Obstructive Airway Disease

1. Obstructive Airway Disease Dr. Khalid Al-Mobaireek King Khalid University Hospital

2. Obstructive airway Disease: • Obstructive diseases are worse during expiration in the thoracic cavity • During inspiration, we have negative pleural pressure leading to airway expansion, and with expiration the opposite happens leading to narrowing of the airways. Therefore, obstructive diseases are worse on expiration. • Reversible = Asthma • Irreversible: Bronchiectasis because the membrane is destroyed therefore the obstruction is permanent. They present with productive cough with high amount of sputum that are more in the morning with clubbing (indicating pus formation). • very important to know if its localized or systemic (diffuse) • Localized: very important to know if its localized or systemic. • Anatomical defect • Airway: Internal, External, • Parenchymal • Examples: foreign body, a lymph node compressing the airway or vascular problem compressing a segment, or a systemic disease starting as local.

3. Diffuse: • Aspiration • Muco-ciliary clearance: primary ciliary dyskinesia (PCD) is an autosomal recessive disease where the ciliary function (clearance of mucous) is impaired and do not have good coordination, with normal mucous secretions. They are at increased risk of bronchiectasis. 50% have kartegner’s syndrome. CF very thick and sticky secretions,, cilia and cough can not clear it out it’s the worse than PCD • Immune deficiency because of recurrent infections. • Post-infectious: Pertussis, TB, adenovirus.. • Swallowing difficulties: Neuromuscular disease, GERD, and congenital defects e.g. palate diseases or congenital defect in the cartilage, T-E fistula. These can cause aspiration leading to bilateral bronchiectasis. • Congenital bronchiatasis born with abnormal cartilage.

4. Bronchiectasis: CT is the diagnostic method of choice, characteristic finding is signet ring appearance. Normally each bronchus is accompanied by a vessel and shouldn’t exceed the vessel diameter. In bronchiectasis, the diameter of the bronchus is larger than that of the vessel. Tram line appearance (two airways running in parallel lines) in cross section.

5. Definition of Asthma • A chronic inflammatory disorder of the airways • Many cells and cellular elements play a role • Chronic inflammation is associated with airway hyper-responsiveness to minor stimuli that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing • Widespread, variable, and often reversible airflow limitation recurrent disease. • The commonest chronic disease in children.

6. Bronchospasm Edema, Mucus Hyper-responsiveness INFLAMMATION!!! (hallmark)

7. Source: Peter J. Barnes, MD Asthma Inflammation: Cells and Mediators

8. Asthma Inflammation: Cells and Mediators Source: Peter J. Barnes, MD

10. NORMAL ASTHMA

12. AIR TRAPPING INSP EXP

13. Air trapping leads to enlargement of the alveoli, if these ruptured the air will leak leading to pneumothorax and air under the skin (sub-cutaneous emphysema). In inspiration the airway pressure is negative and the outside pressure is positive therefore the airway expands and dilate. The opposite happens during expiration and the airways get narrowed. If the obstruction was intra-thoracic, the obstruction will be more evident during expiration (extra-luminal pressure higher than intra-luminal pressure during expiration), because airway will be narrowed and the pressure is positive inside the airway. While obstruction outside the thoracic cavity will be more evident during inspiration (extra-luminal pressure higher than intra-luminal pressure during inspiration e.g. vocal cord paralysis). If the manifestations are present equally in both phases think of sub-glottic stenosis.

14. Ventilation Perfusion (V/Q) Mismatch There will be V/Q mismatch because the blood coming to the lung is not being oxygenized due to obstruction.

15. Burden of Asthma • Asthma is one of the most common chronic diseases worldwide with an estimated 300 million affected individuals • Prevalence increasing in many countries, especially in children almost 1 in 6 are affected. • A major cause of school/work absence

16. Asthma Prevalence 10 - 15%

17. Asthma Prevalence

18. Qaseem 13% Khobar 6% Riyadh 10 % Jeddah 13% Abha 17%

19. Factors that Influence Asthma Development and Expression • Host Factors • Genetic - Atopy- hygiene hypothesis (decreases the use of the immune system (TH1) due to excessive hygiene and indoor life). - Airway hyper-responsiveness • Gender in children males more common unlike adults. • Obesity • Environmental Factors • Indoor allergens are biological and not dose dependent. • Outdoor allergens • Occupational sensitizers (low dose stimulate asthmatics whereas high dose will stimulate asthmatics and non-asthmatics • Tobacco smoke • Air Pollution • Respiratory Infections • Diet

20. Environmental Allergens and Childhood Asthma • Dust mites: fecal material are small enough to pass through the covering of the pillow. Treatment is by air-tight seal of sheets. • Furry pets: isolate the patient from the pet to assure the diagnosis. • Molds • Cockroaches: • Cigarette Smoking: 1st hand, 2nd hand, and 3rd hand from remnant on furniture and from cars. Therefore, smoke in an open space.

21. POLLENS

22. Management of Chronic Asthma • Depends on • Exacerbations and attacks. • Exacerbations requiring steroids. • Night symptoms: how many times you wake up from sleep due to symptoms (if more than twice a month, it is uncontrolled). • Symptoms: cough, etc. • Use of bronchodilators.

23. History • Symptoms (cough, wheeze, SOB) Wheeze: not every patient with a wheeze has asthma. A 2 or 3 months child who has similar asthma symptoms you need to check for structural abnormality compressing the airways as cystic disease. Foreign body is suspected when the child presents with sudden acute cough and wheeze worse in expiration, it needs index of suspicion, when you do CXR the expiratory film will show failure of emptying in the obstructed side (one is larger than the other but you won’t see the obstruction itself) the bronchoscopy is diagnostic and therapeutic. • Onset, duration, frequency and severity • Activity and nocturnal exacerbation • Previous therapy • Triggers • Other atopies • Family history • Environmental history, SMOKING • Systemic review (widen your DDx)

24. Physical Examination • Most important is growth parameter asthma usually doesn’t impair growth if it did then think of another diagnosis as cystic fibrosis or immunological problem (immunodeficiency) . • ENT part of respiratory problem because it is lined by ciliary epithelium examine the ear if there was a ciliary problem the ear will be effected. • Features of atopy. • Chest findings • PEF • Check for clubbing its present its unlikely asthma, think of other suppurative diseases. The diagnosis of asthma should depend on history and examination.

25. Investigations • Don’t usually need investigations, and is mainly history and physical to role out other systemic diseases. • Pulmonary Function Test • Chest X ray: not done except in the suspicion of another disease or severe asthmatics. • Allergy testing in some • PFT is only complementary and is not done to children less than six years.

26. Skin Testing

27. Differential Diagnosis • Infections • Congenital Heart Disease • Foreign body are mostly food because they can’t grind due to lack of molars and are not radio-opaque by CXR, but you see its effect during expiration CXR will show and emptying of one lung only. However, foreign body in the esophagus is not food and tends to be radio-opaque. • GERD • Bronchopulmonary dysplasia • Structural anomalies (any child with severe asthma at the age of 3-4 months think of something else like structural problems because asthma doesn’t start severe early in its course.

29. Levels of Asthma Control

30. REDUCE TREATMENT OF ACTION LEVEL OF CONTROL maintain and find lowest controlling step controlled consider stepping up to gain control partly controlled uncontrolled step up until controlled INCREASE exacerbation treat as exacerbation REDUCE INCREASE TREATMENT STEPS STEP 1 STEP 2 STEP 3 STEP 4 STEP 5

32. Treatment objectives • Achieve and maintain control of symptoms • Maintain normal activity levels, including exercise • Maintain pulmonary function as close to normal levels as possible • Prevent asthma exacerbations • Avoid adverse effects from asthma medications • Prevent asthma mortality • Because asthma is a chronic condition, it usually requires continuous medical care • The primary aim of treatment is control of asthma. According to the GINA guidelines, control is defined in terms of absence of symptoms (acute and chronic), need to use reliever therapy, lung function and freedom from restrictions on physical activity GINA Guidelines 2006

33. Pharmacological therapy • Relievers • Inhaled fast-acting 2-agonists • Inhaled anticholinergics • Theophylline : not used anymore as a relievers coz very toxic and have a low therapeutic index can lead to seizures. • Controllers • Inhaled corticosteroids are good because they are broad spectrum affecting the different inflammatory cells and mediators. • Inhaled long-acting 2-agonists ( never used alone coz of increase mortality must be combined with corticosteroids) • Inhaled cromones not used any more. • Oral anti-leukotrienes (monateleucast singular) • Oral theophyllines • Oral corticosteroids

34. Why don’t patients comply with treatment? A common cause of non-controlled asthma is non-compliance. Therefore, before changing medication check for compliance (60% are non-compliant) • Unintentional • Forget treatment • Misunderstand regimen / lack information • Unable to use their inhaler • Run out of medication • Intentional • Feel better • Fear of side effects • Don’t notice any benefit • Fear of addiction • Fear of being seen as an invalid • Too complex regimen • Can’t afford medication

35. Cromolyn Sodium • Non-steroidal anti- inflammatory • Weak action on Early and late phases • Slow onset of action • If no response in 6 weeks change to ICS • Side effects: Irritation

36. Inhaled Corticosteroids • Effective in most cases • Safe especially at low doses • The anti-inflammatory of choice in asthma ( drug of choice coz they are broad spectrum so they target many cells and mediators)

37. Laitinen LA

38. Inhaled Steroids Side Effects • No systemic side effects with inhaled steroids , candida infection may occur. • Growth: No significant effect at low to moderate doses. • Bones: not important • HPA axis: No serious clinical effect (high doses) • Alteration of glucose and lipid metabolism: Clinical significant is unclear (high doses) • Cataract: No increase risk • Skin: Purpura, easily bruising, dermal thinning • Local side effects

41. MANAGEMENT OF ACUTE ASTHMA

42. Assessment: History • Symptoms • Previous attacks • Prior therapy • Triggers

43. Physical examination: Signs of airway obstruction: • Fragmented speech • Unable to tolerate recumbent position prefer to sit in order to use accessory muscles. • Expiration > 4 seconds • Tachycardia, tachypnea and hypotension • Use of accessory muscles • Pulsus paradoxus > 10 mmHg • Silent hyper=inflated chest • Air leak • Wheezing is a poor sign of obstruction.

44. Physical examination: Signs of tissue hypoxia: • Cyanosis • Cardiac arrhythmia and hypotension (due to increase in thoracic pressure causing a decrease in venous return and consequently hypotension). • Restlessness, confusion, drowsiness and obtundation

45. Physical examination: Signs of Respiratory muscles fatigue: • Increase respiratory rate • Respiratory alterans (alteration between thoracic and abdominal muscles during inspiration) • Abdominal paradox (inward movement of the abdomen during inspiration)

46. Investigations: • Investigations do not help in acute asthma, and blood gases are rarely done except in severe cases • Peak expiratory flow rate • Pulse oximetry • ABG ( its very painful) • CXR • CBC will show leukocytosis because it’s an inflammation. ONLY IN FEW CASES Only done in severe cases X

47. The First Hour

48. Oxygen • Hypoxemia is common • It worsens airway hyperreactivity • Monitor saturation

49. Inhaled β2 agonist Every 20 minutes in the first hour ( 6-8 puffs ) Assess after each nebulizer -better than nebulizer because it’s more localized, less side effects and faster onset of action.

50. Steroids • Do not wait for inhaled B2 agonist response, start immediately on suspicion with oral steroids because it takes 3-4 hours to work. • If not responding to the β agonist • If severe in the beginning • If on PO prednisolone or high dose inhaled steroids. • Previous severe attacks