Chronic bronchitis

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100 Chronic bronchitis

Instruction

Examine this patient’s chest.

Salient features

History

• Productive cough

• Increasing dyspnoea

• Weight loss

• History of smoking

• History of α₁-antitrypsin deficiency.

Examination

• Begin with examination of the sputum pot.

Observe the patient:

• From the end of the bed: for obvious breathlessness, pursed lip breathing and symmetrical chest movements—and count respiratory rate.

• Look for nail changes such as tar staining.

• Feel the palms for warmth and the pulse for rapid bounding pulse (signs of carbon dioxide retention).

• Look at the lips and tongue for central cyanosis.

Examine the neck:

• Comment on the active contractions of the accessory muscles of respiration such as sternocleidomastoids, scaleni and trapezii.

• Palpate for tracheal deviation and measure the distance between the cricoid cartilage and suprasternal notch (less than three fingers’ breadth in emphysema).

• Comment on the raised JVP.

Examine the chest:

Examine the abdomen:

• Palpable liver to look for hepatic displacement (comment on upper border of liver by percussion).

Tell the examiner that this patient is at increased risk for cardiovascular disease, osteoporosis, lung cancer and depression.

Remember: Airflow obstruction as measured by spirometry is defined as a ratio of the postbronchodilator forced expiratory volume in 1 s (FEV₁) to forced vital capacity (FVC) of <0.70.

Diagnosis

This patient has features of COPD (lesion) caused by cigarette smoking (aetiology) and is very cyanosed at rest (functional status).

Questions

What do you understand by the term chronic bronchitis?

Chronic bronchitis is cough with mucoid expectoration for at least 3 months in a year for 2 successive years.

What is the definition of emphysema?

Emphysema is the abnormal permanent enlargement of the airway distal to the terminal respiratory bronchioles with destruction of their walls. Clinical, radiological and lung function tests give an imprecise picture in an individual case but a combination of all these features gives a reasonable picture.

What do you understand by the term chronic obstructive pulmonary disease?

COPD is a condition characterized by airflow limitation that is not fully reversible and is usually progressive and associated with an abnormal inflammatory response. The term COPD encompasses chronic obstructive bronchitis (with obstruction of small airways) and emphysema (with destruction of lung parenchyma, loss of lung elasticity and closure of small airways). Most patients also have mucus plugging (N Engl J Med 2000;343:269).

Advanced-level questions

What is the mechanism reduction in expiratory capacity in chronic obstructive pulmonary disease?

Dynamic hyperinflation is considered to be an important factor in the reduction of exercise capacity and the development of dyspnoea.

COPD is caused by a variable mixture of three processes including loss of alveolar attachments, inflammatory obstruction of the airway and luminal obstruction with mucus. Alveolar attachments ensure a radial tethering effect, which is important for keeping small airways patent in the normal lung. At smaller lung volumes, airways narrow because of decreased lung elasticity and weaker tethering effects. As a result, maximal expiratory airflow decreases as the lung empties and ceases at 25 to 35% of total lung capacity. The remaining air (or residual volume) may account for as much as 60 to 70% of predicted total lung capacity. Patients with COPD must breathe at larger lung volumes to optimize expiratory airflow, but this requires greater respiratory work because the lungs and chest wall become stiffer at larger volumes. These effects are worse with exercise. A normal lung meets the increased ventilatory demands of exercise by increasing both tidal volume and respiratory rate, with little change in the final end-expiratory lung volume. Whereas in COPD the respiratory rate does increase in response to exercise, but with insufficient expiratory time, breaths become increasingly shallow and end-expiratory lung volume progressively enlarges, a phenomenon called dynamic hyperinflation (N Engl J Med 2010;362:1407–16).

What is the role of inflammatory mechanisms in chronic obstructive pulmonary disease?

In COPD, reactive oxygen species (ROS), pathogen associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs) activate families of pattern recognition receptors (PRRs) that include the toll-like receptors (TLRs). This understanding has led to the hypothesis that COPD is also a disease of innate immunity. COPD is characterized by abnormal response to injury, with altered barrier function of the respiratory tract, an acute phase reaction and excessive activation of macrophages, neutrophils and fibroblasts in the lung. Macrophages and epithelial cells in airways are activated by cigarette smoke and other irritants (in developing countries, the inhalation of smoke from biomass fuels is an important cause of COPD, particularly among women who cook in poorly ventilated homes) and these release neutrophil chemotactic factors including interleukin-8 and leukotriene B₄. Neutrophils and macrophages then release proteases that break down connective tissue in the lung parenchyma, resulting in emphysema, and also stimulate hypersecretion of bronchial mucus. The chronic inflammatory process in COPD differs markedly from that seen in bronchial asthma, with different inflammatory cells, mediators, inflammatory effects and responses to treatment.

What is the role of proteolysis in chronic obstructive pulmonary disease?

In COPD, the protease-antiprotease balance is tipped in favour of proteolysis because of either an increase in proteases (including neutrophil elastase, proteinase 3, cathepsins, matrix metalloproteases 1, 2, 9 and 12) or a deficiency of antiproteases (including α₁-antitrypsin, elafin, secretory leukoprotease inhibitor and tissue inhibitors of matrix metalloproteases).

What is the main cause of death and disability in chronic obstructive pulmonary disease?

Mortality and disability from COPD is related to an accelerated decline in lung function over time, with a loss of >50–60 ml/year in the forced expiratory volume in 1 s (FEV₁), compared with a normal loss of 20–30 ml/year. The progressive reduction in FEV₁ and increasing severity of disease over time result in increasing dyspnoea on exertion, which slowly advances to respiratory failure.

What is explanation for the cardiac silhouette on chest radiography in patients with emphysema?

In patients with emphysema, the cardiac silhouette on chest radiography is typically long and narrow (Fig. 100.1). The common explanation for this finding is the altered, more vertical position of the heart in the thoracic cavity. A recent study suggested an alternative explanation for this finding: a decreased left ventricular volume (N Engl J Med 2010;362:217). This study also reported a linear relation to impaired left ventricular filling, reduced stroke volume and lower cardiac output without changes in the ejection fraction.

Fig. 100.1 COPD. (A) The superior aspect of the hemidiaphragms is at the same level as the posterior aspect of the twelfth ribs. (B) Hyperinflation.

(With permission from Mettler 2004.)

What is the role of high-resolution CT in the diagnosis of emphysema?

It is the most sensitive technique for the diagnosis of emphysema. It is useful in evaluating symptomatic patients with almost normal pulmonary function except for a low carbon monoxide diffusing capacity—a combination of findings that occurs in emphysema, interstitial lung disease and pulmonary vascular disease (Radiology 1992;182:817–21).

How would you differentiate emphysema from chronic bronchitis?

	Predominant bronchitis	Predominant emphysema
Age (years)	40–45	50–75
Appearance	Blue bloater	Pink puffer
Dyspnoea	Mild; late	Severe; early
Cough	Early; copious sputum	Late; scanty sputum
Infections	Common	Occasional
Respiratory insufficiency	Repeated	Terminal
Cor pulmonale	Common	Rare; terminal
Airway resistance	Increased	Normal or slightly increased
Elastic recoil	Normal	Low
Chest radiograph	Prominent vessels; large heart	Hyperinflation; small heart

From Kumar et al. Pathologic Basis of Disease, 8th edn. Saunders.

If the patient was between the ages of 30 and 45 years, what would you consider to be the underlying cause of the emphysema?

Smoking, α₁-antitrypsin deficiency.

What medications are commonly used in outpatient treatment of chronic obstructive pulmonary disease?

Note: Influenza and pneumococcal vaccinations and pulmonary rehabilitation (including education, exercise, behaviour modification and interventions to improve social and psychological functioning) are important therapeutic measures in COPD.

How would you treat an acute exacerbation?

• Nebulized bronchodilators: terbutaline, ipratropium bromide

• Intravenous antibiotics (BMJ 1994;308:871–872), initially with amoxicillin and, if no clinical response, then with a second-generation cephalosporin, quinoline or co-amoxiclav. Antibiotics decrease the relative risk of treatment failure by approximately 50% in exacerbations (Cochrane Database Syst Rev 2006;2:CD004403)

• Oxygen (24%)

• Intravenous hydrocortisone and oral steroids (steroids useful in only acute exacerbations and, unlike in asthma, do not influence the course of chronic bronchitis). Systemic steroids reduced the relative risk of treatment failure (as defined by intensification of therapy, rehospitalization or return to the emergency department) by about 30% in patients with acute exacerbations who were hospitalized or seen in the emergency department (N Engl J Med 1999;340:1941–7; N Engl J Med 2003;348:2618–25).

What is the role of inhaled steroids in chronic obstructive pulmonary disease?

Inhaled steroids reduce the frequency of exacerbations by 15–20%. The combination of an inhaled corticosteroid with a long-acting beta-agonist reduces exacerbations compared with either therapy alone.

What are the organisms commonly associated with exacerbations of chronic obstructive pulmonary disease?

Haemophilus influenzae and Streptococcus pneumoniae are the commonest organisms identified in the sputum during exacerbations of COPD, accounting for 43% and 25%, respectively, of positive cultures in one study. Moraxella (previously Branhamella) catarrhalis is also frequently isolated from sputum during exacerbations. Less commonly, Chlamydia pneumoniae or Pseudomonas aeruginosa has been associated with some exacerbations.

What clinical features would suggest that this patient is suitable for long-term domiciliary oxygen therapy?

• COPD: FEV₁ <1500 ml, FVC <2000 ml and stable chronic respiratory failure (Pao <7.3 kPa, that is, 55 mmHg or oxygen saturation <88% at normal blood pH) in patients who have (1) had peripheral oedema or (2) not necessarily had hypercapnia or oedema (New Engl J Med 1995;333:710–14); carboxyhaemoglobin of <3% (i.e. patients who have stopped smoking)

• Terminally ill patients of whatever cause with severe hypoxia (Pao <7.3 kPa).

Note: If the patient’s oxygen saturation is ≤88% at rest in a clinical stable state, long-term oxygen therapy should be prescribed and used for at least 18 h each day.

How can the sensation of breathlessness be reduced?

By the use of either promethazine or dihydrocodeine.

How would you treat acute respiratory failure?

If Pao is <8 kPa, administer 24% oxygen. There is no need for oxygen when Pao is >8 kPa. Monitor blood gases after 30 min. If Paco₂ is rising (by 1 kPa), monitor blood gases hourly. If Paco₂ continues to rise, administer doxapram. If, in spite of this, the patient continues to deteriorate, artificial ventilation may be called for.

What do you know about non-invasive ventilation?

Non-invasive ventilation is an alternative approach to endotracheal intubation to treat hypercapnic ventilatory failure, which occurs in COPD. It reduces the complications of endotracheal intubation such as infection and injury to the trachea. Non-invasive ventilation is pressure-support ventilation delivered with a face mask and a piece of white foam placed in the face mask to reduce the amount of internal dead space. In a recent randomized trial, non-invasive ventilation was shown to reduce the need for endotracheal intubation, length of hospital stay and in-hospital mortality rate in selected patients with acute exacerbations of COPD (N Engl J Med 1995;333:817–22).

What do you know about the BODE index?

The BODE index combines information about several predictors in a score ranging from 0 to 10, including:

• body mass index (BMI)

• airflow obstruction (FEV₁)

• dyspnoea (Medical Research Council dyspnoea scale)

• exercise capacity (6 min walk distance) in a score ranging from 0 to 10.

This prognostic index predicts mortality significantly better than FEV (the traditional prognostic COPD indicator) alone.

What do you know about molecular genetics of chronic obstructive pulmonary disease?

Deficiency of α₁-antitrypsin

• It was first described in Sweden. The patient is deficient in α₁-antitrypsin, with activity approximately 15% of normal values; concentrations of 40% or more are required for health. The patient is homozygous for the gene (Z) encoding a protease inhibitor (Pi). Other genetic combinations and their percentage normal activity are MS (80%), MZ (60%), SS (60%), SZ (40%). Six per cent of the population is heterozygous for S(PiMS) and 4% for Z(PiMZ), making an overall frequency of 1 in 10 for the carriage of the defective gene. Liver transplantation results in conversion to the genotype of the donor.

• In the lung α₁-antitrypsin inhibits the excessive actions of neutrophil and macrophage elastase, which cigarette smoke promotes. When the lung is heavily exposed to cigarette smoke, the protective effect of α₁-antitrypsin may be overwhelmed by the amount of elastase released or by a direct oxidative action of cigarette smoke on the α₁-antitrypsin molecule. The emphysema is panacinar and is seen in the lower lobes of the lungs. Smoking increases the severity of, and decreases the age of onset of, emphysema. Liver disease is a much less common complication. Human α₁-antitrypsin prepared from pooled plasma from normal donors is recommended for patients over 18 years with serum levels below 11 µmol/l and abnormal lung function.

• The siblings of an index case should be screened for this disorder. Their identification should be followed by counselling to avoid smoking and occupations with atmospheric pollution. Children of homozygotes will inherit at least one Z gene and hence will be heterozygotes. They should avoid pairing with another heterozygote if they wish to avoid the risk of producing an affected homozygote.

Tumour necrosis factor-alpha

COPD is 10 times more common in Taiwanese with a polymorphism in the promoter region of the gene for Tumour necrosis factor-alpha, resulting in its increased production (Am J Respir Crit Care Med 1997;156:136–9). However, the same polymorphism in the UK population is not associated with increased risk of COPD (Eur Respir J 2000;15:281–4).

Microsomal epoxide hydrolase

A polymorphism variant of microsomal epoxide hydrolase, an enzyme involved in the metabolism of the epoxides that may be generated in tobacco smoke, has been associated with a quintupling of the risk of COPD (Lancet 1997;350:663).

What is the role of surgery in chronic obstructive pulmonary disease?

• Bullectomy may improve gas exchange and airflow, and reduce dyspnoea in selected patients with bullae larger than one-third of the hemithorax and accompanying lung compression.

• Lung-volume reduction surgery (N Engl J Med 2000;343:239–45) results in functional improvements including increased FEV₁, reduced total lung capacity, improved function of respiratory muscles, improved exercise capacity and improved quality of life (J Thorac Cardiovasc Surg 1999;112:1319–29, Am J Respir Crit Care Med 1999;160:2018–27). The National Emphysema Treatment Trial Group found that lung-volume reduction surgery increased the chance of improved exercise capacity but did not confer a survival advantage over medical therapy. It did yield a survival advantage for patients with both predominantly upper-lobe emphysema and low baseline exercise capacity. Patients previously reported to be at high risk and those with non-upper-lobe emphysema and high baseline exercise capacity are poor candidates for lung-volume reduction surgery because of increased mortality and negligible functional gain (N Engl J Med 2003;348:2059–73).

• Single lung transplantation has been successful for at least 3–4 years in patients with COPD. The criteria for selecting patients for transplantation have not been established. It does not improve survival but improved quality of life (J Thorac Cardiovasc Surg 1991;101:623–32, J Heart Lung Transplantation 2006;25:75–84).

What is the best method for communicating spirometry findings to patients?

Results from studies suggest that providing feedback on lung age with graphic displays may be the best option so far for communicating the results of spirometry. More patients are likely to stop smoking when spirometry results, as communicated using Fletcher and Peto’s diagram (a pictorial representation of how smoking ages the lungs), are shared with the patient (Thorax 2006;61:869–73, BMJ 2008;336:567–8).

What are the general indications for lung transplantation?

The general indication is end-stage lung disease without alternative forms of therapy. Patients should be <60 years of age and should have a life expectancy of <12–18 months; they should not have an underlying cancer or other serious systemic illness. The most common lung diseases are pulmonary fibrosis, emphysema (particularly α₁-antitrypsin deficiency), bronchiectasis, cystic fibrosis and primary pulmonary hypertension.

What is the role of nutrition in chronic obstructive pulmonary disease?

Undernutrition is associated with reduced respiratory muscle function and an increased mortality rate. A high dietary intake of n-3 fatty acids may protect cigarette smokers against COPD.

Mention some newer treatments for chronic obstructive pulmonary disease

• Antagonists of inflammatory mediators: 5-lipoxygenase inhibitors, leukotriene B₄ antagonists, interleukin-8 antagonists, tumour necrosis factor inhibitors and antioxidants

• Protease inhibitors: neutrophil elastase inhibitors, cathepsin inhibitors, non-selective matrix metalloprotease inhibitors, elafin, secretory leukoprotease inhibitor, α₁-antitrypsin

• New anti-inflammatory agents: phosphodieasterase-4 inhibitors, nuclear factor-κB inhibitors, adhesion molecule inhibitors and p38 mitogen-activated protein kinase inhibitors (N Engl J Med 2000;343:1960–1).

Further reading

American Thoracic Society (ATS)/European Respiratory Society (ERS). Standards for the diagnosis and treatment of COPD. www.ersnet.org.

Cochrane Airways Group (up-to-date, accurate systematic reviews and meta-analyses). www.cochrane-airways.ac.uk.

United Kingdom National Institute for Clinical Excellence (NICE). COPD guidelines. www.nice.org.uk.

World Health Organization Global Initiative for Obstructive Lung Disease (GOLD) resources. www.goldcopd.com.

Peter Howard, contemporary chest physician, Sheffield; his chief interest is long-term domiciliary oxygen therapy.

Peter Barnes, contemporary physician and professor, National Heart and Lung Institute London.

Sir Michael Rawlins is the founding chairman of National Institute for Health and Clinical Excellence (NICE). From 1973 to 2006, Rawlins was the Ruth and Lionel Jacobson Professor of Clinical Pharmacology University of Newcastle. Rawlins obtained his medical degree at St Thomas’ Hospital. His post-graduate training in clinical pharmacology and general medicine was completed at St Thomas’ http://en.wikipedia.org/wiki/Hammersmith_Hospital” \o “Hammersmith Hospital” Hammersmith hospitals, with a year at the Karolinska Institute in Stockholm.

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