A 68-year-old woman with breathlessness and yellow sputum

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Problem 31 A 68-year-old woman with breathlessness and yellow sputum

Hubertus P.A. Jersmann

You are working in the emergency department one winter evening. A 68-year-old woman is brought in by ambulance, acutely short of breath. The history is obtained mainly from the patient’s daughter, because the patient is too breathless to talk, very tired and also a little drowsy. She says she has had difficulty with her breathing for many years and can now only walk at a slow pace for 100 metres and then has to stop due to breathlessness. She has had a smoker’s cough for as long as she can remember and has produced phlegm on most days for many years. She has had a number of chest infections this winter despite repeated courses of antibiotics and as a result the local doctor started her on a purple inhaler.
On this occasion the woman has been unwell for 1 week. During this time she has been producing thick yellow-green sputum which she has found difficult to cough up. She has been sitting up at night in a chair and has been unable to do anything due to her breathlessness and extreme fatigue. She has become nauseated and is eating very little. She has not had a temperature or shivers or chest pain. She has not noticed any blood in her sputum and she has not had ankle swelling. The patient has been on antibiotic tablets for 5 days but there has been no improvement.
The woman suffered a myocardial infarction at the age of 60 and underwent coronary bypass surgery. She has not had recurrent angina since then and is not on any cardiac medication. She does not have hypertension or diabetes mellitus. She had experienced pain in the left calf on walking up until the last 6 months when she has been more troubled by breathlessness.
She is on a salbutamol puffer, 2 puffs 4-hourly, fluticasone/salmeterol 250 mg/25 mg 2 puffs bd and amoxicillin 500 mg three times a day for the past 3 days. She currently smokes 5 cigarettes a day, but until 3 months ago smoked 30–60 a day and had done so since the age of 17. She claims she finds benefit from the smoking as it seems to aid the clearing of her sputum.

Q.1

What is the likely diagnosis? What factors may have precipitated her recent deterioration?

You ponder the differentials, and move on to examining the patient.

Q.2

Describe the key components of the examination.

The woman is agitated and looks exhausted and cyanosed. She sits up on the examination couch, in obvious respiratory distress. She is tachypnoeic at 30 breaths/minute. She has prolonged expiration with an audible wheeze, and is coughing frequently, producing thick yellow-green sputum. She has a ruddy complexion, and appears moderately dehydrated.

Her temperature is 38°C, her pulse 140 bpm, regular and bounding, and her blood pressure is 150/100 mmHg with a paradox of 25 mmHg. The patient has a barrel chest with markedly reduced chest expansion and a tracheal tug with use of her sternocleidomastoid muscles and intercostal recession. Precordial dullness is lost. There is no finger clubbing or flap.

Her jugular venous pulse is raised 4 cm. Her apex is not palpable and her heart sounds are inaudible. Her chest is hyper-resonant with globally reduced breath sounds, a prolonged expiratory phase and a loud wheeze. There is no cervical lymphadenopathy and the abdomen is not examined formally due to the patient’s distress. There is mild ankle oedema. She is unable to perform simple spirometry due to the severity of her breathlessness.

Q.3

What investigations would you like at this stage?

The following result is obtained:

Investigation 31.1 Arterial blood gas analysis on air

pO2 41 mmHg
pCO2 75 mmHg
pH 7.25
HCO3 32 mmol/L

Q.4

What does this investigation show?

The patient is placed on 3 L/min oxygen via nasal cannulae. The arterial blood gas estimation is then repeated after 30 minutes. Biochemical analysis, complete blood picture, blood cultures, sputum cultures, CXR and an ECG are also obtained.

Investigation 31.2 Arterial blood gas analysis on 3 L/min O2

pO2 58 mmHg
pCO2 89 mmHg
pH 7.21
HCO3 32 mmol/L

Investigation 31.3 Complete blood picture

image

The electrolytes are normal other than bicarbonate.

The chest X-ray is shown in Figure 31.1.

image

Figure 31.1

An ECG shows a sinus tachycardia with a right axis deviation and a prominent R wave in lead V1.

Q.5

What do these results indicate?

Q.6

How are you going to manage this patient?

The patient is managed in the specialist respiratory ward. Her blood gases are maintained within a satisfactory range using low-flow nasal cannulae at 1 L/min oxygen. Salbutamol nebulizers are given hourly.

After blood cultures have been taken, she is started on oral amoxicillin/clavulanic acid and intravenous clarithromycin. Oral steroids are given starting at 50 mg prednisolone.

Q.7

If her respiratory failure had continued to worsen, what options would have been open to you?

Twenty-four hours later you are called to see the patient because she has an obvious tremor and a temperature of 37.6°C. Her pulse is 140 bpm and her blood pressure is 140/90 mmHg.

Q.8

What are the possible explanations for her deterioration? What should you do?

Her chest findings are unchanged and abdominal examination is unremarkable. A repeat chest X-ray shows no change and an ECG shows a sinus tachycardia with a rate of 146 bpm.

Her nebulized salbutamol is decreased to 4 hourly and the tachycardia slowly improves. The prednisolone dose is decreased and then ceased over 7 days. Tiotropium is instituted as a once-daily inhaler.

Seven days after admission she has improved to the extent where she can walk slowly around the ward. Formal pulmonary function tests are done prior to discharge. The results are as follows:

Investigation 31.4 Forced expiratory volumes

image

Investigation 31.5 Arterial blood gases on air

pO2 50 mmHg
pCO2 61 mmHg
pH 7.40
HCO3 34 mmol/L

The patient is told firmly that she must stop smoking immediately.

Q.9

What do these results tell you? How will you manage the patient before discharge and in the future?

The patient ignores your advice on smoking. She qualifies for home oxygen but is not issued the treatment due to her current smoking. She survived another 18 months, dying of another episode of acute on chronic respiratory failure.

Answers

A.1 She has at least a 100 pack/year history of smoking and chronic obstructive pulmonary disease (COPD) secondary to cigarette smoking is the most likely underlying diagnosis. This includes chronic bronchitis and emphysema and there may also be an element of reversible airways obstruction, i.e. asthma. Infection of the tracheobronchial tree causing an increase in airway inflammation and volume and viscosity of sputum is the most common precipitant of deterioration in these patients.

Cardiac failure, either diastolic failure secondary to ischaemia or decompensation of cor pulmonale secondary to increasing pulmonary artery pressures, are important factors to consider as precipitants or as confounders.

Other factors contributing to deterioration may include increased tobacco use, non-compliance with medication, use of sedative drugs, intercurrent pneumonia, left ventricular failure, pneumothorax, thromboembolism and development of a bronchogenic carcinoma or development of anaemia.

The differential diagnosis includes adult-onset asthma and bronchiectasis, and heart failure.

The occupational history is important as the woman may have pneumoconiosis in addition to her smoking-related disease. Exposure may be indirect, such as having laundered her husband’s clothes contaminated with asbestos material etc. Occupational history including exposure related to hobbies must always be asked about, even with an obvious smoking history. A history of childhood respiratory problems including exposure to pulmonary tuberculosis may also be relevant.

A.2 During the examination of this patient you will focus on:

• Disturbance of the mental state, e.g. agitation or drowsiness, suggesting underlying hypoxia or hypercapnia.
• Cyanosis and polycythaemia.
• Clubbing (which suggests an underlying lung carcinoma).
• Metabolic flap (hypercapnia).
• Fever (suggests systemic infection).
• Tachycardia and arrhythmia (e.g. sudden-onset atrial fibrillation could contribute to decompensation of cor pulmonale).
• Blood pressure including pulsus paradoxus.
• Pursed lips respiration.
• Use of accessory muscles and intercostal recession.
• Chest signs of over-inflation (loss of precordial dullness, increased resonance, reduced breath sounds) and airways obstruction (wheeze). Also evidence of pneumothorax (reduced breath sounds) or consolidation (bronchial breath sounds).
• Evidence of right heart failure (cor pulmonale).
• Evidence of primary and metastatic malignancy (e.g. cachexia, pleural effusion, supraclavicular lymphadenopathy, hepatomegaly).
• Sputum.

A.3 Initial investigations (and reasons why):

• Spirometry (if available).
• Arterial blood gas analysis (an objective measure of the degree of derangement of lung function and to detect respiratory failure).
• Chest X-ray (evidence of emphysema, consolidation, airways thickening, pneumothorax, cor pulmonale and primary lung malignancy).
• ECG (arrhythmia, right ventricular hypertrophy or hypoxia-induced ischaemia/infarction).
• Complete blood picture (anaemia or polycythaemia, leucocytosis).
• Biochemistry (baseline electrolytes).
• Sputum culture and cytology (bacterial pathogens by Gram stain and culture, malignant cells).
• Blood serology (raised titres of antibodies against bacteria, e.g. Legionella and Bordetella pertussis).
• Blood cultures (septicaemia).

A.4 The initial blood gas indicates acute on chronic respiratory failure. The bicarbonate is halfway between what is expected in acute respiratory acidosis (lower bicarbonate) and chronic respiratory acidosis (higher bicarbonate). This suggests renal (metabolic) compensation for chronic hypercapnia and acidosis by bicarbonate retention. This would normalize the pH in the chronic state. With an acute deterioration this compensation cannot occur, resulting in a moderate acidosis.

A.5 With the application of 3 L/min of oxygen there has been improvement in oxygenation but also further CO2 retention and exacerbation of the acidosis.

The patient has a raised haemoglobin, which is likely to reflect a secondary polycythaemia induced by chronic hypoxia. She has a neutrophilic leucocytosis, which indicates bacterial infection.

The chest X-ray reveals a cardiac size within normal limits and prominent pulmonary arteries. The lung fields are grossly inflated and there is some scarring at the lung apices. There is no evidence of consolidation. This suggests chronic obstructive pulmonary disease (COPD) with pulmonary hypertension. This diagnosis is supported by the ECG changes of right ventricular strain (right axis deviation and a prominent R wave in V1).

Overall, the clinical picture indicates that the patient has COPD with probable cor pulmonale. There has been an acute deterioration precipitated by infection but there is no evidence of pneumonia.

A.6 Oxygenation is the key. Patients need oxygen if they are hypoxic, but excessive supplemental oxygen can result in dangerous hypercapnia with mental stupor or coma and respiratory arrest. A compromise is needed. Improvement of the pO2 towards 50–60 mmHg should be attempted using the smallest amount of oxygen possible. At this level pulmonary vasodilatation is achieved. This is when Venturi masks are useful: low-dose oxygen via 24% Venturi mask improves oxygen without causing dangerous respiratory depression. If these cannot be tolerated, nasal cannulae can be substituted at 1 L/min. A modest rise in pCO2 is acceptable provided that the patient remains alert. If a 24% Venturi mask is tolerated, particularly if the patient improves, a 28% mask (or nasal cannulae at 1.5–2 L/min) may be tried. The blood gases will need to be checked to exclude deterioration in ventilation.

In addition to oxygen, the treatment of any reversible airways obstruction by removing secretions and treating infection will help. If these measures to improve ventilation and ventilation–perfusion mismatch fail non-invasive ventilation (NIV) will have to be considered, including with continuous positive airways pressure (CPAP) or bi-level positive airway pressure (BiPAP). Usually endotracheal intubation and mechanical ventilation would be regarded as the last resort.

The patient may only have a small component of reversible airways obstruction but attempted bronchodilatation by frequent salbutamol nebulizers is accepted practice. Salbutamol intravenous infusion is hardly ever used.

Steroids are used in acute exacerbations of chronic airways obstruction, although they are more important in asthma, and their effectiveness in the management of COPD is not uniform. A similar dose is often used during the acute phase of the illness, but unless there is a significant component of bronchospasm in the obstruction, the chronic use of steroids is not recommended.

Clearance of airway secretions in this patient is important. In the acute stage she would not tolerate routine chest physiotherapy, but regular encouragement of coughing and possibly nasotracheal suction should be performed.

Although the patient has no consolidation she has a fever and a severe deterioration associated with purulent sputum; intravenous antibiotics such as amoxicillin (or amoxicillin/clavulanic acid), doxycycline or clarithromycin should be added. It must be remembered that the macrolide antibiotics (erythromycin, roxithromycin, clarithromycin) interact with many medications including warfarin, anticonvulsants, oral contraceptives and any drugs metabolized by hepatic cytochrome P450. Intravenous erythromycin is now avoided wherever possible, as it can be associated with a highly irritant superficial thrombophlebitis.

This patient is critically ill with respiratory failure, and should be admitted to a dedicated respiratory speciality ward or if that is not available to a high dependency unit. If repeated gas measurements are necessary, an arterial line can be considered.

A.7 She would need some form of respiratory support. This would probably be non-invasive in the form of non-invasive ventilation such as BiPAP, or CPAP. Both these forms of ventilatory support are supplied via well-fitting face or nasal masks. If her respiratory failure worsened further or her conscious level decreased then she would need endotracheal intubation.

A.8 The most likely explanation for the tachycardia is the combination of fever and the frequent administration of salbutamol. Potassium levels may have changed, especially if diuresis has occurred. In addition, she may have cor pulmonale which makes her prone to atrial tachyarrhythmias, further exacerbated by hypoxaemia. You should arrange an ECG to rule out ischaemia, given her history, repeat electrolytes and a chest X-ray.

A.9 Her lung function tests show an obstructive pattern with significant reversibility to salbutamol. According to GOLD criteria this lady has severe COPD with respiratory failure, stage IV. The reduced DLCO demonstrates markedly impaired gas exchange and is typical of severe emphysema.

Her gases show a return to her chronic state. She is no longer acidotic and her bicarbonate has risen back to its chronically elevated level.

In the short term she should finish her course of antibiotics and tail off her steroids over the following week.

She should have an assessment of her inhaler technique and if required receive more education on device use. She should be discharged with inhalers of tiotropium and a corticosteroid/long-acting beta agonist combination as well as salbutamol if needed.

She must stop smoking. Tobacco smoke inhibits mucociliary function and hence clearance of airway secretions. Smoking also stimulates increased airway mucus production so cessation of smoking will decrease sputum production and bronchospasm. In addition home oxygen cannot be prescribed if the patient continues to smoke, because of the fire hazard.

This patient should have the pneumococcal vaccine every 5 years and an annual influenza vaccine. Compliance with medication should be ensured and inhaler technique should be checked regularly. Infective exacerbations should be treated early with oral antibiotics, and intensive chest physiotherapy. If manifestations of cor pulmonale (such as ankle swelling) worsen, they may have to be treated with diuretics.

Referral to a respiratory rehabilitation programme is helpful, and provision of home improvements may improve the ability of the chronically breathless person to cope. This patient would fit the criteria for home oxygen provided she can become an established non-smoker and that there is reversal of hypoxaemia with domiciliary oxygen without progressive hypercapnia.

Revision Points

Chronic Obstructive Pulmonary Disease (COPD)

Cigarette smoking is by far the most important aetiological factor in this disease. Smoking cessation slows the progression of the disease and there may be improvement in airway obstruction. Marijuana smoking has been largely undervalued as a risk factor and it is estimated that one marijuana cigarette may be as damaging as 8–15 cigarettes.

Diagnosis

• Clinical examination is a good tool to rule out alternative diagnoses, but notoriously poor to rule in COPD. In addition, patients often deny symptoms or symptoms become manifest only when the disease is quite advanced.
• Thus, suspicion based on history (including smoking status) should lead to early use of spirometry.
• Spirometry shows a reduction in the forced expiratory flow rate (FEV1).
• A low FEV1/FVC ratio will confirm obstruction.
• More complex pulmonary function tests include measurement of the gas diffusion coefficient (DLCO), static lung volumes and lung elastic recoil or compliance.
• Lung function testing provides the data needed to assess the severity of COPD according to GOLD criteria (Global Initiative for Chronic Obstructive Lung Disease – http://www.GOLDCOPD.com).
• Cor pulmonale is a bad prognostic indicator.
• Blood gas analysis in the acute setting must be interpreted in the light of the patient’s chronic status. The renal bicarbonate compensation for chronic hypercapnia will usually cause the pH to be within the normal range. This means that a patient with acidosis has usually had a major decompensation.

Treatment

• Smoking cessation is the only intervention in COPD which has been shown to reduce the rate of decline in lung function.
• There are two inhaled therapies for COPD authorized by the PBS, which reduce exacerbations and, hospitalizations and improve quality of life:

– tiotropium (Spiriva), indicated for all stages of COPD (New England Journal of Medicine 2008;359:1543–1554. ‘UPLIFT’)
– fluticasone/salmeterol (Seretide) indicated for moderately severe and severe COPD, predominantly patients with frequent exacerbations (New England Journal of Medicine 2007;356:775–789. ‘TORCH’).

• When used in combination patients derived an even greater benefit than from treatment with either drug alone (Annals of Internal Medicine 2007;146:545–555. ‘OPTIMAL’).
• The evidence for benefit from inhaled corticosteroids (ICS) alone is less convincing.
• Short-acting bronchodilator drugs such as salbutamol are useful for symptomatic improvement.
• Oral steroids are indicated in acute airflow obstruction exacerbations. They have no role in the long-term treatment of COPD.
• Vaccination against pneumococcus and influenza virus is advisable and early treatment of chest infections is important.
• If the PaO2 is below 55 mmHg long-term oxygen therapy >16 h per day or longer prolongs survival as well as improves the quality of life in COPD.

Issues to Consider

• How do you clinically measure pulsus paradoxus?
• What disorders, other than smoking, can cause chronic respiratory failure?
• How are patients assessed to qualify for home oxygen therapy?

Further Information

, www.COPDX.org.au. The COPD-X Plan, Australian and New Zealand guidelines for the management of chronic obstructive pulmonary disease

, www.GOLDCOPD.com. GOLD – Global Initiative for Chronic Obstructive Lung Disease

, www.lungfoundation.com.au. The Australian Lung Foundation is a key agent of change in Australia for promoting the understanding, management and relief of lung disease

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