Asthma and Vocal Cord Dysfunction

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1 Asthma and Vocal Cord Dysfunction Amy L. Marks DO, FACOP Pediatric Allergy and Immunology Assistant Professor of Pediatrics Oakland University William Beaumont School of Medicine

2 Objectives: Understanding the basic principles of asthma and vocal cord dysfunction Treatment and management of asthma in the pediatric population Treatment and management or vocal cord dysfunction in the pediatric patient population 2

3 Case Presentation 14 year old girl presents to your office with SOB while participating in competitive indoor soccer. This occurs with both practice and competition. Onset is sudden and can happen without overexertion. She reports symptoms of SOB with activity in the past with outdoor travel soccer May thru June. She does have significant seasonal allergies 3

4 Case Presentation Her past medical history is remarkable for a recent soccer injury with a concussion and whiplash. Family history for seasonal allergies Her PCP has given her an albuterol inhaler to use prior to activity without improvement Symptoms now occurring more frequently and onset more sudden, unable to speak with difficulty getting air into her lungs 4

5 Case presentation Spirometry with evidence of mild obstruction 8% reversibility post bronchodilator on FEV1 Skin testing revealed significant positives to tree, grass, weed, and ragweed pollen Negative to mold, dust mite, cat dog and cockroach 5

6 Flow Volume Loop 6

7 Case presentation Started on Beclomethasone dipropionate HFA 40mcg 2 puffs bid with spacer Device instruction with demonstration in the office Albuterol inhaler for rescue Use and symptom diary recommended Treatment of seasonal allergies initiated with detailed trigger discussion Cetirizine, Fluticasone (nasal) 7

8 Asthma A complex disorder with variable and recurring respiratory symptoms -airflow obstruction -bronchial hyper-responsiveness bronchospasm -underlying inflammation -mucous production and plugging

9 Pathogenesis of Asthma -Infiltration of inflammatory cells eosinophils, neutrophils, lymphocytes, mast cells -Hypertrophy of airway smooth muscle in smaller airways -Hyperplastic smooth muscle in larger airways -Increased airway wall thickness -Damages epithelial cells are seen in chronic asthmatics 9

10 10

11 11

12 Diagnosis of Asthma Transient early wheezers ( most prevalent type) Wheeze less than 3 yrs old and resolved by age 6 Persistent wheezers Wheeze less than 3 yrs of age and continues through 6 yrs of age Late-onset wheezers Children whose onset of wheeze was at 6 years of age 12

13 Onset of Symptoms in Children With Asthma 20% 30% 1-2 years <1 year 20% 2-3 years 30% >3 years McNicol and Williams. BMJ. 1973;4:7-11; Wainwright et al. Med J Aust. 1997;167: ; Dodge et al. J Allergy Clin Immunol. 1996;98:48-54.

14 Asthma Affects more than 7 million children in the US 80% of asthmatics diagnosed before the age of 5 Symptoms include Cough, Wheeze, Breathlessness Chest tightness or pressure Chest pain 14

15 Risk factors for development of asthma in children Genetic characteristics Environmental Exposures Contributing Factors 15

16 Genetic characteristics of Asthma Atopy body s predisposition to develop an antibody (IgE) in response to exposure to environmental allergens IL-4 Gene Beta 2 adenoreceptor gene ADAM 33 16

17 Genetic Predisposition and Environmental Interactions are thought to determine Asthma Phenotype -ATOPY: strongest identifiable predisposing factor -Allergen exposure plays a complex roll: both onset and triggering of asthma -A child s sensitization to Alternaria by six years of age is associated with persistent asthma by 11-years-old - In older children, exposure to higher levels of dust mites correlates with wheezing and airway hyper-responsiveness. -Gender differences are seen (eg, boys have a higher prevalence than girls until the ages of 15-17, the opposite is seen after that age)

18 Atopy and Asthma 30% of children with food allergy have asthma and respiratory allergy Food allergy is a risk factor for life threatening asthma Family history Children with one parent asthmatic are 2.6 times more likely to have asthma Both parents 5.2 times more likely 18

19 Asthma Risk Factors Allergy and eczema Food allergy Early RSV infection Parental asthma 19

20 Asthma Symptoms Cough Nocturnal Seasonal cough Cough secondary to exposures Cold air, exercise, laughing, smoke Cough > 3weeks Although wheezing is considered hallmark for asthma, cough is often the sole complaint 20

21 Asthma Symptoms Wheeze High pitched-musical sound Air forced through narrow airways Polyphonic (varied pitch) Central Airway obstruction Harsh expiratory monophonic wheeze tracheobronchomalacia Upper airway obstruction single pitched inspiratory stridor VCD 21

22 Atopic Asthma Atopic Asthma Symptoms worse in certain pollen season Other allergic symptoms typically flare concurrently with chest complaints Rhinitis, conjunctivitis, eczema Essential to treat atopic symptoms to help alleviate asthma exacerbations Oral antihistamines, nasal sprays, eye drop, topical steroids, moisturizers 22

23 Exercise Induced Bronchospasm Exercise induced bronchospasm (EIB) may be the only manifestation of asthma in children Symptoms SOB, chest tightness and cough Several minutes into exercise Resolution of symptoms with rest over minutes EIB that is difficulty to control indicates inadequately controlled underlying asthma 23

24 Diagnostic evaluation for Asthma History PFT with bronchodilators Trial of bronchodilators Testing for aeroallergy sensitization Consider imaging 24

25 Asthma Management Avoidance of triggers and management of comorbidities GERD ( 45-65% of asthmatics) Atopy Sleep apnea Vocal cord dysfunction 25

26 Asthma Pharmacotherapy Step 1 Stepwise approach Short-acting b-agonist as needed (indicated for all patients) Step 2 Low-dose ICSs or leukotriene modifiers Step 3 Low-dose/medium-dose ICS low-dose/medium-dose ICSs plus LABA Step 4 High-dose ICSs and LABA plus systemic oral corticosteroids Biologic therapy Omalizumab (Anti-IgE) Mepolizumab ( Anti-IL-5) 26

27 Omalizumab Anti- IgE therapy Recombinant, humanized, monoclonal IgG1k anti IgE antibody that binds to the Fc region of IgE, preventing IgE from binding to the cell surface receptors of mast cells and basophils Inhibiting the release of inflammatory mediators that can cause an asthma exacerbation 27

28 NIH Guidelines on Asthma 28

29 29

30 30

31 31

32 The Global Initiative for Asthma Classification of Asthma Severity by Clinical Features Before Treatment 32

33 Intermittent Symptoms less than once a week Brief exacerbations Nocturnal symptoms not more than twice a month FEV1 or PEF 80% predicted PEF or FEV1 variability < 20% Mild Persistent Symptoms more than once a week but less than once a day Exacerbations may affect activity and sleep Nocturnal symptoms more than twice a month FEV1 or PEF 80% predicted PEF or FEV1 variability < 20 30% Moderate Persistent Symptoms daily Exacerbations may affect activity and sleep Nocturnal symptoms more than once a week Daily use of inhaled short-acting 2-agonist FEV1 or PEF 60-80% predicted PEF or FEV1 variability > 30% Severe Persistent Symptoms daily Frequent exacerbations Frequent nocturnal asthma symptoms Limitation of physical activities FEV1 or PEF 60% predicted PEF or FEV1 variability > 30% 33

34 34

35 Case presentation Continues to have episodes now more frequent and more severe. No improvement of symptoms on Beclomethasone dipropionate HFA 95% compliance Albuterol not helping with symptoms ER visits twice with one call to 911 from school Now episodes happening outside of sports 35

36 Asthma or something else? Post infectious GERD Smoking Psychogenic Structural Abnormality Vocal cord dysfunction CF 36

37 Case presentation At her most recent ER visit, no wheeze, no cough and no response to bronchodilator CXR normal Evaluated by ENT, no evidence of structural abnormalities No mass visualized 37

38 Vocal Cord Dysfunction (VCD) VCD is a form of functional or nonanatomic upper airway obstruction Characterized by paradoxical or paroxysmal vocal cord movement Vocal cords adduct (close) during inspiration or early expirations rather than abduct (open) Intermittent Diagnosis suspected by history of inspiratory wheeze and throat tightness 38

39 Symptoms of VCD Intermittent onset of: Dyspnea Cough Stridor Wheeze Throat or chest tightness Hoarseness All of variable severity 39

40 VCD Symptoms often mimic asthma however they are typically un-responsive to asthma medications Pathogenesis is still unknown Psychogenic and neurogenic factors Intrinsic or extrinsic irritants on a hyperresponsive larynx Appears to be gender related and highest among females Associated with type A personalities and GERD 40

41 VCD and concurrent diagnosis Asthma Chronic rhinosinusitis with post nasal drainage GERD Atypical (laryngopharyngeal) reflux VCD may masquerade as or coexist with severe asthma 41

42 Diagnosis of VCD Suggested by flow volume loops which may reveal blunting of the inspiratory loop Methacholine challenge Definitive diagnosis made by fiberoptic rhinolaryngoscopy which reveals paradoxical motion of the vocal cords 42

43 Flow Volume Loops 43

44 Flow Volume Loop 44

45 VCD 45

46 VCD 46

47 Treatment of VCD May respond to breathing re-training Diaphragmatic breathing Relaxation of larynx with conscious activation of the diaphragm Speech pathologist are essential for treatment and breathing training exercises for theses patients 47

48 Asthma and VCD Asthma Responds to bronchodilators and inhaled steroids Night time symptoms Atopy Diagnosed at a young age VCD Fail to respond to asthma medications Sensation of airflow obstruction in the upper airway Symptoms in throat with choking and stridor Teenage Excercise related 48

49 Asthma and VCD Questions? 49

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