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Asthma

Asthma. SS Visser, Lung Unit, UP. Contents. Definition Disease Pattern Prevalence Mortality Etiology Pathogenesis Triggers of acute attacks. Contents. Pathophysiology Manifestations of Resp failure Diagnosis: clinical,physiologic,immunologic and radiologic Differential diagnosis

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Asthma

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  1. Asthma SS Visser, Lung Unit, UP

  2. Contents • Definition • Disease Pattern • Prevalence • Mortality • Etiology • Pathogenesis • Triggers of acute attacks

  3. Contents • Pathophysiology • Manifestations of Resp failure • Diagnosis: clinical,physiologic,immunologic and radiologic • Differential diagnosis • Management

  4. Definition • Chronic inflammatory disease of airways (AW) •  responsiveness of tracheobronchial tree • Physiologic manifestation: AW narrowing relieved spontaneously or with BD  Cster • Clinical manifestations: a triad of paroxysms of cough, dyspnea and wheezing.

  5. Disease Pattern • Episodic --- acute exacerbations interspersed with symptom-free periods • Chronic --- daily AW obstruction which may be mild, moderate or severe  superimposed acute exacerbations • Life-threatening--- slow-onset or fast-onset (fatal within 2 hours)

  6. Prevalence • All ages, predominantly early life • Adults: 2-5% population • Children: 15% population • 50% dx <10y,85% dx <40y, 15% dx > 40y • 2:1 male/female preponderance in childhood

  7. Mortality • Fatal asthma 1-7% asthmatics • ing death rate ?abuse of inhaled BDs • Risks for death:previous life-threatening asthma, severe disease, recent hospitalization or emergency room Rx, non-compliant and confusion re Rx, under- treatment with Corticosteroids, discontinued Rx, severe AW hyperreactivity.

  8. Etiology • Allergic/atopic/early onset asthma---rhinitis, urticaria,eczema,(+)skin tests,IgE,(+) response to provocation tests with aeroallergens. • Idiosyncratic/non-atopic/late onset asthma--- no allergic diseases,(-)skin tests,normal IgE, symptoms when upper resp infection, sx lasting days or months. • Mixed group---usually onset later in life

  9. Pathogenesis - 1 • Non-specific AW hyperreactivity: Sx more severe & persistent Nocturnal  early awakening with dyspnea diurnal fluctuation in lung function Unstable lung function  BD response,  therapeutic needs • Cause of hyperreactivity = inflammation

  10. Pathogenesis - 2 • Dual AW response to AG challenge 1.Early bronchospastic response- type1reaction within min after IH of AG: Mechanism: IH of aeroallergensensitizatiom formation of IgE & expression on mast cells re-exposure to AG mast cell degranulation & mediator release bronchospasm

  11. Pathogenesis - 3 2.Late-bronchospastic reaction: in 30-50%, 6-10 hours after AG exposure. Minority only a late response Mechanism: recruitment of E, N, L and macro-phagesrelease lipid mediators(PG E2, F2 ,D2; LT C,D,E , PAF), O2radicals, toxic granule proteins, cytokines (TH1:IL-2, IFN; TH2: IL-4, IL-5) bronchoconstriction, vascular congestion, mucosal edema, mucus production, mucociliary transport.

  12. Pathogenesis - 4 • Chronic asthmatic response: Destruction of AW epithelium by toxic granule contentsepithelial shedding into bronchial lumen exposure of sensory nerve endings and imbalance in cholinergic and peptidergic neuronal control AW remodelling with subendothelial fibrosis, goblet cell hyperplasia, smooth muscle hyper- trophy, vascular changes fixed AW obstruction.

  13. Allergens - pollen Pharmacol stimuli such as aspirin, NSAIDS, - adrenergic blockers, preservatives,col agent Environment pollution- ozone, SO2, NO2 Occupational- metal salts, biol enzymes Infection- resp viruses Exercise –IH cold dry airthermally-induced hyperemia and micro-vascular engorgement Emotional stress Triggers of acute asthmatic episodes

  14. Pathophysiology • Reduction in AW diameterAW resistance  FeV and flow rates hyperinflation work of breathing altered respiratory muscle Fx and elastic recoil abnormal ventilation • Vascular congestion and edema of bronchial walls abnormal perfusion • V/P mismatch altered blood gases hypoxemia and hypocapnia with respiratory alkalosis, but with impending ventilatory failure  normocapnia and later hypercapnia and respiratory acidosis

  15. Manifestations of respiratory failure • Hypoxemia: cyanosis- very late sign, not dependable • Hypercapnia: sweating, tachycardia,widened pulse pressure • Acidosis: tachypnea • Blood gases the only accurate assessment of ventilatory status

  16. DIAGNOSIS : CLINICAL • Episodic asthma: Paroxysms of wheeze, dyspnoea and cough, asymptomatic between attacks. • Acute severe asthma: Upright position, use accessory resp muscles, can’t complete sentences in one breath, tachypnea > 25/min, tachycardia > 110/min, PEF < 50% of pred or best, pulsus paradoxus, chest hyperresonant, prolonged expiration, breath sounds decreased, inspiratory and expiratory rhonchi, cough.

  17. DIAGNOSIS : CLINICAL • Life-threatening features: PEF < 33% of pred or best, silent chest, cyanosis, bradycardia, hypotension, feeble respiratory effort, exhaustion, confusion, coma, PaO2 < 60, PCO2 normal or increased, acidosis (low pH or high [H+]). • Chronic asthma: Dyspnea on exertion, wheeze, chest tightness and cough on daily basis, usually at night and early morning; intercurrent acute severe asthma (exacerbations) and productive cough (mucoid sputum), recurrent respir-atory infection, expiratory rhonchi throughout and accentuated on forced expiration.

  18. DIAGNOSIS : PHYSIOLOGIC • Demonstration of variable airflow obstruction with reversibility by means of FEV1 and PEF measurement (spirometer and peak flow meter). • FEV1 < 80% of pred – PEF < 80% of pred. • Reversibility: A good bronchodilator response is a 12% and 200ml improvement in FEV1 20 min after inhalation of 200ug salbutamol (2 puffs). • Diurnal peak flow variation: Normal variation: Morning PEF 15% lower than evening PEF. With asthma this variation is > 15% (morning dipping).

  19. DIAGNOSIS : PHYSIOLOGIC • Provocation studies: (a) Exercise: A 15% drop in FEV1 post exercise indicates exercise induced asthma. (b) Metacholine challenge: A 20% reduction in FEV1 at Metacholine concentrations < 8mg/ml indicates bronchial hyperreactivity. This is expressed as a PC20 value of eg 0.5mg/ml (= a 20% reduction in FEV1 at 0.5mg/ml Metacholine).

  20. DIAGNOSIS : IMMUNOLOGIC • Skin prick wheal and flare response. • IgE and RAST. • Eosinophil cationic protein (ECP). • Peripheral blood and sputum eosinophilia.

  21. DIAGNOSIS : RADIOLOGY • Chest XR may be normal between attacks. • With attacks hyperinflation may be found. • In complicated asthma segmental lobar collapse (mucous plugs) and pneumothorax can occur.

  22. DIFFERENTIAL DIAGNOSIS • Upper airway obstruction – glottic dysfunction. • Acute LV failure – pulmonary oedema. • Pulmonary embolism. • Endobronchial disease. • Chronic bronchitis. • Eosinophilic pneumonia. • Carsinoid syndrome. • Vasculitis.

  23. MANAGEMENT 1 • Avoidance of allergen and triggers – may be impractical  adjust Rx. • Occasional asthma: Rarely symptomatic  2 agonist prn. • Mild intermittent asthma (episodic): 2 agonist prn + low dose IH corticosteroid. • Mild persistent asthma: 2 agonist prn + high dose IH corticosteroid or long acting 2 agonist + low dose IH corticosteroid. • Moderate persistent asthma: 2 agonist prn + high dose IH corticosteroid + long acting 2 agonist or SR theophylline.

  24. MANAGEMENT 2 • Severe, persistent asthma 2 agonist prn + high dose IH corticosteroid + long acting 2 agonist + SR Theophylline + oral corticosteroids. • Step up: If uncontrolled at any severity level, oral steroids – Prednisone 30-40-mg/day for 7-14 days. • Step down: When stable for at least 3 months – reduce or stop oral steroids first. • Leukotriene antagonists: for patients with aspirin/NSAIDS induced asthma. May also be added on for severe persistent asthma or in pts with steroid related side effects such as growth retardation or non-responsiveness to IHS or to allow low dose IHS instead of high dose.

  25. MANAGEMENT 3 • Acute severe asthma: 1. Immediate Rx: O2 40-60% via mask or cannula + 2 agonist (salbutamol 5mg) via nebulizer + Prednisone tab 30-60mg and/or hydrocortisone 200mg IV. With life-threatening features add 0.5mg ipratropium to nebulized 2 agonist + Aminophyllin 250mg IV over 20 min orsalbutamol 250ug over 10 min. 2. Subsequent Rx: Nebulized 2 agonist 6 hourly + Prednisone 30-60mg daily or hydrocortisone 200mg 6 hourly IV + 40-60% O2.

  26. MANAGEMENT 4 • No improvement after 15-30 min: Nebulized 2 agonist every 15-30 min + Ipratropium. • Still no improvement: Aminophyllin infusion 750mg/24H (small pt), 1 500mg/24H (large pt), oralternatively salbutamol infusion. • Monitor Rx: Aminophyllin blood levels + PEF after 15-30 min + oxymetry (maintain SaO2 > 90) + repeat blood gases after 2 hrs if initial PaO2 < 60, PaCO2 normal or raised and patient deteriorates. • Deterioration: ICU, intubate, ventilate + muscle relaxant.

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