Management of Asthma CME
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Transcript of 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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