Bronchial Asthma Etiology Pathogenesis Clinical features Treatment of Bronchial Asthma
- Asthma is a chronic inflammatory disease of airways characterized by increased bronchial responses to a variety of stimuli.
- There is widespread narrowing of air passages which is relieved by therapy, or by itself.
- The typical clinical picture is paroxysms of dyspnoea, cough; and wheezing.
- Most attacks are short-lived, for minutes to hours and patient recovers completely after an attack.
- The attack comes in episodes lasting for minutes, hours, days or weeks.
- There are symptom-free periods between attacks.
- Status asthmaticus severe obstruction persisting for days or weeks continuously.
- Serious attacks can result in death ,
- Age: Usually occurs before age of 10 years or before 40 years age.
- Sex: Amongst children, it is more common in males.
- Symptoms of recurrent episodes of airway obstruction or airway hyper-responsiveness may include:
- Cough (particularly if worse at night)
- Airflow obstruction is at least partially reversible.
- Alternative diagnoses are excluded.
- Chest tightness
- Difficulty breathing
- Symptoms are typically precipitated or worsened by exercise, viral infections, irritants such as allergens, changes in weather, stress or strong emotions, and/or menstrual cycles.
Bronchial Asthma Etiology
- It is an atopic disease (genetic) where environmental factors have an important role.
- Allergic asthma is associated with rhinitis, urti-caria, eczema, increased IgE, and positive reaction to intradermal antigens.
- Some patients have non-atopic asthma (no history of allergy) or idiosyncratic asthma.
- Asthma of early life usually has allergic basis. Asthma occurring in later life usually has no history of allergy.
Bronchial Asthma Pathogenesis
- The airways are inflamed, edematous, infiltrated with eosinophils, neutrophils, Iymphocytes.
- The cells involved in inflammatory and allergic response are masked cells, eosinophils, Iymphocytes, epithelial lining cells of airways .
- The IgE response is controlled by T and B Iymphocytes in allergic asthma.
Stimuli that can cause asthma
- Environmental factors
- Occupational factors
Drugs which can cause asthma
- Tartrazine – colouring agent .Y Beta adrenergic antagonists y Indomethacin
- Inhalational bronchodilator solutions .v’ IV glucocorticoids.
Pathophysiology Bronchial Asthma
- There is reduction in airway diameter.
- FEV1 is reduced to less than 40% of predicted. .y Peak expiratory flow rate (PEFR) is less than 40% of predicted.
- There is hypoxia and ventilatory failure.
- There may be hypocapn~ and respiratory alkaI~.
- There may be metabolic acidosis in acute severe asthma.
- There may be cyanosis.
Clinical features Bronchial Asthma
- There is a triad of dyspnoea, cough, wheezing.
- · There is tachypnea, sense of constriction in chest,
- nonproductive cough, wheezing in inspiration and expiration, prolonged expiration, tachycardia”
- systolic hypertension. •
- Anteroposterior diameter of thorax is increased.
- Wheezing is high-pitched and there is loss of an . sOUnds in severe cases.
- Accessory muscles become active.
- There is paradoxical pulse due to large negative intrathoracic pressu re.
- There may be productive cough with mucus often as casts called Curschmann’s spirals. These are laden with eosinophils and Charcot-Leyden crystals.
- Respiration may change from tachypnea to gasping.
- Patient then needs ventilatory support.
Complications Bronchial Asthma
- Spontaneous pneumothorax
- In asthma there is reversible airway obstruction.
- Reversibility is a 15% or more increase of FEV1
- after 2 puffs of beta adrenergic agonist.
- The FEV and PEFR are reduced.
Treatment OF Bronchial Asthma
- Quick relief medications: Beta adrenergic agonists, metQylxanthines, anticholinergics.
- Beta adrenergic agonists :
- These are catecholamines, resorcinols and saligenins.
- Catecholamines e.g. epinephrine, isoproterenol.
- They are short acting and given by inhalation or parenterally.
- Resorsinols e.g. Fenoterol.
- Resorsinols have no cardiac side effects.
- Saligenins e.g. Albuterol (salbutamol).
- Long acting beta 2 agonists e.g. Terbutaline, Salmeterol, Formeterol.
- Methyl xanathines e.g.
- Theophylline Common side-effects of theophylline are nervousness, nausea, vomiting, anorexia, headache and even seizures and cardiac arrhythmias.
Long term control medications:
- Glucocorticoids, long acting beta 2 aganists, mast cell stailizing agents, leukotriene modifiers, methylxanthines.
- Glucocorticoids – have anti-inflammatory and preventive role. Its effects are not immediate and only seen after 6 hrs of administration.
- Prednisone is given 60 mg every 6 hours.
- In acute asthma methyl prednisolone IV 120180 mg is given 6 hrly.
- Inhaled glucocorticoids : These are b.eclomethasone, budesonide, fluticasone.
- Mast cell stabilizing agents: Promolin sodium, Nedocromil sodium. Effective in atopic asthma
- Leukotrine modifiers: These reduce the synthesis of leukotrines. E.g. Zileuton, Zafirlukast, Montelukast.
Miscellaneous agents Bronchial Asthma
- Expectorants, mucolytic agents, IV fluids, tranquilizers.
Approach to a Case of Bronchial Asthma
- · Evaluation of symptoms.
- · Monitoring of respiratory parameters.
- · Avoidance of allergens.
- · For acute cases use short-acting drugs – Inhaled Albuterol, IV Aminophylline.
- Beta 2 agonists every 20 minutes by inhalation for 2 – 3 doses.
- · Anticholinergics like ipratropium may be added.
- · Inhalational agents may be given by jet nebulizer, metered dose inhaler, or dry powder inhalers in acute situations.
- · For respiratory emergency like paradoxical pulse, use of accessory muscles, FEV1 <20% and disturbed arterial blood gases-intensive management, glucocorticoids, ventilatory support may be required.
- ·If PaCO2 is elevated, patients need intensive care. In severe airway obstruction 80% helium and 20% oxygen may be useful.
- For chronic asthma – mast cell stabilizing agents, g1Ucocorticoids, methylxnnthines, long-acting !5eta 2 agonists may be used.
- · Cigarette smoking must be stopped in all asthma patients.