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Asthma
Asthma is a reversible airway obstruction often triggered by factors like infections and weather changes, more common in boys before puberty. Its pathophysiology includes inflammation and bronchospasm, with clinical manifestations such as cough, shortness of breath, and wheezing. Management involves acute treatment options like bronchodilators and steroids, and chronic care focusing on patient education, trigger avoidance, and pharmacologic therapy.
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Asthma
- 1. ASTHMA Saad Bin ZafarMahmood Ziauddin University
- 2. Definition • Reversible obstructionof airways due to hyper responsiveness to various immunologic and non-immunologic stimuli
- 3. Epidemiology • Common chroniclung disease in children • Boys > Girls (Before puberty) • More severe in young children
- 4. Etiology / Triggers •Respiratory infections (Viral, Mycoplasma) • Changes in weather • Emotional stress
- 5. Types of Asthma •Extrinsic Asthma ▫ Related to environmental exposures ▫ Inc. conc of IgE antibodies • Intrinsic Asthma ▫ No IgE antibodies ▫ Often in the first 2 years of life
- 6. Pathophysiology • Asthma ischaracterized by airway inflammation and bronchospasm • Pathologic components’ ▫ Bronchospasm ▫ Mucus production ▫ Edema ▫ Infiltration of inflammatory cells ▫ Desquamation of epithelial and inflammatory cells
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- 8. Pathophysiology • Allergens bindto mast cell associated IgE • Release of mediators • Result in bronchoconstriction, edema and immune responses • Early phase reaction results in bronchoconstriction • Late phase reaction results in eosinophilic and neutrophilic infiltration
- 9. Risk factors • Poverty •Small Home / Large family • Frequent respiratory infections • Intense allergenic exposure in infancy • Poor compliance to therapy
- 10. Clinical presentation • History ▫Cough ▫ Shortness of breath ▫ Exercise intolerance ▫ Night time symptoms ▫ Agitation ▫ Lethargy ▫ Inability to speak ▫ Decreased appetite ▫ Tripod sitting position ▫ Diaphoresis
- 11. Examination • WHEEZING • Centralcyanosis • Tachypnea • Tachycardia • Pulsus paradoxus • Flaring of nostrils, use of accessory muscle of respiration and intercostal recessions • Barrel shaped chest • Harrison sulci
- 12. • In severeasthmatic attack (respiratory failure) ▫ Wheezing may disappear ▫ Bradycardia ▫ No pulsus paradoxus
- 13. Diagnosis / Investigations •Mainly clinical • CBC • CXR • ABGs • Radio-allergo-sorbent testing (RAST) • PFTs
- 14. CXR in asthma •Hyper inflated and hyper lucent lungs • Inc antero-posterior diameter of chest • Flattening of diaphragm • Heart appears narrow and elongated • More horizontal ribs
- 15. PFTs • PEFR decreased •FEV1 reduced • FEV1 / FVC reduced • RV, FRC and TLC increase • Diurnal variation in PEFR is characteristic of asthma
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- 17. Differential diagnosis • Acutebronchiolitis • Foreign body in the airway • Cystic fibrosis • Congenital malformations – Vascular ring • Cardiac asthma • Pnemonia, croup and pertussis
- 18. Complications • Delayed maturation •Below average weight and height • Pnemothorax • Pneumomediastinum
- 19. Classification of asthmaon severity basis
- 20. Stepwise approach toasthma medications
- 21. Management on follow-upvisits
- 22. Management – Acuteattack • Oxygen (2-3 L/min) • Adequate hydration • Nebulized salbutamol (with O2) ▫ Stop salbutamol if HR > 180 • Terbutaline (SC inj) • Aminophyline (IV) ▫ To be given if already on theophyline ▫ If unable to tolerate B2 agonists • Hydrocortisone (IV) • Epinephrine (SC inj) • Antibiotics • Ventilatory support
- 23. Status asthmaticus • Continuousrespiratory distress despite administration of sympathomimetic drugs with or without theophyline • Management ▫ Admit in ICU ▫ Investigations done immediately ▫ Same management as acute except Steroids given initially Ipratropium can also be used
- 24. Management – Chronicasthma • Four main components ▫ Assessment and monitoring ▫ Patient education ▫ Avoidance of triggers ▫ Pharmacologic therapy
- 25. Patient education • Improvingpatient skills in use of inhaler • Use of peak flow monitoring • Information about medications • When and how to respond to changes
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- 29. Pharmacologic therapy • Beta2 agonits (Short and long acting) • Theophyline • Ipratropium (used along with Beta 2 agonists) • Cromolyn and nedocromil • Leukotriene antagonists • Inhaled corticosteroids • Oral corticosteroids (short courses)
- 30. Prognosis • Good prognosiswith early aggressive treatment • 50 % of asthmatic children are free of symptoms by 10-20 years • 5 % experience severe disease • In severe asthma (chronic steroid dependant disease + hospitalizations) 95% become asthmatic adults
- 31. Prevention • Reduce therisk of developing allergies • Breast feeding ▫ Reduces wheezing ▫ Protection lasts for up to 6 years • Avoidance of triggers