BRONCHIAL ASTHMA in acute exacerbation case

bronchial asthma

1. CASE PRESENTATION Schneider Klein MD

2. OBJECTIVES To report a case of Bronchial Asthma through presentation of the case’s complete history and physical examination. To discuss the GINA (2019) guidelines for the diagnosis and management of Bronchial Asthma.

3. OUTLINE GENERAL DATA CHIEF COMPLAINT HPI PAST MEDICAL HISTORY PAST PERSONAL HISTORY FAMILY HISTORY SOCIAL and ECONOMIC HISTORY REVIEW OF SYSTEMS PHYSICAL EXAMINATION POMR DISCUSSION

4. GENERAL DATA E.P.P 19y/F Single Student August 21, 2000 Baguio City 116 Lower Quirino Hill, B.C Roman Catholic Patient 90% reliability

5. CHIEF COMPLAINT DIFFICULTY OF BREATHING

6. HISTORY OF PRESENT ILLNESS 2 DAYS PTC (+) Fever ( Tmax : 38.2C) (+) Dry cough (+) Colds, watery (-) Abdominal pain (-) Body weakness (-) change in BM nor urinary pattern Meds: 1. Paracetamol ( Biogesic ), 500mg/tab q4, 3 tabs taken 2. Phenylephrine HCl , CPM, paracetamol ( Neozep Forte) 1 tab q6, 2 tabs taken RELIEF OF FEVER

7. HISTORY OF PRESENT ILLNESS 1 DAY PTC (+) DOB aggravated by physical activity, partially relieved by rest and Salbutamol puff (-) SOB (+) Dry cough & colds, watery (-) Fever NO CONSULT. Meds: Salbutamol (Ventolin) puff, 2 sprays, BID PARTIAL RELIEF OF DOB

8. HISTORY OF PRESENT ILLNESS FEW HOURS PTC (+) DOB aggravated by physical activity, not relieved by rest (+) awakening from sleep (+) SOB (+) Dry cough & colds, yellowish (-) Fever PROGRESSION OF DOB with NO SIGNS OF RESOLUTION ER CONSULT

9. PAST MEDICAL HISTORY

10. FAMILY HISTORY (+) Bronchial asthma paternal side (-) Tuberculosis (+) Hypertension both sides (-) Diabetes mellitus (-) Cancer (-) Arthritis (-) Cerebrovascular disease (-) Coronary artery disease (-) Twinning (-) Congenital diseases

11. SOCIAL & ENVIRONMENTAL HISTORY Student, 1 st year college Non-smoker Non-alcoholic drinker Non-congested neighborhood 2-storey house, 4 rooms 5 occupants No pets Near the road Flushed-type toilet Water for domestic purposes: local water district Drinking water: water-refilling station, not boiled Garbage: collected weekly Good handwashing practice done at home

12. REVIEW OF SYSTEMS GENERAL: (-) weight loss, (+) febrile episodes, (-) chills, (-) sweats, (-) poor oral intake, (-) irritability SKIN: (-) cyanosis, (-) pallor, (-) jaundice, (-) rashes HEAD AND NECK: (-) lesions, (-) dryness, (-) masses EYES: (+) tearing, (-) redness, (-) discharge EARS: (-) discharge NOSE: (+) congestion, (+) colds, (+) sneezing MOUTH AND THROAT: (-) ulcers, (-) gum bleeding

13. REVIEW OF SYSTEMS RESPIRATORY: (+) cough, dry, (+) colds, yellowish, (+) difficulty of breathing, (+) shortness of breath, (-) hemoptysis CARDIAC: (-) edema, (-) cyanosis GASTROINTESTINAL: (+) poor appetite, (-) constipation, (-) diarrhea, (+) nausea, (+) vomiting, (-) hematochezia, (-) melena URINARY AND RENAL: (-) oliguria, (-) hematuria, (-) dysuria GENITALIA: (-) swelling, (-) itchiness

14. REVIEW OF SYSTEMS MUSCULOSKELETAL: (-) swelling, (-) trauma ENDOCRINE AND METABOLIC: (-) hair changes, (-) weight gain, (-) weight loss HEMATOLOGIC: (-) anemia, (-) bleeding, (-) bruising NERVOUS & PSYCHIATRIC: (-) seizures, (-) convulsions, (-) tremors, (-) coordination problems

15. PHYSICAL EXAMINATION GENERAL SURVEY: awake, conscious, oriented to time, place and person, not weak-looking, in mild cardiopulmonary distress, speak in sentences VITAL SIGNS: BP: 120/80 mmHg CR: 91 bpm RR: 23 cpm [tachypneic] T: 36.0 C SpO2: 93% at room air ANTHROPOMETRIC MEASUREMENTS: Weight: 66 kg Height: 1.52 m BMI: 28.6 kg/m2

16. PHYSICAL EXAMINATION SKIN: brown, no cyanosis, no jaundice, no pallor, no rashes, warm and soft to touch, good skin turgor HEAD: No scars, no lesions, with appropriately patterned black terminal hair, no lice noted EYES: Anicteric sclerae , pink palpebral conjunctivae, clear corneal film, non-sunken eyeballs EARS: Normally set and symmetrical ears, no lesions, minimal cerumen noted on both ear canals, intact tympanic membrane

17. PHYSICAL EXAMINATION NOSE: Septum at the midline, boggy turbinates, minimal yellowish mucoid discharge, pink nasal mucosae MOUTH AND THROAT: Dry lips, moist buccal mucosae, no circumoral cyanosis, no tonsillopharyngeal wall congestion, dental caries noted, no tongue deviation NECK: No suprasternal and supraclavicular retractions, no anterior neck mass, no swelling, no neck vein engorgement, no cervical lymphadenopathies

18. CHEST AND LUNGS: Symmetrical chest wall expansion, no lags nor retractions, equal tactile fremitus, resonant on percussion, with diffuse wheezing noted on bilateral lung fields, no crackles, no egophony, no bronchophony HEART: No lifts, PMI at 5th ICS left midclavicular line, no heaves, no thrills, normal rate, regular rhythm, no murmurs and adventitious heart sounds

19. ABDOMEN: Flabby, non-distended, normoactive bowel sounds, tympanitic, soft, no tenderness on all quadrants, no masses palpated BACK: no lesions, no costovertebral angle tenderness EXTREMITIES: no gross deformities, no cyanosis, no edema, full and equal peripheral pulses, 1 sec CRT

20. POMR #1 DOB, SOB, Known asthmatic (02/17/2020)

21. #1 DOB/SOB S Febrile episodes DOB/SOB, fast breathing Dry cough Colds, yellowish Good oral intake No changes in BM nor urinary pattern Known case of bronchial asthma No previous hospitalizations due to asthma Family history of bronchial asthma

22. #1 DOB/SOB O G/S: in mild cardiopulmonary distress, able to speak in sentences VITAL SIGNS: BP: 120/80 mmHg CR: 91 bpm RR: 23 cpm [tachypneic] T: 36.0 C SpO2: 93% at room air ANTHROPOMETRIC MEASUREMENTS: BMI: 28.6 kg/m2 (Overweight)

23. PHYSICAL EXAMINATION NOSE: boggy turbinates, minimal yellowish mucoid discharge, pink nasal mucosae MOUTH AND THROAT: Dry lips, moist buccal mucosae, no circumoral cyanosis, no tonsillopharyngeal wall congestion NECK: No suprasternal and supraclavicular retractions, no cervical lymphadenopathies CHEST AND LUNGS: Symmetrical chest wall expansion, no lags nor retractions, equal tactile fremitus, resonant on percussion on both lungs, with diffuse wheezing noted on bilateral lung fields, no crackles, no egophony, no bronchophony

24. #1 DOB/SOB A Bronchial Asthma in Acute Infectious Exacerbation DDx: Etiology: Viral vs. Bacterial CAP-LR

25. #1 DOB/SOB P Therapeutics Salbutamol + Ipratropium bromide nebulization Budesonide nebulization* ICS-LABA Non-pharmacological therapies and strategies

26. GINA 2019 1993 GOAL -produce recommendations for asthma management based on the best scientific information available The GINA report is not a guideline, but an integrated evidence-based strategy focusing on translation into clinical practice

27. ASTHMA: DEFINITION Heterogeneous disease AIRWAY INFLAMMATION HISTORY Wheeze, shortness of breath, chest tightness & cough that vary overtime in intensity variable expiratory airflow limitation

28. AIRWAY HYPERRESPONIVENESS Hallmark of pathophysiology of asthma: CHRONIC INFLAMATION TRIGGER

29. ASTHMA TRIGGERS 1. ALLERGENS MOST COMMON trigger for asthma: Dust mite or Dermatophagoides 2. VIRAL INFECTIONS The MOST POTENT trigger of asthmatic exacerbations

30. 3. PHARMACOLOGIC AGENTS Beta Blockers: Block the Beta receptor, the receptor that causes bronchodilation -> Bronchoconstriction Topical β- blockers (most common: ophthalmic drugs used in glaucoma) can cause fatal bronchospasm ABSOLUTE CONTRAINDICATION in asthma

31. ACE Inhibitors: Block the Angiotensin Converting Enzyme -> Shift the formation to Bradykinin which causes cough and spasm RELATIVE CONTRAINDICATION (does not directly cause bronchospasm) Aspirin: blocks AA pathway, preferentially generates leukotrienes due to blockage of COX pathway. Leukotrienes B4, D4, E4 re produced causing asthma

32. 4. EXERCISE (EIA) Exercise Induced Asthma Increase airway osmolarity Basic pathophysiologic mechanism for EIA: The airways swells because of the cold air.

33. 5. PHYSICAL FACTORS Change in weather, perfume, laughter 6. FOOD Metabisulfite : is the one that generates sulfur dioxide. - Found in wine, beer – that’s why you get red because it causes vasodilation Converted to Sulfur Dioxide – Sulfur causes vasodilatation. Found in preservatives. Tartrazine yellow: Preservative for FD&C no 5 (Food, Drugs, and Cosmetics) - Seen in drinks: Juice, tetra packs; blush-on

34. 7. AIR POLLUTION Sulfur dioexide , ozone

35. ASTHMA: DESCRIPTION Characterized by Wheeze Shortness of breath Chest tightness Cough VARIABLE airflow imitation Triggered by Exercise Allergens Irritant exposure Change in weather Viral respiratory infection

36. DEVELOPMENT OF ASTHMA HOST FACTORS Genetic Genes predisposing atopy (MAJOR RISK factor for asthma) Genes predisposing to airway hyperresponsiveness Obesity Sex

37. DEVELOPMENT OF ASTHMA B. ENVIRONMENTAL FACTORS Allergens Indoor: Domestic mites, furred animals (dogs, cats, mice), cockroach allergen, fungi, molds, yeasts Outdoor: Pollens, fungi, molds, yeasts Infections (predominantly viral) Tobacco smoke Air pollution Diet

38. THE DIRTY GENE HYPOTHESIS “MENDELIAN CURSE” Gene Th0 During childhood, environmental exposure will determine how the Th0 will develop Environment: DIRTY CLEAN Th0 will develop into: Th1 Th2 That is: Protective Predisposition to allergic antibody response

39. DIAGNOSIS

40. DIAGNOSTIC CRITERIA

41. DIAGNOSTIC CRITERIA

42. OBJECTIVE MEASURES FOR ASTHMA DIAGNOSIS Measurement of lung function: Spirometry pre/post BD: Reversibility of airflow limitation BEST DIAGNOSTIC TEST/GOLD STANDARD Peak flow rate (PEFR) measurement: Variability of airflow limitation For monitoring of therapy Measurement of airway responsiveness Non- invasive markers of inflammation Measurement of allergic status

43. LUNG FUNCTION TEST SPIROMETRY: MOST IMPORTANT DIAGNOSTIC test for obstructive lung disease. FEV1/FVC: Most important parameter FVC: the amount of FORCEFULLY exhaled air after a MAXIMAL inhalation FEV1: the amount of air on the FIRST SECOND of expiration Normal: 80%

44. ASTHMA: REVERSIBILITY TEST o FEV1 improvement ≥ 12% AND ≥ 200ml from pre bronchodilator value (it has to be BOTH) *If no reversibility seen (but good suspicion for asthma)? Do not exclude asthma Suggest: Repeat testing or monitor response to empiric therapy or do Methacoline challenge test

45. METHACHOLINE CHALLENGE TEST An allergen, which is the methacholine , is given to the patient to induce bronchospasm *Only give small concentrations enough to trigger asthma to asthmatic patients and not in normal patients If (+) bronchospasm: (+) 20% drop of FEV1 even in low dose of methacholine

46. NON-INVASIVE MARKERS OF AIRWAY INFLAMMATION Tests to evaluate airway inflammation associated with asthma: o Sputum (included) eosinophilia o Levels of exhaled nitric oxide (FENO): NO is released when there is inflammation in the airways

47. ALGORITHM FOR VENTILATORY DEFECTS RESTRICTIVE LUNG DISEASE OBS TRUCTIVE LUNG DISEASE

48. TREATMENT GOAL: achieve and maintain clinical control to a period of ALMOST NEAR NORMANCY. The patient, when on treatment, should perform or function the same way as a non-asthmatic and the only difference is that he/she has medication.

49. GOALS OF ASTHMA MANAGEMENT

50. PARAMETERS OF CONTROL 1 Daytime symptoms 2 Nighttime awakening/symptoms 3 Limitation of activities 4 Need for Reliever/Rescue Treatment 5 Exacerbation 6 Abnormal Lung Function

51. ASSESSING LEVELS OF ASTHMA CONTROL

52. CONTROL-BASED ASTHMA MANAGEMENT CYCLE

53. REVIEW RESPONSE ASSESS ADJUST * Off-label; data only with budesonide-formoterol (bud-form ) † Off-label; separate or combination ICS and SABA inhalers STEP 2 Daily low dose inhaled corticosteroid (ICS), or as-needed low dose ICS-formoterol * STEP 3 Low dose ICS-LABA STEP 4 Medium dose ICS-LABA Leukotriene receptor antagonist (LTRA), or low dose ICS taken whenever SABA taken † As-needed low dose ICS-formoterol * As-needed short-acting β 2 -agonist (SABA) Medium dose ICS, or low dose ICS+LTRA # High dose ICS, add-on tiotropium, or add-on LTRA # Add low dose OCS, but consider side-effects As-needed low dose ICS-formoterol ‡ STEP 5 High dose ICS-LABA Refer for phenotypic assessment ± add-on therapy, e.g.tiotropium, anti-IgE, anti-IL5/5R, anti-IL4R Symptoms Exacerbations Side-effects Lung function Patient satisfaction Confirmation of diagnosis if necessary Symptom control & modifiable risk factors (including lung function) Comorbidities Inhaler technique & adherence Patient goals Treatment of modifiable risk factors & comorbidities Non-pharmacological strategies Education & skills training Asthma medications 1 © Global Initiative for Asthma, www.ginasthma.org STEP 1 As-needed low dose ICS-formoterol * Low dose ICS taken whenever SABA is taken † ‡ Low-dose ICS-form is the reliever for patients prescribed bud-form or BDP-form maintenance and reliever therapy # Consider adding HDM SLIT for sensitized patients with allergic rhinitis and FEV >70% predicted PREFERRED CONT R OLLER to prevent exacerbations and control symptoms Other controller options Other reliever option PREFERRED RELIEVER Box 3-5A Adults & adolescents 12+ years Personalized asthma management: Assess, Adjust, Review response Asthma medication options: Adjust treatment up and down for individual patient needs

54. ANTI-ASTHMA DRUGS B2 Agonists – Reliever Pathway: Adenylyl cyclase Preferential generation of cAMP → protein kinase A → PROMOTE BRONCHODILATION Salbutamol, Terbutaline, etc. ADR: Tachycardia, Tremors, Tachyphylaxis (too much dose)

55. B. Anti- Cholinergics - Reliever Blocks acetylcholine to PREVENT BRONCHOCONSTRICTION Ipratropium, Tiotropium bromide, etc. *For maximum dilation: Use B2 agonists + Anticholinergics

56. C. Theophylline – Reliever and Controller Inhibition phosphodiesterase (PDE) In the adenylyl cyclase mechanism, the cAMP is metabolized into AMP by PDE. Inhibition of PDE, will shift the flow to the generation of protein kinase A → PROMOTE BRONCHODILATION

57. D. Inhaled Corticosteroids – THE TREATMENT FOR ASTHMA , Controller Anti-inflammatory Acts directly on the airways Can cause very little adrenal insufficiency Systemic absorption: 5-10% (almost negligible: will not cause any effects of chronic steroid use)

58. E. Systemic corticosteroids – Reliever Chronic use of steroid may lead to adrenal insufficiency leading to death Only be used during ACUTE exacerbation

59. F. Antileukotrienes - Controller “- lukast ” Zilueton

60. G. Cromones – Controller Stabilizes mast cells no release of eosinophils Prevents degranulation of mast cells that causes severe inflammation Used more in pediatrics Used in super allergies, e.g. hay fever

61. H. Anti- IgE – Controller Step 5 component Omalizumab SQ every 2 weeks Blocks antibody that neutralizes circulating IgE without binding to cell bound IgE ; thus inhibits IgE - mediated reactions Used in patients who did not improve with other medication

62. RISK FACTORS: FAMILY HISTORY OBESITY POOR COMPLIANCE Hx OF EMERGENCY VISIT IN < 1 YEAR PMHX: - KNOWN ASTHMATIC TRIGGER: INCREASE PHYSICAL ACTIVITY COUGH & COLDS P A TIENT WHEEZING DOB SOB COUGH AWAKENING FROM SLEEP USE OF RELIEVER POOR CONTRO L SABA + LOW DOSE ICS SALBUTAMOL NEB FLUTICASONE 44ug, 2 puffs BID