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com
 BRONCHIAL
ASTHMA
BY
DR ESSAM EL-GAMAL
PROFESSOR OF CHEST DISEASES
MANSOURA FACULTY OF MEDICINE
2009

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 DEFINITION
 Chronic inflammatory disorder of the
airways in which many cells play a role
including mast cells, eosinophils and T-
lymphocytes.
 Chronic inflammation is associated with :
- Airway hyperresponsiveness that → recurrent
episodes of wheezing, breathlessness, chest
tightness, and coughing, particularly at night or
in the early morning.
- Widespread, but variable, airflow obstruction
within the lung that is often reversible either
spontaneously or with treatment.
 Asthma is a chronic inflammatory disorder
associated with BHR + widespread variable AWO.

Asthma

BHR AWO
Airway inflammation

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 : Asthma Triggers

Host Factors Environmental Factors

 Genetic
. Allergens (indoor, outdoor).
- Atopy . Air Pollution with irritants.
- BHR . Occupational sensitizers.
. Tobacco smoke.
 Gender
. RT Infections.
 Obesity
. Diet.
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 ATOPY
allergic hypersensitivity affecting
parts of the body not in direct
contact with the allergen. Associated
with :
- a strong hereditary component.
- elevated serum levels of total and
allergen-specific IgE, → positive skin-
prick tests to common allergens.
 Includes atopic dermatitis, allergic
rhinitis, conjunctivitis, and asthma.
Common Allergens & Irritants :

Allergens Irritants
• Food. • Secondhand sk.
• Pollen / Molds. • Strong odors.
• Animals/Pets. • Ozone.
• Cockroaches. • Chem compounds
• Dust.

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 Asthma triggers

Viruses and
other pathogens
Occupational Allergens
PETS
chemicals

Smoking Drugs (aspirin) Stress

Exercise
 ?Is it Asthma
 Recurrent episodes of wheezes.
 Recurrent cough at night.
 Wheeze or cough after exercise.
 Wheeze, cough or chest tightness after
exposure to airborne allergens or
pollutants.
 Colds “go to the chest” or take > 10
days to clear
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 Pollen

• Grass ‫ عشب‬, pine‫ صنوبر‬, oak

trees. ‫بلوط‬
• Transported by wind
and can get indoors
during pollen season.
• Close windows during
pollen season.
• Weather-strip doors and
windows.
Dust Mites
• Found everywhere, too
small to be seen.
• Live in soft bedding, in
warm, humid places.
• Feed on dead skin cells.
• Mites & mite droppings
can trigger asthma.
 Pets/Animals

• Skin flakes, urine, and saliva of warm

blooded animals trigger asthma.
• Triggers remain inside for several Mns
after an animal is removed.
Molds

• A type of fungus.
• Grow on damp
surfaces by
releasing spores.
• Grow on organic
materials: wood,
drywall, carpet,
foods, wallpaper.

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 Other Indoor Triggers:
Household Products
• Vapors from cleaning
solvents paint, liquid
bleach, mothballs, glue.
• Spray deodorants,
perfume.
• bleach, pesticides, oven
cleaners, aerosol spray
products.
 Pathogenesis of Asthma

 Immunologic mechanism.
 Neural mechanism.

 Genetic mechanism.

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 1) Immunologic Mechanism :
Occur in atopic pts due to
 Immediate R :

Ag/Ab R on the surface of MC → cell

disruption & release of mediators
(histamine, bradykinin) → BC.
 Late R :
PAF & MBP → oedema & cell infiltratin of
br wall.
 MCP & eosinophils and lymphocytes : play
role in the inflam reaction in BA.
2) Neural Mechanism :

.ANS plays a role in the control of airway

contraction, relaxation and secretions.
. Symp NS → BD.
. Parasymp NS → BC and ↑↑ secretions.
. NANC system →inhib innervation to AW
smooth Ms (BD), neurotransmitter is VIP.

3) Genetic Mechanism :
BA occurs in families, heredity may play a
role in determination of BHR.
 Association of the ADAM33
gene with asthma and BHR :
 Genome scan (of 460 Caucasian families)
identified a locus on chromosome 20p13
(ADAM33).
 ADAM proteins are membrane bound
metalloproteases with diverse funtcions; eg.
Release of cytokines.
 It will shed light on molecular pathway
involved & new ttt strategies.
PATHOGENESIS

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Histologic Features In Asthma

 Shedding of airway epithelium.

 Collagen deposition of in basal membrane.
 Hyperplasia of goblet cells.
 Hypertrophy of smooth muscles.
 Inflammatory cell infiltration (N,E,L).
What happens during an
?asthma episode

Airways narrow due to :

. tightening of the ASM
. swelling of inner lining.
. ↑↑ mucous production.

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 Asthma Diagnosis
 History and patterns of symptoms.
 Measurements of lung function :
- Spirometry
- Peak expiratory flow
 Measurement of airway
responsiveness.
 Measurements of allergic status to
identify risk factors.
 : C/P of Bronchial Asthma
Symptoms : recurrent attacks of :
 Breathlessness and chest tightness.
 Chest Wheezes.
 Cough more at night.

Signs : during asthma attacks :

 Tachycardia>120/min,tachpnea>30/min.
 Pulsus paradoxus > 20 mm Hg.
 Cyanosis.
 Inability to speak in sentences.
 Use of accessory respiratory muscles.
 Chest wheezes or Silent chest.
 Pulsus paradoxus
 Definition :
an exaggeration of normal variation in the pulse
during respiration, in which the pulse becomes
weaker as one inhales & stronger as one exhales.
 Occurs in several conditions including :
asthma, COPD, cardiac tamponade, pericarditis,
chronic sleep apnea and croup.
 Detection :
by measuring variation of SBP with respiration :
. Normal SBP variation (with respiration) is
considered to be ≤10 mmHg.
. Pulsus paradoxus is an inspiratory reduction in
systolic pressure > 10 mmHg.
:CLASSES OF ASTHMA SEVERITY

Severity intermittent mild persistent

Symptoms once per week > once per week ≤

but < once per day

EXB brief ( few hr: few days) may affect activity and
asymptomatic between EXB sleep

Night times per month 2 > times per month 2 <

Symptoms
FEV1 ≥ 80% OPV, ,OPV 80% ≤
or PEF variability < 20% variability < 20%
 CLASSES OF ASTHMA SEVERITY:

Severity moderate severe persistent

persistent
Symptoms daily use of SABA continuous; physical
activities limited
EXB affect activity & frequent
sleep
Night once per week < frequent
Symptoms
FEV1 to < 80% 60% < OPV 60% =>
or PEF OPV variability > variability > 30%
30%
 Levels of Asthma
Control
Partly controlled
Characteristic Controlled (Any present in Uncontrolled
(any wk
Daytime
None ( ≤/ wk) twice / wk >
symptoms
Limitations of
activities
None Any ≥3
Nocturnal features of
symptoms / None Any partly
awakening
controlled
Need for rescue
None (≤( / wk twice /wk > asthma in
/ “reliever” ttt
any week
Lung function OPV or 80% <
Normal personal best on
((PEF or FEV1
any day

Exacerbation None One or more / y 1 in any week

 Investigation In Bronchial
Asthma:
 Pulmonary function tests.

m
Chest X-ray.

co


s.
ABG.

an


sF
 Serum IgE.

an
Detection of allergen.

.M


w
 Sputum Exam.
ww
 Others : CBC, ECG.
 Pulmonary function tests In
Bronchial Asthma
■ Obstructive Hypoventilation :
• FEV1 < 80% OPV & FEV1/FVC < 65%.
• Coved pattern of F-V loop : maximal exp
begins & ends at higher lung volumes &
lower flow rates than normal.

■ Reversibility of AWO:
∀ ↑ FEV1 ≥ 12% (↑ 200 mLs) after 2 puffs of
SABA.
 Pulmonary function tests In
Bronchial Asthma
■ PEFR Variability :
. Shows > 20% diff ( ) the highest & lowest
values with morning dipping.
. Used to monitor EXB : to assess their
severity and guide management decisions.

■ Bronchoprovocation Challenge Test :

. With methacholine histamine or exercise in
cases with normal spirometry.
 OBSTRUCTIVE & RESTRICTIVE
HYPOVENTILATION

OBSTRUCTIVE RESTRICTIVE
FEV1/ FVC
RATIO Reduced Normal or ↑
LUNG . FEV1 markedly ↓ . FEV1 markedly ↓
VOLUMES . FVC decreased . FVC markedly
. VC normal or ↓ ↓ . VC
moderately ↓
F-V LOOP coved pattern witch's hat
appearance
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 Peak Flow Meter
How to use PEF meter:
 Stand up or sit up straight.

 Slide indicator to base of meter.

 Take in deep breath.

 Place mouthpiece in mouth and seal lips

around it.
 Blow out as hard and fast as you

can (one quick blow).

 Repeat process 2 times more.

 Select highest number of the 3 efforts.

 :MANAGEMENT OF ASA

A E R O S O L TH E R A P Y

A F T E R 2 0 M IN A F T E R 2 0 M IN A F T E R 2 0 M IN
P E FR P E FR P E FR
> 7 0 % -----> D IS C H A R G E > 7 0 % -----> D IS C H A R G E > 7 0 % -----> D IS C H A R G E
< 7 0 % ----> R E P E A T < 7 0 % ----> R E P E A T < 7 0 % -----> IV C S T

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 :MANAGEMENT OF ASA

PEFR < 70%

40 - 70 % 2 5 -4 0 % < 25 %
IV C S T IV C S T IV C S T
6 0 M IN ---> A E R O S O L IN T U B A T IO N
M V

> 7 0 % -----> D IS C H A R G E A D M IT T O H O S P IT A L A D M IT T O IC U
< 7 0 % ------> A D M IT
 Flow-volume curve variations

Flow-volume curves from

(A) a healthy person.
(B) severe obstruction (emphysema).
(C) severe restriction (interstitial fibrosis).
(D) upper airways obstruction (tracheal stenosis).
(E) poor effort.
 Investigation In Bronchial
:Asthma
 CXR :
. May show a cause or C/O of BA :
pneumonia, pnx, collapse, # ribs.
 ABG :
. For hypoxemia, hypercapnia and need of MV.
 Total serum IgE :
. ↑ in cases with atopy.
 Detection of Allergen :
. Serum specific IgE, skin prick test, BPT using
inhaled allergens.
 Investigation In Bronchial
:Asthma
 Sputum Exam :
. May show eosinophilia, Curchman spirals,
Charcot-Leyden crystals and Creola bodies.

 CBC :
. Eosinophilia in allergic diseases, Leucocytosis in
infection.

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 :Curschmann's spirals
 Yellow-white wavy long
threads represent
bronchial casts
composed of :
- shed epithelium.
- spiral aggregates of
eosinophils.
- mucus.
in a fibril network.
 Charcot-Leyden crystals
 Breakdown
product of
eosinophils.
 Appear : slender
and pointed and
stain purplish-
red in the
trichrome stain.
 : Creola Bodies
 compact clumps
or strips of
columnar
epithelial cells
shed from the
bronchus.

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 Alternative causes of
recurrent wheezing (Other
(D. Dx
considered and excluded. These include:
• Chronic rhino-sinusitis.
• Recurrent viral lower RTI.
• TB.
• COPD.
• GERD.
• FB aspiration.
• Primary ciliary dyskinesia syndrome.
• Cystic fibrosis.
• Congenital malformation causing narrowing of the
intrathoracic airways.
• Congenital HD.
• Immune deficiency.
 COMPLICATIONS OF ACUTE
SEVERE ASTHMA
 Pneumothorax, pneumomediastinum,
pneumopericardium, subcutaneous
emphysema.
 ABPA.

 Rib Fracture.

 Respiratory Failure.

 tracheoesofageal fistula (with MV).

 Death.
 GINA GUIDELINES FOR
Stepwise Approach to
Therapy :

G-IN-A : Global Initiative for

Asthma Management

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 GINA GUIDELINES FOR
Stepwise Approach to Therapy :
 PRN : Quick Relievers :
iSABA : given PRN
 Daily or increasing use indicates need for
long-term control therapy.
 Intensity of ttt depends on severity of EXB.

 Daily : Long-term Control Therapy:

ICS and other drugs in schedule
NB : Step 1 Intermittent asthma : no LTC.
 GINA GUIDELINES FOR
Stepwise Approach to Therapy :
Daily LTC
Step 2 Mild ICS/LD OR Cromolyn OR nedocromil OR
Persistent SR–theo OR LTM
Step 3  ICS/MD OR

Moderate  ICS/LD-MD + iLABA (OR SR-theo)

Persistent - If needed ↑ dose (ICS/HD, iLABA)

asthma - Consider refrral to a specialist
Step 4  ICS/HD + all :

Severe  LABD:iLABA OR SR_theo OR oral LABA

Persistent  Oral CT: long-term.

Asthma - Recommended refrral to a specialist.
 Stepwise Approach to Therapy
: Maintaining Control
STEP 4 ■ Step down if
Multiple long-term-control possible
medications, include ■ Step up if
oral corticosteroids necessary
■ Pat education &
STEP 3
environm control
> 1 Long-term-control
at every step
medications
■ Recommend
STEP 2 referral to
1 Long-term-control specialist at
medication : anti-inflammatory
Step 4;
■ consider referral
STEP 1
at Step 3
Quick-relief medication :PRN
 Step 1 Treatment :
Mild Intermittent
1) Daily Long-Term
Control : Not needed
2) PRN Quick Relief
–iSABA : PRN
– use, or use > 2 /
wk, may indicate need
for long-term-control
– Intensity of ttt
depends on severity of STEP 1
EXB
 Step 2 Treatment :
Mild Persistent
1) Daily Long-Term Control
– Anti-inflammatory
■ ICS (low dose) or
■ Cromolyn or
nedocromil OR
– SR theophylline (to
STEP 2
serum conc 5-15
mcg/mL) is an alternative
but not preferred.
– Leukotriene modifier
may be considered
 Step 2 Treatment :
Mild Persistent (continued)

2) PRN Quick Relief

■ iSABA : PRN
■ Daily or increasing
use indicates need
STEP 2
for long-term-
control
■ Intensity of ttt
depends on severity www.MansFans.com
of EXB
 Step 3 Treatment :
Moderate Persistent

1) Daily Long-Term Control

■ ICS (medium dose)
OR
■ ICS (low-to-medium dose)
STEP 3
AND
■ LABA or SR theophylline.
IF NEEDED, increase to:
■ ICS (medium-to-high dose)
and LABA.
Consider referral to a
specialist
 Step 3 Treatment :
( Moderate Persistent(continued

PRN Quick Relief

■ iSABA : PRN
■ Daily or increasing use
STEP 3
indicate need for long-
term-control therapy
■ Intensity of ttt depends

on severity of EXB
 Step 4 Treatment :
Severe Persistent
1) Daily Long-Term Control
■ ICS (high dose) AND
■ Long-acting STEP 4
bronchodilator
– iLABA OR
– SR theophylline OR
– LABA tablets AND
■ Long term Oral CST
Recommend referral to a
specialist

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 Step 4 Treatment :
Severe Persistent ( continued)

2) PRN Quick Relief

■ iSABA : PRN
■ Daily or increasing STEP 4

use indicates need

for long-term control
therapy
■ Intensity of ttt

depends on severity
of EXB.
those who care for the patients can be taught to“
”.manage cases well with what is available
E Parry
The Tropical Health & Education Trust
London
Thorax1997;52:589
Without actions asthma drugs
are available only for rich patients and
for animals in rich countries!

New Zealand.
Sunday Star. Times
January 4,2004
Photo : Kevin Stent

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Thank you
 New changes in asthma
medications
 Leukotriene modifiers now have a more
prominent role as controller treatment in
asthma, particularly in adults.
 LABA alone are no longer presented as an
option for add- on treatment at any step of
therapy, unless accompanied by ICS.
 Monotherapy with cromones is no longer
given as an alternative to monotherapy with
a low dose of ICS in adults.
 Some changes have been made to the tables
of equipotent daily doses of ICS for both
children and adults.
 How serious is it, as a health
? problem
 A very common AW disease.
 About 155 million individuals
worldwide are affected.
 Number one chronic illness
among children and young adults
 From 1979 to 1996, the no. of
children dying from asthma
increased 300%
 What is asthma ?
 Caused by hypersensitivity of airways
to a number of triggers
Dust-pollen-smoke-cold air-excercise

 The airways are obstructed leading to

difficulty in breathing
 Can lead to death in severe cases
 Usually associated with atopy,
elevated IgE in serum and bronchial
hyper- responsiveness
ACUTE SEVERE ASTHMA TERMINAL ASTHMA

pt is alert, distressed drowsy, confused

hot sweats, pale cold sweats, cyanosed

wants to sit up wants to lie down

says few words can not speak
hyperinflation with hyperinflation with
insp & exp movements no expansion
audible wheezes silent chest

tachycard., P alternans bradycar., no pulsus

 FLOW-VOLUME LOOP
. Normal Loop → rapid rise to the PEFR,
followed by a nearly linear fall.

. Obstructive → maximal exp begins & ends

at higher lung volumes and lower flow rates
than normal → coved pattern.

. Restrictive → lung volumes & flow rates are

↓ but the flow in relation to lung volume is
> normal → witch's hat" appearance with a
steep descending limb.
 LEVELS OF ASTHMA CONTROL
PARTLY
CONTROLLED CONTROLLED
CHARACTERISTIC All of the) Any measure) UNCONTROLLED
(following (present in any wk

Daytime Symptoms None twice /wk ≤

(twice /wk ≥)
features/wk 3 ≤
Need For Reliever None of partly
twice /wk ≤
ttt controlled
(twice /wk ≥)
Nocturnal Symptoms asthma
None Any
Limitations Of
Activity Non Any
(PFT (PEF or FEV1 Normal OPV 80% >

EXB
None One /year ≤ One in any wk
 Atopy
 Definition : an allergic hypersensitivity
affecting parts of the body not in direct
contact with the allergen. Associated
with :
1 - a strong hereditary component.
2 - elevated serum levels of total and
allergen-specific IgE, → positive skin-
prick tests to common allergens.
 Includes atopic dermatitis, allergic
rhinitis, conjunctivitis, and asthma.
 Atopic syndrome can be fatal in serious
allergic reactions such as anaphylaxis,
due to reaction to food or environment.
 Pulsus paradoxus
 How to elicit the sign :

 Can be measured by listening to Korotkoff sounds

during blood pressure measurement -- slowly
decrease cuff pressure to SBP level where sounds
are first heard during expiration. Then, cuff
pressure is slowly lowered further until Korotkoff
sounds are heard throughout the respiratory cycle,
during both inspiration and expiration.
 If the pressure difference between hearing the
first sounds and hearing them throughout the
respiratory cycle is > 10mmHg, it can be classified
as pulsus paradoxus.
 INDUCERS
:Pathogenesis Allergens,Chemical sensitisers,
Airway Air pollutants, Virus infections
Hyperresponsiveness
Genetic*

INFLAMMATION
Airflow Limitation

SYMPTOMS
TRIGGERS Cough Wheeze
Exercise, Cold Air Dyspnoea
:Mucous plug in asthma
 Additional Tests
The Tests Reasons for Additional Tests
Patient has symptoms spirometry
but is normal or – Assess diurnal variation of peak flow over 1
near normal. to 2 weeks.

– Refer to a specialist for

bronchoprovocation withmethacholine,
histamine, or exercise; negative test may hel
rule out asthma.

Suspect infection, large airway lesions, heart – Chest x-ray

disease, or obstruction by foreign object

Suspect coexisting chronic obstructive pulmonary

– Additional pulmonary function studies
disease, restrictive defect, or central airway – Diffusing capacity test
obstruction

Suspect other factors contribute to asthma – Allergy tests—skin or in vitro

(These are not diagnostic tests for asthma.) – Nasal examination
–Gastroesophagealreflux assessment
 Severe episode
 Subcutaneous emphysema
 ·Significant reduction of breath sounds

suggesting mucus plugging or

pneumothorax.
 ·Pulsus paradoxus greater than 20 mm Hg

 ·Agitation

 Unable to lie flat

 PEF after therapy less than 50%.

 Treatment: First-line Drugs
Oxygen to keep SaO2 > 92%
Inhaled Beta2 Agonists: Salbutamol (Albuterol)

MDI: 4-8 puffs (100 ug/puff) q15-20 min

with spacer, increase by one puff
q 30-60 sec
Wet Nebulizer: 2.5-5 mg (0.5-1 ml) in 2.5 ml
normal saline q15-20 min
Corticosteroids
Oral: prednisone 40-60 mg
Intravenous: methylprednisolone 125 mg bolus
then 120-180 mg/day in 3-4 divided doses for 48 hrs
 Step 1: Initial Assessment
Vital Signs
 Heart Rate
 Respiratory Rate
 Peak Expiratory Flow Rate (PEF) or FEV1
 Oxygen Saturation
 Respiratory Status

 Lung auscultation
 Assess accessory muscle use
 Chest X-Ray has low yield in acute
exacerbations
 Assessment if patient in extremis

 Arterial Blood Gas

 Step 2: Initial Management
 Inhaled Short-acting Beta Agonist (Nebulized Albuterol)
One dose up to every 20 minutes for one hour
 Anticholinergic (Ipratropium bromide or Atrovent)
Indication: FEV1 or PEF <50% of predicted (Severe)
Add to Nebulized Albuterol
 Systemic Corticosteroid IV Indication :
Severe episode (FEV1 or PEF <50% predicted)
No immediate response
 Oxygen indication Oxygen Saturation <91%
 Consider Additional measures for severe exacerbation
 Step 3: Reassess
Repeat measures in step 1
 Moderate episode ( PEF 60-80% of predicted )
Nebulized Albuterol hourly
Consider Systemic Corticosteroids
Continue management for 1-3 hours while improving
 Severe episode ( PEF <60% predicted )
 Nebulized Albuterol hourly or continuous
 Consider adding ipratroprium bromide to nebulizer
 Oxygen
 Systemic Corticosteroids
 Prednisone 1-2 mg/kg/day qd-bid
 Maximum: 40-60 mg/day for 5-10 days
 No tapering needed if use less than 2 weeks
 Emergency Room Management of Asthma
,O2 to keep Sat >91% •

nebulized b2 agonists up to every 20 min •

Systemic steroids and Ipratropium in severe cases •

Good Response Partial Response Poor Response

PEF > 70% PEF 50-70% PEF <50%

Continue
1-2 hrs
Disch arge PEF >70% PEF <70% Admit to the
Home Hospital
 Managing Exercise-Induced
( Bronchospasm(EIB )(continued

■ Management Strategies
• Short-acting inhaled beta2-agonists used
shortly before exercise last 2 to 3 hours
• Salmeterol may prevent EIB for 10 to 12 hours
• Cromolyn and nedcromil are also acceptable
• A lengthy warmup period before exercise may
preclude medications for patients who can
tolerate it
• Long-term-control therapy, if appropriate
 Hospitalized patients:

1 mg / kg of prednisone equiv. / 6 – 12 hrs

for 48 hrs
or FEV1 or PEFR reaches 50 % of predicted
or of
baseline
then decrease dose to 60-80 mg / d. to
achieve
PEF 70 %

 ICS to be started at beginning of tapering

 If patient discharged from ER : 40 mg x 5 d.

short courses:

• 0.5 – 1 mg / kg / d prednisone in a single or bid

dose

( 40-60 mg / d for 5-10 days )

Bid regimen decreases side effects

1 more week of a reduced dose can be added

relatively little dose-related toxicity

( mood disturb. – increased appet. – loss of

glucose control in DM – candidiasis –
cough )
 Longer courses :
 for more protracted bouts of severe asthma
 slower rate for tapering
( avoid exacerbations & adrenal
suppression )
 repeated efforts to decrease dose to min.
needed
 alternate days is preferred
Alternate days :
in severe persistent asthma
( high dose ICS )
I.V.
methyl predn.
In ER:
125 mg stat decreases rate of
return to er

In ward :
40-60 mg qid
 INHALED CORTICOSTEROIDS

• 1st line therapy for persistent asthma

• High concentration directly to site of
inflammation
• Therapeutic index of drugs greatly
enhanced
leading to less side effects
Members:
beclomethasone triamcinolone
flunisolide budesonide
fluticasone
• MDI
PROPER TECHNIQUE
INHALATION CHAMBER

DRUG POWDER INHALERS

NON – CFC PERPELLANT SYST.

• NEBULIZERS
Dose :
• 400 – 1000 ug of beclomethasone dipropionate or
equivalent
• Increase dose as necessary guided by:
symp. ( frequency of B2 agonists – signs of
poorly
controlled asthma )
PEF
50-100 % till symp. Are controlled
In case of: severe symp. – night awakening –
PEFR > 65% of predicted give a short course of
OCS