Bronchial

BRONCHIAL ASTHMA

Collins Kadiboh UMB/17-A/165

Favor Kisienya UMB/2024/3145

Facilitator Prof F.E Onyango

Outline
INTRODUCTION
AETIOLOGY
EPIDEMIOLOGY
PATHOGENESIS
PATHOLOGY
PATHOPHYSIOLOGY
CLINICAL PRESENTATION
DIAGNOSIS
TREATMENT
COMPLICATIONS
PROGNOSIS
PREVENTION
DEFINITION
Bronchial asthma is a chronic respiratory condition characterized by
inflammation, narrowing of the airways and hyper responsiveness of
the bronchial.
AETIOLOGY
• The exact cause of asthma is not fully understood, but it is believed to
result from a complex interplay of genetic and environmental factors.
These include:
1. Environmental allergens like dust mites etc
2. Viral respiratory infection like influenza
3. Exercise and hyperventilation
4. GERD
5. Iatrogenic like use of beta blockers,ASA
6. Stress and emotional factors
EPIDEMIOLOGY
• a. Burden of disease:

• Asthma is a significant public health burden worldwide, affecting an

estimated 339 million people globally in 2020. It is a leading cause of
chronic illness and disability, and is associated with substantial
healthcare costs and lost productivity.
• Asthma affected an estimation of 262 million people in 2019(1) and
caused 455000 deaths
• b. Distribution and trends of disease:

• Asthma prevalence varies widely across different countries and

regions, with higher rates reported in developed countries. The
prevalence of asthma has been increasing over the past few decades,
particularly among children and adolescents.
...distribution and trends of disease
• Currently, there are about 4.8 million children with asthma
• Prevalence: occurs more frequently in boys before puberty and in girls
after puberty.
• More than 8.5%of children in US have been diagnosed with asthma-
www.msdmanuals.com
• Higher percentage of black than white children
c. Risk factors
• Host factors • Non host factors
• Genetic:atopy and airway • Parents asthma
hyperresponsiveness • Inhalant allergen sensitization
• Male gender • Formula feeding be4 4 months
• Obesity • Maternal smoking
• Prematurity • Stress to mother
• Low birth weight • Delivery by caesarian section
• ≥4% peripheral blood eosinophilia • Young maternal age
• Poor maternal nutrition
• Other allergies
• Urban environment
PATHOPHYSIOLOGY/PATHOGENESIS
This is discussed under three subheadings
1. Airway inflammation
2. Intermittent airflow obstruction
3. Bronchial hyperresponsiveness.
The mechanism maybe acute, subacute or chronic depending on the
inflammatory cells involved.
This leads oedema, mucus secretion and Bronchial reactivity in acute to
subacute phase.
In chronic phase, varying degree of mononuclear cells and eosinophils
infiltration may lead to desquamation of epithelium, hyperplasia of SM hence
airway remodeling.
AIRWAY INFLAMMATION
• Activation of mast cells, eosinophil, epithelial cells, Macs and T
lymphocytes.
• Release of various cytokines via T lymphocytes leading to airway
remodeling.
• Bronchial response to exogenous and endogenous stimuli is what
causes the hyperresponsiveness therefore the degree of the response
is reliable on the clinical severity of the asthma.
• In chronic state, fibroblasts, endothelial cells and epithelial cells are
the major contributors.
AIRWAY OBSTRUCTION
• Maybe caused by the following:-
1. Oedema
2. Chronic mucus plug from exudate of serum proteins and cell debris
3. Airway remodeling coz of hyperplasia
4. Acute bronchoconstriction because of IgE
This leads to inflow resistance and decreased expiratory rate hence
hyperinflation which may help in temporary relief in exhalation.
However this leads to laboured breathing.
BRONCHIAL HYPERRESPONSIVENESS
• The compensation which is Ltd to tidal volume resulting in alveolar
hypoventilation.
• Uneven air distribution, altered circulation, vasoconstriction due to
alveolar hypoxia leads to ventilation perfusion mismatch.
• In early stages, hypercarbia is prevented by CO2 readily dissolving
across alveolar capillary membranes.
• As things worsen, CO2 retention occurs, increased cardiac activity,
increased O2 consumption all results to metabolic acidosis.
• As CO2 retention worsen further, respiratory failure is imminent
leading to respiratory acidosis.
Pathogenesis of asthma
Inflammation mediators

•primary mediators: histamine, proteases, eosinophil chemotactic

factor, neutrophil chemotactic factor
•secondary mediators: leukotrienes, prostaglandins,bradykinins
IL3,4,5,9 and 13
CLINICAL PRESENTATION
• 80% of asthmatic children develop symptoms before 5th year of life.
• Symptoms: recurrent attacks of dry cough, dyspnea and wheeze
(worse at night)
• Chest tightness
• In between attacks, patient is either free or wheezing
• Signs:refer to signs of severe asthma or mild) moderate asthma plus
• Irritability and restlessness, respiratory distress
DIAGNOSIS-
Working Diagnosis
Symptoms Signs
• Expiratory wheezing
Chest tightness • Prolonged expiratory phase
Cough • Decreased breath sounds
Shortness of breath • Crackles/rales
Difficulty breathing • Accessory muscle use
Wheezing-whistling noise while • Nasal flaring
breathing • Absence of wheezing in severe
cases
Physical findings
On Inspection
Tachypneic.wheezing,drowsiness,central cyanosis,hyper inflated chest,head
nodding,using accessory muscles when breathing,hyperexpanded chest
Palpation
Decreased symmetrical chest wall expansion
Limited chest expansion
Percussion
Resonance
Auscultation
Reduced breath sounds,rhonchi,vesicular breath sounds with prolonged expiration
• Typical clinical features of Asthma
• Demonstration of reversible bronchoconstriction
by use of PFTs
Spirometry
reduced FEV1
reduced FEV1/FVC
reduction in FEV1 by 20% is diagnostic of asthma
Bronchial provocation-methacholine
still on diagnosis
• Bronchial reversibility test
Helps differentiate from COPD
Inhalation of albuterol 200-400mcg will cause an increase if FEV1 by
more than 12% will show the patient has athma and unlikely its COPD
Investigatios
Immunologic:elevated IgE,IL 4,5
chest X-ray: during attack may show:
• Hyperinflation
• Increased bronchovascular marking

Pulmonary functional tests

Arterial blood gases
Oxygen sat less than 92%
Baseline tests-CBC-eosiniphilia,UECS
spirometry

• Variable expiratory airflow limitation

• The grater the variations, the more confident the diagnosis

• Reduced FEV1/FVC ratio < 0.75

• Positive bronchodilator reversibility test- increase FEV1≥ 12%/ > 200ml from baseline.

• Significant increase in lung function after 4 weeks of anti inflammatory treatment

Other tests

• Exercise tolerance test

• Allergen skin prick test
• Bronchial challenge test with methacholine or histamine[20% fall in
FEV1]
DIFFERENTIAL DIAGNOSIS
• Allergic diseases such as eczema, rhinitis or urticaria
• Upper airway obstruction by tumor or laryngeal edema
• Acute left ventricular failure
• COPD
• Foreign bodies in the airway
• Infectious bronchiolitis
• Cystic fibrosis
• Hypersensitivity pneumonitis
• Allergic bronchopulmonary aspergillosis
• Alpha-1 antitrypsin deficiency
• Tropical eosinophilia/ parasitic infections
CLASSIFICATION
Severe Asthma
Any of these
• Oxygen saturation<90%
• Central cyanosis
• Inability to drink or breastfeed
• AVPU= "V" " P" or "U' or
• Inability to talk or complete sentences
• Pulse rate>200bpm(0-3years) and 180bpm(4-5years)
• Silent chest on auscultation.
Mild or Moderate Asthma
• Wheeze plus
• Lower chest wall in drawing OR
• Fast breathing
• RR≥50breaths/min(age 2-11months)
• RR≥40 breaths/min(age12-59 months)
TREATMENT
Supportive Treatment

Supportive treatment of asthma involves the use of bronchodilators, which help to relax the airway
smooth muscle and relieve symptoms. Oxygen therapy may also be used in severe cases.
Assess for emergency signs,ABCDs
If emergency signs present, immediately transfer to emergency area
-start life support procedures
-give oxygen ,weigh if possible
• Resuscitation: ensure airway is clear and safe-suction any secretions
• Position the airway:head tilt -chin lift manoeuver
• Ensure proper hydration
• Identify and minimize exposure to risk factors
• Manage asthma exacerbation
Specific Treatment
Pharmacotherapy

• Beta-adrenergic agonists e.g. albuterol, salbutamol[Ventolin]

• Acts in minutes, lasts 4 to 8 hours
• Short term relief of bronchoconstriction.
• Treatment of choice in acute exacerbations.
• Useful in preventing bronchospasm precipitated by exercise and other
stimuli
• Overuse may cause rebound bronchospasm.
• Longer-acting- lasts 8-12 or 24 hr;useful for nocturnal asthma.
• Can be used in combination with inhaled corticosteroids.
INHALED CORTICOSTEROIDS

Agents currently available are

beclomethasone,budesonide,flunisolide,fluticasone
propionate ,ciclesonide and triamcinolone acetonide.
Suppress inflammatory response.
Local side effects-rare in young children
-thrush, dysphonia-minimize by wiping perioral skin and rinsing mouth
after inhalation
LONG ACTING BETA-AGONIST[LABA]
• LABAs relax airway smooth muscle but no anti inflammatory effect.
• Add LABA or medium-dose ICS as step-up in poorly controlled child.
• Potential adverse effects:
• Tachycardia,tremor,insomnia
• Paradoxical increase in serious asthma in some pts due to down
regulation of B2-receptors
• Examples;salmeterol,formoterol
• bottomline:always combine with ICS/LABA
LEUKOTRIENE RECEPTOR
ANTAGONISTS
• Used as step-up in addition to ICS
• Have bronchodilator and anti inflammatory effects
• Zileuton –modest bronchodilator but has limited effectiveness against
allergens.
• Paediatric formulations of LTRA-monteleukast,zafirluekast
• 4mg sachets[sweet granules]
• 5mg chewable tab[sweet]
MAST CELL STABILIZERS
• Inhibit release of histamine
• Inhibit late phase response
• Long term administration can prevent and reduce bronchial hyper-
reactivity
• Effective in exercise-induced asthma when used 10 to 20 minutes
before exercise.
ANTICHOLINERGICS
• Atropine sulfate produce bronchodilation in asthma pts but limited by
systemic side effects
• They are also slow to act[60-90 min] and are only of modest potency.
COMPLICATIONS
• Status asthmaticus
• Severe life threatening attack refractory to usual treatment where pt poses risk of
respiratory failure
• Pneumonia
• Growth retardation
• Long-term uncontrolled asthma may also lead to irreversible changes in the
airways, known as airway remodeling
• Death

• Mngt:reverse obstruction, correct hypoxemia

PROGNOSIS
• The prognosis of asthma varies among individuals and depends on
the severity of the disease and response to treatment.
Although asthma is considered a chronic disease, the large majority of
patients have good control of the disease if prevention measures are
applied and the inhaled treatment is done correctly. Only a small
percentage of patients have asthma refractory to conventional treatment.
With proper management, most individuals with asthma can achieve
good control of symptoms.
Prevention
• Prevention of bronchial asthma can be classified into three categories: primary, secondary, and
tertiary.
• Primary prevention :
• Primary prevention aims to prevent the development of asthma in individuals who have not yet
developed the condition. The following are some strategies that can be used for primary prevention:
① Avoidance of triggers: Individuals at risk of developing asthma should avoid exposure to common
triggers such as allergens (e.g., pollen, animal dander), irritants (e.g., smoke, air pollution), and
respiratory infections.
② Immunization: Vaccination against respiratory viruses, including influenza and pneumococcus,
may reduce the risk of developing asthma.
③ Breastfeeding: Studies have shown that breastfeeding may reduce the risk of developing asthma in
children.
④ Healthy lifestyle: Maintaining a healthy lifestyle, including regular exercise and a balanced diet,
may reduce the risk of developing asthma.
• Secondary prevention aims to detect and treat asthma early in individuals
who have already developed the condition. The following are some
strategies that can be used for secondary prevention:
• Regular monitoring: Individuals with asthma should undergo regular
monitoring of their symptoms and lung function to detect any changes that
may require treatment adjustments.
• Education: Patients with asthma should receive education on how to
manage their condition, including proper use of medications and
recognition of early warning signs of an asthma attack.
• Environmental control: Patients with asthma should be advised to reduce
exposure to triggers in their environment, such as allergens and irritants.
• Tertiary prevention aims to prevent or reduce the severity of exacerbations and
complications in individuals who have already developed asthma. The
following are some strategies that can be used for tertiary prevention:
• Medications: Patients with asthma should be prescribed appropriate
medications, including bronchodilators and inhaled corticosteroids, to manage
their symptoms and prevent exacerbations.
• Self-management: Patients with asthma should be educated on self-
management strategies, including monitoring their symptoms, using a peak
flow meter, and knowing when to seek medical attention.
• Follow-up: Patients with asthma should undergo regular follow-up with their
healthcare providers to monitor their condition and adjust treatment as needed.
MERCI