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Chest medicine 

Chest medicine
Chapter:
Chest medicine
Author(s):

Lesley K Bowker

, James D Price

, and Sarah C Smith

DOI:
10.1093/med/9780199586097.003.0011
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  • The ageing lung [link]

  • Respiratory infections [link]

  • Influenza [link]

    • HOW TO . . . Treat influenza-like illness in older people [link]

  • Pneumonia [link]

  • Pneumonia: treatment [link]

    • HOW TO . . . Manage the patient with pneumonia who fails to respond to treatment [link]

  • Vaccinating against pneumonia and influenza [link]

  • Pulmonary fibrosis [link]

  • Rib fractures [link]

  • Pleural effusions [link]

    • HOW TO . . . Aspirate a sample of pleural fluid [link]

  • Pulmonary embolism [link]

  • Aspiration pneumonia/pneumonitis [link]

  • Chronic cough [link]

  • Lung cancers [link]

  • Tuberculosis: presentation [link]

  • Tuberculosis: investigation [link]

    • HOW TO . . . Perform and interpret a tuberculin skin test [link]

  • Tuberculosis: treatment [link]

  • Asthma and COPD: assessment [link]

  • Asthma and COPD: drug treatment [link]

    • HOW TO . . . Improve drug delivery in asthma or COPD [link]

  • Asthma and COPD: non-drug treatment [link]

  • Oxygen therapy [link]

  • Asbestos-related disease [link]

The ageing lung

Most of the functional impairment of the lungs that is seen in older people is due to disease, often smoking-related. Intrinsic ageing leads only to mild functional deterioration. The respiratory system has a capacity well in excess of that required for normal activity, so intrinsic ageing:

  • Does not lead to symptoms in the non-smoker without respiratory disease

  • In those with respiratory disease (eg emphysema) will cause progressively worsening symptoms with age even if the disease itself remains stable

  • In acute disease, eg pneumonia, may cause earlier decompensation or a more severe presentation

Specific respiratory changes

Seen in healthy older people are similar to those seen in mild chronic obstructive pulmonary disease, and include:

  • Decreased elastic recoil causing small airways to collapse at low lung volumes and increased residual volume

  • Increased chest wall stiffness, due to:

  • Degenerative change in intercostal, intervertebral and costovertebral joints

  • Osteoporosis and kyphoscoliosis

    • Weaker respiratory muscles that may have lower endurance

    • Reduced gas exchange and increased ventilation-perfusion (V/Q) mismatch, due to collapse of peripheral airways while perfusion remains intact

    • Impaired chemoreceptor function, leading to lessened ventilatory response to decreased PaO2 or increased PaCO2

  • Impaired microbial defence mechanisms. Less effective mucociliary clearance and less sensitive cough reflex

Observed consequences of these changes

These include:

  • Increased susceptibility to infection (underventilation of and inability to clear sputum from dependent lung zones)

  • Lower maximum minute ventilation (weaker musculature acting against a stiffer chest)

  • An approximately linear fall in PaO2 with age (~0.3%/year). Since alveolar oxygen tension remains stable, the alveolar-arterial (A-a) oxygen gradient rises

  • Reduced exercise capacity. However, oxygen consumption and cardiac output decline in proportion to lung function, so the lungs are rarely the limiting factor in exercise performance

Breathlessness in older people is often multifactorial

  • Chronic breathlessness in an individual may be the result of, eg, decreased fitness, obesity, an inefficient gait (osteoarthritis or stroke), kyphosis, previous lung damage (eg apical fibrosis due to tuberculosis (TB)) and intrinsic ageing. In this example, note that only one of the factors is specific to the lung

  • In the acutely breathless patient, pathologies commonly coexist, eg infection, fast AF, and heart failure. The classic treatment triad of digoxin, furosemide, and amoxicillin is not a sign of diagnostic indecision but is often entirely appropriate treatment

Respiratory infections

Cough with or without sputum, shortness of breath, fever or chest pain is a very common presentation in older patients. It is very important to try to distinguish which part of the airway is primarily affected because this implies completely different pathogens, prognoses, and treatment strategies. Try to avoid aggregating all such patients together using the imprecise term ‘chest infection’.

Upper respiratory tract infections

These are caused by viruses, eg rhinovirus, respiratory syncytial virus, influenza, and parainfluenza. Symptoms include nasal discharge and congestion, fever, and sore throat. These may extend to the lower tract and then include cough, wheeze, sputum production, or worsening of existing cardiopulmonary disease.

With increasing age:

  • Upper respiratory tract infection becomes less frequent, but more severe

    • The risk of complications increases. These include:

    • Lower tract infection such as bronchitis or pneumonia, which may be bacterial or viral

    • Bronchospasm

    • Extrapulmonary manifestations such as falls, immobility, and delirium

    • Postinfection weakness, fatigue, and anorexia is more severe and prolonged, maybe lasting several weeks

  • Frequency of hospital admission and death increases substantially

Acute bronchitis

Occurs with inflammation of the bronchial tree with little or no involvement of lung parenchyma (which is pneumonia). Is commoner in those with chronic airways disease (see Chest medicine ‘Asthma and COPD: assessment’, [link]).

Compared with pneumonia, bronchitis:

  • Has fewer systemic features and a better prognosis

    • Has no chest symptoms and signs, eg pleuritic pain or crepitations, but may have prominent cough and wheeze

    • CXR not routinely indicated

  • Can be managed less aggressively, with more reliance on supportive treatment and bronchodilators than antibiotics. Often viral in origin, if an antibacterial is thought appropriate, give amoxicillin to cover Streptococcus pneumoniae (erythromycin or clarithromycin if penicillin sensitive)

Influenza

This is the most serious viral respiratory tract infection, and is often a severe, systemic illness with pulmonary bacterial superinfection (Staphylococcus aureus, Haemophilus influenzae, Strep. pneumoniae). It occurs most commonly in December-February. Antigenic shifts result in periodic pandemics (large-scale epidemics).

Presentation is similar in young and old, ie rapid onset of fever (rigors, chills), myalgia, headache, and fatigue with variable degrees of prostration. Compared with less threatening viruses such as rhinovirus:

  • Nausea, vomiting, diarrhoea, high fever, rigors and ocular symptoms (eg photophobia) are more common

  • Rhinorrhoea is less common

Less common serious complications include myocarditis and meningoencephalitis. Mild meningism is common, and if combined with other sinister features (eg altered conscious level) is an indication for CSF sampling.

Diagnosis is usually based on combining clinical assessment with epidemiological data, particularly current influenza incidence. Some other viruses can cause an identical clinical syndrome, and serological test results are not immediately available. Thus an initial assessment cannot produce an absolutely confident microbiological diagnosis. The syndrome may therefore most precisely be labelled ‘influenza-like illness’.

Positive virological diagnosis in the context of increased community incidence or a care home outbreak is helpful by prompting vigorous attempts to reduce transmission of infection.

Reducing viral transmission

Mass outbreaks of respiratory viral infection are common in care homes and hospitals. They can occur at any time of year but are commonest from autumn to spring, Viruses are spread by aerosol or hand-to-hand contact (sometimes indirect, via fomites such as cutlery or drinking vessels).

During an outbreak

  • Reduce transfers of healthy patients into, or symptomatic patients out of, the affected area

  • Reduce staff movement across work areas (especially applicable to short-term staff who may work in many clinical areas in a short time)

  • Care for symptomatic patients in single rooms, or in ward bays with similarly infected patients

  • Exclude visitors with respiratory or viral symptoms from the ward

  • Ensure that care staff have been immunized against influenza

  • Ensure that scrupulous hand-washing procedures are followed

  • Consider using face masks for staff caring for symptomatic patients

HOW TO . . . Treat influenza-like illness in older people

The following guidance is generic, and should be tailored to the patient, their illness, and their care environment. If the highest quality care cannot be provided, then a prompt step-up of care should be arranged. This may include hospital admission.

  • Do not underestimate the disease. Mortality and morbidity increases exponentially with age and frailty

  • Give excellent supportive and symptomatic care. Its effectiveness should not be underestimated

    • Fluids. Reduced intake and increased losses (fever) lead to volume depletion and end organ dysfunction. Encourage frequent oral fluid and suspend any diuretic treatment. Consider early initiation of s/c or iv fluids if a vicious spiral of dehydration and poor intake seems likely to ensue

  • Nutrition. Encourage high-calorie, high-protein drinks or solids. If the illness is especially severe, prolonged, or complicated, or if the patient is especially frail or malnourished, consider a period of NG feeding. Involve a dietician early

  • Paracetamol. If fever, discomfort, or pain occur

  • Maintain mobility. Bed rest may sentence the patient to death or dependency. Carers may need clear, firm advice about this

  • Identify and treat complications promptly

    • Carers may need information about important warning signs and the need to seek prompt medical advice

    • Perform regular observations of BP, pulse, and temperature where possible

  • Common serious complications include delirium, secondary bacterial infection, bronchospasm, pressure sores, and circulatory collapse

  • Antiviral agents (the neuraminidase inhibitors zanamivir and oseltamivir) can reduce both the severity and duration of influenza

  • They are indicated in patients >65 years who have an influenza-like illness during a period of high community incidence, provided they present early (<48hr)

  • They are well tolerated, reduce symptom severity and duration and they may reduce mortality

  • Zanamivir is inhaled, oseltamivir is taken orally

Further reading

NICE. Amantadine, oseltamivir and zanamivir for the treatment of influenza (2009). Online: Chest medicine www.nice.org.uk/ta168.

Pneumonia

Pneumonia

  • This is a syndrome of acute respiratory infection with shadowing on CXR

  • May be primarily lobar, bronchial or mixed pattern

  • Symptoms may be mild and are often non-organ specific eg fever, malaise

  • Common presenting scenarios include cough (often unproductive), delirium, reduced conscious level, lethargy, anorexia, falls, immobility and dizziness. Rarely patients can present with shock, coma and adult respiratory distress syndrome (ARDS)

  • Chest pain, dyspnoea and high fever are less common than in younger people. Signs may be minimal:

    • The patient may be well or unwell. Assess severity using the CURB criteria (see Chest medicine ‘Characteristics of severe pneumonia: the CURB-65 score’, [link])

  • Fever is often absent, but vasodilatation is common

  • Tachypnoea is a sensitive sign, as is at least moderate hypoxaemia (≤95% on air) on oximetry

  • Tests often guide management

  • Chest radiograph often reveals minimal infective infiltrate. Associated problems can include malignancy, effusion, or heart failure

  • Blood cultures should be sent, but sputum culture is rarely useful unless TB is suspected

  • White cell count may be raised, normal, or even depressed

  • CRP is often normal early in the illness. A very high CRP suggests pneumococcal disease or severe sepsis of any cause

  • U,C+E guide fluid management. Renal impairment is a sign of poor prognosis

  • Arterial blood gas (ABG) sampling is not usually necessary, unless oxygen saturations are <90%; oximetry is much better tolerated and usually sufficient to guide oxygen therapy

  • Organisms (see Table 11.1)

    • Often no causative organism is identified

    • Pneumococcus is a common pathogen in all settings, including hospital

    • Viral pneumonia, especially influenza, is under-recognized, and is the second most common cause of community-acquired pneumonia

  • Legionella and Mycoplasma pneumonias are uncommon. Mycoplasma is much more frequent during epidemics, occurring every 3 years or so

  • Unusual organisms are more common in frail patients, in higher dependency environments and in those who have recently received courses of antibiotics. These organisms include Gram negatives (which colonize the oropharynx) and anaerobes (a result of aspiration of gut contents). MRSA pneumonia and septicaemia is an increasing problem and may be contracted in the community, ie not just a hospital problem

Table 11.1 Pneumonia pathogens in various care settings; in approximate order of frequency

Community-acquired

Care home

Hospital

Strep. pneumoniae (>30% of cases)

Strep. pneumoniae (>30% of cases)

Gram-negative aerobic bacilli, eg Klebsiella, Pseudomonas aeruginosa

Viral, eg influenza, parainfluenza, respiratory syncytial virus

Viral, eg influenza, parainfluenza, respiratory syncytial virus

Anaerobes, eg Bacteroides, Clostridium. Especially in those at risk of aspiration, eg immobility, swallowing difficulty, prolonged recumbency or impaired conscious level

Haemophilus influenzae

Gram-negative aerobic bacilli, eg Klebsiella, P. aeruginosa

Staph. aureus

Gram-negative aerobic bacilli, eg Klebsiella, P. aeruginosa

H. influenzae

Strep. pneumoniae and H. influenzae. NB These may be the most common pathogens—in non-acute settings, eg rehabilitation wards—in the well, less frail patient

Legionella pneumophila. Mycoplasma pneumoniae if epidemic

Anaerobes eg Bacteroides, Clostridium. Especially in those at risk of aspiration, eg immobility, swallowing difficulty, prolonged recumbency or impaired conscious level

Viral, eg influenza, parainfluenza, respiratory syncytial virus

Other, eg TB

Other, eg TB

Following influenza, think of secondary bacterial infection, especially with Strep. pneumoniae (most common), H. influenzae or Staph. aureus

Following influenza, think of secondary bacterial infection, especially with Strep. pneumoniae (most common), H. influenzae or Staph. aureus

Pneumonia: treatment

Treatment is much more than antimicrobials alone:

  • Assess and optimize fluid volume status; give oral, s/c, or iv fluid as appropriate. Concurrent heart failure is common, but volume depletion more so

  • If there is subjective dyspnoea or moderate/severe hypoxaemia, then supplement oxygen, titrating the inspired oxygen concentration upwards to achieve arterial oxygen saturations >90% (see Chest medicine ‘Oxygen therapy’, [link]). For lesser degrees of hypoxaemia, it is not necessary to subject patients to claustrophobic, uncomfortable oxygen masks: simply monitoring saturations may be sufficient

  • Exercise caution in COPD: observe the patient closely, both clinically and with serial ABG sampling

  • Avoid the use of nasal specs acutely: if ventilatory drive is poor, inspired oxygen concentrations are very uncontrolled

  • Encourage mobility. If immobile, sit upright in bed, and sit out in a chair

  • Request physiotherapy if there is a poor cough, or lobar/lung collapse

  • Use saline nebulizers to loosen secretions which are difficult to expectorate and bronchodilator nebulizers when wheeze suggests associated bronchoconstriction

  • Minimize risk of thromboembolism unless contraindicated through prophylactic heparin, early mobilization, and compression stockings

  • Assess pressure sore risk and act accordingly (see Chest medicine ‘Pressure sores’, [link])

  • If dyspnoea, anxiety or pain is very distressing, consider opiates. Side effects include respiratory depression, sedation and delirium, so begin with small doses and assess effect

  • Anticipate possible deterioration, and judge in advance the appropriate levels of intervention. Would renal dialysis, ventilation and/or cardiopulmonary resuscitation be effective and appropriate? (See Chest medicine ‘Diagnosing dying and estimating when treatment is without hope’, [link])

  • Keep the family informed. Where possible, enlist their help, eg in encouraging eating and drinking

Characteristics of severe pneumonia: the CURB-65 score

Five key criteria (acronym ‘CURB-65’) determine prognosis:

  • Confusion (AMTS ≤8)

  • Urea (serum urea >7mmol/L)

  • Respiratory rate (≥30/min)

  • Blood pressure (<90 systolic and/or ≤60mmHg diastolic)

  • 65 years of age or more

The score has a six point scale (0–5 adverse prognostic features):

  • 0 or 1: Low risk of death (0–3%). Possibility of home treatment (but consider other factors, eg functional status, hypoxaemia

    • 2: Intermediate risk of death (13%). Hospital treatment is indicated

  • 3, 4, or 5: Severe pneumonia, with high risk of death (score 3: mortality 17%, 4: 41%, 5: 57%). Consider intensive care admission.

A five-point scale using only four criteria (CRB-65; urea excluded) can be applied outside hospital and also discriminates effectively between good and poor prognoses (eg mortality score 1: 5%, score 3: 33%).

Antimicrobials

Refer to local guidelines, reflecting pathogen sensitivities, and drug costs.

Community or care home settings

  • Amoxicillin orally is usually effective (vs. Strep. pneumoniae and H. influenzae). Erythromycin or clarithromycin if penicillin-allergic

  • Add clarithromycin (or erythromycin which has more gastric side effects) if there are features of atypical pneumonia, there is a Mycoplasma epidemic, or the patient may have had influenza

  • Co-amoxiclav orally has added activity against some Gram-negatives and Staph. aureus, and may be more effective in the frail patient or where aspiration is likely

  • Ciprofloxacin alone should be used rarely—it has Gram negative activity, but is less effective against Strep. pneumoniae, an important pathogen in most settings. If an antimicrobial is sought that will cover both chest and urinary sepsis, a better choice may be co-amoxiclav or trimethoprim

  • iv antibiotics are only necessary if the patient is very unwell (CURB-65 score of 3 or above) or unable to swallow. Co-administration of cefuroxime and erythromycin is a good choice in the unwell patient, treating all likely pathogens effectively. If you suspect MRSA pneumonia, add vancomycin. Convert to oral therapy and change broad to narrower spectrum drugs when the patient's condition improves and/or culture results are known to minimize complications, eg CDAD (see Chest medicineClostridium difficile-associated diarrhoea’, [link]). Often, only 48hr or less of broad spectrum, iv therapy is needed

Hospital-acquired infection

This presents a difficult dilemma. Hospitalized patients, especially those who are more frail and have spent longer in hospital, are prone to Gram-negative and anaerobic pulmonary infections. However, they are also susceptible to the adverse effects (especially diarrhoea) of broad spectrum antimicrobials.

A hierarchical approach is sensible, considering likely pathogens and illness severity;

  • In the less frail patient who remains well, begin amoxicillin alone, co-amoxiclav or a combination of amoxicillin and ciprofloxacin (all po). Broaden the spectrum only if the patient deteriorates or culture results suggest that the likely pathogen is insensitive

  • If a patient is at high risk of Gram-negative infection (frail, dependency, prolonged stay, invasive procedures, aspiration risk), begin with iv cefuroxime (or equivalent). Narrow the antimicrobial spectrum when the patient's condition improves and/or a pathogen is identified

  • If the patient has received multiple courses of treatment, seek microbiology advice

  • In all cases take blood cultures, and monitor the patient carefully

Further reading

British Thoracic Society guidelines online: Chest medicine www.brit.thoracic.org.uk.

HOW TO . . . Manage the patient with pneumonia who fails to respond to treatment

Is the diagnosis correct?

  • Consider other chest pathology such as heart failure, pulmonary embolism, pleural effusion, empyema, cancer or cryptogenic organising pneumonia. Extrathoracic pathology mimicking pneumonia includes acidosis (tachypnoea), and biliary or pancreatic pathology

  • Review the history, examination and investigations

  • Consider admission to hospital and further tests

Is there a complication?

For example effusion, empyema, heart failure, silent myocardial infarction or pulmonary embolism

Is the antibiotic being taken regularly and in adequate dose?

  • Is concordance a problem? Could a friend or relative help prompt tablet-taking, or would a dosette box help?

  • Syrups may be swallowed more easily than tablets. An experienced nurse can help where there are swallowing difficulties

  • If swallowing remains ineffective, or drug absorption in doubt (eg vomiting) then consider iv therapy

Is the organism resistant?

  • Take more blood cultures

  • Consider a change in antimicrobial, taking into account likely pathogens and their known sensitivities

  • Consider atypical infection; send urine for Legionella antigen test, especially if the patient is immunocompromised or if a patient appears disproportionately unwell. Remember MRSA pneumonia especially in those known to be previously colonized

Could other elements of care be more effective?

For example: fluid balance, oxygenation, nutrition, posture, and chest physiotherapy.

Is this an end-of-life situation?

  • Is treatment to extend life now inappropriate, the failure to respond a sign that the diagnosis is of ‘dying’ (see Chest medicine ‘Diagnosing dying and estimating when is treatment without hope’, [link])? If the patient cannot tell you their wishes, determine their likely views by discussing with family and friends, a decision informed by your judgement of where in their life trajectory your patient sits

  • In determining prognosis consider comorbidity—is this an abrupt, potentially reversible illness in an otherwise fit person, or a further lurch downhill for a patient with multiorgan failure. Not for nothing is pneumonia referred to as ‘the old man's friend’, sometimes bringing to a brisk and welcome end a period of irrevocable decline and suffering

Vaccinating against pneumonia and influenza

Vaccine delivery

  • Both vaccines should be offered simultaneously in October or early November to all aged >65 years, especially:

  • The frail

    • Care home residents

    • The immunosuppressed

    • Those with comorbidity, eg heart failure, COPD

  • Reliable delivery of these vaccinations depends upon effective information management systems in general practice, and substantial efforts by patients, carers, district nurses, and GP nurses

  • A common reason to have missed immunization is to have been a long-term inpatient (eg undergoing rehabilitation) during the autumn immunization period. Hospitals should ensure that these inpatients are immunized

  • Vaccinating healthcare workers, especially those working in long-term care settings, reduces the spread of infection and therefore death due to influenza among patients

Pneumococcal vaccine

  • Pneumovax® II, a multivalent pneumococcal polysaccharide vaccine, is effective against 65% of serotypes

  • Immunity remains for at least five years, perhaps for life

  • Bacteraemia is reduced by at least 50%. The effect on incidence of pneumonia itself is less clear

Influenza vaccine

  • The trivalent vaccine is prepared from currently prevalent serotypes

  • Immunity develops in <2 weeks, and it is therefore useful during epidemics

  • Immunity remains for up to 8 months

  • The risk of pneumonia, hospitalization, or death due to influenza is reduced by over half

Postexposure antiviral prophylaxis

  • Pharmacological prophylaxis of influenza is currently recommended when an unimmunized, high-risk group adult (eg care home resident) has had close contact with a person with influenza-like illness during a period when flu is prevalent (NICE 2008)

  • Treatment with neuraminidase inhibitors must be initiated within 24hr (for oseltamivir) or 24hr (for zanamivir) (see Chest medicine ‘Upper respiratory tract infections’, [link])

  • Consider why immunization was not performed. Is it too late to administer this year (this contact may not have ‘flu, but the next one might)? If not, then optimize the chances of immunization next year

Pulmonary fibrosis

This common problem is much underdiagnosed in older people due to a combination of under-investigation and overlap of clinical signs with common pathologies such as heart failure.

Consider when breathlessness coexists with profuse fine chest crepitations, with or without clubbing. On CXR, there may be bilateral pulmonary shadowing consistent with pulmonary oedema, but with little supporting evidence (eg normal heart size, absent Kerley B lines).

Causes

  • Idiopathic. The most common type in older people, known as usual interstitial pneumonia

  • Connective tissue disease, eg rheumatoid arthritis (most common), systemic lupus erythematosus, sarcoidosis. Lung involvement is sometimes the first manifestation of the multisystem disease

  • Drugs, eg amiodarone, nitrofurantoin rarely

    • Occupational exposure, eg asbestos, silica

    • If localized, consider TB, bronchiectasis, and radiotherapy

Tests

  • The diagnosis is usually confirmed by high-resolution CT scanning, which can also help distinguish subgroups likely to respond to immunosuppressive treatment

  • Respiratory function tests may be useful (a restrictive picture with decreased transfer factor is usual) but typically adds little in the frail older person

  • Refer to a respiratory physician to confirm diagnosis and guidance on management

Prognosis

This is very variable—about a third are clinically stable, a third improve and a third deteriorate at rates that vary greatly between individuals. Some can live with pulmonary fibrosis for years without significant functional impairment.

Treatment

  • Treat or remove any underlying cause, eg drugs

  • A minority respond slowly (over weeks) to immunosuppression (eg prednisolone and azathioprine). Monitor closely for side effects. In non-responders, tail off and stop. In responders, reduce dose cautiously. Ensure bone protection with calcium, vitamin D, and bisphosphonates

  • Home oxygen therapy is often useful

  • Give opiates for distressing dyspnoea

  • In those in whom dyspnoea progresses, consider end-of-life issues including treatment limitation, and a change of focus from life-extending measures to a purely palliative approach

Rib fractures

Common in older people.

  • Often a result of falls or even minimal bony stress such as coughing in a person with osteoporosis

  • Consider the possible contribution of alcohol, which causes both falls and osteoporosis

Diagnosis

Rib fractures should be diagnosed clinically.

  • Point tenderness and crepitus are often found

  • Pressure over the sternum may provoke the pain in a lateral rib

  • CXR, even with multiple projections, may miss the fracture, but is useful in excluding early complications such as pneumo- or haemo-thorax

  • Radioisotope bone scans are very sensitive but not specific (hot spots are often found without clinical fracture) so they are rarely indicated

Management

Rib fractures heal without specific treatment. The major problem is pain, which commonly leads to voluntary splinting of the injured area. There is hypoventilation and a failure to clear secretions, and secondary pulmonary infection can occur.

  • The patient should be encouraged to breathe deeply and to cough. Supporting the injured area when coughing, using a small pillow, minimizes pain. Strapping of the affected area is no longer done, as it increases complication rates

  • Regular analgesia should include paracetamol, plus a weak opiate in most cases. A short course of NSAIDs may be helpful

  • Admit to hospital if pain is severe and the patient unable to cough, or if complications (usually infection) have occurred

  • In cases of severe pain (eg multiple fractures), consider strong opiates or intercostal/paravertebral blocks. Involve the local pain team

Reassure the patient that the injury itself is not severe, will heal without immobilization and that coughing will prevent complications, not cause further damage.

Pleural effusions

A frequent (clinical or radiological) finding, sometimes incidental. Common causes are heart failure, post-pneumonia, PE, and malignancy (especially lung primary, mesothelioma, leukaemia, lymphoma, and metastatic adenocarcinoma (ovary, stomach)).

The differential diagnosis is wide, but narrowed when the results of CXR and pleural fluid aspiration are known (Table 11.2).

  • Empyemas, malignancy, and TB produce exudates with low pH (<7.2), low glucose (<3.3mmol/L) but high lactate dehydrogenase (LDH)

  • Transudates are usually not due to focal lung pathology, and so usually affect both lungs. Unilateral effusions due to transudates occasionally do occur, more commonly on the right side

  • Effusions due to heart failure are typically small and bilateral, with cardiomegaly; they can be unilateral, but usually a tiny contralateral effusion is seen, manifesting as blunting of the costophrenic angle; if the angle remains sharp, other causes are more likely

  • A massive unilateral effusion is usually due to malignancy

  • A uniformly bloodstained effusion is usually due to infection, embolism, malignancy or trauma

Table 11.2 Differentiating cause, by protein level

Transudate (protein <25g/L)

Exudate (protein >35g/L)

Heart failure

Malignancy

Hepatic cirrhosis

Infection, including TB

Hypoproteinaemia,

eg malabsorption, sepsis

Gastrointestinal causes,

eg pancreatitis

Nephrotic syndrome

Multisystem disorders, eg rheumatoid

(Exudative causes if low serum protein)

(Heart failure after diuresis)

Chronic effusions

  • If bilateral transudates, should be treated as for heart failure

  • If the diagnosis is not clear after CXR and aspiration consider chest physician referral and tests including CT, pleural biopsy (CT-guided rather than blind), video-assisted thoracoscopy with biopsy (VATS), and echocardiogram

  • For large, recurrent effusions, consider chest physician referral for continuous outpatient external fluid drainage via a semipermanent intrapleural (‘Pleuryx’) catheter

  • Frail patients may not tolerate, or desire, the more invasive tests. In this case, consider:

  • Repeated aspiration, combining diagnostic with therapeutic taps and sending larger volumes of fluid for cytology and acid-fast bacillus culture

  • ‘Watching and waiting’, with regular clinical review

  • A trial of diuretics, especially if the effusion is a transudate

HOW TO . . . Aspirate a sample of pleural fluid

Although aspiration is increasingly conducted under ultrasound guidance it remains a safe procedure in selected patients (compliant with good sized effusions) without ultrasound guidance. Simple aspiration in an outpatient or community setting remains a useful tool for the geriatrician:

  1. 1. Sit the patient leaning forwards and resting comfortably. Make yourself comfortable

  2. 2. Clinically identify the effusion (review the CXR; percuss to find maximum dullness)

  3. 3. Using permanent ink, mark this point

  4. 4. Clean and disinfect the skin. Attach a green hub (21-gauge) needle to a 10ml syringe

  5. 5. Using aseptic technique, insert the needle close to the marked point, but above a rib in order to avoid the neurovascular bundle

  6. 6. Advance slowly, applying moderate suction to the syringe, until the pleural space is entered and fluid flows

If a larger volume of aspirate is needed, swap to a larger syringe, holding the needle quite still.

Ultrasound detects small effusions (50–100ml) and aids diagnostic aspiration in patients with a small effusion.

Tests on the aspirate should usually include microscopy/culture, cytology, protein, LDH, glucose, and pH. If tuberculosis or cancer is suspected, then send larger volumes (eg 50ml) to microbiology and cytology, respectively.

Pulmonary embolism

Pulmonary embolism (PE) is common, yet as ‘the great pretender’ (of other pathology), is underdiagnosed and underreported on death certificates. It commonly coexists with and is confused with other lung disease eg pneumonia, heart failure and COPD—and is a common cause of deterioration in such patients.

Presentation

The classic symptom triad of pain, dyspnoea and haemoptysis is seen less commonly in older people.

Common presentations include:

  • Brief paroxysm(s) of breathlessness, or tachypnoea

  • Collapse, cardiac arrest, syncope, presyncope, or hypotension

  • Pulmonary hypertension and right heart failure, presenting as chronic unexplained breathlessness

  • Puzzling signs eg fever, wheeze, resistant heart failure, arrhythmia, confusion, or functional decline

Investigations

Determining the likelihood of PE rests on combining clinical judgement (the product of history, examination, and immediately available tests such as CXR) with appropriate imaging such as V/Q scan or CT pulmonary angiogram (CTPA). The common clinical features of PE—tachypnoea, tachycardia, and modest degrees of hypoxaemia—are common in ill older people, so clinical judgement alone is rarely enough.

Moreover, a confident diagnosis is essential because in older people:

  • The risk of anticoagulation is higher

  • The risk of a missed diagnosis is higher (less physiological reserve)

Possible PE in older people should be investigated in the usual way, with the choice of tests guided by local facilities and expertise. The following issues are especially relevant:

  • In a patient without known lung disease, the combination of breathlessness and a CXR showing clear lung fields strongly suggests PE. Further test(s) (V/Q or CTPA) are indicated

  • CXR abnormalities may be minor (atelectasis, raised hemidiaphragm, small effusions), or major (usually reflecting comorbid conditions rather than PE itself). Classical wedge shadows or unilateral oligaemia are rare

  • PE in the absence of lower limb deep vein thrombosis is common (10–20% of cases), so do not be put off by an absence of clinical signs of the leg, or a negative Doppler ultrasound

  • D-dimer can be a useful screening test to rule out PE but because many older people have coexisting conditions, eg infection false positives are very common (ie sensitivity high, specificity low)

  • Arterial blood gases have some value in diagnosis, but the common abnormalities (low PaO2, low PaCO2, and increased alveolar-arterial (A-a) oxygen gradient) are neither sensitive nor specific

  • In healthy older people, an increased A-a gradient is common

    • In older people following PE, a normal A-a gradient is seen in >10%

  • Echocardiogram may be normal following PE. However, in a patient with a high clinical probability, typical features of PE on echocardiogram usually provide sufficient diagnostic confidence to permit anticoagulation without further imaging

  • In the patient with unexplained right heart failure, consider PE: obtain an ECG and echocardiogram (ask for PA pressures) and request imaging that details the lung parenchyma (high-resolution CT: pulmonary fibrosis?) and the vasculature (CTPA: pulmonary embolism?)

  • In the patient who does not respond to treatment for chest infection, heart failure or acute exacerbation of COPD, consider whether PE may be responsible

Treatment

Anticoagulation

Standard treatment is low molecular weight heparin (eg dalteparin, enoxaparin) followed by warfarin with goal INR 2–3. Once the possibility of PE is raised, it is essential to treat with low molecular weight heparin pending investigation results, unless there are particular treatment risks.

To minimize bleeding risk:

  • Anticoagulate with caution. Check baseline clotting. Give 5mg (not 10mg) warfarin dose on day 1 (see Chest medicine ‘HOW TO . . . Initiate warfarin’, [link])

  • Beware the older patient with mild anaemia or a low MCV—do they have occult blood loss?

  • In the very frail, sick, unstable patient in whom anticoagulation with warfarin would present significant risk, consider a period of anticoagulation with low molecular weight heparin. Start warfarin when clinical stability returns

Thrombolysis

Consider thrombolysing, balancing risks and benefits, where there is life-threatening PE, manifesting as acute right heart strain and systemic hypotension. Both risk and benefit increase with age, so age itself is not a contraindication.

Inferior vena cava (IVC) filter

An IVC filter (‘Greenfield filter’) can be inserted under local anaesthesia by an interventional radiologist. Most cannot be removed once in situ but some of the newer ones are potentially retrievable.

Indications include:

  • Strong contraindication to anticoagulation, eg

  • Active bleeding

  • A high risk of bleeding, eg newly diagnosed peptic ulcer or very recent haemorrhagic stroke

  • Massive thromboembolism with contraindication to thrombolyis

  • Ongoing thromboembolism despite anticoagulation

  • Embolism from a septic focus

Aspiration pneumonia/pneumonitis

The involuntary entry of extrinsic material into the pulmonary airways. This is a common problem, ranging from subclinical micro-aspiration of oropharyngeal mucus to major inhalation of gastric contents.

Risk factors

  • Swallowing problems

  • Gastro-oesophageal disorders leading to reflux

  • Impaired conscious level including seizures

  • Sedative drugs

  • Previous aspiration or non-aspiration pneumonia

  • Clinically assisted nutrition—either NG or gastrostomy

Diagnosis

Commonly, the occurrence of pneumonia in a patient with risk factor(s) suggests the diagnosis.

CXR may show consolidation in dependent lung zones, eg R lower lobe, although any zone may be affected.

Treatment

  • The role of antibiotics is debated. Much of the radiographic response may be a chemical pneumonitis, ie inflammatory reaction to caustic gastric contents, rather than infective pneumonia

  • The choice of antibiotics is also contentious. Many cases respond well to amoxicillin or co-amoxiclav, but consider broad spectrum iv antibiotics to cover Gram-negatives and anaerobes in:

    • The unwell

    • The especially frail

  • High-dependency settings

  • Where aspiration has been major

  • If possible, treat the underlying cause. If risk factors persist (eg impaired swallow or continual seizures), consider a ‘nil by mouth’ order until they are addressed.

  • Where the swallow may be impaired, perform a formal swallowing assessment (see Chest medicine ‘HOW TO . . . Manage swallow after stroke’, [link]) and manage according to the results

  • In palliative care;

    • Consider anticholinergics to dry secretions

  • In advanced dementia, it is often appropriate to accept the risk of aspiration. Insertion of a gastrostomy (commonly a PEG) risks medicalizing the final months while achieving nothing—aspiration is common in patients with a PEG

  • It is often cruel and futile to deny a dying patient food that he or she may enjoy, even if the risk of aspiration and a life-shortening pneumonia exists. ‘Nil by mouth’ orders are usually inappropriate in end-of-life situations. Instead consider using thickened fluids, pureed diet, supervised feeding, and avoiding eating in recumbent position, with straws or feeder cups

Chronic cough

A common problem, with causes ranging from the trivial to the sinister. Even where the underlying cause is benign, chronic cough can be both distressing and disabling.

Causes

  • Asthma. Cough is a common presenting symptom in older people

  • Silent pulmonary aspiration

  • GORD

  • Postnasal drip can be due to sinusitis or chronic rhinitis. Frequently allergic in origin, but in older people, symptoms are often not seasonal

  • Drugs, eg ACE inhibitors (may take weeks or months to develop), β‎-blockers (leading to bronchospasm)

    • Persistent benign cough following upper respiratory tract infection. May persist for 2–3 months

    • Chronic pulmonary pathology eg COPD, TB, bronchiectasis

  • Heart failure, with high pulmonary pressures

  • Thoracic malignancy, either primary or secondary

Investigation

Consider both tests and trials of treatment. Their pace and extent depends on the differential diagnosis following careful history and examination. Consider the following tests:

  • CXR (mandatory)

  • Sinus X-ray

  • Spirometry, with assessment of response to bronchodilators

  • Regular monitoring of PEFR, looking for morning drops suggesting asthma

  • Sputum microscopy and culture is unlikely to be helpful

Next, consider a trial of treatment for the most likely cause, eg:

  • Bronchodilators (and inhaled steroids) for possible asthma

  • A PPI for possible GORD

  • Assess the effect of treatment of possible chronic rhinitis with:

  • Nasal corticosteroids. Probably the treatment of choice, eg beclometasone, budesonide

    • Decongestants. Should be used in short courses only (since rebound phenomenon)

    • Antihistamines. Most useful for obviously allergic rhinitis. Can be topical spray or tablet. Should be used with caution; select those with fewer anticholinergics properties, eg cetirizine or loratadine

In all cases, trials of treatment need to be prolonged (≥8 weeks).

Treatment

This is of the underlying cause. Where this cannot be treated effectively (eg advanced malignancy), specific treatments aimed at reducing cough may be of benefit. These include opiates such as codeine or morphine. Simple cough linctus may be useful for irritating dry cough following an upper respiratory tract infection.

Lung cancers

The commonest cause of cancer deaths, and largely a disease of older people.

  • Symptoms may be non-specific (eg fatigue, weight loss), or else pulmonary in origin but attributed to existing non-malignant pathology (eg dyspnoea in a patient with COPD)

  • Have a high index of suspicion and a low threshold for further investigation. Have an even higher degree of suspicion in older smokers presenting with pneumonia

Sinister features in those presenting with pneumonia include:

  • Haemoptysis, especially if significant, eg with persistent blood clots

  • Regional or generalized symptoms of cancer (eg hoarse voice, weight loss)

  • Cough and consolidation without obvious infective symptoms (eg fever)

  • Symptoms that continue to be troublesome despite antibiotics

If sinister features are present, it is unacceptable to wait (up to 6 weeks) before repeating a CXR to confirm resolution. Refer promptly for urgent specialist assessment and consider CT scanning, bronchoscopy, or lung biopsy.

Treatment

  • Treatment has improved and is now more effective, both in extending life and in palliating symptoms. Therefore, ‘benign neglect’, ie simply observing an older person with probable lung cancer, is now only rarely acceptable. It may be appropriate, for example, in cases of extreme frailty or severe cognitive impairment

  • Older people with probable lung cancer remain under-investigated and under-treated:

  • Tests such as bronchoscopy and a histopathological diagnosis are less commonly obtained. This makes palliative treatment and prognostication difficult

  • Treatment such as surgery or chemotherapy are less commonly considered or administered. To an extent this reflects appropriate decision making based on functional status

  • Treatment decisions should be made by expert MDTs that consider the patient's functional status, comorbidities, and cancer characteristics

▸Refer all patients with suspected or confirmed lung cancer for a specialist opinion.

Non-small cell carcinoma (squamous cell, adeno-, and large cell carcinoma)

  • Surgery may lead to cure if:

  • There is adequate pulmonary function (arbitrarily, FEV1 ≥1.5L)

  • There is no distant spread (but >50% of cancers have spread at presentation)

  • The patient is relatively well with good functional status and no serious comorbidity

  • Surgical procedures are high risk (eg at 70 years, lobectomy has 10% perioperative fatality, and pneumonectomy 20%). However, the condition is always fatal without treatment, so the patient's view is critical

  • Radiotherapy. When surgery is not feasible, either because of the nature of disease, or the fitness of the patient, then radiotherapy may be used either:

  • Palliatively, to control symptoms (see Chest medicine ‘Palliative interventions’, [link])

  • Curatively, in high dose (CHART). Success rates are lower than for surgery

  • Neoadjuvantly, to reduce tumour volume and sometimes to convert a non-operable tumour into an operable one

  • Chemotherapy. Oral agents can be used if EGFR mutation found

Small cell carcinoma

  • Relatively more common in older people: >20% of cases

  • Most cases are advanced at presentation, and treatment is palliative

  • Most tumours are chemoresponsive. Frail patients are unlikely to tolerate aggressive treatment and it risks reducing the quality of the brief life that remains. Therefore, chemotherapy regimens are tailored to the patient, determined by structured assessment of performance status. In general, frail patients undergo fewer but similar chemotherapy cycles compared to the more robust

  • Surgery is the treatment of choice, but is seldom useful because tumours are rarely localized at presentation

Palliative interventions

  • Radiotherapy for superior mediastinal obstruction, bronchial obstruction, chest pain, haemoptysis, or painful bony metastases. This is generally well tolerated, although 710% develop radiation pneumonitis weeks after treatment, and it is on average more severe in older people

  • Opiates for cough

  • Aspiration of pleural effusion for breathlessness

  • Endobronchial therapy (eg stenting, diathermy)

Tuberculosis: presentation

In older people, TB:

  • Incidence is much higher, especially in the very old

  • Outcomes, including mortality, are much less good

  • Is most commonly due to reactivation of previous disease, the primary infection having been asymptomatic or unrecognized. In the early twentieth century, primary infection of young adults was common. By the mid-late twentieth century, primary infection in younger people had diminished. When this cohort reaches old age, TB reactivation will be much less common

  • Reactivation (postprimary disease) occurs due to decreased immunity itself due to intrinsic ageing, disease (eg diabetes mellitus, renal failure), malnutrition (eg chronic alcohol excess) or drugs (eg steroids)

  • A few patients develop new infection from open cases. Care home residents are most vulnerable, infection passing from fellow residents or from care home staff

  • Consider HIV infection when TB diagnosed

Presentation

Pulmonary disease

  • Sometimes similar to that in younger people, ie cough, sputum, fatigue, weight loss and anorexia

  • Night sweats, fevers and pulmonary symptoms may be less common

  • May present as pneumonia that fails to resolve, or as an incidental finding, suggested on CXR

Extrapulmonary disease

Most (>75%) presentations are pulmonary, but extrapulmonary cases are relatively more common in older people, eg:

  • Miliary. Diffuse, overwhelming infection with fever, weight loss and hepatosplenomegaly. Pancytopenia can occur

  • Urogenital and renal. May affect any part of the renal tract. Sterile pyuria, haematuria, abdominal or back pain, genital sinuses, or pelvic masses may occur, or disease may be asymptomatic

  • Meningeal. Consider this in the very frail, malnourished or immunosuppressed patient with non-specific cerebral signs (eg confusion, dementia-like syndrome, headache, or reduced conscious level). Meningism may be absent, and the CSF virtually acellular

  • Skeletal. Bone infection most commonly affects the spine (usually thoracic or lumbar), presenting as pain and tenderness. TB arthritis usually affects large weight-bearing joints

  • Other eg lymph nodes, intestine

Sequelae of previous treatment

Lung collapse therapy was used widely in the treatment of pulmonary TB in the 1930–50s. Procedures included therapeutic pneumothorax, thoracoplasty, and plombage (expanding the extrapleural space with artificial materials). Sequelae include empyema, sinus formation, bronchopleural fistulae, and ventilatory failure. TB, pyogenic or fungal organisms may be isolated. Early specialist input is essential.

Tuberculosis: investigation

Chest X-ray

Changes are more variable than in younger people, and may mimic other benign or malignant disease (eg bacterial pneumonia, cancer)

  • Usually upper zone infiltrates with cavities, but more common features in older people include mid/lower zone infiltrates, miliary (diffuse nodular) and bilateral change

  • Healed old disease is usually seen, ie calcified hilar nodes, a peripheral primary complex, pleural thickening, and diffuse apical fibrosis and calcification

  • Pleural effusions are common

  • Rare changes include mass lesions or isolated lymphadenopathy

  • Very rarely the CXR may be normal, eg occasionally in miliary or endobronchial disease

Sputum for microscopy and culture

The standard method of confirming TB.

  • Conventionally, three early morning sputum specimens are obtained and stained by acid fast staining (eg Ziehl-Neelsen). The quality and persistence of the microscopist is important, as the scanty organisms can be easily missed on cursory examination

  • If a patient cannot expectorate, obtain ‘induced sputum’, through physiotherapy, or nebulized normal saline (rarely nebulized hypertonic saline). If this fails, or clinical suspicion is high despite negative smear and culture, consider bronchoscopy with washings

Other tests

  • Raised ESR and CRP are usual

  • FBC. Mild (normocytic) anaemia and reduced white cell count are more common in older people. Lymphocytosis or pancytopenia can occur

    • Obtain three early morning urine specimens in case of possible genitourinary infection

  • Tissue sampling. Where possible, sample tissue eg lymph node, pleura, bone marrow. Send samples to both microbiology (microscopy and culture) and to histology. Typical histological features, of caseous necrosis with granuloma formation (with or without acid fast bacilli) support strongly the diagnosis of TB

  • Tuberculin skin testing is complex

HOW TO . . . Perform and interpret a tuberculin skin test

In these diagnostic tests, tuberculin purified protein derivative (PPD) is injected in a standardized manner, and the reaction assessed quantitatively.

Heaf's test has been used in screening larger numbers of younger patients, often as pre-vaccination screening programmes. Tiny droplets of high-concentration PPD are administered using a multiple tine (Heaf) apparatus. High-concentration PPD is no longer manufactured, and the test is not further described here.

Mantoux's test is most commonly performed where TB is suspected in an individual patient. Fixed volumes of less concentrated PPD are injected intradermally.

  • The standard dose is 5 tuberculin units (0.5mL of 1 in 10 000 dilution)

  • Examine the skin after 48–72hr and measure the diameter of induration, reflecting the extent of the cell-mediated immune response

  • A positive test indicates immunity, not necessarily infection. This may be a result of previous (probably asymptomatic) TB infection, or immunization (although reactivity to the bacille Calmette Guérin (BCG) vaccine often disappears after 10 years)

  • The degree of induration correlates approximately with the likelihood of infection. However, the post-test probability of infection is a product of both the pre-test probability and the test result.

    • ≥15mm indicates a significant reaction and the probability of active infection

    • 5–15mm may be significant if pre-test probability is high eg close contacts, suggestive CXR. Consider causes of a false negative reaction

    • <5mm is negative, usually indicating a low probability of active infection. However, if the pre-test probability is very high, consider treatment

  • The test may be falsely negative (or equivocal) with steroid use, lymphoma, malnutrition, sarcoid, overwhelming TB infection or when there is concurrent other infection

  • Ageing itself impairs the immunological reaction to tuberculin, and may produce a false negative or equivocal test in patients previously infected with TB. Giving a second (booster) tuberculin dose within 20 weeks of the first often produces a positive test, defined as when induration >10mm and augmentation of induration (test 1–test 2) exceeds 6mm

Tuberculosis: treatment

Given the complexities of treatment, specialist referral is mandatory. This is a notifiable disease and public health local authorities will investigate contacts, especially in the care home setting. Respiratory isolation precautions are necessary for patients with pulmonary TB treated in hospital.

Pulmonary disease is treated for a total of 6 months

  • Usually 6 months of rifampicin and isoniazid, with pyrazinamide (and ethambutol) for the first 2 months only

  • Ethambutol may be omitted if the risk of resistance to isoniazid is low

  • Longer treatment periods may be needed for extrapulmonary disease

In older people:

  • Drug resistance is rare, as most infections are recurrences of primary disease, contracted decades ago

  • Failures of treatment are usually due to poor concordance. Combination drug preparations may improve this (eg Rifater® = rifampicin + isoniazid + pyrazinamide)

  • Side effects are more common, including ocular toxicity from ethambutol (reduce dose in renal impairment) and hepatitis from isoniazid. Close monitoring is important

  • Atypical mycobacteria, eg Mycobacterium avium intracellulare or kansasii can occur in those with structural lung disease such as bronchiectasis. This requires even broader and more prolonged courses of antibiotics but isolation is not required as it does not spread from person to person

Asthma and COPD: assessment

Presentation

Asthma and COPD (Table 11.3) in older people:

  • Are both diseases characterized by airflow obstruction

  • Commonly coexist, eg in the childhood asthmatic who has smoked

  • May both be mimicked by other common diseases eg cancer, pulmonary embolism, heart failure

  • May present late: older people are less aware of hypoxaemia, breathlessness or bronchoconstriction

  • Are underdiagnosed and undertreated, especially in older people

Table 11.3 Distinguishing Asthma from COPD

Asthma

COPD

Modest degree of fixed airways obstruction (this is uncommon in younger people)

Greater degree of airways obstruction

Significant or full reversibility

No, or only minimal, reversibility

≥20% variability in PEFR

<20% variability in PEFR

Greater age

Significant smoking history

Asthma

  • May present in old age as true ‘late onset asthma’. There are also increasing numbers of people who have grown old with their asthma

  • In older people, cough may dominate, symptoms fluctuate less, triggers (eg cold, smoke, allergens) are less frequent and the association with hay fever or eczema is less strong

  • Nocturnal cough or dyspnoea, including paroxysmal nocturnal dyspnoea, may be caused by asthma

  • NSAIDs and β‎-blockers (oral or ocular) may worsen bronchoconstriction

COPD

  • Is much more common in older age, the consequence of intrinsic ageing and progressive disease

  • Is caused by environmental exposure, usually to tobacco smoke, in genetically susceptible people. Significant disease can develop in those who have not smoked for years, as acquired lung damage depends more on ‘total pack years’ smoked rather than duration alone

  • Symptoms are usually more chronic and slowly progressive, without significant variability

  • If bronchitis is significant, there is a productive cough (most days of at least 3 months of 2 consecutive years). Fatigue and sleep disturbance are common. Daytime somnolence suggests ventilatory failure

  • There may be associated anaemia of chronic disease, osteoporosis, malnutrition, and depression

Investigations

  • Oximetry will determine the presence and degree of hypoxaemia. In moderately or severely hypoxaemic patients (O2 saturation <92%), consider ABGs to determine whether long-term oxygen therapy may be of benefit (see Chest medicine ‘Oxygen therapy’, [link]) and, in the acutely unwell, to guide oxygen administration

  • CXR, ECG, and FBC will help to exclude other pathology, eg anaemia, dysrhythmia

    • PEFR, measured regularly (bd—qds) for up to 2 weeks, helps determine whether variable airways obstruction (asthma) exists. Variability ≥20% is significant. Older people may find using PEFR meters and charting the results difficult. Ask them to demonstrate technique, reading the device, and charting in clinic

  • Spirometry. Obtain at least FEV1 and forced vital capacity (FVC). An FEV1: FVC ratio of <70% suggests obstruction

    • Older people often have difficulty performing pulmonary function tests; an experienced technician in a respiratory laboratory will help provide accurate results

    • Assessments for bronchodilator responsiveness using inhaled bronchodilators are now considered less helpful, as they are poorly predictive of the response to treatment, and do not distinguish reliably between asthma and COPD. However, airflow obstruction that completely and repeatedly resolves after bronchodilator administration does exclude COPD

    • Assessments for steroid responsiveness can be helpful in distinguishing between asthma and COPD (response is greater in asthma than COPD, although there is overlap). Perform spirometry before and after steroids (either 2 weeks of prednisolone 30mg od, or 6 weeks of inhaled beclometasone 400micrograms bd)

  • Some patients show improvement in FVC or functional status (walking distance or speed) despite no significant change in FEV1

Asthma and COPD: drug treatment

In general, treatment principles are similar to those in younger people, and are described in detail in British Thoracic Society guidelines. However some differences and some similarities benefit from emphasis.

Bronchodilators

  • Older people perceive symptoms less reliably, so where there is evidence of variable airways obstruction, give bronchodilators regularly rather than as required

  • In older age, response to anticholinergics, eg ipratropium, tiotropium, may be better than to β‎-agonists, eg salbutamol

  • High dose β‎-agonists, eg from nebulizers, may cause tremor, tachycardia or rate-related angina. Nebulizers may not be required—try higher inhaled doses via a spacer (eg salbutamol 400–800micrograms (4–8 puffs of a standard metered dose inhaler)), or long-acting β‎-agonists, eg salmeterol

  • Anticholinergic bronchodilators uncommonly cause side effects such as dry mouth or blurred vision, more often with higher (nebulized) doses and with long-acting preparations. Acute glaucoma is a rare but important complication—reduce ocular exposure by nebulizing via a mouthpiece rather than a face mask

Corticosteroids

  • Long-term oral steroids are rarely beneficial

  • In those receiving regular courses of oral steroids for acute exacerbations, give osteoporosis prophylactic treatment. Inhaled steroids alone probably do not cause osteoporosis

Theophylline

  • Toxicity is common in older people. Plasma levels are increased by febrile illness, heart failure and drugs, eg erythromycin/ciprofloxacin. Serious side effects, eg convulsions may be the first sign of toxicity

  • Check levels when titrating dose. Most of the therapeutic effect is seen by the lower end of the therapeutic range, so target this first

  • Before introducing oral theophylline, optimise inhaled bronchodilator and steroid therapy, including the use of long-acting and higher dose preparations if necessary

Other

  • Influenza and pneumococcal vaccine should be given

  • Exercise extreme caution in the use of respiratory depressants, eg benzodiazepines or opiates. In general:

  • In acutely unwell patients with CO2 retention, stop them, reintroducing only if withdrawal effects occur

  • In stable patients with or without CO2 retention, withdraw or reduce them where possible

  • In severe, end-stage COPD, if dyspnoea or cough are distressing and cannot be otherwise relieved, consider giving opiates. Give small doses initially, but increase as needed to relieve distress, even if respiratory function deteriorates. Explain the rationale to staff, relatives and the patient if appropriate

HOW TO . . . Improve drug delivery in asthma or COPD

  • The traditional metered dose inhaler alone is rarely adequate, due to difficulties in coordinating device activation and the onset of inhalation

  • Adding a large volume spacer device reduces the need to coordinate activation with inhalation, improving drug delivery and reducing side effects (eg oral thrush). Spacers are generally better tolerated by older patients who don't tend to consider them such a social handicap as youngsters

  • Breath-activated devices provide an alternative to the metered dose inhaler, although lung volumes may not be adequate to activate the device. They vary widely in design, and patients vary greatly in ability to use them

  • Assess and advise on technique regularly, involving both hospital and community teams (doctor, nurse, and pharmacist) as well as the family and other carers

  • Nebulizers are rarely required. A metered dose inhaler via a large volume spacer device is usually just as effective. Patients in whom nebulized drugs are being considered should be referred for specialist assessment

  • Where concordance is an issue, eg in a person with dementia living alone

    • Give long-acting preparations where possible, eg salmeterol in place of salbutamol, tiotropium in place of ipratropium

    • Give combined preparations eg Combivent® in place of salbutamol and ipratropium

    • Once daily inhaled steroid is better than none

    • Supervise taking of medication as often as possible, but accept that taking for pulmonary drugs, taking medications irregularly is probably better than taking them not at all

  • Rarely, inhaled drugs are administered too frequently by cognitively impaired people. This very rarely causes side effects, but relatives may need reassurance that this is the case

  • Occasionally, oral β‎-agonists are useful, in patients in whom all inhaled preparations have been unsuccessful

Further reading

British Thoracic Society guidelines online: Chest medicine www.brit-thoracic.org.uk.

Asthma and COPD: non-drug treatment

  • Smoking cessation should be advised, except in the very advanced or terminal phase, where it may lack benefit and be unkind. Consider referring for support and/or nicotine replacement therapy

  • Exercise is beneficial, sometimes available as part of a pulmonary rehabilitation scheme. Elements should include aerobic and strength-based exercises as well as specific breathing exercises

  • Pulmonary rehabilitation is as effective as inhaler therapy, and should be a key part of treatment. It is a complex intervention tailored to the individual, with exercise, behavioural and educational components. Individual action plans can be followed by older people, facilitating self-management and early intervention

  • Weight reduction is beneficial in the obese. However weight commonly falls in advanced disease as the work of breathing exceeds calorific intake, and nutritional supplements may be needed

  • Comorbidities including depression are common and should be treated aggressively

  • Social and practical interventions. A comprehensive multidisciplinary assessment may be warranted. Provide appropriate mobility aids, eg electric wheelchairs, stairlifts, and alarm systems, eg pendant alarms. Treat social isolation

Assisted ventilation

  • Consider this in cases of respiratory arrest, respiratory acidosis, delirium, exhaustion or deteriorating respiratory function despite full treatment. Hypercapnia rather than hypoxaemia is usually the key contributor to delirium; sedation is likely to worsen ventilation and precipitate coma

  • For some patients with acute-on-chronic deterioration, ventilation will be futile and inappropriate. Make such a decision after considering:

  • The nature of the chronic illness and recent deterioration

  • The presence of reversible factors

    • The patient's current physiological status

  • The views of the patient or others who represent them

    • If in doubt, request guidance from the ITU team

  • Non-invasive ventilation (NIV), eg nasal intermittent positive pressure ventilation provides an acceptable alternative to invasive ventilation (usually endotracheal intubation). NIV is often well tolerated, can be delivered on specialist or high-dependency wards, and provides a modest level of ventilatory support that can be weaned promptly as the patient recovers

Palliative interventions

  • Reassure—many patients are frequently terrified. Assure them that their symptoms of suffocation can, and will be treated. Consider advance care planning

  • Positioning—sit up, day and night

  • Involve the palliative care team. Their advice and support is often valuable and can continue into the community if discharge occurs

Oxygen therapy

  • Oxygen is a drug—it has clear indications, and common and important side effects

  • Precision and care in prescribing maximizes benefit and reduces harm

  • In older people, dyspnoea may be more frequently accepted, leading to underprescribing

  • However, indiscriminate prescribing, particularly the use of high-concentration oxygen, risks respiratory depression, and CO2 narcosis. This is common in older people with COPD

Long-term oxygen therapy (LTOT)

This improves prognosis in severe COPD and in moderate COPD with features of cor pulmonale. To reduce pulmonary hypertension, arterial pO2 should be raised above 8kPa for at least 15hr each day. Concentrations of inspired oxygen (FiO2) of 24–28% usually achieve this. Respiratory depression is very rarely a problem in patients with stable respiratory failure who receive low oxygen concentrations.

Specific criteria must be met before prescribing LTOT. Measure arterial blood gases twice, on air, at least 3 weeks apart, and at least 4 weeks after an acute exacerbation.

Criteria include:

  • PaO2 7.3–8.0kPa in COPD with complications such as peripheral oedema, evidence of pulmonary hypertension, or polycythaemia

  • PaO2 <7.3kPa in COPD without the complications already listed

Intermittent oxygen therapy (IOT)

This is useful for a variety of cardiorespiratory conditions, eg COPD, advanced heart failure, lung cancer. It relieves distress and improves exercise tolerance and mobility. Low concentrations (24–28%) can achieve significant symptomatic benefit. Prognosis is unaltered.

High concentration oxygen therapy

Oxygen at 40–60% is useful for short-term use in respiratory failure without hypoventilation and CO2 retention, commonly seen in acute heart failure, PE, and pneumonia. Even in these cases, high-flow oxygen may reduce respiratory drive, leading to CO2 narcosis. This is especially common in older people, those with a smoking history, the acutely unwell and where respiratory depressants (eg opiates, benzodiazepines) are co-administered.

Avoid this by:

  • Keeping saturations just below normal (90–94%) rather than normal or above normal (98–100%)

  • Avoiding respiratory depressants

  • Monitoring closely for signs of CO2 retention

Oxygen delivery systems

Supply patients with an administration device applicable to their circumstances. Latest guidelines for hospital are that clinicians should prescribe the target saturation range and state whether controlled/constant performance is required and that nurses should monitor the patient and determine the most suitable delivery system within those parameters.

Constant performance oxygen delivery systems (eg Ventimask 28%) provide a stable FiO2 (24%, 28%, 32%, etc.) for a range of ventilation rates. 28% is suitable for most patients receiving LTOT. These must always be used for hypoventilating patients with elevated PaCO2.

Variable performance oxygen delivery systems. FiO2 varies. The system delivers oxygen at a given rate which mixes with room air at rates dependent on ventilation. Systems include

  • Nasal cannulae. Often better tolerated by patients, and allow them to eat and talk. With oxygen flows of 1–2L/min, FiO2 is usually low (less than 28%), but can approach 30% if the patient hypoventilates

  • Simple face mask, eg Hudson. Provides variable FiO2 up to 40%

  • Non-rebreathing mask with reservoir bag. Provides variable FiO2 up to 60%

Oxygen gas supply

Oxygen concentrators are costly to purchase but running costs are low. They are cost-effective when needing low flow oxygen for prolonged periods (≥8hr per day). Oxygen is piped to convenient position(s) in the home, and usually administered via nasal cannulae. Urgent installations can usually be arranged within 24hr.

Oxygen bottles are useful for:

  • Patients on LTOT via an oxygen concentrator who wish to leave their home for short periods

  • Patients needing oxygen as required, who do not meet the LTOT criteria

  • Patients who are likely to have a short-term need for continuous oxygen, eg for end-of-life palliation, for whom installation of an oxygen concentrator may not be worthwhile

A small oxygen cylinder (‘PD oxygen cylinder’; 300L, lasting 2hr) is available which is convenient for wheelchair excursions, or travel in a car.

▸Smokers should stop smoking before beginning oxygen therapy. The risk of burns and household fires is substantially increased.

Asbestos-related disease

The period between asbestos exposure and overt (or covert) disease is usually long, often over 20 years. Almost all new cases are in older people because asbestos exposure is so carefully regulated now. The exposure may not be clearly recollected by the patient but always consider in high-risk occupations including builders, dock work and heavy engineering. Confirming the diagnosis is important because compensation may be due if disease can confidently be shown to have arisen as a consequence of asbestos exposure. If the diagnosis could not be confirmed during life, then post-mortem confirmation may lead to compensation payments to relatives.

Pleural plaques

Discrete areas of thickening of the pleura that often calcify. Benign. A marker of asbestos exposure, but of no further clinical significance. However, compensation is payable for this alone, if the claim is made promptly following diagnosis.

Asbestosis

Progressive fibrosis, clinically and radiographically similar to idiopathic pulmonary fibrosis. Usually due to prolonged and substantial occupational exposure.

Mesothelioma

A malignant, incurable tumour of the pleura, presenting as cough, chest pain, effusion, or dyspnoea. Very poor prognosis; few survive over 2 years. Treatment is nearly always palliative; the tumour is not resectable, and is relatively insensitive to chemotherapy or radiotherapy. Asbestos exposure may have been only transient.

Bronchial carcinoma

There appears to be a synergistic effect between asbestos and tobacco.