Chapter 49: Dyspnoea

Dyspnoea is the subjective sensation of breathlessness that is excessive for any given level of physical activity. It is a cardinal symptom affecting the cardiopulmonary system and can be very difficult to evaluate. Appropriate breathlessness following activities such as running to catch a bus or climbing several flights of stairs is not abnormal but may be excessive due to obesity or lack of fitness.

It is important to emphasise that dyspnoea or breathlessness is a subjective sensation of the desire for increased respiratory effort and must be considered in relation to the patient’s lifestyle and individual tolerance of discomfort. It also depends on the age, physical fitness and physical expectations of the person. Patients may complain of tightness in the chest and this must be differentiated from angina.

The American Thoracic Society guide for grades of dyspnoea is:

The distinguishing features between dyspnoea due to heart disease and to lung disease are presented in TABLE 49.1.

The history is a good indication and a useful guideline is that dyspnoea at rest is typical of lung disease, especially asthma, while it tends to be present on effort with heart disease as well as with COPD.

Wheezing is any continuous musical expiratory noise heard with the stethoscope or otherwise. Wheeze includes stridor, which is an inspiratory wheeze.

Common causes of wheezing

Localised:

• partial bronchial obstruction:

  • – impacted foreign body

  • – impacted mucus plugs

  • – extrinsic compression

  Generalised:

• asthma

• obstructive bronchitis

• bronchiolitis

The term ‘cardiac asthma’ is used to describe a wheezing sensation such as that experienced with paroxysmal nocturnal dyspnoea. Differentiating features are presented in TABLE 49.2.

Is it asthma or COPD?

This question is often asked, especially in the middle-aged or elderly person with dyspnoea. Differentiating features are presented in TABLE 49.3.

A summary of the diagnostic strategy model is presented in TABLE 49.4.

Probability diagnosis

The common causes of dyspnoea are lung disease, heart disease, obesity, anaemia (tissue hypoxia) and functional hyperventilation. More specifically, bronchial asthma, COPD, acute pulmonary infections and left heart failure (often insidious) are common individual causes.

Serious disorders not to be missed

Severe cardiovascular events such as acute heart failure, which may be precipitated by myocardial infarction (may be silent, especially in diabetics), a life-threatening arrhythmia, pulmonary embolism, dissecting aneurysm or a cardiomyopathy (such as viral myocarditis) require early diagnosis and corrective action. Recurrent pulmonary embolism may present a diagnostic problem. There may be a history of deep venous thrombosis, pregnancy, malignancy or taking the contraceptive pill.⁴

Severe infections such as lobar pneumonia, tuberculosis and myocarditis must be considered. In children acute epiglottitis, croup, bronchiolitis, pneumonia and bronchitis are serious infections responsible for respiratory distress.

Primary carcinoma is an important consideration, especially in dyspnoea of gradual onset. Other malignant conditions to consider are metastases, lymphangitis carcinomatosis, lymphomas and pleural mesothelioma. Pleural effusion may be the mode of presentation of some of these serious disorders.

Pitfalls

Interstitial pulmonary disease can be a diagnostic dilemma because the physical signs and X-ray appearances can be minimal in the early stages despite the presence of significant dyspnoea. Allergic alveolitis, such as that caused by birds (e.g. hypersensitivity to their droppings) can be a pitfall. The diagnosis is easier if a known disease associated with pulmonary infiltration, such as sarcoidosis, is present. Measuring the diffusing capacity will help with diagnosis.

Pericardial tamponade may cause difficulty in diagnosis either with an acute onset, such as malignancy involving pericardium, or insidiously. The patient usually has a weak pulse with pulsus paradoxus, hypotension and a raised jugular venous pressure.

It is important to be careful not to attribute dyspnoea simply to obesity or lack of fitness when it could have a true organic disorder such as heart failure.

Seven masquerades checklist

Most of the masquerades have to be considered as underlying causes. Depression can be associated with dyspnoea, anaemia is an important cause of dyspnoea, thyrotoxicosis can rarely present with dyspnoea, and diabetic ketoacidosis can cause rapid deep breathing.

Drugs must also be considered, especially as a cause of interstitial pulmonary fibrosis that presents with dyspnoea, cough and fever. Drugs that cause this disorder include several cytotoxic agents (especially bleomycin, cyclophosphamide, methotrexate), amiodarone, sulphasalazine, penicillamine, nitrofurantoin, gold salts and adrenergic nasal sprays.³ Poisons that may cause hyperventilation are salicylate, methyl alcohol, theophylline overdosage and ethylene glycol. Anaemia must be considered especially in those at risk. Dyspnoea is unlikely to be caused solely by chronic anaemia unless the haemoglobin level is less than 8 g/dL.⁴ It is more likely to occur if another predisposing cause, such as ischaemic heart disease, is present.

Psychogenic considerations

Functional dyspnoea or hyperventilation is common. However, it is important to exclude organic causation such as asthma, drugs and thyrotoxicosis before settling with the psychogenic label and to reassure the patient strongly if there is no organic cause. Any uncomfortable sensation in the chest may be interpreted as dyspnoea by anxious patients. Depression, anxiety and panic attacks may be underlying the problem. Characteristic associated features of hyperventilation with anxiety include dizziness, faintness, palpitations, yawning, paraesthesia of the hands and legs, inability to take a deep breath or a sensation of smothering. These patients may exhibit sighing and irregular breathing on examination. In true psychogenic dyspnoea, chest X-rays and pulmonary function tests are normal but symptoms are often reproduced after 15–30 seconds of voluntary hyperventilation. It is important to remember that it may be present in a patient who has organic disease of a mild degree such as asthma.

History

Special attention should be paid to evaluating exactly what the patient means by breathlessness or restriction of breathing. The analysis should then include provoking factors and associated symptoms with a view to differentiating between pulmonary causes such as asthma and COPD. Wheeze is often (but not always) present in asthma and chronic airflow obstruction. Most respiratory causes of dyspnoea also produce cough. The rate of development of dyspnoea gives an indication of the possible cause (see TABLE 49.5).⁵ The sudden onset of dyspnoea at rest is suggestive of pulmonary embolism or pneumothorax. Severe dyspnoea developing over 1 or 2 hours is most likely due to left heart failure or bronchial asthma. Bronchial asthma is usually easily distinguished from left heart failure by the history of previous attacks, by the absence of chest pain and the absence of cardiac murmurs. ‘My breathing feels tight’ indicates asthma. A complaint of ‘suffocation or feeling smothered’ or ‘just not getting enough air’ may be a pointer to functional dyspnoea.

The dyspnoea of asthma tends to occur at rest and at night, while that with chronic airflow obstruction occurs with exertion.

Examination

The routine findings from inspection, percussion and auscultation will determine whether the underlying lung disease is localised or generalised. The generalised findings for various disorders of the lungs are summarised in TABLE 49.6.

Careful inspection is mandatory. The patient should be stripped to the waist and observed for factors such as cyanosis, clubbing, pallor, mental alertness, dyspnoea at rest, use of accessory muscles, rib retraction and any other abnormalities of the chest wall. A coarse tremor or flap of the outstretched hands indicates carbon dioxide intoxication.⁶ To obtain maximum value from auscultation, request the patient to open his or her mouth and take deep breaths. Adventitious sounds that are not audible during tidal breathing may then be heard. Wheezes are high-pitched continuous sounds heard either in expiration or inspiration, being more pronounced in expiration.

Crackles are short interrupted sounds heard mainly at the end of inspiration, resembling the crackling sound of hair being rubbed between the fingers near the ear. Fine crackles, previously referred to as crepitations, occur typically in lobar pneumonia and diffuse interstitial fibrosis, and are not cleared by coughing. Medium crackles are typical of congestive cardiac failure, and coarse crackles indicate airway mucus and usually clear on coughing.

Causes of pulmonary crackles

• Left ventricular failure

• Idiopathic pulmonary fibrosis

• Extrinsic allergic alveolitis

• Pneumonia

• Bronchiectasis

• Chronic bronchitis

• Asbestosis

• Pulmonary fibrosis

Investigations

The two most important initial investigations for respiratory disease are chest X-ray and pulmonary function tests.

Pulmonary function tests (PFTs)

These relatively simple tests provide considerable information.

The most practical instrument for office use to detect chronic airway obstruction due to asthma or chronic bronchitis is the mini peak flow meter, which measures peak expiratory flow rate (PEFR).

The interpretation of the tests, which vary according to sex, age and height, requires charts of predicted normal values. A chart for PEFR in normal adult subjects is presented in Appendix V. The value for a particular patient should be the best of three results.

Spirometry is the gold standard test. The measurement of the forced vital capacity (FVC) and the forced expiratory volume in one second (FEV₁) provide a very useful guide to the type of ventilatory deficit. Both the FVC and the FEV₁ are related to sex, age and height.

The FEV₁ expressed as a percentage of the FVC is an excellent measure of airflow limitation. In normal subjects it is approximately 70%. A normal spirometry pattern is shown in FIGURE 49.1 and abnormal patterns in FIGURE 49.2. FIGURE 49.3 summarises the relative values for these conditions.

Tidal volume (TV) and vital capacity (VC) can be measured by a simple spirometer but the total lung capacity and the residual volume are measured by the helium dilution method in a respiratory laboratory.

This test measures the carbon monoxide uptake by a single breath analysis for whole lungs. In normal lungs the transfer factor is a true measure of the diffusing capacity of the lungs for oxygen and depends on the thickness of the alveolar-capillary membrane.⁵ Gas transfer is usually reduced in patients with severe degrees of emphysema and fibrosis, anaemia and congestive cardiac failure. Useful for COPD and interstitial lung disease. Normal in asthma.

The outstanding monitoring aid, transcutaneous pulse oximetry, estimates oxygen saturation (SpO₂) of capillary blood. The estimates are generally very accurate and correlate to within 5% of measured arterial O₂ saturation (SaO₂).⁷ The ideal level is 97–100%; median levels—neonates 97%, children 98%, adults 98%. <92% is very serious.

This test indicates the presence of airway or bronchial hyper-reactivity, which is a fundamental feature with asthma. The test should not be performed on those with poor lung function and only performed by a respiratory technician under medical supervision. The test is potentially dangerous.

Other investigations (to select from)

• Haemoglobin, red cell indices and PCV

• White blood cell count (e.g. eosinophilia of asthma)

• Sputum, culture and cytology

• Tuberculosis tests

• ESR/CRP

• Arterial blood gas analysis

• Cardiological investigations:

  • – ECG, including exercise

  • – echocardiography (technically difficult in emphysema)

  • – nuclear gated blood pool scan to assess heart function

  • – cardiac enzymes

• Other medical imaging:

  • – high-resolution CT

  • – MRI

  • – ventilation and perfusion radionuclide scan (pulmonary embolism)

• Bronchoscopy, especially fibre-optic bronchoscopy

• Thoracocentesis and pleural biopsy

• Open lung biopsy

• Alpha₁-antitrypsin measurement (normal range 1.1–2.2 g/L)

Pleural effusion

Key points

• Normal pleural space has 10–20 mL fluid

• Can be detected on X-ray if >300 mL fluid in pleural space

• Can be detected clinically if >500 mL fluid

• Can be subpulmonary—simulates a raised diaphragm

• May be asymptomatic

• Dyspnoea common with large effusion

• Chest pain in setting of pleuritis, infection or trauma

• Signs: refer TABLE 49.6

• The fluid may be transudate or exudate (diagnosed by aspirate)

• If blood stained—malignancy, pulmonary infarction, TB

Transudate

Protein content <25 g/L; lactic dehydrogenase <200 IU/L.

• Heart failure (90% of cases)

• Hypoproteinaemia, e.g. nephrotic syndrome

• Liver failure with ascites

• Constrictive pericarditis

• Hypothyroidism

• Ovarian tumour—right-sided effusion (Meigs syndrome)

Exudate

Protein content >35 g/L; lactic dehydrogenase >200 IU/L

• Infection—bacterial pneumonia, pleurisy, empyema, TB, viral

• Malignancy—bronchial carcinoma, mesothelioma, metastatic

• Pulmonary infarction

• Connective tissue diseases (e.g. SLE, RA)

• Acute pancreatitis

• Lymphoma

• Sarcoidosis

• HIV with parasitic pneumonia

Management

Aspiration if symptomatic: may require repeats and pleurodesis. Treat the underlying cause.

There are numerous causes of dyspnoea in children but the common causes are asthma, bronchiolitis and pulmonary infections. The important infections that can be fatal—croup, epiglottitis and myocarditis—must be kept in mind and intensively managed.

Bronchiolitis is an important cause of respiratory distress in infants under 6–12 months. It should not be confused with asthma (refer to CHAPTER 96).

Sudden breathlessness or stridor may be due to an inhaled foreign body. Signs of lobar collapse may be present but physical examination may be of little help and a chest X-ray is essential.

Cardiovascular disorders, including congenital heart disease, can cause dyspnoea. Extra respiratory causes include anaemia, acidosis, aspiration, poisoning and hyperventilation.

Dyspnoea in the elderly is common and is caused usually by heart failure and COPD. The other associations with ageing, such as lung cancer, pulmonary fibrosis and drugs, are relevant. The classic problem of the aged is acute heart failure that develops typically in the early morning hours. The acute brain syndrome is a common presentation of all these disorders.

Respiratory disease in the elderly

The respiratory system, like most other bodily systems, matures until about the age of 25 years and subsequently slowly loses efficiency due to a variety of factors such as disease, smoking, pollution and ageing. There is a decline in lung function and gas exchange and decreased ventilatory responses to hypoxia and hypercapnia.

Heart failure

Heart failure occurs when the heart is unable to maintain sufficient cardiac output to meet the demands of the body. Dyspnoea is a common early symptom as pulmonary congestion causes hypoxia (increased ventilation) and decreased compliance (increased work). The incidence of congestive cardiac failure (CCF) has been increasing steeply, partly due to the ageing population.

Symptoms

• Increasing dyspnoea progressing to (in order):

  • – fatigue, especially exertional fatigue

  • – paroxysmal nocturnal dyspnoea

  • – weight change: gain or loss

It is convenient to divide heart failure into left and right heart failure but they rarely occur in isolation and often occur simultaneously. Right failure is invariably secondary to left failure. Furthermore, some cardiologists stress the importance of differentiating between systolic and diastolic dysfunction. Both present in the same way clinically and hence referral for cardiac studies to obtain measurement of the left ventricular function is required. This permits an accurate diagnosis and guide to treatment and an accurate prognosis.

Refer to Chronic heart failure (CHAPTER 88).

Chronic obstructive pulmonary disease

Chronic bronchitis and emphysema should be considered together as both these conditions usually coexist to some degree in each patient. An alternative, and preferable, term—chronic obstructive pulmonary disease (COPD)—is used to cover chronic bronchitis and emphysema with chronic airflow limitation.⁶

For more detail on the management of COPD refer to CHAPTER 83.

Interstitial lung diseases comprise a group of disorders that have the common features of inflammation (pneumonitis) and fibrosis of the interalveolar septum, representing a non-specific reaction of the lung to injury of various causes.^8,9

In many there is a hypersensitivity reaction to various unusual antigens. The fibrosis may be localised as following unresolved pneumonia, bilateral as with tuberculosis or widespread.

Consider the possibility of fibrosis of the lungs in chronic dyspnoea and a dry cough with normal resonance.

Causes of widespread interstitial pulmonary fibrosis include:

• idiopathic pulmonary fibrosis

• hypersensitivity pneumonitis (extrinsic allergic alveolitis)

• drug-induced

• lymphangitis carcinomatosis

• various occupational lung disorders

• rheumatoid arthritis

• sarcoidosis

• acute pulmonary oedema

• immunological/multisystemic disease (e.g. connective tissue disorders, RA, vasculitis, inflammatory bowel disease)

Common clinical features:

• dyspnoea and dry cough (insidious onset)

• fine inspiratory crackles at lung base with faint breath sounds

• cyanosis and finger clubbing may be present

• PFTs:

  • – restrictive ventilatory deficit

  • – decrease in gas transfer factor

• characteristic X-ray changes

High-resolution CT scanning has been a major advance in diagnosis. May show ‘honeycomb lung’.

Idiopathic pulmonary fibrosis

Idiopathic pulmonary fibrosis, also known as idiopathic fibrosing interstitial pneumonia and cryptogenic fibrosing alveolitis, is the most common diagnosis among patients presenting with interstitial lung disease.

Patients usually present in the fifth to seventh decade with the clinical features as outlined under interstitial lung diseases such as slowly progressive dyspnoea over months to years. Chest X-ray abnormalities are variable but include bilateral diffuse nodular or reticulonodular shadowing favouring the lung bases. High-resolution CT scans are effective for diagnosis. Open lung biopsy may be needed for diagnosis and staging. The usual prognosis is poor, with death occurring about 3.5–5 years after diagnosis. The usual treatment is high doses of oral corticosteroids with azathioprine and no smoking.^9,10

If refractory, refer to a palliative care service.¹¹

Pulmonary sarcoidosis

Sarcoidosis is a multisystemic disorder of unknown aetiology, which is characterised by non-caseating granulomatous inflammation that involves the lung in about 90% of affected patients. A characteristic feature is bilateral hilar lymphadenopathy, which is often symptomless and detected on routine chest X-ray (CXR). Radiological lung involvement can be associated with or occur independently of hilar lymphadenopathy.

Clinical features^8,9

• May be asymptomatic (one-third)

• Onset usually third or fourth decade (but any age)

• Bilateral hilar lymphadenopathy (on CXR)

• Cough

• Fever, malaise, arthralgia

• Skin lesions: erythema nodosum, lupus pernio

• Ocular lesions (e.g. anterior uveitis)

• Other multiple organ lesions (uncommon)

• Overall mortality 2–5%

Erythema nodosum with an acute swinging fever, malaise and arthralgia in a young adult female is diagnostic of sarcoidosis.

Diagnosis

Histological evidence from biopsy specimen, usually transbronchial biopsy (essential if an alternative diagnosis, e.g. lymphoma, cannot be excluded) or skin biopsy in cases of erythema nodosum. A better modern diagnostic method is biopsy via video-assisted thoracoscopy.

Supporting evidence:

• elevated serum ACE (non-specific)

• PFTs: restrictive pattern; impaired gas transfer in advanced cases

• ±ve Kveim test (not recommended these days)

• serum calcium

Treatment

Sarcoidosis may resolve spontaneously (hilar lymphadenopathy without lung involvement does not require treatment).

Indications for treatment with corticosteroids:

• no spontaneous improvement or worsening after 3–6 months

• symptomatic pulmonary lesions

• eye, CNS and other systems involvement

• hypercalcaemia, hypercalciuria

• erythema nodosum with arthralgia

• persistent cough

• Prednisolone 0.5 mg/kg (up to 50 mg) (o) daily for 4–6 weeks, then reduce to lowest dose that maintains improvement.⁹ If there is a response, taper the dose to 10–15 mg (o) daily as a maintenance dose for 6–12 months.⁹

• Prednisolone 20–30 mg for 2 weeks for erythema nodosum of sarcoidosis.

Hypersensitivity pneumonitis

Hypersensitivity pneumonitis (extrinsic allergic alveolitis) is characterised by a widespread diffuse inflammatory reaction in both the small airways of the lung and the alveoli, due to the inhalation of allergens, which are usually spores of micro-organisms such as thermophilic actinomycetes in ‘farmer’s lung’ or (more commonly) avian protein from droppings or feathers in ‘bird fancier’s lung’. Occupational causes of extrinsic alveolitis have been described by Molina¹² (see TABLE 49.7).

Illness may present as acute or subacute episodes of pyrexia, chills and malaise with dyspnoea and a peripheral neutrophil several hours after exposure.¹² Management is based on prevention, namely avoiding exposure to allergens or wearing protective, fine-mesh masks. Prednisolone can be used (with caution) to control acute symptoms. It should be pointed out that this allergic disorder is different from the infection psittacosis.

Drug-induced interstitial lung disease⁹

Drugs are an important cause of this disorder and have three main effects:

1. Alveolitis with or without pulmonary fibrosis. This is mainly due to cytotoxic drugs, nitrofurantoin and amiodarone. The drug should be removed and consideration given to prescribing prednisolone 50 mg (o) daily for several weeks, depending on response.

2. Eosinophilic reactions. This is presumably an immunological reaction, which may present as wheezing, dyspnoea, a maculopapular rash and pyrexia. The many implicated drugs include various antibiotics, NSAIDs, cytotoxic agents, major tranquillisers and antidepressants, and anti-epileptics. Treatment is drug removal and a short course of prednisolone 20–40 mg (o) daily for 2 weeks.

3. Non-cardiogenic acute pulmonary oedema. This is rare and has been reported to occur with opioids, aspirin, hydrochlorothiazide, β2-adrenoceptor agonists (given IV to suppress premature labour), cytotoxics, interleukin-2, heroin.

Various types of acute and chronic pulmonary diseases are related to exposure to noxious substances such as dusts, gases and vapours in the workplace. Common chemical causes include formaldehyde used in processed woods, e.g. chipboard and medium-density fibre. GPs have a crucial role in the identification of the possible work-relatedness of lung disease.

Disorders due to chemical agents include:

• obstructive airways disorders, such as occupational asthma, acute bronchitis, (chronic) industrial bronchitis, byssinosis (asthma-like condition due to cotton dust)

• hypersensitivity pneumonitis

• pulmonary fibrosis (pneumoconiosis) due to mineral dust

• lung cancer due to industrial agents such as asbestos, various hydrocarbons

• pleural disorders, usually associated with asbestosis

Pneumoconiosis

The term ‘pneumoconiosis’ refers to the accumulation of dust in the lungs and the reaction of tissue to its presence, namely chronic fibrosis. The main cause worldwide is inhalation of coal dust, a specific severe variety being progressive massive fibrosis (complicated coal worker’s pneumoconiosis) in which the patient suffers severe dyspnoea of effort and a cough often productive of black sputum. TABLE 49.8 summarises the important causes.

Of particular concern are diseases caused by inhalation of fibres of asbestos, which is a mixture of silicates of iron, magnesium, cadmium, nickel and aluminium. These diseases include asbestosis, diffuse pleural thickening, pleural plaques, mesothelioma and increased bronchial carcinoma in smokers. Pulmonary asbestosis has classic X-ray changes but high-resolution CT scans may be required to confirm the presence of calcified pleural plaques. It usually takes 10–20 years from exposure for asbestosis to develop and 20–40 years for mesothelioma to develop,⁸ while bronchial carcinoma is caused by the synergistic effects of asbestosis and cigarette smoking.

Acute respiratory distress syndrome (ARDS)

ARDS, also known as acute lung injury and formerly called ‘adult respiratory distress syndrome’, refers to acute hypoxaemic respiratory failure following a pulmonary or systemic insult with no apparent cardiogenic cause of pulmonary oedema. This occurs about 12–48 hours after the event.¹³ The most common cause is sepsis, which accounts for about one-third of ARDS patients. The mortality rate is 30–40%, increasing if accompanied by sepsis. Management is based on early diagnosis, early referral, identification and treatment of the underlying condition and then optimal intensive care.¹⁴

• Sudden onset of respiratory distress

• Stiff lungs—reduced lung compliance

• Refractory hypoxaemia

• Bilateral pulmonary infiltrates on X-ray

• No apparent evidence of congestive heart failure

• Absence of elevated left atrial pressure

• Specific gas exchange abnormalities

• Signs: tachypnoea, laboured breathing, rib retraction, central cyanosis, fine crackles on auscultation

The differential diagnoses are pneumonia and acute heart failure. Common risk factors/associations for ARDS include (indirectly—systemic)—sepsis, shock, trauma, burns, drug overdose (e.g. heroin), multiple transfusions, obstetric complications (e.g. eclampsia, amniotic fluid embolism), and many direct causes such as pulmonary aspiration, toxic gas inhalation, blast injury and pneumonia (e.g. SARS). Admit patient to an intensive care unit.

Severe acute respiratory syndrome (SARS)⁷

SARS is a respiratory illness of varying severity (mild to severe) with a known mortality rate of about 10% of clinically established cases. All cases to date exhibit a high fever of >38°C. It is considered to be an atypical pneumonia caused by a quite unique coronavirus (SARS–CoV). Cases have acquired SARS following exposure to endemic areas of South-East Asia. Severe cases (up to 10% mortality) can progress to ARDS.

Suspected case = fever >38°C + cough, breathing difficulty or dyspnoea + contact with SARS person/area. Plain X-rays may show pulmonary infiltrates while high-resolution CT scans may show typical patterns.

Key features

• Symptoms of atypical pneumonia: fever, cough, dyspnoea

• Associated may be myalgia, diarrhoea, headache, sore throat, rhinorrhoea, confusion, malaise, rash

• Virulent virus—droplet spread by close contact

• Incubation period 2–7 days

• Crackles and wheezes may be present on auscultation but no hallmark sign

• Non-specific X-ray signs

• Prime CT scans may show typical changes

• Diagnosis confirmed by PCR studies or isolation of the virus on culture

• Complications appear to be confined to the lung

Optimal treatment for SARS by drugs is still being evaluated. Management is supportive; supplemental oxygen is required. Preventive measures, including wearing of face masks (NIOSH standard mask best) and appropriate infection control procedures, are important. Wear a mask, gloves, goggles and gown for clinical assessment of suspected cases and switch off air-conditioning (refer to CHAPTER 28).

Dyspnoea is associated with about 60% of cases of lung cancer³ (see CHAPTER 42). It is not a common early symptom unless bronchial occlusion causes extrinsic collapse. In advanced cancer, whether primary or secondary, direct spread or metastases may cause dyspnoea. Other factors include pleural effusion, lobar collapse, metastatic infiltration, upper airway obstruction due to superior vena cava (SVC) obstruction and lymphangitis carcinomatosis. A special problem arises with coexisting chronic bronchitis and emphysema.

• Patients with acute onset of severe dyspnoea

• All patients with heart failure resistant to initial therapy or where the diagnosis is in doubt

• Patients with pulmonary disease of uncertain aetiology, especially those requiring respiratory function tests

• Those in whom lung cancer is suspected

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Asthma

• Asthma in children

• Chronic obstructive pulmonary disease

• Asthma: dangerous asthma

• Heart failure