OBSTRUCTIVE LUNG

DISEASE

GUIDE: DR. POOJA K

PRESENTOR: VIJAYALAXMI K
 DEFINITION
• The ATS and ERS define COPD as a preventable and treatable disease state
characterised by airflow limitation that is not fully reversible. The airflow
limitation is usually progressive and associated with a chronic
inflammatory response of the lungs to noxious particles or gases.

• The major site of obstruction is in the small airways.

• COPD forms a spectrum with pure chronic bronchitis at one end and pure
emphysema at the other end

An official American Thoracic Society/European Respiratory Society statement: research questions in COPD
Bartolome R. Celli
AETIOLOGY
 PATHOLOGY
• Airflow limitation is a major physiologic change in COPD, can result from
small airway disease and/or emphysema.

• Small airways become narrowed by cells (hyperplasia and accumulation),

mucus, and fibrosis, and extensive small airway destruction is a hallmark of
advanced COPD.

• Changes in large airways cause cough and sputum production, while changes
in small airways and alveoli are responsible for physiologic alterations.
 Pathophysiology of COPD
• Airflow limitation is progressive, associated with abnormal
inflammatory response to noxious particles or gases

• Chronic inflammation damages tissue

• Scar tissue in airways results in narrowing

• Scar tissue in the parenchyma decreases elastic recoil(compliance)

• Scar tissue causes thickened vessel lining and hypertrophy of smooth

muscle(pulmonary hypertension)
PATHOPHYSIOLOGY

■ AIRFLOW OBSTRUCTION
Key parameters obtained from spirometry include the volume of air
exhaled within the first second of the forced expiratory maneuver
(FEV1 ) and the total volume of air exhaled during the entire spirometric
maneuver (forced vital capacity [FVC]).
Patients with airflow obstruction related to COPD have a chronically
reduced ratio of FEV1 /FVC.
■ HYPERINFLATION

In COPD there is often “air trapping” (increased residual volume and

increased ratio of residual volume to total lung capacity) and progressive
hyperinflation (increased total lung capacity) late in the disease.

Hyperinflation pushes the diaphragm into a flattened position with a

number of adverse effects.
 CLINICAL FEATURES
• The three most common symptoms in COPD are cough, sputum production, and
exertional dyspnea.
• Cough and associated sputum production often referred to as a ‘smoker’s cough’.
• Breathlessness measured using modified Medical Research Council (MRC)
dyspnoea scale
 PHYSICAL FINDINGS
• In the early stages of COPD, patients usually have an entirely normal physical
examination.
• In patients with more severe disease, the physical examination of the lungs
is
1. notable for a prolonged expiratory phase
2. expiratory wheezing
3. signs of hyperinflation: include a barrel chest and enlarged lung volumes
with poor diaphragmatic excursion.
4. use of accessory muscles of respiration, sitting in the characteristic
“tripod” position to facilitate the actions of the sternocleidomastoid,
scalene, and intercostal muscles.
5. Cyanosis: visible in the lips and nail beds.
• Advanced disease may be accompanied by cachexia, with significant
weight loss, bitemporal wasting, and diffuse loss of subcutaneous
adipose tissue.

• Some patients with advanced disease have paradoxical inward

movement of the rib cage with inspiration (Hoover’s sign), the result of
alteration of the vector of diaphragmatic contraction on the rib cage as
a result of chronic hyperinflation.
 INVESTIGATIONS
• chest X-ray

• Pulmonary function test: spirometer

• ABG analysis:
decreased of PaO2 and pH
increase of PaCO2
 ACUTE EXACERBATIONS
• Exacerbations are episodic acute worsening of respiratory symptoms,
including increased dyspnea, cough, wheezing, and/ or change in the
amount and character of sputum.

• They become more frequent as the disease progresses and are usually
triggered by bacteria, viruses or a change in air quality.

• They may or may not be accompanied by other signs of illness, including

fever, myalgias, and sore throat.

• The strongest single predictor of exacerbations is a history of a previous

exacerbation.
CHRONIC BRONCHITIS
• Chronic bronchitis is defined as a condition associated with excessive
tracheobronchial mucus production to cause cough with
expectoration for at least 3 months of the year, for more than 2
consecutive years

Medicine: Prep Manual for Undergraduates

Mathew K.G.
INCIDENCE
• Middle and late adult life.
• More in males than in females.
• More in smokers than in non-smokers.
• More in urban than in rural dwellers.
AETIOLOGY (RISK FACTORS)
• Cigarette smoking:
• Air pollution with dust, smoke and fumes, sulphur dioxide and particulate
matter
• Low socio-economic status
• Sluggish ciliary movement.
• Bronchoconstriction (through smooth muscle constriction).
• Hypertrophy and hyperplasia of mucus-secreting glands.
• Release of proteolytic enzymes from polymorphonuclear leucocytes.
• Release of inflammatory mediators in lungs.
• Inhibition of the function of alveolar macrophages
 PATHOLOGICAL CHANGES
• Hypertrophy and hyperplasia of the
mucus-producing glands.
• Goblet-cell hyperplasia.
• Reduction in the ciliated cells.
• Mucosal oedema and intraluminal mucus
plugs.
• Increased smooth muscle.
• Reduction in the calibre of the air
passages.
 CLINICAL FEATURES
History
• The most striking features: impressive history of cough with sputum production for
many years and a relatively late onset of breathlessness.
• Initially, the cough is present only in the winter seasons ("winter cough" or
"smoker's cough"), especially in the mornings ("morning cough"). Over years, cough
increases in frequency, severity and duration until it is present all round the year.
• The sputum is usually scanty, mucoid and more in the mornings. Sputum is
occasionally blood-stained (haemoptysis) and occasionally frankly purulent
("mucopurulent relapse").
• Breathlessness is late in onset in chronic bronchitis. It is due to airflow obstruction
and is aggravated by infection, excessive smoking and adverse atmospheric
conditions.
• Other symptoms include fever during mucopurulent relapses, wheezing and
tightness in the chest.
 PHYSICAL SIGNS
• Usually the patient is overweight.

• At rest, there is no respiratory distress. Respiratory rate is normal and

accessory muscles of respiration are not acting.

• Percussion note is normally resonant over the lungs. Liver dullness and
cardiac dullness are normal in position.
Auscultation

• Vesicular breath sounds with prolonged expiration.

• Inspiratory and expiratory rhonchi.

• Crepitations that either disappear or change in location and intensity

after coughing.
Systemic Features

• Decreased free-fat mass.

• Impaired systemic muscle function and muscle wasting.

• Anaemia.

• Osteoporosis.

• Depression.

• Increased risk of angina, acute myocardial infarction and heart failure.

• Metabolic syndrome.
 INVESTIGATIONS
• Radiological examination:

Chest radiograph does not show any characteristic abnormality in chronic

bronchitis.

• Pulmonary function tests:

FEV 1 is reduced.

FVC is decreased.

Ratio of FEV 1 to FVC is subnormal.

BRONCHIECTASIS
• Bronchiectasis is defined as a permanent abnormal dilatation of one or
more bronchi due to the destruction of elastic and muscular
components of the bronchial wall.

Medicine: Prep Manual for Undergraduates

Mathew K.G.
AETIOLOGY
 CLASSIFICATION
• The dilated airways, depending upon their gross or bronchographic
appearance, have been subclassified into the following different
types:
i) Cylindrical: the most common type characterised by tube-like
bronchial dilatation.
ii) Fusiform: having spindle-shaped bronchial dilatation.
iii) Saccular: having rounded sac-like bronchial distension.
iv) Varicose: having irregular bronchial enlargements
PATHOLOGY
• Three common mechanisms include

1. bronchial wall injury/structural weakness of bronchial walls

2. traction from adjacent lung fibrosis, and
3. bronchial lumen obstruction
 PATHOLOGY
• The bronchiectatic cavities are lined by granulation tissue, squamous
epithelium or normal ciliated epithelium.
• There may be inflammatory changes in the deeper layers of the
bronchial wall and hypertrophy of the bronchial arteries.
• Chronic inflammatory and fibrotic changes are usually found in the
surrounding lung tissue, resulting in progressive destruction of the
normal lung architecture in advanced cases.
• Common sites of involvement are lower lobes, lingula and middle lobe.
Pathogenesis
CLINICAL
FEATURES
 CLINICAL FEATURES
• The hallmarks of bronchiectasis are chronic cough with sputum
production, haemoptysis and recurrent pneumonias.
• Cough is chronic and worse in the mornings.
• Sputum is characteristically copious, purulent and foul-smelling due
to anaerobic infections.
• Haemoptysis is due to rupture of the thin-walled vessels on the walls
of dilated bronchi.
• Chest pain, which is pleuritic
• dyspnoea and wheezing
• Systemic symptoms include fever, weight loss, anaemia, night
sweats and weakness.
• Acute exacerbation is characterised by increase of sputum
with cough, increased dyspnoea, fever, increased wheezing,
fatigue and radiological signs of infection
PHYSICAL FINDINGS
• General examination may reveal anaemia, clubbing of the digits, fever,
halitosis and sinusitis.

• Respiratory signs may be unilateral, but are usually bilateral and basal.

• Presence of large amounts of secretion is responsible for the

characteristic "bilateral, basal, coarse, leathery crepitations" of
bronchiectasis.
 Investigations

• Bacteriological and mycological examination of sputum

• Radiological examination In advanced disease, thickened airway walls,
cystic bronchiectatic spaces, and associated areas of pneumonic
consolidation or collapse may be visible.
CT is much more sensitive, and shows thickened dilated airways
• Assessment of ciliary function A screening test performed in patients
suspected of having a ciliary dysfunction syndrome by measuring the
time taken for a small pellet of saccharin placed in the anterior
chamber of the nose to reach the pharynx, when the patient can taste
it.
• ABG studies may show respiratory alkalosis or hypoxaemia.
 CYSTIC FIBROSIS
• Cystic fibrosis (CF) is the most common fatal genetic disease with
autosomal recessive inheritance
• A carrier rate of 1 in 25 and an incidence of about 1 in 2500 live births
• CF is the result of mutations affecting a gene on the long arm of
chromosome 7 which codes for a chloride channel known as cystic
fibrosis transmembrane conductance regulator (CFTR), that influences
salt and water movement across epithelial cell membranes.
• The genetic defect causes increased sodium and chloride content in
sweat and increased resorption of sodium and water from respiratory
epithelium.
• The gene defect also causes disorders in organs like the gastrointestinal
tract, pancreas, liver and reproductive tract.
Davidson’s Principles and Practice of Medicine
21st edition
Clinical features
• The lungs are macroscopically normal at birth, but bronchiolar
inflammation and infections usually lead to bronchiectasis in childhood.
• At this stage, the lungs are most commonly infected with Staphylococcus
aureus; however, many patients become colonised with Pseudomonas
aeruginosa by the time they reach adulthood.
• Recurrent exacerbations of bronchiectasis, initially in the upper lobes but
subsequently throughout both lungs, cause progressive lung damage
resulting ultimately in death from respiratory failure.
 INVESTIGATIONS
• The indications for diagnostic tests are
(1) an existing child with cystic fibrosis in the family, or
(2) a clinical history of otherwise unexplained lung disease and/or
intestinal malabsorption due to pancreatic insufficiency.
• Diagnosis of cystic fibrosis is based on the determination of elevated
levels of chloride ions in sweat.
• The chloride concentration in stimulated sweat from healthy children is
less than 50 mmol/litre, whereas levels above 60 mmol/litre are seen in
children with cystic fibrosis.
• The sweat test recognizes more than 98% of children with cystic fibrosis.
• Blood tests. For pancreatic function tests
• chest radiography: With advancing pulmonary disease, the following
findings may be noted:
• Pulmonary nodules resulting from abscesses
• Infiltrates with or without lobar atelectasis
• Marked hyperinflation with flattened domes of the diaphragm
• Thoracic kyphosis
• Bowing of the sternum
• CF show mild decreases in arterial PO2, with oxygenation declining
slowly throughout life.8 Elevation of arterial PCO2 generally occurs with
FEV1 volumes of <30% of predicted and constitutes an end-stage event
for most patients
• Pft
 EMPHYSEMA
• The word "emphysema" means inflation or distension with air
• The WHO has defined pulmonary emphysema as combination of permanent
dilatation of air spaces distal to the terminal bronchioles and the destruction
of the walls of dilated air spaces.

Textbook of PATHOLOGY Seventh Edition

Harsh Mohan
CLASSIFICATION
Emphysema can be classified based on the anatomical site:
• Pulmonary emphysema
• Mediastinal emphysema
• Subcutaneous emphysema.
CLASSIFICATION
As per WHO definition of pulmonary emphysema, it is classified
according to the portion of the acinus involved, into 5 types:
• centriacinar
• panacinar (panlobular)
• para-septal (distal acinar),
• irregular (paracicatricial) and
• mixed (unclassified) emphysema
AETIOLOGY
• Smoking
• Occupational causes-furnace blowers, goldsmiths, exposure to
cadmium
• a-1 antitrypsin deficiency
PATHOLOGY
CLINICAL FEATURES
History
• The most striking feature is steadily progressive exertional
breathlessness with minimal cough and expectoration.
• Breathlessness is insidious in onset, initially only exertional, but
gradually and steadily progressive, ultimately ending in breathlessness
on trivial exertion and even at rest.
• Cough with expectoration of scanty mucoid sputum is
characteristically minimal.
• Weakness, anorexia, lethargy and weight loss can occur with advanced
disease
CLINICAL FINDINGS
Inspection and Palpation .
• Body build is asthenic.
• Neck is short and thick.
• Neck veins may distend during expiration, but they collapse briskly
during inspiration.
• Patient sits leaning forwards, extending the arms to brace himself.
• Patient appears distressed and tachypnoeic.
• Accessory muscles of respiration (sternomastoid and scalene muscles)
are hypertrophied. They lift the sternum in an anterosuperior direction
during inspiration.
• Prolonged expiration through pursed lips ("pursed lip breathing").
• Expiration begins with a grunting sound.
• Exaggerated tracheal descent during inspiration (Campbell's sign).
• Reduction in the length of trachea above the suprasternal notch.
• Apical impulse is usually invisible or feeble.
• Excavation of the suprastemal and supraclavicular fossae during
inspiration.
• Indrawing of the costal margins during inspiration.
• Chest appears cylindrical or barrel like ("barrel-shaped chest").
Anteroposterior diameter of the chest is markedly increased, and the
normal ratio of anteroposterior to transverse diameter of 5:7 is
altered.
• Whole of the chest is in a fixed state of full inspiration.
• Sternum is arched forwards and angle of Louis is unduly
prominent.
• Subcostal angle is widened (normal: 70° ).
• Ribs are placed more horizontally and widely.
• Kyphosis of the thoracic spine.
• Chest expansion is symmetrically diminished.
Percussion
• Hyper-resonant percussion note over the lungs.
• Cardiac dullness is reduced or obliterated.
• Liver dullness is pushed down or absent.

Auscultation
• Intensity of the breath sounds is diminished.
• Breath sounds are vesicular in character with prolonged expiration.
• Scattered, faint, high-pitched, end-expiratory rhonchi may be audible
 INVESTIGATIONS
Radiological features PA view :
• Bullae.
• Low set, flat diaphragm.
• Unusually translucent lung fields.
• Loss of peripheral vascular markings.
• Widely placed and horizontal ribs.
• Long and narrow heart ("tubular heart").
• Prominent pulmonary artery shadows at the hilum.

Chest radiograph lateral view may show a large retrostemal translucency

Pulmonary function tests:
• FEV1 is decreased.
• FVC is decreased.
• FEV 1 :FVC ratio is reduced.
• TLC is increased.
• RV is increased.
• RV:TLC ratio is increased.
• Gas transfer factor for carbon monoxide (diffusion) is reduced.
ABG studies usually reveal a slightly reduced Pa02 and normal or mildly
elevated PaC02
TREATMENT
• There is no specific treatment for established generalised emphysema
• one can prevent its further progression, and treat the aggravating
factors and complications.
• Prevention of progression of emphysema includes cessation of smoking
and avoidance of occupational exposure.
• Treatment of aggravating factors and complications include prompt
treatment of infections, respiratory failure and right heart failure.
• A trial with bronchodilators and steroids is given
• Surgical ablation of giant bullae may bring about improvement in
pulmonary function.
• Lung volume reduction surgery reduces hyperinflation of one or both
lungs by surgical and/or laser resection.
• Heart and lung transplantation may be considered in young patients
with severe emphysema due to a-1 antitrypsin deficiency.
• For patients with a-1 antitrypsin deficiency, intravenous replacement
therapy using a1 -antitrypsin derived from pooled human plasma is
being used but its efficacy is not clear.
blue bloaters
• it is a distinctive clinical pattern seen in chronic bronchitis.
• Marked cyanosis ("blue") and peripheral oedema ("bloated") are
dominant.
• These patients have prominent cough with expectoration,
mucopurulent relapses, repeated episodes of right ventricular failure
and respiratory failure, arterial hypoxaemia and hypercapnia.
pink puffers
• This is a distinctive clinical pattern seen in pulmonary emphysema.
• They have marked dyspnoea ("puffer") and no cyanosis (hence
"pink").
• The clinical course is characterised by steadily progressive dyspnoea.
They maintain a near-normal Pa02 and PaC02 .
• The occurrence of respiratory failure and right heart failure are late
and often terminal.
Asthma
• Asthma is an inflammatory disorder with airway hyperresponsiveness
leading to recurrent episodes of wheezing, breathlessness, chest
tightness and coughing

The effectiveness of physiotherapy in patients with asthma: A systematic review of the literature
Marjolein L.J.Bruurs
epidemiology
• according to WHO 2016, Asthma affects 235 million people
worldwide, out of which 15–20 million people are from India.

• In India, the prevalence of self-reported Asthma is 2.00%

among women aged 15–49 years
• 1.00% among young women aged 15–19 years and men aged 15–
49 years as per the latest report.
Pathophysiology
inhales an allergen to which he or she is sensitized

the antigen cross-links to IgE molecules attached to the surface of mast cells

The mast cells degranulate rapidly (within 30 minutes)

Mast cells Releases multiple mediators including leukotrienes, histamine,

prostaglandins, platelet activating factor, and other mediators.

mediators lead to smooth muscle contraction, vascular congestion, and leakage,

resulting in airflow obstruction

This is the early (acute) asthmatic response, which is an immediate

hypersensitivity reaction that usually subsides in approximately 30 to 60 minutes
 Clinical features
• Wheezing
• Dyspnea
• Coughing
• increased mucus production
• chest tightness
• increased ventilation and use of accessory muscles of ventilation
• hyperinflation.
• Symptoms worse at night
• physical signs are inspiratory, and to a greater extent expiratory,
rhonchi throughout the chest
 diagnosis
• Lung Function Tests: Simple spirometry confirms airflow limitation with a
reduced FEV1 , FEV1 /FVC ratio, and PEF.

• Elevated serum IgE levels

• levels of sputum eosinophils

• ABG analysis shows hypoxaemia and hypocarbia during acute attack. In

severe acute asthma, hypercarbia develops.
• Imaging Chest is usually normal but in more severe patients may show
hyperinflated lungs.

• Skin prick tests to common inhalant allergens are positive in allergic

asthma and negative in intrinsic asthma.

• Fractional exhaled nitric oxide (FENO) is Elevated and now being used
as a noninvasive test to measure eosinophilic airway inflammation.
 Exacerbations of asthma
• Exacerbations are characterised by increased symptoms, deterioration in lung
function, and an increase in airway inflammation.

• Exacerbations are most commonly precipitated by viral infections, but moulds,

pollens and air pollution are also implicated.

• Most attacks are characterised by a gradual deterioration over several hours to days
but some appear to occur with little or no warning: so-called brittle asthma.
 Clinical features of acute exacerbation
• Patients are aware of increasing chest tightness, wheezing, and dyspnea that are often
not or poorly relieved by their usual reliever inhaler.
• In severe exacerbations patients may be so breathless that they are unable to complete
sentences and may become cyanotic.
• On Examination: increased ventilation, hyperinflation, and tachycardia. Pulsus
paradoxus may be present.
• There is a marked fall in spirometric values and PEF.
• Arterial blood gases on air show hypoxemia, and PCO2 is usually low due to
hyperventilation.
• A normal or rising PCO2 is an indication of impending respiratory failure and requires
immediate monitoring and therapy.
empyema
• Abnormal accumulation of fluid between parietal pleura and visceral
pleura is called pleural effusion.
• Accumulation of purulent fluid is called empyema
• The accumulation of frank pus is termed empyema
• An empyema may involve the whole pleural space or only part of it
(‘loculated’ or ‘encysted’ empyema) and is usually unilateral.
 Aetiology
• Lung diseases: Pneumonia (the most common cause) Lung abscess,
tuberculosis.
• Subphrenic abscess (accumulation of infected fluid between the diaphragm,
liver, and spleen)
• Post traumatic: penetrating chest injury
• Post-operative: chest tube placement and thoracic surgery.
• Iatrogenic
• Blood spread
 Pathology
• Both layers of pleura are covered with a thick, shaggy inflammatory exudate. The pus in
the pleural space is often under considerable pressure, and if the condition is not
adequately treated, pus may rupture into a bronchus causing a bronchopleural fistula and
pyopneumothorax, or track through the chest wall with the formation of a subcutaneous
abscess or sinus, so-called empyema necessitans. An empyema will only heal if infection is
eradicated and the empyema space is obliterated, allowing apposition of the visceral and
parietal pleural layers. This can only occur if re-expansion of the compressed lung is
secured at an early stage by removal of all the pus from the pleural space. Successful re-
expansion and resolution will not occur if: • the visceral pleura becomes grossly thickened
and rigid due to delayed treatment or inadequate drainage of the infected pleural fluid •
the pleural layers are kept apart by air entering the pleura through a bronchopleural
fistula • there is underlying disease in the lung, such as bronchiectasis, bronchial
carcinoma or pulmonary TB preventing re-expansion. In these circumstances an empyema
tends to become chronic, and healing will only occur with surgical intervention.
• During an inflammatory process such as pneumonia, there is an
increase in fluid production in the pleural cavity known as the exudate
stage. As the disease progresses microorganisms, usually bacteria, can
colonize the fluid and generated an empyema. This fluid is
characterized by elevated lactate dehydrogenase, proteins, neutrophils,
and dead cells. Macroscopically is a thick opaque fluid found in
the fibrinopurulent stage. After the resolution of the infection and as a
consequence of the inflammation, there is a process of fibrosis that can
lead to restriction of the lung parenchyma. Appropriate and early
intervention is vital to decrease complications and mortality.
Clinical Features
• Patients with aerobic bacterial infection often present with acute
onset of symptoms while immunocompromised or elderly patients or
those with anaerobic infections present with chronic features.
• Systemic symptoms like high-grade, remittent fever with chills and
rigors, malaise and weight loss.
• Respiratory symptoms like pleuritic chest pain, breathlessness and dry
cough are present. Copious and purulent sputum indicates the presence
of a bronchopleural fistula.
• Physical examination reveals digital clubbing, oedema of the chest
wall, intercostal tenderness and signs of fluid in the pleural space.
 Investigations
• Polymorphonuclear leucocytosis and raised ESR.
• Chest radiographic findings are similar to that of pleural effusion.
• Aspiration and examination of the pus.
The pus may vary from very thin to very thick in consistency.
The pus contains large numbers of polymorphonuclear leucocytes.
Gram staining may identify the organism.
The causative organism may be cultured from the pus.
Tubercle bacilli may be seen and culture for tubercle bacilli may be
positive in tuberculous empyema