Management of Asthma CME

By Dr. Mutabazi Sharif MBchB Date: 18th/May/2012 Venue: BMC

Presentation Outline
Aetiology Brief Overview of Pathophysiology How to make a diagnosis of Asthma

Management of Acute Exacerbations

Out Patient Management of Asthma

Aetiology of Asthma
Genetic . Single nucleotide polymorphism in 17 q 21. Environmental. Respiratory tract viral infections increase the

risk in children, Stress and drugs like beta blockers. Maternal tobacco smoking during pregnancy. Socio-economic factors, see Hygiene Hypothesis

The Hygiene Hypothesis of Asthma

Asthma or allergic diseases during childhood related to

predominance of Th2 over Th1 cells.

Factors enhancing Th1 activation: - reduce Th2 activity - decrease frequency of allergic diseases and asthma.

Hypothesis supported by: - Epidemiologic evidence reduced frequency of allergy or asthma in those exposed to: Mycobacterium tuberculosis, measles, hepatitis A virus. Asthma more prevalent among affluent societies.

Aetiology Continued
Asthma is defined as chronic inflammation of the airways that is

characterized by increased responsiveness of the tracheobronchial tree to a multiplicity of stimuli. Allergic/atopic/early onset asthma---rhinitis, Urticaria , eczema ,(+)skin tests , Ig E,(+) response to provocation tests with aeroallergens.
Idiosyncratic/non-atopic/late onset asthma--- no allergic

diseases,(-)skin tests, normal Ig E, symptoms when upper resp infection, sx last days or months.

Mixed group---usually onset later in life

Pathophysiology of Asthma
1.Early bronchospastic response- type1reaction within min after inhalation( IH) of AG:
Mechanism: IH of aeroallergen sensitization

formation of IgE & expression on mast cells re-exposure to AG mast cell degranulation & mediator release bronchospasm

Pathophysiology
2.Late-bronchospastic reaction: in 30-50%, 6-10 hours after AG exposure. Minority only a late response
Mechanism: recruitment of E, N, L and macrophages

release lipid mediators (PG E2, F2 ,D2; LT C,D,E , PAF), O2radicals, toxic granule proteins, cytokines (TH1:IL-2, IFN; TH2: IL-4, IL-5) bronchoconstriction, vascular congestion, mucosal edema, mucus production, mucociliary transport.

Chronic Asthmatic response

Destruction of AW epithelium by toxic granule Contents epithelial shedding into bronchial lumen exposure of sensory nerve endings and imbalance in cholinergic and peptidergic neuronal control AW remodeling with subendothelial fibrosis, goblet cell hyperplasia, smooth muscle hypertrophy, vascular changes fixed AW obstruction.

Triggers of Acute Episodes

Allergens - pollen Pharmacological stimuli such as aspirin, NSAIDS,

blockers Environment pollution ozone,SO2, NO2 Occupational- metal salts, biological enzymes Infection- resp viruses Exercise IH cold dry air thermally-induced hyperemia and micro-vascular engorgement Emotional stress

How to Make A diagnosis of Asthma

History Examination Investigations

History
Chest tightness Cough Sputum

Breathlessness
Family history of asthma, eczema, rhinitis SYMPTOMS ARE EPISODIC AND VARIABLE

History of provoking factors

Exercise Cold air Viral respiratory infection

Allergens
Cigarette smoke Drugs

Emotion and stress

Investigations
FBC Sputum Chest X-ray

Allergy skin testing

Serum Ig E levels

Procedures
Pulmonary function testing Metacholine and histamine challenge Exercise testing

Peak flow monitoring

Adult Asthma Diagnostic guide

Diagnosis of Asthma (British Thoracic Society Guidelines 2011)

Clinical Features that increase the probability of asthma. More than one

of the following; i. Wheeze ii. Breathlessness iii. Chest tightness iv. Cough. Especially if symptoms are worse at night or precipitated by known asthma triggers. Other clinical features include; i. History of atopic disorder ii. Family history of asthma iii. Wide spread wheeze on auscultation. iv. Otherwise unexplained low peripheral blood eosinophilia

Classification of Severity
Severity in patients 12 years of age [15] Symptom frequency Night time symptoms %FEV1 of predicted FEV1 Variability Use of shortacting beta2 agonist for symptom control 2 days per week

Intermittent

2 per week

2 per month

80% 80%

<20% 2030%

Mild persistent
Moderate persistent Severe persistent

>2 per week but not daily

Daily Throughout the day

34 per month
>1 per week but not nightly Frequent (often 7/week)

>2 days/week but not daily

Daily Several times per day

6080%

>30%

<60%

>30%

Classification of Acute Exacerbations

Near-fatal asthma High PaCO2 and/or requiring mechanical ventilation Any one of the following in a person with severe asthma:Clinical signs Altered level of consciousness Life threatening asthma Exhaustion Arrhythmia Measurements Peak flow < 33% Oxygen saturation < 92% PaO2 < 8 kPa

Low blood pressure Cyanosis Silent chest Poor respiratory effort

Any one of:Peak flow 3350% Acute severe asthma

"Normal" PaCO2

Respiratory rate 25 breaths per minute

Management of Acute Asthma Exacerbations

Give oxygen if hypoxemic( if SPO2 less than 94%). Nebulised salbutamol 5mg/4ml NS repeated every 15 minutes if

no improvement Add ipratropium bromide 0.5mg 4-6 hourly if there is poor response to nebulised salbutamol Prednisolone 40-60 mg daily for 14 days or until recovery. Give IV if unable to swallow but efficacy is the same. Give the following if there is no response; i. IV Magnesium 1.2-2g over 20 minutes ii. Adrenaline sc 0.1 mg repeated hourly 2-3 iii. Ketamine /Inhalational anaesthetics in ICU NB: IV aminophyline is no longer recommended as studies have not shown any benefits.

Outpatient Mgt of Chronic AsthmaBritish Thoracic Society Guidelines

Start treatment at then step most appropriate to initial

severity. Achieve early control Maintain control by; by stepping up as necessary and stepping down when control is good. Complete control is defined as ; no daytime symptoms, no night awakening due to asthma, no exacerbations, no exercise limitation, minimal side effects from medication, and PEF >80% of the predicted.

Step 1: Inhaled SABA

Quick reliever (SABA) PRN for every asthmatic. No regular

schedules. When to start controller drugs? relievers used 2d/week. or 2x night time awakenings.

Step 2: Inhaled corticosteroids

Cornerstone of long term control. Anti inflammatory (gene transcription). Benefits: Improve morbidity, QOL. Dose 200-800

mcg/day, start at a dose appropriate to severity of disease. Unequal benefits in individuals: Cigarette smoking, neutrophillic
inflammation, pharmacogenetics.
Side effects -local, prevention measures.

-systemic - at high doses.

Management continued
Give either of the following if no response to the above; IV Magnesium sulphate 1.2-2g over 20 minutes Adrenaline 0.1mg sc every 30 minutes for 2-3 times.

Ketamine /inhalational anaethetics in ICU if all the above

fails.

Step 3: Inhaled LABA

Bronchodilators. Pharmacogenetics. MUST be used with an anti inflammatory agent.

LABA/inhaled steroid combos available (adv/disadv), more

favourable outcome. Regular use, S/Es.

Step 4: High Dose of Inhaled corticosteroids.

Increase corticosteroid dose up to 2000 mcg/day or add

LTRA

Step 5: Continuous / frequent use of oral steroids.

Use oral steroid tablets in lower dose providing adequate

control. Maintain the high dose of inhaled steroid at 2000 mcg/day. Educate patients on avoiding triggers , adherence and when to seek immediate care.