166.)⁵

► Worrying signs CURB-65 score ≥3 (see ‘Severity’, p. 282).

Symptoms Cough, purulent sputum, pleuritic chest pain, breathless, haemoptysis, fever, unwell, confusion, anorexia.

Signs ↑temp, ↑ RR, ↑ HR, ↓sats, unequal air entry, reduced expansion, dull percussion, bronchial breathing.

Severity The CURB-65 criteria (see Fig. 8.1) are a validated set of variables that support (but do not replace) clinical judgement in community-acquired pneumonia on whether to admit.⁶ In the out-patient setting, omit urea to get a CRB-65 score; patients scoring 0 (and possibly 1–2) are suitable for home treatment.

Investigations blds ↑ WCC; ↑ neutrophils; ↑ CRP; bld cultures. If CURB-65 ≥2; Sputum cultures If CURB-65 ≥3 (or CURB-65=2 and not had antibiotics); Urine If CURB-65 ≥2 test for pneumococcal antigen; if CURB-65 ≥3 or clinical suspicion, test for legionella antigen; ABG ↓PaO₂ (±↓PaCO₂ due to hyperventilation but not if tiring or COPD); CXR MAY show focal consolidation; repeat at 6wk if ongoing symptoms or high risk for malignancy/empyema.

Treatment Sit up and give O₂ as required. Give antibiotics according to local policy or p. 181 for empirical treatment. Look for dehydration and consider IV fluids. Most patients who require IV antibiotics can safely be switched to PO therapy by day 3.⁷ Offer a 5d course of antibiotic therapy for patients with low-severity CAP; consider a 7–10d course of antibiotic therapy for patients with moderate and high severity CAP. If symptoms not resolving by day 3, repeat CRP and CXR to exclude pleural effusion/empyema.

Complications Empyema, respiratory failure, sepsis, confusion.

Hospital-acquired pneumonia Pneumonia developing ≥48h after admission and not felt to have been incubating at time of admission. Causative organisms will include Gram –ve bacilli (eg Pseudomonas or Klebsiella species, E. coli.) as well as S. pneumoniae and S. aureus (including MRSA). Symptoms and signs can be severe, particularly in frail patients with other comorbidities, and lung necrosis and cavitation may develop. Empirical antibiotic selection should be guided by local policy ±discussion with a microbiologist.

Aspiration pneumonia Aspiration of gastric contents refluxing up the oesophagus and down the trachea may lead to a sterile chemical pneumonitis. Alternatively, oropharyngeal bacteria may be aspirated causing a bacterial pneumonia. Risk factors include ↓GCS (eg sepsis, anaesthesia, seizures), oesophageal pathology (eg strictures, neoplasia), neurological disability (eg dementia, MS, Parkinson’s disease), or iatrogenic interventions (eg NG tube, OGD, bronchoscopy). At-risk patients can be identified by bedside swallow evaluation ( p. 356). Care is supportive, with O₂ supplementation, suctioning of secretions, and attention to prevention of further aspiration (involve SALT and chest physio). Empirical antibiotics can be of benefit if bacterial pneumonia suspected (eg persistent fever, purulent sputum)—eg co-amoxiclav 625mg/8h PO or 1.2g/8h IV with metronidazole 400mg/8h PO or 500mg/8h IV.

Fig. 8.1 Severity assessment and investigations in community-acquired pneumonia. Adapted by permission from BMJ Publishing Group Limited. British Thoracic Society guidelines for the management of community acquired pneumonia in adults: update 2009, Lim, W.S. et al. Thorax 2009 64 (Suppl 3):iii1.

Pulmonary embolism ( OHAM4 p. 120.)

Symptoms Often none except breathlessness; may have pleuritic chest pain, haemoptysis, dizziness, leg pain; consider risk factors in Table 8.5.⁸

Signs ↑ JVP, ↑ RR, ↑ HR, ↓ BP, RV heave, hypotension, pleural rub, ±pyrexia. Tachycardia and tachypnoea may be the only clinical signs.

Investigations D-dimer Will be raised in many situations (infection, malignancy, MI, CVA to name a few) while a normal D-dimer must be interpreted in the clinical context (Box 8.3); ECG (sinus tachycardia commonest finding), RBBB, inverted T waves V1–V4 or S₁Q₃T₃; ABG type 1 RF (↓ CO₂, ± ↓ O₂₎ (if large PE); CT-PA Is the definitive imaging modality, though V/Q scan may be used, eg in those with renal failure, pregnancy.

Acute treatment Sit up (unless ↓ BP) and give 15L/min O₂. If life-threatening (hypotension +shock) seek immediate senior support, arrange an urgent CT-PA + echo and consider thrombolysis. Otherwise parenteral anticoagulation ( pp. 420–422), eg enoxaparin 1.5mg/kg/24h SC and pain relief; IV fluids if ↓ BP.

Chronic treatment Anticoagulation ( pp. 420–422) eg warfarin/ DOAC. Length of treatment will depend on risk factors/context.⁹

Box 8.3 Clinical risk assessment for PE

PEs are common and potentially fatal, but associated with non-specific clinical signs. The CT-PA offers excellent diagnostic accuracy but exposes your patient to 3.6yr of background radiation, along with nephrotoxic IV contrast medium, while taking up significant resources. So can D-dimer testing help? Remember, the negative predictive value of any test is determined by the prevalence of whatever disease you are testing for: the value of D-dimer testing lies in the excellent negative predictive value when the risk of a PE is low. In those at high risk, negative D-dimer levels do not provide sufficient reassurance.

The Wells score for PE (Table 8.5) is a clinically reliable method of identifying the risk of PE, and hence deciding on further testing.

• Those scoring ≤4 are low risk: test for D-dimers.¹⁰ If elevated, proceed to CT-PA; if negative, then consider alternative diagnoses

• Those scoring >4 are high risk: proceed to CT-PA testing and start treatment dose of LMWH.

Table 8.5 Wells score for pulmonary embolism

Clinical feature	Points
Signs/symptoms of DVT (leg swelling and pain on deep vein palpation)	3
PE most likely clinical diagnosis	3
HR >100	1.5
>3d immobilization or surgery in past 4wk	1.5
Previous DVT/PE	1.5
Haemoptysis	1
Malignancy (current treatment or treatment in past 6mth or palliative)	1

Source: data from Wells et al. Thromb Haemost 2000;83:358.

Spontaneous pneumothorax (OHAM4 p. 204)¹¹

May occur apparently spontaneously (primary) or in the presence of underlying lung disease or injury (secondary).

Risk factors Primary Tall, thin, male; Marfan’s; recent central line, pleural aspiration or chest drain; Secondary COPD, asthma, infection, trauma, mechanical ventilation.

Symptoms Breathlessness ±chest pain.

Signs Hyper-resonant and reduced air entry on affected side, tachypnoea, may have tracheal deviation or fractured ribs.

Investigations CXR Lung markings not extending to the peripheries, line of pleura seen away from the periphery.

Treatment Sit up and give 15L/min O₂. Chest drain/aspiration as directed by BTS guidelines ( p. 286). In essence, primary pneumothoraces can potentially be discharged, while secondary pneumothoraces require admission and either aspiration ( p. 552) or, more usually, drainage ( pp. 554–555).

►► Tension pneumothorax

If air trapped in the pleural space is under positive pressure (eg following penetrating trauma or mechanical ventilation) then mediastinal shift may occur, compressing the contralateral lung and reducing venous return. The patient may be hypotensive, tachycardic, tachypnoeic, with unilateral hyper-resonance and reduced air entry; ↑ JVP and may have tracheal deviation away from the side of the pneumothorax. ► This is an emergency, it will rapidly worsen if not treated. Sit up and give 15L/min O₂. Treat prior to CXR. Insert a large cannula (orange/grey) into the 2nd intercostal space, midclavicular line. Listen for a hiss and leave it in situ; insert a chest drain on the same side. If there is no hiss, leave the cannula in situ and consider placing a 2nd cannula or consider alternative diagnoses; a chest drain is usually still required to prevent a tension pneumothorax accumulating.

Pleural effusion ( OHAM4 p. 216.)¹¹

Excessive fluid within the pleural space reflects an imbalance between hydrostatic and oncotic pressures within the pleural vasculture, and/or disruption to lymphatic drainage.

Causes Pleural effusion may be divided into those causing transudates (where pleural fluid protein <25g/L—tend to be bilateral) pulmonary oedema, cirrhosis, nephrotic syndrome, hypothyroidism, intestinal malabsorption/failure and exudates (protein >35g/L—may be unilateral or bilateral) malignancy, infection, vasculitides, rheumatoid; if purulent and pH <7.2, this is empyema reflecting infection.

Light’s criteria These help differentiate, especially when protein >25g/L but <35g/L. Consider the effusion an exudate if pleural protein:serum protein >0.5, pleural LDH:serum LDH >0.6, or pleural LDH >2/3 of upper limit of normal serum value.

Symptoms The patient may be breathless with pleuritic chest pain.

Signs Stony dull to percussion with reduced air entry, tachypnoea.

Investigations CXR Loss of costophrenic angle with a meniscus pp. 596–597.

Treatment Sit up and give 15L/min O₂. Investigate the cause; if the effusion is large, pleural aspiration ( p. 552) may relieve symptoms and aid diagnosis (draining >1.5L/24h may cause re-expansion pulmonary oedema).

Algorithms for the treatment of spontaneous pneumothorax

Fig. 8.2 Treating spontaneous pneumothorax in patients over 50 with no significant smoking history or evidence of underlying lung disease. Adapted by permission from BMJ Publishing Group Ltd, Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010, MacDuff, A. et al. Thorax 2010 65 (Suppl 2):ii18.

Fig. 8.3 Treating pneumothorax in patients over 50 with significant smoking history or evidence of underlying lung disease. Adapted by permission from BMJ Publishing Group Ltd, Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010, MacDuff, A. et al. Thorax 2010 65 (Suppl 2):ii18.

Pulmonary oedema ( OHAM4 p. 87.)

Symptoms Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, frothy sputum; coexistent dependent oedema or previous heart disease.

Signs ↑ JVP, tachypnoea, fine inspiratory basal crackles, wheeze, pitting cold hands and feet; oedema (ankles and/or sacrum) suggests right heart failure.

Investigations blds (Look specifically for anaemia, infection or MI): fbc, U+E, CRP, cardiac markers; BNP (normal levels unlikely in cardiac failure); ABG May show hypoxia; ECG Exclude arrhythmias and acute STEMI, may show old infarcts, LV hypertrophy or strain ( pp. 586–588); CXR Cardiomegaly (not if AP projection), signs of pulmonary oedema ( pp. 596–597); Echo Poor LV function/ejection fraction.

Acute treatment Sit up and give 15L/min O₂. If the attack is life-threatening call an intensivist early as CPAP and ICU may be required. Otherwise monitor HR, BP, RR, and O₂ sats while giving furosemide 40–120mg IV ±diamorphine (repeat every 5min up to 5mg max, watch RR) 1mg boluses IV (repeat up to 5mg, watch RR). If further treatment is required, be guided by blood pressure:

• Systolic >100 Give 2 sprays of sublingual GTN followed by an IV nitrate infusion (eg GTN starting at 4mg/h and increasing by 2mg/h every 10min, aiming to keep systolic >100; usual range 4–10mg/h; p. 203)

• Systolic <100 The patient is in shock, probably cardiogenic. Get senior help as inotropes are often required. Do not give nitrates

• Wheezing Treat as for COPD alongside above-mentioned treatment

• No improvement Give furosemide up to 120mg total (more if chronic renal failure) and consider CPAP (see Box 8.4). Insert a urinary catheter to monitor urine output, ±CVP monitoring. Request senior help. Consider HDU/ICU.

Once stabilized, the patient will need daily weights ±fluid restriction. Document LV function with an echo and optimize treatment of heart failure ( p. 274). Oral bumetanide may be preferred to oral furosemide for diuresis since absorption is said to be more predictable in the presence of bowel oedema, though evidence for this is lacking. Always monitor U+E during diuresis: The heart-sink patients are those with simultaneously failing hearts and kidneys who seem fated to spend their last days alternating between fluid overload and AKI—close liaison with the patient’s GP and palliative care teams is as essential as ever here.

Box 8.4 Continuous positive airway pressure (CPAP)

Application of positive airway pressure throughout all phases of the respiratory cycle limits alveolar and small airway collapse, though the patient must still initiate a breath and have sufficient muscular power to inhale and exhale. Pursed-lip breathing has a similar effect, and is often observed in patients with chronic lung disease. CPAP is often used in the acute treatment of pulmonary oedema or the chronic treatment of sleep apnoea (may use nasal CPAP).

SVC obstruction ( OHCM10 p. 528.)

Symptoms Breathlessness, orthopnoea, facial/arm swelling, headache.

Signs Facial plethora (redness), facial oedema, engorged veins, stridor.

Pemberton’s test Elevating the arms over the head for 1min results in increased facial plethora and ↑ JVP.

Investigations CXR/CT Mediastinal mass, tracheal deviation, venous congestion distal to lesion; Other Sputum cytology for atypical cells.

Treatment Seek senior input early. Sit up and give 15L/min O₂. Dexamethasone 4mg/6h PO/IV. Consider diuretics to decrease venous return and relieve SVC pressure (eg furosemide 40mg/12h PO). Otherwise symptomatic treatment while arranging for tissue diagnosis.

Acute respiratory distress syndrome (ARDS) ( OHAM4 p198.)

Acute-onset respiratory failure due to diffuse alveolar injury following a pulmonary insult (eg pneumonia, gastric aspiration) or systemic insult (shock, pancreatitis, sepsis). Characterized by the acute development of bilateral pulmonary infiltrates and severe hypoxaemia in the absence of evidence for cardiogenic pulmonary oedema.

Symptoms Breathlessness, often multiorgan failure.

Signs Hypoxic, signs of respiratory distress, and underlying condition.

Investigations CXR Bilateral infiltrates.

Treatment Sit up and give 15L/min O₂. Refer to HDU/ICU early and treat underlying cause. Often requires ventilation.

► Stridor in a conscious adult patient

► Airway	Acute stridor—CALL ANAESTHETIST AND ENT URGENTLY
► Breathing	If poor respiratory effort—CALL ARREST TEAM
► Circulation	If no palpable pulse—CALL ARREST TEAM

►► Call for senior anaesthetics and ENT help immediately.

► Life-threatening causes

• Infection (epiglottitis, abscess)

Fig. 8.4 Adult choking treatment algorithm, 2015 guidelines. Reproduced with the kind permission of the Resuscitation Council (UK).

Cough

Box 8.5 Causes of coughs

*Acute*	URTI, post-viral, post-nasal drip (allergy), pneumonia, LVF, PE
*Chronic*	Asthma, COPD, bronchitis, bronchiectasis, smoking, post-nasal drip, oesophageal reflux, pneumonia, TB, parasites, interstitial lung disease, heart failure, ACEi, lung cancer, sarcoid, sinusitis, cystic fibrosis, habitual
*Bloody*	Massive Bronchiectasis, lung cancer, infection (including TB and aspergilloma), trauma, AV malformations Other Bronchitis, PE, LVF, mitral stenosis, aortic aneurysm, vasculitides, parasites

Usually, the cause of coughing is obvious (Box 8.5). Chronic (>8wk), unexplained coughing with a normal CXR and the absence of infective features requires a considered approach. Is there diurnal or seasonal variation in coughing (cough-variant asthma; do PEFR diary, lung function testing, and a trial of inhaled steroids)? Is there a history suggestive of gastro-oesophageal reflux (trial of PPI)? Does the onset of a dry cough follow the introduction of an ACEi (consider an AT II receptor blocker)? Or is there a sensation of mucus accumulation at the back of the throat (consider chronic/allergic rhinitis and ‘post-nasal drip’ and a trial of nasal steroids or antihistamines)?

Haemoptysis Coughing up blood, >500mL over 24h is massive.

Management ABC, establish patent airway; FBC, U+E, LFT, clotting, G+S, sputum C+S and cytology, ABG, ECG, CXR. Sit up, 15L/min O₂. Codeine 60mg PO (may ↓cough) If massive Good IV access (≥green), monitor HR and BP, immediate referral to respiratory team for urgent bronchoscopy ±CT thorax.

Bronchiectasis ( OHCM10 p. 172.)¹²

Abnormal and permanently damaged and dilated bronchi caused by destruction of the elastic tissue of the bronchial walls.

Causes Cystic fibrosis, infection (pneumonia, TB, HIV), tumours, immunodeficiency, allergic bronchopulmonary aspergillosis, foreign bodies, aspiration, asthma, rheumatoid arthritis, idiopathic.

Symptoms Chronic cough with purulent sputum ±haemoptysis, halitosis.

Signs Clubbing, coarse inspiratory crepitations ±wheeze.

Investigations FBC, immunoglobulins, aspergillus serology; blood or sweat test (for CF); Sputum C+S; CXR Thickened bronchial outline (tramline and ring shadows) ±fibrotic changes; CT thorax (‘high-resolution CT’) Bronchial dilatation; spirometry; Bronchoscopy for other diagnoses.

Acute treatment O₂ ±BIPAP as required, ±bronchodilators ±cortico-steroids. Typical recurrent infections include Pseudomonas (consult local antibiotic guidelines). Chest physiotherapy to mobilize secretions.

Chronic treatment Chest physio, inhaled/nebulized bronchodilators, antibiotics, consider prophylactic, rotating antibiotics if ≥3 exacerbations/yr. NIV and surgery may be considered where medical management fails.

Complications Recurrent pneumonia, pseudomonal infection, massive haemoptysis, cor pulmonale.

¹ Patients with chronic lung disease may normally have sats <92%. 88–92% is a better target. See BTS guidelines on emergency use of oxygen in adults at www.brit-thoracic.org.uk

² NICE guidelines available at guidance.nice.org.uk/CG101

³ Global Initiative for Chronic Obstructive Lung Disease. 2017 report. http://goldcopd.org/wp-content/uploads/2016/12/wms-GOLD-2017-Pocket-Guide.pdf

⁴ Summarized at https://www.brit-thoracic.org.uk/document-library/clinical-information/pulmonary-rehabilitation/bts-quality-standards-for-pulmonary-rehabilitation-in-adults/

⁵ NICE guidelines available at guidance.nice.org.uk/CG191

⁶ Lim WS, et al. Thorax 2003;58:377 full-text available free at: www.ncbi.nlm.nih.gov/pmc/articles/PMC1746657

⁷ Oosterheert JJ, et al. BMJ 2006;333:1193 full-text available free at: www.ncbi.nlm.nih.gov/pmc/articles/PMC1693658

⁸ NICE guidelines available at guidance.nice.org.uk/CG144

⁹ 3mth may suffice if low risk (eg 1st PE with identified risk factor now removed); if higher risk (recurrent or unprovoked PEs, or thrombophilia) treatment may need to be long term.

¹⁰ In pregnancy, D-dimer testing is uninterpretable. If clinical suspicion, then a Doppler U/S of leg veins is the safest initial investigation—treat if DVT seen. If this is negative, a half-dose V/Q scan provides an acceptable balance of diagnostic utility with radiation exposure. The risk of CT-PA is not to the foetus (which can be shielded) but to proliferating maternal breast tissue.

¹¹ British Thoracic Society guidelines available at https://www.brit-thoracic.org.uk/standards-of-care/guidelines/bts-pleural-disease-guideline/

¹² British Thoracic Society guidelines available at https://www.brit-thoracic.org.uk/standards-of-care/guidelines/bts-guideline-for-non-cf-bronchiectasis/

Chapter 8

Respiratory

► Breathlessness and low sats emergency

Breathlessness and low sats

Asthma

► Stridor in a conscious adult patient

Cough