Obstructive pulmonary diseases

Asthma

• Asthma is a chronic inflammatory disorder of the airways, in which many cells and cellular elements play a
role.
• Chronic inflammation is associated with airway hyper-responsiveness that leads to recurrent episodes of
wheezing, breathlessness, chest tightness and coughing, particularly at night and in the early morning.
• These episodes are usually associated with widespread but variable airflow obstruction within the lung that is
often reversible, either spontaneously or with treatment.
Pathophysiology:
• Airway hyper-reactivity (AHR) – the tendency for airways to narrow excessively in response to triggers that
have little or no effect in normal individuals is integral to the diagnosis of asthma and appears to be related,
although not exclusively, to airway inflammation.
• Other factors likely to be important in the behavior of airway smooth muscle include the degree of airway
narrowing and neurogenic mechanisms.
• The relationship between atopy (the propensity to produce IgE) and asthma is well established and in many
individuals there is a clear relationship between sensitization and allergen exposure, as demonstrated by skin-
prick reactivity or elevated serum-specific IgE.
Clinical features:
• Typical symptoms include recurrent episodes of wheezing, chest tightness, breathlessness and cough.
• Asthma is commonly mistaken for a cold or a persistent chest infection (e.g. longer than 10 days).
• Classical precipitants include exercise, particularly in cold weather, exposure to airborne allergens or
pollutants, and viral upper respiratory tract infections.
• Wheeze apart, there is often very little to find on examination.
• An inspection for nasal polyps and eczema should be performed.
• Rarely, a vasculitic rash may suggest eosinophilic granulomatosis with polyangiitis (EGPA, formerly known
as Churg–Strauss syndrome).
• Patients with mild intermittent asthma are usually asymptomatic between exacerbations
• Asthma characteristically displays a diurnal pattern, with symptoms and lung function being worse in the
early morning.
• When poorly controlled, symptoms such as cough and wheeze disturb sleep
• Cough may be the dominant symptom in some patients, and the lack of wheeze or breathlessness may lead to
a delay in reaching the diagnosis of so-called ‘cough-variant asthma’.
• In some circumstances, asthma is triggered by prescription drugs such as Beta-adrenoceptor antagonists (β-
blockers), even when administered topically as eye drops, may induce bronchospasm, as may aspirin and
other non-steroidal anti-inflammatory drugs (NSAIDs).
Diagnosis:
• The diagnosis of asthma is predominantly clinical and is based on the combination of history, lung function
and ‘other’ tests, which allows high, intermediate or low probability of asthma to emerge.
• The approach may vary from patient to patient and may need to be re-evaluated following the introduction of
treatment.
• Supportive evidence is provided by the demonstration of variable airflow obstruction, preferably by using
spirometry
• to measure FEV1 and FVC. This identifies the obstructive defect, defines its severity, and provides a baseline
for bronchodilator reversibility
• If spirometry is not available, a peak flow meter may be used.
Management
Severe asthma ( Status Asthmaticus)
Chronic obstructive pulmonary disease

• Chronic obstructive pulmonary disease (COPD) is defined as a preventable and treatable disease
characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar
abnormalities, usually caused by significant exposure to noxious particles or gases.
• The spectrum of COPD includes chronic bronchitis and emphysema. Chronic bronchitis is defined as cough
and sputum for at least 3 consecutive months in each of 2 consecutive years.
• Emphysema is abnormal permanent enlargement of the airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls.
• Exacerbations and comorbidities contribute to the overall severity in individual patients.
• Extrapulmonary effects include weight loss and skeletal muscle dysfunction.
• Commonly associated comorbid conditions include cardiovascular disease, cerebrovascular disease, the
metabolic syndrome, osteoporosis, depression and lung cancer.
• COPD has both pulmonary and systemic components. The presence of airflow limitation combined with
premature airway closure leads to gas trapping and hyperinflation, adversely affecting pulmonary and chest
wall compliance.
• Pulmonary hyperinflation also results, which flattens the diaphragmatic muscles and leads to an increasingly
horizontal alignment of the intercostal muscles, placing the respiratory muscles at a mechanical disadvantage.
The work of breathing is therefore markedly increased – first on exercise, when the time for expiration is
further shortened, but then, as the disease advances, at rest.
• Emphysema may be classified by the pattern of the enlarged airspaces: centriacinar, panacinar and paraseptal.
• Some individuals develop bullae; permanent air-filled spaces within the lung that are more than 1 cm in
diameter. This results in impaired gas exchange and respiratory failure.
Clinical features:
• Cough and associated sputum production are usually the first symptoms, and are often referred to as a
‘smoker’s cough’.
• Hemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough
investigation.
• Breathlessness usually prompts presentation to a health professional.
• Physical signs are non-specific, correlate poorly with lung function, and are seldom obvious until the disease
is advanced.
• Breath sounds are typically quiet; crackles may accompany infection but, if persistent, raise the possibility of
bronchiectasis.
• Finger clubbing is not a feature of COPD and should trigger further investigation for lung cancer or fibrosis.
• Right heart failure may develop in patients with advanced COPD, particularly if there is coexisting sleep
apnea or thromboembolic disease.
• Two classical phenotypes have been described: ‘pink puffers’ and ‘blue bloaters’.
• Pink puffers: are typically thin and breathless, and maintain a normal PaCO2 until the late stage of disease.
• Blue Bloaters: develop hypercapnia earlier and may develop edema and secondary polycythemia.
• In practice, these phenotypes often overlap.
Investigations:
• Although there are no reliable radiographic signs that correlate with the severity of airflow limitation, a chest
X-ray is essential to identify alternative diagnoses such as cardiac failure, lung cancer and the presence of
bullae.
• The diagnosis requires objective demonstration of airflow obstruction by spirometry and is established when
the post-bronchodilator FEV1/FVC is <70%. The severity of COPD may be defined in relation to the post-
bronchodilator FEV1
Assessment of severity
• The severity of COPD has traditionally been dedined in relation to the FEV% predicted.
Management:
The management of COPD focuses on improving breathlessness, reducing the frequency and severity of
exacerbations, and improving health status and prognosis.
1- Reducing exposure to noxious particles and gases
2- Pulmonary rehabilitation
3- Bronchodilators: Long-acting beta-agonists (LABA) and long-acting muscarinic-antagonists (LAMA) are
available in single agent or combination inhalers.
• Significant improvements in breathlessness may be reported despite minimal changes in FEV1, probably
reflecting improvements in lung emptying that reduce dynamic hyperinflation and ease the work of breathing.
• Oral bronchodilator therapy, such as theophylline, is only recommended when other long-acting
bronchodilators are not available.
4- Combined inhaled glucocorticoids and bronchodilators:
Those with frequent exacerbations and/or persistent breathlessness despite long-acting bronchodilators, may
benefit from inhaled glucocorticoids (usually abbreviated to ICS, for ‘inhaled corticosteroids’), in the form of
either a LABA/LAMA/ICS or LABA/ICS combination inhaler.
5- Oral anti-inflammatories:
Oral glucocorticoids are useful during exacerbations but maintenance therapy contributes to osteoporosis and
impaired skeletal muscle function, and should be avoided.
Roflumilast, a phosphodiesterase-4 inhibitor, improves lung function and reduces moderate to severe
exacerbations in patients with severe or very severe COPD.
Azithromycin 500 mg three times weekly can reduce the number of exacerbations, but non-tuberculous
mycobacterial infections must first be excluded, and LFTs, QTC and hearing should be monitored.
• Oxygen therapy and home ventilation
Long-term domiciliary oxygen therapy (LTOT) improves survival in selected patients with COPD complicated
by severe hypoxaemia (arterial PaO2 <7.3 kPa (55 mmHg)
• Surgical intervention: Bullectomy may be considered when large bullae compress surrounding normal lung
tissue. Patients with predominantly upper lobe emphysema, preserved gas transfer and no evidence of
pulmonary hypertension may benefit from lung volume reduction surgery (LVRS).
• Palliative care: Addressing end-of-life needs is an important aspect of care in advanced COPD. Hand-held
electric fans and morphine preparations may be used for palliation of breathlessness and low-dose
benzodiazepines may reduce anxiety. Decisions regarding resuscitation and escalation of care should be
addressed in advance of critical illness
• Prognosis: COPD has a variable natural history but is usually progressive.
• The prognosis is inversely related to age and directly related to the post-bronchodilator FEV1.
• Additional poor prognostic indicators include weight loss and pulmonary hypertension.
• A composite score comprising the body mass index (B), the degree of airflow obstruction (O), a measurement
of dyspnoea (D) and exercise capacity (E) (BODE index) may assist in predicting death from
• respiratory and other causes
• Respiratory failure, pneumonia, cardiac disease and lung cancer represent common modes of death.
• Specific challenges with the diagnosis and management of obstructive pulmonary disease in older people
Acute exacerbations of COPD

• Acute exacerbations of COPD (AECOPD) are characterised by an increase in symptoms and deterioration in
lung function and health status.
• They become more frequent as the disease progresses and are usually triggered by infection or a change in air
quality.
• accompanied by the development of respiratory failure and/or fluid retention and represent an important
cause of death.
• Many patients can be managed at home with the use of increased bronchodilator therapy, a short course of
oral glucocorticoids and, if appropriate, antibiotics.
• The presence of cyanosis, peripheral oedema or an alteration in consciousness should prompt referral to
hospital
Management of COPD Exc.

Oxygen therapy: In patients with an exacerbation of severe COPD, high concentrations of oxygen may
cause respiratory depression and worsening acidosis.
• Controlled oxygen at 24% or 28% should be used with the aim of maintaining SaO2 of 88%–92% or PaO2 of
more than 8 kPa (60 mmHg) without worsening acidosis

Bronchodilators: Nebulized short-acting β2-agonists combined with an anticholinergic agent (e.g.

salbutamol and ipratropium) are routinely administered.

• Glucocorticoids: Oral prednisolone reduces symptoms and improves lung function.

Doses of 30 mg for 5 days are currently recommended but weaning courses are required if the patient has had a
recent course of steroids. Prophylaxis against osteoporosis should be considered in patients who receive
repeated courses of glucocorticoids.
Antibiotic therapy
The role of bacteria in exacerbations remains controversial. There is little evidence for the routine
administration of antibiotics, but they are recommended for patients reporting an increase in sputum purulence,
sputum volume or breathlessness. In most cases simple regimens are advised, such as an aminopenicillin, a
tetracycline or a macrolide. However, local practice will depend on local guidance and epidemiology.
Non-invasive ventilation
Non-invasive ventilation (NIV) reduces mortality and invasive ventilation rates in patients with an acute
exacerbation of COPD complicated by mild to moderate respiratory acidosis (pH <7.35 and PaCO2 >6.5 kPa).
Additional therapy diuretics.
Bronchiectasis

• Bronchiectasis means abnormal dilatation of the bronchi. Chronic suppurative airway infection with sputum
production, progressive scarring and lung damage occur, whatever the cause.

Aetiology and pathology

• Bronchiectasis may result from a congenital defect affecting airway ion transport or ciliary function, such as
cystic fibrosis, or may be acquired secondary to damage to the airways by a destructive infection, inhaled
toxin or foreign body
• Localised bronchiectasis may occur due to the accumulation of pus beyond an obstructing bronchial lesion,
such as enlarged tuberculous hilar lymph nodes, a bronchial tumour or an inhaled foreign body.