Bronchial Asthma

1. Bronchial Asthma Alena Vlachová

2. Definition Chronic inflammatory disease with inflammation due to complex interaction between inflammatory cells,mediastors and airways cells The chronic inflammationis associated with hyperresponsivenes that leasd to reccurent episodes of wheezing,breathlessness,chest tightess and coughing,particulary at night or in the early morning These epizodes are usually associated with widespread but variable airflow obstruction withing the lung, that is often reversible either spontaneously or with treatment.

3. Airway structure Mucosais composed of epithelial cells that are capable of specialized mucous production and a transport Basement membrane Smooth-muscle matrix extending to the alveolar entrances Predominantly fibrocartilaginous or fibroelastic -supporting connective tissue

4. Cellular elements Mast cells are involved in the complex control of releasing histamine ad other mediators Basophils, eosinophils and macrophages are responsible for extensive mediastors release in the early and late stage bronchial asthma

5. Stretch and irritans receptors Cholinergic motors nerves which innervate the smooth muscle and glandular units

6. Patophysiology is complex involves following components: airway inflammation intermitent airflow obstruction bronchial hyperresponsiveness

7. Airway inflammation Eosinophilic 50% of all patientsmay have atopic history IgE mediated reaction -Th2cell produce cytokines (IL -5,IL-6,IL-4,IL-9,IL-13) eosinophils,epithelial cells, macrophages

8. Airway inflammation Neutrophilic -usually severe asthma -IL-8, matrix-metaloproteinasis -often non immunologic ( smoking, infection) -often irreversible obstruction - poor response to inhal.steroids Paucigranulocytic marker of inflammation does not exist no response to steroids

9. Airflow obstruction Variable : Acute -bronchoconstriction -airway edema -mucus production Airway remodeling during chronic inflammation

10. Bronchial hyperresponsivenes Airflow obstruction ..hyperinflation.. increased intra-alveolar pressure with alteration in circulation ...ventilation-perfusion mismatch ..compensatory vasocontriction in early stage of airflow obstruction : hypoxemia without hypercapnia - respiratory alkalosis later increased work of breathing, increased oxygen consumption: hypoxemia with hypercapnia - respiratory acidosis

11. Etiology Enviromental allergens – house dust mites, animal allergens, fungi... Viral respiratory tract infection Exercise,hyperventilation Gastroesophageal reflux disease Chronic sinusitis or rhinitis Aspirin or nonsteroidal anti-inflammatory drugs,sulfit sensitivity Obesity Enviromentall pollutans,tobacco smoke

12. Etiology Occupational exposure Irritans -eggs,household sprays, paint fumes Various high and low-molecular weight compounds -eggs,nsects,plants, latex, rubber, diisocyanates,anhydrides,wood dust,.. Emotional factors or stress Perinatal factors-prematurity and increased maternal age, maternal smoking,genetics

13. Epidemiology 5-10% of the population 40% asthmatics are smokers! common in industriazed countries prevalence raises in developing countries In US asthma prevalence is higher in black In childhood predominantly in boys (m:f..2:1) 2/3 of asthma cases are diagnosed under the age of 18 After puberty predominantly in females In older than 40 predominantly females

14. Dg and assessment of asthma History– family, occupation, drugs, hobbies,diseases Physical examination Pulmonary function tests Sputum analysis

15. Dg and assesment of asthma Laboratory: blood tests, IgE, ECP, ABG FeNO CXR, CT Examination of upper airways Allergic screening Examination of expired air or sputum: leukotriens ( B4,D4,C4...)

17. Clinical features May be normal Dry cough Shortness of breath Wheezes,classically expiratory Chest tightness Chest deformity / hyperinflation –long-lasting or poorly controlled asthma Severe -life threatening asthma may have no wheezing and a silent chest , tachypnoea, tachycardia or bradycardia, cyanosis,use of accessory respiratory muscles, anxiety, general distress, pulsus paradoxus , exhaustion, confusion or coma. PO2 low to 8kPa,pCO2 up to 5-6 kPa!!!

18. Differential diagnosis of asthma COPD Tumours Upper airway obstruction Thromboembolic disease Vocal cord dysfunction Foreign body aspiration Infection Left heart failure Gastroesophageal reflux disease

19. Vasculitis PAH ILD Hyperventilation sy Cystic fibrosis Differential diagnosis of asthma

20. Classification according to severity Intermittent Mild persistent Moderate persistent Severe persistent Patient with asthma of any level of severity can have mild, moderate or severe exacerbation

21. Pharmacologic management Control agent :inhaled or systematic steroids leucotriens modifiers inhaled cromones long acting bronchodilatators theophylline-long acting anti IgE specific immunoterapy Relief agent: short acting bronchodilatators systemic steroids short acting theophylline

22. Stepwise managementof chronic asthma 1.step:mild intermitent:avoid alergen, RABA on demand 2.step: regular preventive terapy: RABA+ add: ICS or leucotriens modifiers 3.step: RABa +ICS +add LABA or long acting theophylline or leucotrien modifiers RABA + increase ICS 4.step: step 3 + increase ICS + leucotrien modifiers + long acting theophyline 5.step: step 4 + systemic CS + anti IgE

23. Non pharmacologic management Allergen avoidance No smoking ! Dietary factors Weight reduction Physiotherapy - breathing techniques Patient education Bronchial thermoplasty

24. Hospital treatment of acute asthma B2agonists -nebulised 5-10 mg/h Anticholinergic drug- nebulised Steroid IV or oral MgSO4 Theophylline -IV aminophyllin 5mg/kg Antibiotics –in case of infection Rehydratation Oxygen

25. Acute severe asthma Severe bronchospasm refractory to usual treatment Identification of high risk asthmatics : History: Previous life threatening attacs (CO2,intubation) Frequent ER visits Hospitalization in last year Recent steroid use Deterioration on steroids

26. Acute severe asthma Clinical features : HR more than 130,RR more than 25 PEF 33-50% of predicted or best Paradoxical thoracoabdominal motion Silent chest Confusion, lethargy,fatigue Patient can´t speak Bradycardia Respirarory insuficiency

27. Treatment of acute severe asthma Oxygen Beta (2) agonists - in almost all situations inhaled b2 terapy schould be given prior to parenteral (!side effects). But in little airflow parenteral : epinephrine: SC: 0,3-0,5mg q20-30 min IV: 4-8 ucg/min Via ETT: 5 ml of 1:10000 salbutamol : nebulizace 5-10 mgq 15 min 0,1-0,2 ucg/kg/min

28. Treatment of acute severe asthma Anticholinergic agens -in severely obstructed patient drug deposit in the more proximal airways where cholinergic receptorsare located ipratropium MDI 4-9puffs q 15min or cont. atropine IV 20mg /kg -! side effects ! glycopyrrolate IV 10 mg/kg ! Side effects! Corticosteroids -take 4-12 hours to show an effect hydrocortison 10-15mg/kg/day- 500 mg =metylprednisolone 40-120 mg 4-6 h

29. Treatment of severe acute asthma Theophyllines : loading dose 3-6 mg/kg, IV 0,2-0,9 mg/kg/hr !side effects ! Magnesium sulfate: 10-12 mmol/20 min

30. Intubationdecision Progressive exhaustion Respiratory arrest Decreased level of consciousness Persistent respiratory acidosis (pH <7,2) Hypoxemia (SaO2 < 90%) Hypercapnia is not indication for intubation ?-studies show improvement after aggresive use of bronchodilatators

31. Alternative treatments of severe acute asthma Volatile anestetics Heliox ECMO Pulmonary lavage