Bronchial Asthma PDF

Bronchial Asthma Epidemiology ◼ Affects between 10-15 % of people in Europe, UK, New Zealand, Australia and US; incidence is increasing worldwide. Although it is much less in China, Malaysia, Africa etc. ◼ Peak age of onset is under 5 years ◼ There is an allergic component in 1/3 to ½ of all case...

Bronchial Asthma Epidemiology ◼ Affects between 10-15 % of people in Europe, UK, New Zealand, Australia and US; incidence is increasing worldwide. Although it is much less in China, Malaysia, Africa etc. ◼ Peak age of onset is under 5 years ◼ There is an allergic component in 1/3 to ½ of all cases ◼ About 2000 patients die from asthma in UK each year; many deaths are preventable In Malaysia, asthma affects children and has high prevalence in urban areas. The estimated asthma prevalence in Malaysia had increased from 6.4-9.4% in children aged 6-7 years old and from 9-13% in children aged 13-14 years old. Introduction: STILL a CHALLENGE to TREAT ? Definition In the recent Global Initiative for Asthma (GINA) Guidelines 1 asthma is defined as follows: a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation causes an associated increase in airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible, either spontaneously or with treatment. Definition ◼ Chronic inflammatory disorder of the airways, presents with reversible airflow obstruction causing cough, wheeze, chest tightness and shortness of breath ◼ In chronic asthma the bronchial wall inflammation may lead to irreversible obstruction of airflow ◼ airflow limitation ◼ airway hyperresponsiveness ◼ inflammation of the bronchi Aetiology and types ◼ Early onset ( extrinsic / atopic) asthma ◼ Late onset (idiopathic / non- atopic adult) asthma Trigger factors ◼ URTI ◼ Dust ◼ Pets-cats ◼ Exercise ◼ Cold air ◼ Laughter / Emotional stress ◼ Irritants (smoke, chemical fumes) ◼ Drugs (Beta blockers, NSAIDs) ◼ Industrial causes Airway inflammation ◼ Eosinophils, lymphocytes, mast cells, neutrophils ◼ Submucosal oedema ◼ Smooth muscle hypertrophy and hyperplasia ◼ Thickening of basement membrane ◼ Mucous plugging in the lumen ◼ Epithelial damage Clinical features ◼ Cough - may be the only symptom ◼ Breathlessness - Wheeze ◼ Worse at night and will feel tight in the morning –diurnal variation Case History HOPI should elicit the typical symptoms of asthma: wheeze, cough and breathlessness.?cause of acute attack Chronic History • Duration of asthma • Allergic history • Severity of asthma- frequency of attacks / how often pt. uses his rescue inhaler • Control : nocturnal attacks, daytime symptoms • Past admissions/ICU? • Treatment history ; compliance • Home and occupational environment • Progress of disease Physical Examination Vital Pulse Rate Increased heart rate in acute severe episode Pulsus paradoxus (a fall of SBP between 10-20mmHg during inspiration) in moderately severe episode Respiratory Rate Increased respiratory rate greater than 30 cycles per minute in moderately severe and acute severe episodes Skin Profuse sweating in imminent respiratory failure Severe hypoxia resulting in central cyanosis and hypoventilation in imminent respiratory failure Eyes Conjunctival congestion as a consequence of constant rubbing are suggestive of associated allergic rhinitis. Nose Nasal examination is mandatory to rule out associated conditions such as, aspirin sensitivity or allergic rhinitis. Use of accessory muscles of respiration such as sternocleidomastoid and scalene muscles Loud prolonged expiratory wheeze In between attacks, chest is clear and no abnormal physical signs may be detectable. Presentation ◼ acute asthma ◼ Chronic asthma – episodic ◼ ◼ ◼ mild moderate severe ACUTE ASTHMA Life threatening attack Severe acute asthma Moderately severe Mild attack Life threatening ◼ Cannot speak ◼ Central cyanosis ◼ Exhaustion, confusion, reduced conscious level ◼ Bradycardia ◼ Silent chest ◼ Unrecordable PEF ◼ ABG : Normal / high CO2, Hypoxemia (< 8 kPa), Low pH Indications for assisted ventilation ◼ Coma ◼ Respiratory arrest ◼ Exhaustion, confusion, drowsiness ◼ Deterioration of arterial blood gas tensions despite optimal therapy: PaO2 < 60 mm Hg and falling PaCO2 > 45 mm Hg and rising pH < 7.3 and falling Causes of death ◼ Mucus plug( eosinophils, epithelial cells, and bronchial casts) obstructing the airway ◼ Patient exhausted by prolonged attack leading to alveolar hypoventilation and severe arterial hypoxemia Mucous plug Acute severe asthma Assessment : Severe: ◼ Pulse rate > 110 / min ◼Pulsus paradoxus Systolic blood pressure normally falls during quiet inspiration in normal individuals. Pulsus paradoxus is defined as a fall of systolic blood pressure of >10 mmHg during the inspiratory phase. ◼ Unable to speak in sentences ◼ PEF < 50% of expected Nebuliser and Oxygen therapy Treatment of acute attack Nebulised Beta 2 agonist every 15-30 minutes, reduce to 4 hourly once clear Refractory cases: Ipratropium bromide 0.5 mg added to nebulised Beta 2 –agonist IV Hydrocortisone 200 mg 6 hourly / methyl pred. intravenous magnesium sulfate was given as a single dose of 1.2 g or 2 g over 15 to 30 minutes Aminophylline infusion or i.v. Salbutamol or terbutaline clinical response General ◼ Hydration, nutrition ◼ Avoid drugs like sedatives ◼ Antibiotics Monitoring ◼ Vital signs, conscious level, PEF ◼ ABG / Pulse oximetry ◼ Serum theophylline level ◼ S. potassium, glucose Investigations CXR: ◼ Normal / Hyperinflation, ◼ Collapse due to mucous plug, ◼ Transient infiltrates (eosinophilia), ◼ Pneumothorax Blood: ◼ FBC infection ◼ Eosinophilia ◼ ABG during acute attack Tests for specific hypersensitivity ◼ Skin testing: Intradermal / Modified prick skin test ◼ Increased serum Ig E ◼ Bronchial challenge: Exercise test / Histamine or Methacholine bronchial provocation test / occupational exposure test Skin test PEF meter The peak expiratory flow, The peak expiratory flow, also called peak expiratory flow rate, is a person's maximum speed of expiration, as measured with a peak flow meter, a small, hand-held device used to monitor a person's ability to breathe out air MANAGEMENT of CHRONIC ASTHMA Drugs ◼ Beta 2 adrenoceptor agonists SABA/ LABA ◼ Anticholinergics ◼ Corticosteroids ◼ Theophylline / Aminophylline ( phosphodiesterase inhibitors) ◼ Leukotriene antagonists ◼ Disodium cromoglycate (mast cell stabiliser) Drugs ◼ Relief drugs- rescue inhalers (bronchodilators) ◼ Prevention /contollers (inhaled corticosteroids/LABA /muscarinic) ◼ Reserve (oral prednisolone) CHRONIC ASTHMA SEVERITY intermittent mild moderate severe symptoms <2days/wk >2days/wk daily Through day Limitation of activity none minor some extreme SABA use ≤ 2 days/week daily > 2 days/week but not Daily Several times a day Night time awakening 0 3–4x/month > 1x/week treatment Step 1 Step 3 Step 4/5 1–2x/month Step 2 ASTHMA Education ! NEGLECTED issue !! SPACE HALER or INHALER ? JUGGALARY of Treatment OPTIONS ! Short course oral corticosteroid ◼ Prednisolone 30-60 mg / day, each morning until 2 days after control is re-established Indications: ◼ Symptoms and PEF progressively worsening ◼ Fall of PEF below 60% of personal best ◼ Onset or worsening of sleep disturbance by asthma ◼ Persistence of morning symptoms until midday ◼ Progressively diminished response to an inhaled bronchodilator Prognosis ◼ Generally good; occasional fatal outcome if treatment is inadequate or delayed ◼ About 50% of children grow out of their asthma in early adult life ◼ Late onset asthma is almost always chronic, more severe and needs aggressive treatment ◼ Atopic asthma – Worse in summer ◼ Chronic asthma – Worse in winter Which of the following is NOT a characteristic of asthma? a Increase in IgG immunoglobulins b Airway hyperresponsiveness c Infiltration of eosinophils into the airways d Increased mucus production. Chronic asthma is associated with a activation of eosinophils b activation of TH1 lymphocytes c reduced function of goblet cells d decreased permeability of submucosal capillaries. Which drug is the most commonly prescribed preventer therapy in asthma? a β2-adrenoreceptor agonists b Xanthines such as theophylline c Muscarinic receptor antagonists d Inhaled steroids. Thank You Most common cause of a chronic slightly productive cough in the adult population is: A. B. C. D. Asthma Chronic bronchial inflammation Heart failure None of the above