Management of Asthma CME

7/31/2019 Management of Asthma CME

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By Dr. Mutabazi Sharif

MBchB

Date: 18th/May/2012

Venue: BMC


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Aetiology

Brief Overview of Pathophysiology

How to make a diagnosis of Asthma

Management of Acute Exacerbations Out Patient Management of Asthma


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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


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Asthma or allergic diseases during childhood related topredominance 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.


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Asthma is defined as chronic inflammation of the airways that ischaracterized by increased responsiveness of the tracheobronchialtree 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 allergicdiseases,(-)skin tests, normal Ig E, symptoms when upper respinfection, sx last days or months.

Mixed group---usually onset later in life


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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

releasebronchospasm


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2.Late-bronchospastic reaction: in 30-50%, 6-10hours 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.


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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.


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Allergens - pollen

Pharmacological stimuli such as aspirin, NSAIDS, -

blockers

Environment pollution ozone,SO2, NO2

Occupational- metal salts, biological enzymes

Infection- resp viruses

ExerciseIH cold dry air thermally-induced hyperemia

and micro-vascular engorgement Emotional stress


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History

Examination

Investigations


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Chest tightness

Cough

Sputum

Breathlessness Family history of asthma, eczema, rhinitis

SYMPTOMS ARE EPISODIC AND VARIABLE


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Exercise

Cold air

Viral respiratory infection

Allergens Cigarette smoke

Drugs

Emotion and stress


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FBC

Sputum

Chest X-ray

Allergy skin testing Serum Ig E levels


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Pulmonary function testing

Metacholine and histamine challenge

Exercise testing

Peak flow monitoring


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Clinical Features that increase the probability of asthma. More than oneof the following;

i. Wheeze

ii. Breathlessness

iii. Chest tightnessiv. Cough.

Especially if symptoms are worse at night or precipitated by knownasthma triggers. Other clinical features include;

i. History of atopic disorder

ii. Family history of asthmaiii. Wide spread wheeze on auscultation.

iv. Otherwise unexplained low peripheral blood eosinophilia


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Severity in

patients

12 years of

age [15]

Symptom

frequency

Night time

symptoms

%FEV1 of

predicted

FEV1

Variability

Use ofshort-

acting

beta2

agonist for

symptom

control

Intermittent 2 per week2 per

month80% 2 per week

but not daily

34 per

month80% 2030%

>2

days/week

but not daily

Moderate

persistentDaily

>1 per week

but not

nightly

6080% >30% Daily

Severe

persistent

Throughout

the day

Frequent

(often7/week)

30%

Several times

per day
http://en.wikipedia.org/wiki/Asthmahttp://en.wikipedia.org/wiki/Asthma


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Near-fatal asthma High PaCO2 and/or requiring mechanicalventilation

Life threatening asthma

Any one of the following in a person with severe asthma:-

Clinical signs Measurements

Altered level of

consciousness Peak flow < 33%

Exhaustion Oxygen saturation < 92%

Arrhythmia PaO2 < 8 kPa

Lowblood pressure "Normal" PaCO2

CyanosisSilent chest

Poor respiratory effort

Acute severe asthma

Any one of:-

Peak flow 3350%

Respiratory rate 25 breaths per minute
http://en.wikipedia.org/wiki/Arterial_blood_gashttp://en.wikipedia.org/wiki/Arterial_blood_gashttp://en.wikipedia.org/wiki/Level_of_consciousnesshttp://en.wikipedia.org/wiki/Level_of_consciousnesshttp://en.wikipedia.org/wiki/Peak_flowhttp://en.wikipedia.org/wiki/Oxygen_saturationhttp://en.wikipedia.org/wiki/Arrhythmiahttp://en.wikipedia.org/wiki/Arterial_blood_gashttp://en.wikipedia.org/wiki/Arterial_blood_gashttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Cyanosishttp://en.wikipedia.org/wiki/Cyanosishttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Arterial_blood_gashttp://en.wikipedia.org/wiki/Arterial_blood_gashttp://en.wikipedia.org/wiki/Arrhythmiahttp://en.wikipedia.org/wiki/Oxygen_saturationhttp://en.wikipedia.org/wiki/Peak_flowhttp://en.wikipedia.org/wiki/Level_of_consciousnesshttp://en.wikipedia.org/wiki/Level_of_consciousnesshttp://en.wikipedia.org/wiki/Arterial_blood_gashttp://en.wikipedia.org/wiki/Arterial_blood_gas


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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 poorresponse to nebulised salbutamol

Prednisolone 40-60 mg daily for 14 days or until recovery. GiveIV 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 2-3iii. Ketamine /Inhalational anaesthetics in ICU

NB: IV aminophyline is no longer recommended as studies have notshown any benefits.


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Start treatment at then step most appropriate to initialseverity.

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.


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Step 1: Inhaled SABA

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

When to start controller drugs?

relievers used 2d/week.

or

2x night time awakenings.


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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, neutrophillicinflammation, pharmacogenetics.

Side effects -local, prevention measures.

-systemic - at high doses.


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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 abovefails.


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Step 3: Inhaled LABA

Bronchodilators.

Pharmacogenetics.

MUST be used with an anti inflammatory agent.

LABA/inhaled steroid combos available (adv/disadv), morefavourable outcome.

Regular use, S/Es.


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Management of Asthma CME

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