Bronchial asthma

3.  Definition
 Epidemiology
 Triggers
 Risk factors
 Types (Extrinsic & Intrinsic)
 Pathophysiology
 Clinic
 Diagnosis
 DDX
 Complications
 Management
 Prognosis
 Prevention
 References
WHAT TO EXPECT?

4. It is defined as reversible obstruction of large
and small airways due to hyper-responsiveness
to various immunologic and non-immunologic
stimuli
Definition

5.  Chronically in kids
 Before puberty male female ratio 2:1
 At puberty ration 1:1
 Young kids Î due viral infections, small airways
size and resistance
Epidemiology

6.  Respiratory infections
 Irritants
 Exercise
 Inhaled
 Ingested allergens
 Changes in weather
 Emotional stress
 Medications (Aspirin)
 GER
 Sinusitis
Triggers

7.  Poverty
 Small house size
 Large family
 Intense allergic exposure in childhood (>10
microgram of dust)
Risk Factors

8.  Extrinsic (allergic) Asthma: IgE total and
specific raised
 Intrinsic Asthma: IgE normal, in first 2 yrs of
childhood
Types

9.  Inflammation then bronchospasm
 Pathogenic components:
1. Bronchospasm
2. Mucus production
3. Edema and inflammation of the airways
mucosa
4. Infiltration of inflammatory cells (eosinophils,
neutrophils, basophils, macrophages)
5. Desquamation of epithelial and inflammatory
cells
Pathophysiology

10.  Obstruction during expirations and gas trapping ,
hyperinflation
 Raised ITP – venous return less – CO less
 Ventilation mismatch – hypoxia – interferes conversion of
lactic acid to water and CO2 – metabolic acidosis
 Hypercapnia - dissociates into H+ and HCO3- respiratory
acidosis
 Risk of developing asthma associated with serum IgE level
(allergen binds to specific mast cell, new and stored local
mast cells release mediators – leukotrienes C4, D4, E4, PAF,
histamine and then initiate bronchoconstriction, mucosal
edema and immune response)
PathoPhysiology

12.  Early Immune Response: Results in
Bronchoconstriction
 Treated with beta2 receptor agonists
 Prevented with mast cell stabilizing agent (cromolyn
or nedocromil)
 Late Phase Reaction: 6-8 hours later –
continued state of airway hyper-
responsiveness with Eosinophil and neutrophil
infiltration
 Treated and prevented with steroids. Also
prevented with mast cell stabilizing agents
Pathophysiology

13.  Wheeze (main)
 Cough
 Shortness of breath (dyspnea or chest congestion)
 Tachypnea (Hypoxia)
 Exercise intolerance
 Night attacks in kids (airways patency less)
 Mild or absent symptoms (prolonged expiration)
 Severe attack (+/- wheeze and ronchi – poor air movement)
 Severe obstruction (nasla flaring and use of accessory muscles)
 Central cyanosis (hypoxia)
 Signs of respiratory failure(agitation, lethargy, inability to speak,
tripod sitting position, diaphoresis)
 Asthma kids ( W and H below average and increased AP diameter)
Clinic

16.  Clinical (mainly)
 Blood Exam ( leukocytosis in Acute + severe asthma,
eosinophilia, IgE raised)
 Sputum (eosinophilia)
 CXR (hyperinflation, AP increased, flat diaphragm,
more horizontal ribs, narrow and elongated heart)
 Arterial blood gases (PO2 less, early PCO2 less then
raised as hypoventilation and respiratory failure
occurs)
 RAST : identifies allergen
 PFT: PEFR, FEV1 and VC decreased and RV, FRC and TLC
increased
Diagnosis

17.  Wheezy bronchitis: croup, acute bronchiolitis,
pneumonia, pertussis (continuous)
 Foreign body in airway (wheeze during ins and exp,
history of choking)
 Endobronchial TB or lymph node pressing bronchi(F:M
3:1)
 Cystic fibrosis (Multisystem disorder- resp, biliary tree,
sweat glands, GIT)
 Congenital malformation as vascular ring (+digestive
problems)
 Cardiac asthma (test for CHF)
Differential Diagnosis

18.  Pneumothorax
 Pneumomediastenum
 Delayed maturation
 Slow pubertal growth velocity
Complications

19.  Oxygen (2-3L/min)
 Salbutamol nebulizer (0.5mg/kg/dose)
 adrenaline (0.01ml/kg – subcut)
 Terbutaline (0.01ml/kg/dose)
 Aminophylline (5mg/kg –IV diluted)
 Hydrocortisone (5-10mg/kg)
 Adequate hydration (20ml/kg in 1-2hrs)
 Antibiotics
 Ventilatory support
 Subsequent management: oral/inhaled salbutamol,
steroid, theophyllin)
Management of AAA

20.  For hypoxia: Oxygen so saturation >92%
 Steroid user: steroid given initially
 Other: salbutamol neb, sal+ipratropium neb,
aminophylline infusion, adequate hydration, steroids
as in AAA management
 Respiratory failure: mechanical ventilation
Management Status Asthmaticus

21.  Components of therapy:
 Patient education
 Assessment and monitoring asthma severity
 Avoidance or asthma triggers
 Establishment of comprehensive pharmacologic therapy
including managing exacerbation
 Cromolyn and nedocromil (inh bronchospasm)
 Corticosteroid inhaler (reduce airway hyper-reactivity)
 Beta2 adrenergic agonist (relax airway smooth muscles, inhance
mucocilliary clearance decrease mediator release)
 SABD(e.g.sabutamol)
 LABD
Management of Chronic Asthma

22.  Good with aggressive therapy
 Death rare and due to under treatment
 Remission due to cross-sectional diameter
growth
 Resolution is rare in kids with severe asthma
Prognosis

23.  Reduce risk of developing allergies
 Breastfeeding in first 2 months of life and
helps till 6 years of age
 Reduce triggers
Prevention

24.  Basics of Pediatrics
 Eighth edition (2015)
 Parvez Akbar
Reference

25. THANK YOU