Fortunately, the emergency crew recognised the problem and tried to clear the airway. There was no improvement so the Heimlich manoeuvre was performed and a large bone was expelled with immediate relief of the man’s respiratory distress. He was taken to A&E for assessment but discharged after 2 hours.

Remember

The Heimlich manoeuvre is used to expel an inhaled foreign body:

• Stand behind the patient

• Encircle the upper part of the abdomen, just below the patient’s rib cage, with your arms

• Give a sharp, forceful squeeze, forcing the diaphragm sharply into the thorax.

This should expel sufficient air from the lungs to force the foreign body out of the trachea. If this fails, urgent assessment by experienced ENT or cardiothoracic clinician is required. Fibre optic or rigid bronchoscopy will be required if obstruction beyond vocal cords.

Other causes of upper airway obstruction are shown in Table 11.1, all of which require emergency management, which is also shown.

Table 11.1 Causes of upper airways obstruction (with management strategies)

Cough

Cough is common and when persistent can cause considerable fear and distress. Apart from the immediate discomfort of coughing, paroxysmal cough can interrupt sleep, provoke retching or vomiting and, if severe, result in rib fractures or syncope. Always enquire about sputum and its colour.

Case history

A 67-year-old man is admitted to hospital with a myocardial infarct. Following successful coronary intervention he is discharged on anti-platelet therapy, atorvastatin and enalapril. When seen again 2 weeks later, he was very well but complained of a persistent hacking cough. This had been keeping him awake at night.

In this case, as the patient has only a cough and is not breathless, the cause is very likely to be the ACE inhibitor (enalapril). This should be stopped and an ACE receptor antagonist, e.g. vasartan started. Unlike ACE inhibitors, angiotensin receptor antagonists do not affect bradykinin metabolism and do not produce a cough.

Cough is provoked by stimulation of mucosal and stretch receptors of the lung. Accordingly it has a number of causes:

Investigations

All patients with persistent cough should have a CXR

Other investigations will depend on the likely cause, e.g. serial peak flow in asthma, contrast studies if gastro-oesophageal reflux or aspiration is suspected and sputum culture, including request for Mycobacterium tuberculosis isolation if the cough is productive.

Breathlessness and wheeze

Asthma causes breathlessness, cough and wheeze. However, all that wheezes is not asthma.

Information

• Asthma provocation tests might be required to exclude mild–moderate and variable bronchial irritability

• Bronchoscopy will be required in all chronic cases remaining undiagnosed

Differential diagnosis of asthma:

Figure 11.1 shows causes and triggers of asthma.

Figure 11.1 Causes and triggers of asthma. RSV, respiratory syncytial virus; NSAIDs, non-steroidal anti-inflammatory drugs.

Information

Causes of stridor:

• Tumour

• Foreign body

• Bilateral vocal cord palsy

• Laryngeal oedema

• Thyroid goitre

Case history

A 24-year-old female was admitted to MAU with breathlessness for 6 h. She has had a ‘cold’ for 2 days. Past history revealed her being ‘chesty’ as a child. It was noticed that she could not complete sentences easily. Heart rate was 126/min and respiratory rate was 30/min. There was expiratory wheeze over the lung fields. This patient has severe acute asthma.

Remember

Severe acute asthma:

• Increased breathlessness/cannot complete sentences

• Respiratory rate > 25/min

• Heart rate > 100/min

• PEFR 30–50% of best

• Arterial oxygen saturation (SaO₂) < 92%

30 min later there has been no significant improvement in her breathlessness and PEFR. What would you do next?

• Call for senior help.

• Continue with nebulised β₂ agonist, now with added ipratropium (500 µg). Repeat every 30 min if necessary.

• Intravenous aminophylline infusion can be used if patient does not respond to repeated nebulisation with β₂ agonist and ipratropium. However, do not use this if oral aminophylline has been taken.

Information

Indications for HDU or intensive care

Presence of life-threatening features and:

• PaO₂ < 8 on 60% oxygen

• PaCO₂ >6 kPa

• Previous history of requiring ventilation.

Remember

• Beware of the SILENT CHEST!

If asthma is very severe, air entry will be minimal and breath sounds quiet or absent.

There is now improvement in PEFR and breathlessness with nebulised β₂ agonist and ipratropium. What treatment should be offered to her now?

Continuing management should be:

• Keeping SaO₂ > 90% with oxygen supplementation

• Corticosteroids: prednisolone 20–40 mg daily, on a reducing dose

• 2–4-hourly nebulised short acting β₂ agonist (SABA) therapy.

When could she be discharged?

The patient can be discharged when:

• Symptoms, particularly nocturnal symptoms, have improved

• Ideally, PEFR should be 75% of best and diurnal variation (i.e. ‘morning dips’) < 25%. If patient is improving and compliance expected to be good, an earlier discharge is reasonable.

24–48 h before discharge

• Add inhaled corticosteroids, e.g. beclometasone, to oral steroids.

• Replace nebulised bronchodilators with inhalers.

• Introduce long-acting inhaled β2 agonists, e.g. salmeterol.

• Check inhaler technique (? might need spacer).

• Determine the cause of this attack (non-compliance, infection, allergen exposure).

Further reading

2009 British Thoracic Society Guidelines for asthma. www.brit-thoracic.org.uk, 2009.

Hyperventilation

Case history

A 15-year-old schoolgirl is brought by her teacher to the A&E department with dizziness and feeling faint. You notice that she is anxious, sighing and has erratic ventilation. There are no other physical signs on examination. Her teacher volunteered that the girl was anxious about impending examinations.

What should you do?

Full examination, CXR, PEFR or spirometry, and arterial blood gases (even if oximetry is normal).

You have decided that her symptoms are due to hyperventilation. This should be confirmed by demonstration of a respiratory alkalosis with a low PaCO₂ and [H⁺] in the arterial blood. Reassure the patient and ask her to breathe into a closed paper bag: when settled she can be discharged with further reassurance. Note: mild asthma is a common provocative cause and might require further investigation.

Hyperventilation syndrome refers to a condition of recurrent attacks of anxiety, sometimes phobic in nature, and provoking such profound hyperventilation to cause a reduction in arterial pCO₂ that tetany occurs. Other features include perioral and digital paraesthesia, carpopedal spasm, muscle weakness, dizziness and a sense of impending loss of consciousness or fear.

An attack of hyperventilation can be induced by a strong emotional experience in otherwise normal individuals, e.g. witnessing an accident.

In many patients, the label of hyperventilation syndrome is inappropriately given when mild asthma or other conditions, such as heart failure, lie behind the respiratory sensation. Indeed, hypocapnia resulting from hyperventilation might further provoke bronchoconstriction.

Clinically obvious hyperventilation can also result from a metabolic acidosis and will be recognised by arterial blood gas analysis: a reduced pH and bicarbonate contrary to the alkalosis of respiratory hyperventilation.

Tetany: see p. 451; overbreathing can cause tetany (p. 451).

Progress.

This patient settled quickly. She was reassured that there was nothing seriously wrong with her. She was taken home to her parents with a pamphlet explaining the hyperventilation syndrome.

Haemoptysis

Case history

A 63-year-old male smoker presents with a 4-month history of cough. Recently he has been coughing up blood in his sputum. He has also been breathless on exertion.

Coughing up blood is a dramatic symptom and can be frightening to patients and their families.

Colour of blood – this can differ with different causes

• Pink frothy sputum: pulmonary oedema.

• Rusty sputum: pneumonia.

• Make sure it is not haematemesis, which would be suggested by:

• History of retching

• Altered blood (resembling coffee grounds)

• Low pH of contents.

Enquire about epistaxis, which may cause confusion. Blood-stained saliva suggests bleeding from gums.

Common conditions presenting with haemoptysis

• Carcinoma of the bronchus:

• Smoker

• Age > 40 years

• Usually abnormal chest X-ray.

• Pulmonary embolism:

• Risk factors for DVT

• Chest X-ray often negative

• History of acute breathlessness.

• Pulmonary tuberculosis:

• More common in Asian people (in the UK), people drinking alcohol in excess, patients with HIV infection

• Age often < 40 years

• Chest X-ray usually shows patchy opacities in the upper lobes.

• Bronchiectasis:

• History of purulent sputum and/or possibly recurrent haemoptysis over years

• Cystic lesions on chest X-ray at lung bases in some but not all patients

• High-resolution CT scan of the lungs is diagnostic, with bronchial dilation, loss of airway tapering at the periphery, bronchial wall thickening and thickening and cysts at the end of the bronchioles

• Bronchiectasis is also a feature of cystic fibrosis.

Remember

• Chest X-ray might be normal, e.g. pulmonary embolism

• Large opacity: consider malignancy or tuberculosis.

Less common causes of haemoptysis are:

Management of this case

A chest X-ray was taken (Fig. 11.2 and Information box) which showed a pleural effusion and a hilar mass. The pleural effusion was aspirated and sent for cytology. A pleural biopsy was taken under ultrasound control and showed no evidence of malignancy on histology.

Figure 11.2 Chest X-ray showing a left pleural effusion and a hilar mass.

Video-assisted thoracoscopy was then performed and this allowed visualisation of the pleura. A biopsy taken showed a squamous cell carcinoma.

The patient was referred to the multidisciplinary team for discussion of treatment options.

Information

Chest X-rays

A standard chest X-ray (CXR) is taken posteroanteriorly (PA), with the patient facing the X-ray plate; the beam is directed at the patient’s back at a standard distance.

An emergency department film is often taken anteroposteriorly (AP), with the patient lying down (supine) on the X-ray plate; the beam is directed at the patient’s front – the distance from X-ray source can vary.

In an AP:

• Heart size and mediastinum are magnified.

• Pleural effusion which lies along back of chest cavity when patient supine might be missed.

• Film quality may be poor.

Don’t request an AP ‘portable’ film unless it would be unsafe for the patient to have a PA film.

Management of massive haemoptysis

As little as 250 mL can fill the bronchial tree and be life threatening. Happily, this is uncommon but nevertheless frightening for everyone involved:

• Monitor: oxygen saturation with oximetry, blood pressure and pulse rate.

• Perform CXR. Exclude coagulation defects.

• Endotracheal intubation and suction might be required.

• Urgent bronchoscopy by an experienced doctor is sometimes required.

• A cuffed tube can be employed to protect the unaffected lung. It is inserted into the bronchus via a bronchoscope.

• Bronchial artery embolisation is highly effective if the bleeding vessel can be identified.

Information

Massive haemoptysis can occur in the following conditions:

• Tuberculosis

• Bronchiectasis

• Aspergilloma

• Carcinoma of the bronchus

Remember

Only a minority of patients have a malignant cause of massive haemoptysis.

Chest pain

Diagnosing the cause of a chest pain is often difficult; it can be straightforward or take days to diagnose correctly. A careful history (eliciting site, character and radiation of the pain) is often more useful than tests:

• Exercise-induced central chest pain is usually cardiac in origin.

• Rest pain might be: cardiac, pleuritic, musculoskeletal, nerve root irritation, oesophageal, mediastinal or referred pain from abdomen.

• Lung diseases only cause pain if the pleura, mediastinum, intercostal nerves or bones are involved.

Is it pleurisy?

Sharp pain in the sides of the chest, which ‘catches’ with breathing. This is often accompanied by fever, cough ± sputum or haemoptysis, indicating underlying lung disease.

Think of:

• Pneumonia and pleurisy

• Pulmonary infarction/embolism

• Pneumothorax

• Malignant invasion of pleura.

Is it nerve root irritation?

• Typically in a dermatome distribution around the chest. Might be unilateral.

• Vertebral OA, osteomyelitis, prolapsed disc.

• Malignant nerve root compression.

• Herpes zoster (shingles): is there a vesicular rash? (pain may precede rash).

Is it oesophageal?

Reflux causes retrosternal burning pain, usually after food. Worse lying flat and eased by antacid. Can be severe and mimic myocardial infarction.

Oesophageal rupture

Central pain with shock. Might have associated pleural effusion. Occurs after severe vomiting or more commonly endoscopy at which dilatation has been performed for a malignant lesion.

Is it referred pain from outside the chest?

Diaphragm irritation may cause shoulder tip pain. Localisation might be difficult for the patient. Several abdominal emergencies might have chest pain with or without abdominal pain.

Think of:

• Acute cholecystitis

• Acute duodenal ulceration

Is it genuine?

Yes – nearly always. Exclude organic disease in all cases.

A tiny minority might be attention seeking or have psychiatric disease. Even patients with Munchausen’s syndrome might have genuine disease.

Respiratory failure

Respiratory failure (PaO₂ < 8 kPa) is a common medical emergency often presenting with non-specific symptoms such as mild confusion or agitation. Recognition requires arterial blood gas (ABG) analysis (see below). Oximeters that estimate arterial oxygen saturation from the finger or ear lobe are useful in assessment or monitoring.

Oximeters might be falsely reassuring in the patient breathing oxygen. Importantly, they will not detect alveolar hypoventilation, producing high pCO₂.

Remember

All breathless patients should have oximetry checked at triage in A&E.

Respiratory failure commonly results from either a problem with the respiratory pump or because of intrinsic lung disease.

Remember

All unconscious patients should have ABG analysis at initial assessment.

With respiratory pump failure the arterial pCO₂ (PaCO₂) is raised. You should think of:

• Severe air-flow limitation, e.g. COPD

• Neurological depression, e.g. coma, sedatives, overdose

• Chest wall problem, e.g. flail chest, pneumothorax

• Neuromuscular disease, e.g. Guillain–Barré, old poliomyelitis.

In intrinsic lung disease (apart from COPD) hypoxaemia is often combined with a reduced PaCO₂

The hypoxaemia arises primarily from a mismatch of ventilation and perfusion in the pulmonary alveolar bed. Hypoxic stimulation of ventilation, coupled with abnormal respiratory sensation, then leads to a reduced arterial pCO₂ (alveolar hyperventilation). A raised PaCO₂ indicates impending respiratory arrest as it suggests either a reduction in ventilatory effort or failure of the respiratory pump.

In hypoxaemia with reduced PaCO₂ consider

• Infection, e.g. pneumonia

• Shock, e.g. sepsis, hypovolaemia, acute lung injury

• Asthma

• Cardiac disease, e.g. LVF, pulmonary hypertension

• Pulmonary embolism.

In respiratory failure arterial blood gas sampling is necessary to

• Assess severity

• Identify type, i.e. alveolar hypo- or hyperventilation

• Appreciate the degree of compensation (i.e. the chronicity of the condition)

• A coexisting metabolic acidosis commonly causes confusion and can be recognised by the base excess value (see below).

Information

ABG sampling is painful. Contrary to common belief, the use of local anaesthetic does not make the procedure more difficult. Heparin has a low pH and should be expelled from the syringe. Heparin-bonded microsamplers are available and small-diameter needles make local anaesthetic unnecessary. When taking ABG samples it is essential to note the inspiratory O₂ concentration (FiO₂).

Summary of acid–base changes (Fig. 11.3)

In a respiratory acidosis

Carbon dioxide clearance is reduced – there is alveolar hypoventilation. The PaCO₂ and [H⁺] rise. The HCO₃ is also increased due to renal compensation.

Figure 11.3 The Flenley acid–base nomogram. The bands show the 95% confidence limits representing the individual varieties of acid–base disturbance. The central white box shows the approximate limits of arterial pH and pCO₂ in normal individuals.

Examples: exacerbation of COPD, flail chest injury, Guillain–Barré syndrome.

In a respiratory alkalosis

There is alveolar hyperventilation and both the PaCO₂ and [H⁺] are decreased. The HCO₃ is slightly decreased. Examples: acute asthma, anxiety attack.

In a metabolic acidosis

There is disturbance of bicarbonate regulation or excessive H⁺ production. The HCO₃ is reduced and the PaCO₂ falls because of respiratory compensation.

Example: diabetic ketoacidosis, renal failure, shock.

Common ABG abnormalities

Life-threatening asthma

Supplemental O₂ is being provided (note the high PaO₂). There is a metabolic acidosis (note the pH and BE) as a result of metabolic demands exceeding O₂ delivery and producing a lactic acidosis. Airflow limitation limits the normal respiratory compensation to this profound acidosis.

Acute or chronic respiratory failure in a patient with COPD

Acute or chronic respiratory acidosis exacerbated by a high F_iO₂ using variable performance mask (40–60% O₂) (note high PaO₂ and PaCO₂). The high HCO₃ results from renal compensation. The patient was changed to 28% oxygen.

Severe pneumonia (F_iO₂ 60%)

Despite high F_iO₂ this patient is hypoxaemic because of ventilation: perfusion mismatch. The profound hypoxia despite oxygen and the associated metabolic acidosis indicate the need for urgent intubation and IPPV and are a reflection of circulatory failure resulting from septic shock.

Management

Respiratory failure can be difficult to assess or manage. Always review the CXR. Discuss with your consultant or other more senior staff. If you feel that the situation is unstable, do not hesitate to call an anaesthetist. Semi-elective intubation is much preferred to a respiratory arrest. It should be performed in the ward before transfer of the patient to the ICU.

How do I recognise impending respiratory arrest?

• Tachycardia > 120

• Tachypnoea, respiratory rate > 30

• Hypotension

• Sympathetic activation: pale and sweaty, agitation, confusion

• Progressive increase in PaCO₂ or fall in PaO₂

• Rapid desaturation on disconnection from O₂, e.g. when drinking or coughing.

Evaluation is often at the ‘end of the bed’: is the patient getting tired? Be sensitive to subtle changes or a failure to improve.

Treating the cause

• Individual causes will require different actions: for instance, an intercostal drain for a tension pneumothorax or large pleural effusion (see p. 364).

• In neurological coma, intubation might be necessary for airway protection or to manage raised intracranial pressure by hyperventilation.

• Drug-induced respiratory failure can be confirmed by a therapeutic trial with a specific antidote, i.e. a bolus injection of naloxone for opiates and flumazanil for benzodiazepines. Infusions will be required if a positive response is obtained as antidotes have short half life.

• Oxygen supplementation should be aimed at raising the PaO₂ to beyond the steep part of the oxygen dissociation curve (Fig. 11.4). Very high PaO₂ values are unnecessary but controlled O₂ therapy via a fixed performance mask is only necessary in chronic respiratory failure resulting from COPD.

Figure 11.4 Oxygen dissociation curve. BPG, bisphosphoglycerate; a, arterial point; v, venous point; x, arterial venous difference; HbO₂, oxygen saturation of haemoglobin.

Case history

A 65-year-old man with advanced COPD was admitted with a 1-week history of cough, breathlessness and purulent sputum. In the previous 24 h he had become mildly confused. He was agitated with a respiratory rate of 35, BP 170/90, sweaty with an oximeter reading on air of 72%. There was widespread wheeze and coarse crackles suggestive of retained secretions. ABG analysis revealed pH 7.32, PaO₂ 5.8, PaCO₂ 8.1, and HCO₃ 28.

What do these blood gases mean?

Hypoxaemia with mild acute respiratory acidosis. No evidence of chronic respiratory failure with chronically elevated pCO₂ as HCO₃ is normal, i.e. no compensation.

The initial treatment in A&E was:

• Nebulised bronchodilators (salbutamol 5 mg nebulised + ipratropium bromide 500 µg).

• 28% O₂ by controlled mask.

• IV amoxicillin (erythromycin if patient penicillin allergic).

• IV steroids (this is conventional treatment but there is limited evidence for effectiveness). Hydrocortisone 100 mg × 3 daily.

• Encouragement to clear secretions including sitting patient up and the attention of the physiotherapist.

• CXR to exclude pneumothorax or demonstrate associated pneumonia.

Information

Controlled oxygen via Venturi mask commonly leads to intermittent therapy as the mask is poorly tolerated by agitated, breathless patients. Oxygen via nasal prongs at 1 or 2 L/min is more effective and continuous but is not ‘controlled’.

Repeat ABGs were requested: pH 7.20, PaO₂ 6.5, PaCO₂ 12.5, HCO₃ 30.

These results show further CO₂ retention and a deteriorating situation. Oxygen should not be removed – its removal will precipitate severe hypoxaemia. Alveolar ventilation must be increased. Despite using a nasal airway to stimulate cough and aid suction of respiratory secretions there was no improvement. Furosemide was given because it was difficult to exclude coexistent LVF. Intubation was considered appropriate but a trial of non-invasive ventilation (NIV), BiPAP with tight-fitting facial mask was first tried with repeat gases at 1 h. On NIV the respiratory rate slowed and the acute respiratory acidosis resolved.

Non-invasive ventilatory support employs a nose- or face-mask to provide ventilatory assistance to breathing (this is termed ‘spontaneous pressure support’) or timed breaths (‘pressure controlled ventilation’). An exhalation valve reduces re-breathing. NIV is successful in approximately 70% of patients with respiratory failure resulting from COPD. It should not be employed if intubation would be more appropriate.

Information

Contraindications/cautions to non-invasive ventilation (NIV):

• Unconscious or uncooperative

• Vomiting

• Large amount of respiratory secretions

• Cardiovascularly unstable (beware hypotension)

• Recent facial or upper airway surgery

• Recent upper GI tract surgery

• Inability to protect airway

Mechanical ventilation

In an unstable situation it is essential to maintain oxygenation. As intubation of an acutely unwell patient requires experience, refer to ITU outreach team.

Aims of intubation and mechanical ventilation

• Immediate correction of hypoxaemia

• Slower correction of hypercapnia

• Allow effective suctioning of respiratory secretions.

Hypotension after intubation is very common and relates to

• High airway pressures limiting venous return and causing a fall in cardiac output

• Vasodilation directly caused by sedatives

• A fall in sympathetic tone.

Progress.

This patient was seen by the ITU team who felt, despite his confusion, that he should first be tried on non-invasive ventilatory support. He was put on BiPAP and his blood gases were monitored. These gradually improved on this regimen and antibiotics. He was discharged and advised to see his doctor as soon as he develops a chest infection.

Further reading

British Thoracic Society. Non-invasive ventilation in acute respiratory failure. Available online www.thoraxjnl.com

Roberts CM, Brown JL, Reinhardt AK, et al. Non-invasive ventilation in COPD: management of acute type 2 respiratory failure. Clin Med. 2008:517–521. 8

COPD – acute exacerbation

Chronic obstructive pulmonary disease (COPD) is used to describe a number of clinical syndromes associated with destruction of the lung and airflow obstruction.

Case history (1)

A 63-year-old male ex-smoker has had a chronic productive cough for 20 years. For 10 years he has had gradually increasing breathlessness on exertion. His usual exercise tolerance is 200 yards on the flat. One week previously he became breathless on walking between rooms and his sputum became purulent. His normal medication is salbutamol and beclometasone inhalers.

On examination his chest expanded poorly and he was wheezy, but there were no localising signs, no evidence of cor pulmonale or heart failure.

• His usual FEV₁/FVC was 1.9/3.2 (predicted 3.4/4.4) but on arrival was 0.9/2.6

• His CXR showed no acute lesion.

It was decided not to admit him to hospital because:

• He was able to cope at home with aid of his wife

• He was not cyanosed: oximetry showed SaO₂ 97%

• His general condition was good and he had a normal level of consciousness.

He was discharged home with:

• Amoxicillin 500 mg × 3 daily for 1 week

• Prednisolone 30 mg daily for 2 weeks

• Advice to increase his inhaled bronchodilators to salbutamol four puffs, 4-hourly via a spacer

• A follow-up appointment at the chest clinic for 2 weeks.

Key points

• The patient did not need admission because:

• No evidence of respiratory failure

• No evidence of cor pulmonale

• Able to cope at home.

• Antibiotic was broad spectrum and, in particular, covered the majority of Haemophilus influenzae and Streptococcus pneumoniae organisms (the most common causes of acute exacerbation). Erythromycin was unnecessary because Mycoplasma was unlikely.

• Oral steroids were used as adjunct to antibiotics because the patient was already on inhaled steroids and possibly had a degree of steroid responsiveness. This is conventional treatment but there is limited evidence to support it.

• Patient was given a spacer (and shown how to use it) in order to increase the lung deposition of aerosol.

• Salbutamol dose was increased and given 4-hourly because the effect lasts only 4–6 h and is partly dependent on dose.

• Follow-up at chest clinic because patient had moderately severe COPD and had never been assessed:

• Advise pneumococcal and influenza vaccination

• Consider referral for pulmonary rehabilitation.

However, the patient’s doctor, when seeing the patient 1 week later, cancelled the outpatient appointment believing it unnecessary. He wrote to the chest physician saying that he was able to manage the patient himself. He had a spirometer in the surgery and when well the patient had an FEV₁ of > 50% predicated normal. Furthermore, the doctor said that the patient:

• Had a definitive diagnosis

• Had only moderately severe COPD

• No cor pulmonale

• No respiratory failure and did not need oxygen

• Did not have bullous lung disease

• Did not have a rapidly declining FEV₁.

The patient’s doctor was arranging to perform bronchodilator tests himself using a spirometer and checking the response to both salbutamol and ipratropium inhalers. He would arrange vaccination.

Remember

Spirometry is required to assess the severity of COPD. Most COPD patients can be satisfactorily managed in the community.

Prognosis of COPD

Predictors of a poor prognosis are increasing age and worsening of airflow limitation, i.e. a fall in FEV₁.

A patient with a BODE index (Table 11.2) of 0–2 has a mortality rate of 10%; one with a BODE index of 7–10, a mortality rate of 80% at 4 years.

Table 11.2 BODE index (Body mass index, degree of airflow Obstruction, Dyspnoea and Exercise capacity)

Scores on the modified Medical Research Council (MMRC) dyspnoea scale range from 0 to 4, with a score of 4 indicating that the patient is breathless when dressing.

Case history (2)

A 68-year-old female smoker with a chronic productive cough and 5 years of gradually increasing breathlessness on exertion had a usual exercise tolerance of 40 yards on the flat and was breathless bending and washing. She was virtually housebound and lived alone. She developed a cough with purulent sputum and had been breathless at rest for 2 days. She was sent as an emergency to the A&E Department. She was admitted to the medical assessment unit immediately because she:

On examination

Key points

• Patient in respiratory failure with raised PaCO₂: give oxygen via fixed performance mask 24, initially increasing to 28 or 35% if no rise in PaCO₂.

• Cor pulmonale (right heart failure secondary to lung disease) is difficult to improve while the patient remains hypoxic.

• Atrial fibrillation may only be secondary to hypoxaemia and might revert to sinus rhythm when PaO₂ improves.

There was no improvement

She was therefore given:

• Doxapram as a respiratory stimulant (1.5–4 mg/min infusion) which sometimes helps.

• Non-invasive intermittent positive pressure ventilation (NIV) (see p. 343). The best technique is using a tight-fitting facial mask to deliver bilevel positive airway pressure ventilation support (BiPAP).

Progress

• Patient more alert

• PaO₂ 8.0, PaCO₂ 8.4, pH 7.35 now on 2 L nasal oxygen

• In sinus rhythm.

Key points

• Oxygen should be prescribed on treatment sheet and given continuously, not ‘as required’.

• Management of oxygen is the most helpful and difficult component of treatment.

• Although oxygen by a Venturi mask gives a known concentration it is uncomfortable and claustrophobic. It has to be removed to eat, talk and cough and for nebulised treatment.

• Oxygen by nasal spectacles is more comfortable and can be kept on continuously.

• Nasal oxygen gives variable F_iO₂ depending on pattern of breathing and flow rate between 24% and 35%. It worked on this patient but in many patients with COPD, a 24% oxygen via a mask is preferable when PaCO₂ > 8.0 kPa.

• It takes 30–40 min to equilibrate blood gases with any change in F_iO₂ and blood gases should not be checked earlier.

• It is unnecessary to get the PaO₂ normal: aim to get it at the top of the steep slope of the oxygen saturation curve (see Fig. 11.3).

• If PaO₂ is > 7.5 kPa, a small fall in PaO₂ has little effect on O₂ saturation: this is safe.

• If PaO₂ is 6.5 or less, a small fall produces a dangerous fall in SaO₂. Note: the sigmoid shape of oxygen dissociation curve (see p. 342).

• Increasing the inspired oxygen may cause a small rise in PaCO₂ (mostly because of relaxation of hypoxic vasoconstriction in relatively poorly ventilated alveoli). A pH change of < 0.1 or PaCO₂ < 1 kPa is not significant, so do not reduce or remove the oxygen.

• If, on increasing F_iO₂, this patient had not clinically improved and ABGs showed PaO₂ 6.8, PaCO₂ 12.0:

• Action: patient still needs oxygen but at a more controlled concentration. Increase F_iO₂ to 35%

• Get help from senior, preferably from respiratory team and discuss transfer to HDU for non-invasive ventilation or to ITU for assisted ventilation.

Progress.

Over the next few days the patient improved and felt well by 1 week. Her Hb came back as 180 g/L, Hct 55. What would you do now?

Action

Venesect cautiously under Haematology guidance. Three to four units venesected over next few weeks starting before discharge from hospital aiming for a Hct of 50. Continue bronchodilators as inhalers via spacing device, oral steroids continued for 2 weeks and diuretics, e.g. furosemide given.

Key points

• Before discharge blood gases were checked on air and showed a PaO₂ 7.0, PaCO₂ 6.3. The respiratory nurse was asked to visit to:

• Discuss disease/risk factors, especially to urge to stop smoking and refer to smoking cessation clinic

• Explain mechanism of action of drugs

• Explain use of aerosol devices and spacers

• Give chest clinic follow-up for 2 weeks.

A follow-up in chest clinic was arranged to:

• Optimise bronchodilator treatment.

• Monitor for polycythaemia and cor pulmonale.

• Assess for long-term domiciliary oxygen (indication PaO₂ < 7.3 on two occasions 3–4 weeks apart when patient stable).

• Consider obstructive sleep apnoea in view of marked polycythaemia.

Further reading

British Thoracic Society. Guidelines for COPD. Available online www.brit-thoracic.org.uk

Pneumonia

Pneumonia is an inflammation of the substance of the lungs. It can be classified by site (e.g. lobar, diffuse, bronchopneumonia) or by aetiological agent (e.g. bacterial, viral, fungal, aspiration, or due to radiotherapy or allergic mechanisms). Pneumonias can be community-acquired (CAP; commonest Strep. pneumoniae), hospital-acquired (often Gram-negative bacteria) or ventilator-associated (multiple organisms, e.g. Pseudomonas, Klebsiella, Acinetobacter).

Case history (1)

A 33-year-old female non-smoker was admitted to the medical assessment unit with a 2-day history of fever, sweating and cough, productive of yellow, lightly blood-stained sputum. She had pleuritic pain in the left axilla. Herpes labialis was present.

This is the typical history of community-acquired pneumonia.(CAP).

Signs

• Fever 39°C.

• Respiratory rate 28/min.

• Dullness to percussion left lung base; consolidation.

• Bronchial breathing left lung base; consolidation.

How ill is this patient?

The following CURB-65 criteria indicate the severity of CAP.

Progress.

This patient was young, previously fit, not breathless or shocked. The chest X-ray (Fig. 11.5) showed a left lower lobe pneumonia and the WBC was 11 500. Normal urea. PaO₂ 10.5 kPa.

Figure 11.5 Lobar pneumonia.

This pneumonia is not severe on the CURB criteria.

The patient was treated with oral antibiotics and was discharged in 24 hours (see Antibiotic choices, p. 353).

Investigations show

• CXR (Fig. 11.6):

• Diffuse opacification in both lungs

• Ring opacities in right lung

• Urea 9 mmol/L

• WBC 28 000

• ABG: PaO₂ 9.0 kPa, PaCO₂ 5.3 kPa, on FiO₂ 40%.

This is a high-risk case. He has influenza and a superinfection with Staphylococcus aureus causing severe community-acquired pneumonia with early abscess formation (ring opacities on the CXR). He needs:

• Rehydration: intravenous fluid

• Intravenous antibiotics: see Antibiotics, below – severe CAP

• Pulse oximetry: give O₂ to try to keep O₂ sat > 90%

• Nursing where he can be easily observed or in an HDU (hourly BP, pulse, RR)

• To be watched for respiratory failure: IPPV might be needed

• Physiotherapy if difficulty coughing up sputum.

Figure 11.6 Diagram of chest X-ray showing bilateral diffuse opacities and ring opacities in the right lung.

Information

Indications for intensive care monitoring and assisted respiration:

• PaO₂ < 8 kPa on 60% O₂

• PaCO₂ > 6.4 kPa

• Patient exhausted, drowsy or unconscious

• Shock

• Hypotension or circulatory failure

Antibiotic choices for CAP

Consult your Hospital Formulary or select from below:

Uncomplicated mild community-acquired pneumonia

• Treat for 5 days with oral medication unless patient not swallowing or not absorbing.

• Oral amoxicillin 500 mg × 3 daily + erythromycin 500 mg × 4 daily (or clarithromycin).

In penicillin allergic patient with underlying lung disease (H. influenzae suspected)

• Clarithromycin 500 mg × 2 daily.

Severe CAP

• IV antibiotics until significant improvement. Co-amoxiclav 1.2 g IV x 3 daily and clarithromycin 500 mg IV × 2 daily.

• Antibiotics for up to 10 days.

Staphylococcal pneumonia

• Treat for 10 to 14 days.

• Flucloxacillin 2 g × 4 daily IV + fusidic acid oral 0.5–1 g × 3 or gentamicin 3.0–5.0 mg/kg IV daily as single dose (check gentamicin levels before second dose).

Legionnaire’s disease

• Treat for 3 weeks.

• Clarithromycin 500 mg × 2 daily (for severe cases IV).

Mycoplasma pneumonia N.B.

• Treat for 2 weeks.

• Erythromycin 500 mg × 4 IV or oral daily.

• If allergic to erythromycin give doxycycline 200 mg orally then 100 mg daily or ciprofloxacin 500 mg × 2 daily.

Q fever and psittacosis

• Tetracycline 500 mg × 3 daily for 10 days.

Progress.

This patient made a signficant improvement on his IV antibiotics. He was switched to oral antibiotics and made a slow recovery.

You should think this patient may have HIV infection with a Pneumocystis jiroveci pneumonia because of country of origin, 6-month history of illness, lymphadenopathy, low white cell count and appearance on CXR (Fig. 11.7).

Figure 11.7 Chest X-ray showing bilateral perihilar shadowing. Pneumocystis.

On investigation, the CXR had:

• Ground glass appearance of lung fields

• Bilateral and perihilar shadowing.

Treatment should start in this patient for pneumocystis jiroveci

• High-dose IV co-trimoxazole.

• Add IV cefuroxime and erythromycin if in doubt as to cause of the pneumonia.

• Refer to HIV specialist.

• May need high-dose steroids IV if deteriorates.

• Give O₂ to keep O₂ sat > 90%.

• Arrange for induced sputum collection next day.

Progress.

This patient improved on antibiotics and his care was taken over by the HIV team.

Investigations

• CXR: patchy opacification right lung base

• ABGs: PaO₂ 7.3, PaCO₂ 4.6

• WBC 16 × 10⁹/L

• Urea 10 mmol/L

• ECG sinus tachycardia

What is the diagnosis?

Severe hospital-acquired pneumonia

However, for all cases, think of:

• DVT with pulmonary emboli might coexist.

• Inhalation of vomiting causing aspiration pneumonia.

• Previous antibiotics could have selected out Gram-negative organisms.

• Infected intravenous cannulae.

• Pre-existing lung disease – smoker.

Lung abscess

This is a severe localized suppuration in the lung. The CXR shows cavity formation, often with the presence of a fluid level (not due to tuberculosis).

The causes of lung abscess include aspiration, particularly amongst alcohol users. Lung abscesses also frequently follow the inhalation of a foreign body into a bronchus. They can also occur when the bronchus is obstructed, e.g. a bronchial carcinoma. Chronic or subacute lung abscesses can also follow an inadequately treated pneumonia.

Case history

A man of 74 presented with a 1-month history of a productive cough with offensive-tasting sputum, malaise and weight loss. His dentition was very poor. He had just stopped smoking.

On examination he had a temperature of 39.8°C, a few crackles at the right base but no other respiratory signs. A chest X-ray (Fig 11.8) shows a cavity.

Figure 11.8 Diagram of chest X-ray showing a cavity (lung abscess).

Differential diagnosis

• Lung abscess

• Cavitating lung cancer

• Tuberculosis.

Bronchoscopy showed thick secretions in right lower lobe. No bronchial obstruction. Cytology negative.

Diagnosis: Pyogenic abscess

Progress.

The patient responded to antibiotics (cefuroxime and metronidazole) and the abscess resolved in 6 weeks. This probably resulted from aspiration with mouth anaerobes contributing to the unpleasant smell and taste of sputum. Aspiration usually occurs on the right side as the right bronchus is more vertical.

Tuberculosis

Case history (1)

An 18-year-old man who came to the UK 2 years ago from the Indian sub-continent presented with general malaise, photophobia, unproductive cough, weight loss and night sweats.

On examination his temperature was 39.5°C. He looked unwell and appeared rather vague. There was no neck stiffness or any abnormal chest signs.

Investigations revealed Na 120, K 2.6 and urea 2.8, Hb 104 g/L and WBC 6.4; serum ALT and alkaline phosphatase were slightly raised. Portable AP chest film appeared normal.

He was admitted with the diagnosis of pyrexia of unknown origin. He had blood and urine cultures and CSF examination. CSF showed an increased cell count, mostly lymphocytes, raised protein and low glucose. No organisms were seen but cultures sent. A departmental PA chest X-ray was performed after 2 days, which showed miliary mottling.

This patient has miliary tuberculosis with meningitis (TBM). It carries a high morbidity if not treated early. The hyponatraemia is dilutional secondary to inappropriate ADH secretion.

Treatment.

This is with anti-tuberculous drugs – rifampicin, isoniazid and pyrazinamide. These must commence before cultures are available. Continue for at least 9 months. Ethambutol should not be used because of its eye complications. Corticosteroids, e.g. prednisolone 60 mg are given for the first 3 weeks as they reduce mortality. Relapses and complications (e.g. seizures, hydrocephalus) are common in TBM. The mortality remains over 60% even with early treatment.

Progress.

This patient was started on anti-TB therapy as above. His mental state improved and temperature settled. He was discharged after 3 weeks with an appointment in 3 weeks in outpatients.

Case history (2)

A 50-year-old man who was a heavy drinker, with no fixed abode, was brought to A&E ‘collapsed’. He had stopped drinking alcohol 1 week previously because he had run out of money. He was confused, hallucinating and coughing, and was transferred to the MAU.

On examination he was unkempt and emaciated, confused and jaundiced:

• Temperature: 37.9°C

• Pulse: 100

• BP: 100/60.

On further examination, right upper chest; bronchial breathing + coarse crackles; trachea deviated to the right.

Liver enlarged 3 cm below costal margin. Ascites.

A provisional differential diagnosis was made of:

• Delirium tremens

• Pulmonary tuberculosis

• Alcoholic liver disease.

Urgent sputum was sent for staining with auramine-phenol fluorescent test and culture + sensitivities for AFB (if no organisms found send at least three more good sputum specimens). TB bacilli were found in the third sputum specimen (smear +ve).