Asthma and status asthmaticus

This presentation contains a summary of the pathophysiology, clinical features and mainstay management of both asthma and acute severe asthma.

1. Asthma and status asthmaticus Presentor : Hosanna W Asfaw

2. Outline Asthma definition Epidemiology Risk factors Pathogenesis Clinical features Diagnosis Status asthmaticus Treatment

3. Definition by the Global Initiative in Asthma (GINA) “ a heterogeneous disease, usually characterized by airway inflammation . It is defined by the presence of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity , together with variable expiratory airflow limitation. ”

4. Epidemiology affects approximately 300 million people worldwide (Harrisons 19E) can present at any age, with a peak age of 3 years . In childhood , M:F ration is 2: 1 By adulthood the sex ratio has equalized

5. Characterized by Airway hyperesponsiveness Airway inflammation Reversible airway obstruction

6. Risk factors

7. Triggers Atopy allergic rhinitis (80%) atopic dermatitis (eczema ) Genetic predisposition Determines severity, is polygenic Novel genes: ADAM -33 , and DPP-10 Infections Atypical bacteria, such as Mycoplasma and Chlamydophila

8. Triggers Obesity BMI> 30 kg/ m 2 more difficult to control Others Air pollution Cold air In utero exposure to environmental tobacco smoke Pharmacologic agents ( ẞ blockers)

9. Hygiene hypothesis

10. Typical of asthma GINA

11. I ncrease the probability >1 sx ( wheeze, shortness of breath, cough, chest tightness ) Symptoms often worse at night or in the early morning Symptoms vary over time and in intensity Symptoms are triggered by viral infections (colds), exercise, allergen exposure, changes in weather, laughter, or irritants

12. D ecrease the probability Isolated cough Chronic production of sputum SOB associated with dizziness, light-headedness or peripheral tingling ( paresthesia ) Chest pain Exercise-induced dyspnea with noisy inspiration.

13. Pathogenesis

14. P henotypes

15. Phenotypes Allergic asthma : starts in past and/or family history of allergic disease such as eczema, allergic rhinitis, or food or drug allergy. Examination of the induced sputum reveals eosinophilic airway inflammation Respond well ( ICS) treatment. Non-allergic asthma : Sputum neutrophilic , eosinophilic or contain only a few inflammatory cells Respond less well to ICS.

16. Phenotypes Late-onset asthma particularly women non-allergic require higher doses of ICS or are refractory to corticosteroid treatment. Asthma with fixed airflow limitation : some patients with long-standing asthma develop fixed airflow limitation that is thought to be due to airway wall remodeling. Asthma with obesity : obese patients have prominent respiratory symptoms little eosinophilic airway inflammation.

17. D iagnosis

18. Clinical features classically present with a history of episodes of coughing, chest tightness, shortness of breath, and wheezing onset of symptoms with specific triggers Family history  Social history home characteristics, smoking, workplace or school characteristics, educational level, social support, non-adherence of asthma medications, and illicit drug use .

19. Prodromal symptoms Prodromal symptoms may precede an attack Itching under the chin discomfort b/n scapula unexplained fear.

20. Physical findings Hyperexpansion of the thorax Wheezing during normal breathing Prolonged phase of forced exhalation Increased nasal secretion, mucosal swelling, and/or nasal polyps Atopic dermatitis/eczema

21. Investigations Lung function tests Spirometry  forced expiratory volume in 1 second (FEV 1 ) FEV 1 /FVC < 0.7 generally defines obstruction.  peak expiratory flow (PEF) Reversibility increase in FEV1 of ≥12% or >200 mL after inhalation of a short-acting bronchodilator Flow volume loop

22. Investigations

23. Investigations Provocation studies airway hyperresponsiveness Metacholine / histamine challenge A 20 % reduction in FEV1 Exhaled NO – to measure air way inflammation Total serum IgE and specific IgE to inhaled allergens Skin prick test to common inhalant allergens

24. Investigations Airway Hyperresponsiveness Methacholine or histamine challenge Laboratory tests: not usually helpful Blood eosinophilia Sputum eosinophilia  Serum IgE levels Chest X- ray: usually normal, may show hyperinflated lungs Exhaled nitric oxide (F E NO ) Allergy skin testing

25. Differential diagnosis Upper airway obstruction  flow-volume loop Endobronchial obstruction Vocal cord dysfunction COPD Congestive heart failure Pulmonary embolism Pulmonary infiltration with eosinophilia Cough secondary to drugs ( e.g.,ACE inhibitors )

26. Condition Characteristics COPD Airway obstruction is less reversible; typically seen in older patients with smoking history Vocal cord dysfunction Abrupt onset and end of symptoms; monophonic wheeze; more common in younger patients; confirm with laryngoscopy or flow-volume loop Heart failure Dyspnea and often wheezing; crackles on auscultation; limited response to asthma therapy; cardiomegaly; edema Bronchiectasis Cough productive of large amount of purulent sputum; rhonchi and crackles are common; may have wheezing and clubbing; confirmed by CT imaging ABPA Recurrent infiltrates on chest radiograph; eosinophilia; positive skin testing to Aspergillus antigens, high IgE levels Mechanical obstruction More localized wheezing; if central in location, flow-volume loop may provide a clue Eosinophilic granulomatosis with polyangiitis  Autoimmune small-vessel vasculitis presents with peripheral eosinophilia, lung symptoms similar to asthma

27. T reatment

28. BRONCHODILATOR THERAPIES ẞ 2 - Agonists  Relax airway smooth-muscle cells No effects on inflammatory cells  SABAs: 3–6 h Salbutamole - useful in preventing EIA if taken prior to exercise   LABAs: >12h salmeterol  and  formoterol (Important to use ICS when LABAs are given Anticholinergics prevent cholinergic nerve-induced bronchoconstriction and mucus secretion. once- daily tiotropium bromide Theophylline- Side Effects

29. C ONTROLLER THERAPIES Inhaled corticosteroids (ICSs) Most effective controllers for asthma Anti-inflammatory ↑ expression of β 2 -receptors Reduce AHR First-line therapy for patients with persistent asthma Local side effects hoarseness (dysphonia) oral candidiasis Antileukotrienes , Cromones , Anti- IgE

30. Intermittent Persistent Components of Severity Mild Moderate Severe Symptoms ≤2 days/week >2 days/week but not daily Daily Throughout the day Nighttime awakenings ≤2 ×/month 3-4 ×/month >1 ×/week but not nightly Often 7 ×/week SABA use for symptom control  ≤2 days/week >2 days/week but not more than 1 ×/d Daily Several times a day Lung function FEV 1  ≥80% of predicted FEV 1 /FVC normal FEV 1  ≥80% of predicted FEV 1 /FVC normal FEV 1  ≥60% but <80% of predicted FEV 1  <60% of predicted Exacerbations 0-1/year >2/year >2/year >2/year

31. Stepwise approach to asthma therapy

32. ACUTE SEVERE ASTHMA Also known as STATUS ASTHMATICUS

33. Acute Severe Asthma Formerly known as status asthmaticus Acute exacerbation of asthma that does not respond to standard treatment (Bronchodilators, inhalers, steroids) Medical emergency

34. Causes 50% due to URTIs Non adherence NSAID exposure in ASA-allergic patients Allergen exposure Irritant inhalation

35. Clinical features Chest tightness, wheezing, use of accessory muscles and dyspnea that are often not or poorly relieved by their usual reliever inhaler breathless that they are unable to complete sentences cyanotic

36. Clinical features General appearance: alteration of consciousness fatigue upright posture diaphoresis Respiratory system tachypnea (>30\min) use of accessory muscles for breathing reduced respiratory excursion diffuse expiratory wheezing Cyanotic

37. Clinical features Cardiovascular system Tachycardia (>120/min) pulsus paradoxus SPIROMETRY PEFR < 120L /MIN FEV 1 < 1L Arterial blood gas analysis hypercapnia or normal CXR: over inflated lung

38. Complication Cardiac arrest Respiratory failure or arrest Hypoxemia with hypoxic ischemic central nervous system (CNS) injury Pneumothorax or pneumomediastinum Toxicity from medications

39. Prognosis Good prognosis if appropriate therapy is administered. …unless a complicating illness such as CHF COPDis present A delay in initiating treatment is probably the worst prognostic factor

40. Treatment

41. Treatment H igh concentration of oxygen + High doses of SABA S everely ill patients with impending respiratory failure , IV β2-agonists Nebulized anticholinergic- if unsatisfactory response to β2- agonists patients who are refractory to inhaled therapies, a slow infusion of aminophylline Magnesium sulfate given intravenously or by nebulizer with inhaled β2-agonists Prophylactic intubation for impending respiratory failure, when the PCO 2 is normal or rises . Patients with respiratory failure  necessary to intubate

42. Treatment These patients may benefit from an anesthetic such as halothane if they have not responded to conventional bronchodilators. Sedatives are C/I  depress ventilation. Antibiotics not required unless there are signs of pneumonia .

43. Thank you for your attention

44. References Harrison’s principles of internal medicine 19 th e/o Global asthma initiative for asthma Review article Chapter 14: Acute severe asthma(status asthmaticus ) Review article [Status asthmaticus ]