Bronchial Asthma

• Learning Objective: At the end of this unit the student will be able to
• 1. Define bronchial asthma
• 2. Understand the epidemiology of bronchial asthma.
• 3. Describe the etiology of bronchial asthma.
• 4. Understand the pathophysiology of bronchial asthma .
• 5. Identify the clinical manifestations of bronchial asthma.
• 6. List the signs of severity of bronchial asthma.
• 7. Make an accurate diagnosis of bronchial asthma.
• 8. Manage most cases of bronchial asthma.
• 9. Refer complicated cases of bronchial asthma.
Definition:

Bronchial asthma is defined as chronic inflammatory disease

of airways
characterized by increased responsiveness of the
tracheobronchial tree to a multiplicity of stimuli.
It is associated with widespread airway obstruction that is
reversible (but not completely in some patients), either
spontaneously or with treatment
Epidemiology:
Asthma is a common disease The prevalence of asthma is
rising in different parts of the world.
 It can occur at any age; but it usually starts early in life.
About 50% of patients develop asthma before the age of 10
and another 35% before the age of 40.
Males are affected twice as common as females in early
life; this sex difference equalizes by age 30.
Most cases of asthma are associated with personal or
family history of allergic disease such as eczema, rhinitis
and urticaria.
Etiology

Asthma is a heterogeneous disease and genetic ( atopic ) and

environmental factors such as viruses , occupational exposure
and allegens contribute to its initiation and continuance
Atopy is the single most important risk factor for asthma
Asthma can be classified in to 3 types Allergic (atopic) ,
Nonallergic ( idiosyncratic ) and Mixed
 Factors important for the genesis of asthma
Genetic factors
 Asthma has strong genetic predisposition or familial tendency Stimuli
that incite Asthma
 Allergens : Seasonal allergens such as pollen green
 Non seasonal animal feathers , dust mites , molds
Pharmacologic stimuli: Aspirin , Tatrazin (coloring agent), Beta blockers
such as Propranolol etc
 Environmental and air pollution: in industrial and heavily populated
areas.
The common pollutants are ozone, nitrogen dioxide and sulfur dioxide.
Pathophysiology:

Asthma results from a state of persistent subacute

inflammation of the airways.
 The airways obstruction in asthma is due to a combination
of factors.
The cells thought to play important part in the inflammatory
response are mast cells, eosinophils, lymphocytes and airway
epithelial cells.
These cells release inflammatory mediators which may result
Bronchoconstriction (spasm of airways smooth
muscles )
Vascular congestion and edema of airways mucosa
 Increased mucus production
Injury and desquamation of the airways epithelium
and impaired muco-ciliary transport
Symptom and Signs
The symptoms of each asthmatic patient differ greatly in
frequency and degree.
Some asthmatics are symptom free, with an occasional
episode that is mild and brief; others have mild coughing and
wheezing much of the time, punctuated by severe
exacerbations of symptoms following exposure to known
allergens, viral infection, exercise etc.
 Psychological factors particularly those associated with
crying, screaming or hard laughing may precipitate
symptoms.
Symptom and Signs
An attack usually begins acutely with paroxysms of
wheezing, coughing, and shortness of breath, or
insidiously with slowly increasing manifestations of
respiratory distress.
The asthmatic first notices dyspnea, tachypnea, cough
and tightness in the chest and may even notice audible
wheezes.
 On physical examination

Varying degrees of respiratory distress tachypnea,

tachycardia, and audible wheezes are often present.
Dehydration may be present because of sweating and
tachypnea.
 Chest examination shows a prolonged expiratory phase
with relatively high pitched wheezes throughout
inspiration and most of expiration.
In more severe episodes, patients may be unable to speak
more than a few words without stopping for breath.
On physical examination
Cyanosis is usually a late sign of hypoxia.
 Confusion and lethargy may indicate the onset of
progressive respiratory failure.
Less wheezing (silent chest) might indicate mucous plug or
patient fatigue with less airflow.
 And it is a sign of impending respiratory failure.
 The presence, absence, or prominence of wheezes does not
correlate precisely with the severity of the attack.
On physical examination
The most reliable clinical signs include the degree of dyspnea
at rest, cyanosis, difficulty in speaking and use of accessory
muscles of respiration.
 This is confirmed by arterial blood gas analysis.
 Between acute attacks, breath sounds may be normal during
quiet respiration.
However, low grade wheezing maybe heard at any time in
some patients, even when they claim to be completely
asymptomatic.
Complications during an Acute Attack of Asthma

Pneumothorax: It may present as sudden worsening of

respiratory distress, accompanied by sharp chest pain and on
examination, hyperresonant lung with a shift of mediastinum.
Chest x-ray confirms the diagnosis.
Mediastinal and subcutaneous emphysema due to alveolar
rupture Atelectasis due to obstruction
 Dilated right heart chambers (Corpulmonale) : from chronic
hypoxemia and pulmonary hypertension
Respiratory failure
 Laboratory Findings
Eosinophilia is a common finding.
Sputum is tenacious, rubbery and whitish or may be
yellowish; eosinophils are presentin the sputum.
Chest x-ray: varies from normal to hyperinflation.
Atelectasis and pneumothorax may be seen in complicated
cases.
 Pulmonary function tests are valuable in differential
diagnosis and in known patients to assess the degree of
airways obstruction.
 Diagnosis
Asthma should be considered in anyone who wheezes. A family
history of allergy, rhinitis or asthma can be elicited in most asthmatics.
Differential diagnosis includes:
In children: foreign body obstruction, viral URTI involving the
epiglottis (croup), and bronchiolitis (RSV infection);
In adults: COPD, heart failure, endobronchial TB, and malignancies.
Physical examination should search for heart failure and signs of
chronic hypoxemia (clubbing).
Unilateral wheezes usually indicate obstruction by foreign bodies or
tumor.
Prevention of attacks
The role of environmental factors (e.g. animal dander, dust,
airborne moulds, and pollens) in acute exacerbations is clear.
Allergens that can be controlled by avoidance should be
eliminated.
Nonspecific exacerbating factors (e.g. cigarette smoke,
odors, irritant fumes, and change in temperature, atmospheric
pressure, and humidity) should also be investigated and
avoided if possible.
Treatment

General principles
Assessing the severity of the attack is paramount in
deciding management
Bronchodilators should be used in orderly progression
 Decide when to start corticosteroids
 Treatment of the Acute Attack
 Salbutamol aerosol (Ventolin ) two puffs every 20 minutes for
three doses is the 1st line of treatment.
 Adrenaline 1:1000 can be given in doses up to a maximum of 0.2
ml in children and 0.3 ml in adults, repeated once or twice in 20 to
30 min (if there is no hypertension or any other contra indication).
If the initial treatment fails, Aminophylline 250 mg IV diluted in
dextrose in water should be given slowly over 10-15 minutes, once.
In patient management

Patients who are diagnosed to have severe and life threatening asthma
need in patient management. Some may even need admission to ICU.
Signs of Severity of acute asthmatic attack
1) Tachycardia HR > 120/min , Tachypnea RR.30 min
2) Presence of pulsus paradoxus
3) Use of accessory muscles of respiration
4) Cyanosis
5) Altered state of consciousness ( confusion , drowsiness )
6) Silent chest
In patient management
5) Altered state of consciousness ( confusion , drowsiness )
6) Silent chest
7) Paradoxical movement of the chest and the abdomen
8) Presence of complications : Pneumothorax , atelectasis
9) Unable to finish a sentence with single breath ( frequent interruption
of speech to take a breath )
 Specific drug Treatment
Aminoplylline in doses of 1mg/kg/hr in a continuous IV infusion
should be given.
Corticosteroids should also be given IV e.g. Hydrocortisone
4mg/kg IV every 4 hrs.
When the patient improves the hydrocortisone be changed to
Prednisolone PO and the dosage should be tapered up on
discharge.
 Patients who do not respond to aggressive drug therapy are
candidates for endotracheal intubation and Mechanical
Ventilation for which they should be admitted to an ICU.
Specific drug Treatment
Respiratory tract infections precipitating acute asthmatic
attack are predominantly viral; but if patients expectorate
yellowish, green or brown sputum, antibacterial therapy is
indicated.
 Ampicillin is the first line; alternatives are TTC,
erythromycin or cotrimoxazole.
Chest x-ray is taken if there is suspicion of pneumonia or
complications.
 Supportive Treatment
O2 therapy is always indicated for hospitalized patients
Fluid and electrolyte balance requires special attention because of
frequent occurrence of dehydration during acute asthmatic attack.
 However, over hydration may cause pulmonary edema and one
should be cautious in fluid administration.
 Anxiety is common in patients with severe acute asthmatic attack.
However this can be overcome when underlying hypoxia and
feeling of asphyxiation is treated.
Health personnel should be considerate and reassure the patient.
Maintenance Therapy for Asthma (Chronic Treatment
Chronic obstructive pulmonary diseases (COPD)

• Learning Objective: At the end of this unit the student will be able to
• 1. Define chronic obstructive pulmonary diseases (COPD
• 2. List the etiologies of COPD
• 3. Explain the epidemiology of COPD
• 4. Describe the pathophysiology of COPD
• 5. Identify the clinical manifestations of COPD
• 6. Outline the main differences between c. bronchitis and emphysema
• 7. Describe the most commonly used tests for the diagnosis of COPD
• 8. Make a diagnosis of COPD
 Definition:
Chronic obstructive pulmonary diseases are conditions
characterized by chronic irreversible airway obstruction
causing an increased resistance to outflow of air due to
chronic bronchitis and emphysema.
Both these diseases occur together in the same individual in a
variable proportion but the manifestations of one often
predominates the clinical picture.
1) Chronic bronchitis: is a condition associated with excessive
tracheobronchial mucus production sufficient to cause cough
with expectoration of sputum for at least 3 months in a year for
over 2 consecutive years.
 Etiology
Emphysema: Any factor leading to chronic alveolar inflammation
would encourage development of an emphysematous lesion.
Smoking has adverse effects on lung defenses, leading to
emphysematous change.
Congenital enzyme defects such as α1- antitrypsin deficiency are
also risk factors for the disease.
 Chronic bronchitis: with sufficient exposure to bronchial irritants,
particularly cigarette smoke, most persons develop some degree of
chronic bronchitis with signs of inflammation of the airways.
In developing countries household smoke from fire wood is said to
be a major contributing factor.
Prevalence:

COPD is a major health problem especially in western

societies because of the effect of cigarette smoking and
aging.
Males are affected more than females which could be
attributed to the higher prevalence of smoking in males.
Nowadays, the incidence of this disease in females is
increasing because of the increasing smoking habit.
 Pathological changes and pathophysiology
Chronic bronchitis is characterized by hypertrophy of mucus
glands in both large and small airways with thickening of walls
and accompanying excess production of mucus and narrowing of
airway lumen.
In C. bronchitis, alveoli are often spared, and no vessel loss and
lung perfusion remains normal but ventilation is very much
reduced.
This leads to abnormal V/Q (arteriovenous shunt) and patients
usually suffer from hypoxemia (manifested with cyanosis) and
acidosis, which causes pulmonary hypertension and right heart
failure in the long term.
 Pathological changes and pathophysiology
 On the other hand emphysema is characterized by destruction of
alveolar septa and distension of alveoli resulting in reduced surface area
and loss of vessels, the later causing reduced perfusion.
 Moreover, emphysema causes mucus production and airway narrowing
with accompanying reduction in ventilation.
This leads to retention of carbon dioxide in the blood and severe
dyspnea from reduced tissue perfusion.
However, these patients don’t suffer from hypoxia and acidosis, and
have less chance of development of pulmonary hypertension and cor-
pulmonale.
 Clinical features:
COPD is thought to begin early in adult life but significant
symptoms and disability do not appear until middle age.
A mild "smoker's cough" is often present many years before
onset of exertional dyspnea.
Gradual progressive exertional dyspnea is the most
common presenting complaint.
 Cough, wheezing, recurrent respiratory infections or,
occasionally weakness, weight loss, or reduced libido may
also be initial manifestations.
Physical findings:

in COPD are very variable especially in early stages.

A consistent abnormality is obstruction to expiratory airflow
manifested by prolonged forced expiration (normally < 4
seconds).
 Typical findings including gross pulmonary hyperinflation,
prolonged expiration during quiet breathing, pursed-lip
breathing, stooped posture, and marked use of accessory
muscles of respiration are seen in later stages of COPD.
 Physical findings:
Other findings are rhonchi, diminished vesicular breath sounds,
tachycardia, distant heart sounds, and decreased diaphragmatic
excursion.
The chest may be remarkably "quiet" in advanced stages of
emphysema but is usually "noisy" in patients with chronic
bronchitis.
In advanced cases, frank cyanosis may be there from
hypoxemia; a plethoric appearance associated with secondary
erythrocytosis and, signs of right-sided heart failure in patients
with cor-pulmonale.
 Mild edema may be there even without heart failure.
Diagnosis:

COPD should be suspected in any patient with chronic

productive cough and/or exertional dyspnea of uncertain
etiology, or whose physical examination reveals evidence of
prolonged forced expiration.
Pulmonary function tests (spirometric testing) are done at
specialized hospitals to determine the type of pulmonary
obstruction.
Red cell counts may reveal erythrocytosis and elevated
hematochrit in chronic hypoxemic patients.
Diagnosis:
The pattern of physiologic abnormality in each patient
depends to some extent on the relative severity of
intrinsic bronchial disease and emphysema.
In patients with severe emphysema, resting
hypoxemia is usually mild (i.e. no or less cyanosis). In
patients with chronic bronchitis, severe hypoxemia
may be noted relatively early.
Course and Prognosis

In the early stage of COPD, some reversal of airway

obstruction and considerable
symptomatic improvement can often be obtained with
therapy, but the long-term prognosis is
less favorable in such patients.
Course and Prognosis
Treatment: so far no curative treatment.
Therapy is directed at relieving symptoms, controlling
potentially fatal exacerbations, and slowing of the
progression of the disorder.
Avoidance of bronchial irritants, especially cessation
of smoking, is of primary importance.
• Thus, the treatment is outlined as follows:
1) Treatment of infection: COPD patients with purulent
sputum should be treated with a broad spectrum antibiotic.
Commonly used drugs include co-trimoxazole 980mg POBID
or TTC or Ampicillin 250 - 500mg four times a day for 10
days. The course can be repeated at the first sign of
recurrence of bronchial infection.
2) Control of bronchospasm: β-agonists like salbutamol, or
one of the theophyllines can be used. Corticosteroids do not
have a major role in maintenance treatment.
3) Facilitation of drainage of bronchial secretion: adequate
hydration with oral fluids is essential to prevent drying of
secretions. Inhalation of mist, postural drainage, and chest
exercise may help.
4) Hypoxemia: this will lead to cor-pulmonale in
patients with predominant c.bronchitis.
Oxygen should be given in such patients with hypoxia,
and in severe cases a portable oxygen therapy ( 16
hrs /day) for home use is recommended.
5) Control of heart failure: the most important measures
are correction of hypoxemia, administration of diuretics
and restriction of sodium intake.
6) Exercise: prolonged inactivity leads to exercise
intolerance. Regular exercise as long as there is no
severe heart disease is recommended.
• Thank you