Internal medicine

Topic: bronchial Asthma

Lec #: 3

Dr: mousa malkawy

Date: 26-10-2009

Asthma-Definition
A chronic inflammatory disorder of the airways associated with airway
hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest
tightness, and coughing. These episodes are usually associated with reversible airway
obstruction

Inflammation of the Airway: inflammation with T lymphocytes(mainly TH2), mast
cells, eosinophils with associated plasma exudation, smooth muscle hypertrophy, matrix
deposition, mucus plugging and epithelial damage

Airway hyperresponsiveness: Asthmatic's airways do constrict to usual stimuli which
don't cause constriction in normal people. As if they are exposed to cold air, dust, smoke or
if they exercise.

reversible airway obstruction : The obstruction is usually reversible (spontaneous or
with treatment) in contrast to COPD which is a progressive irreversible disease  so in
asthma if you give bronchodilator and treat the underlying disease, the airway obstruction
will be relieved, while in COPD it's permanent airway limitation.

Most patients have all these symptoms but some may have one symptom alone as cough
alone or SOB alone.

Epidemiology
 Asthma is a common disease and affects people worldwide, with an estimated prevalence
of 300 million or (5-20) % people affected worldwide.

 The highest prevalence present in Wales (17 %), Newzealand and Ireland (15 %). And the
mortality is higher in underdeveloped countries being highest in Russian federation due to
poor management.

 Prevalence increasing in many

countries, especially in children

 Asthma is considered as a cause

of significant number of
preventable deaths  if we treat
those pts with asthma we can
prevent there deaths..

 A major cause of school/work

absence
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Factors influencing asthma

1- Host factors
A- Genetic:
Asthma is not a disease that is inherited by a single gene; it is polygenic.
Where we have Genes that code for IgE production, Genes for airway hyperresponsiveness
even genes responsible for the response to steroids (some patients respond others don't)  so
these genes affect pathogenesis, severity and treatment.

B- Atopy :
Means overproduction of IgE specific to common aero-allergens that normally not cause IgE
production
those persons who are atopic are more likely to develop asthma
Not every atopic is asthmatic also not every asthmatic is atopic  we have atopic asthma and
non atopic asthma.
Atopy can be tested either by measuring total IgE level or specific IgE level or by simple skin
prick test and this is type I immune reactions so will appear & disappear in few minutes .
Examples of major atopic disease include : Allergic rhinitis, eczema and asthma

C- Airway hyperresponsiveness:
Those persons who have airway hyperresponsiveness are more likely to develop asthma
You might have airway hyperresponsiveness without asthma but you cannot find asthmatic
patient without airway hyperresponsiveness  bcz airways hyperresponsiveness is one of the
three characteristic of asthma that must be found to consider this disease as asthma.
This differs from Atopy because you might be atopic and asthmatic or atopic and non
asthmatic.

D-Lung function in infancy:

Premature babies who are born before 9 months might have Bronchopulmonary dysplasia
(BPD)  those are more likely to develop asthma later in life.

E-Sex:
The sex plays a role in asthma.
In pediatric age group  boys are affected more than girls, boys have smaller calliper of
airway than girls
In adulthood  equal predominance
After age of 40  females are more affected. The process of this variation might be related to
estrogens level.

F-Obesity:
There is a relation between obesity and asthma; obese females are more likely to get bronchial
asthma and have poor response to asthma medications but if they lose weight their response to
treatment improves.

G-Rhinitis:
Recent study from France that was published last year found that rhinitis alone is a risk factor
for asthma.
In this study , 6000 person ( adults from 20-40 years old) was followed from 8 10 years, this
study revealed that : those who are non atopic & non rhinitis 1% develop asthma , those who
are atopic & rhinitis 4 % develop asthma, those who are rhinitis alone 3 % develop asthma .

2- Environmental factors
A- Exposure to allergens (indoor and outdoor allergens):
Common allergens worldwide are dust, grass pollens , mixed tree pollens , animals ( cats ,
birds ) , peanut allergens ( in the West ).
Some studies showed that the more exposure to allergens the more probable one gets asthma.

B- Infections (RCV, Parainfluenza, RV) :

Some studies showed that children with proved infection to respiratory syncytial virus (RCV),
about 40% of them develop asthma-like symptoms when they grow up.

C- Hygiene hypothesis:
Growing up in clean environment may predispose toward an IgE response (mediated by TH2)
to allergens, conversely growing up in dirtier environment may allow the immune response to
avoid developing allergic response
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The hypothesis claims that Children who are exposed to recurrent infections are protected
against asthma  bcz infections direct cells from CD4 to CD8, TH2 to TH1 & Treg which
both have protective role.
Some studies found that children who attend daycare facilities are less likely to develop
asthma, because of the higher chance of getting infected.
Even in families the more the number of the family members plays a protective role i.e. a
family of 9 members has less chance compared to a family of 4 members. Even in the family
the first child has a higher chance than the second and the second more than the third and so
on.
A study was done to compare the prevalence of asthma in East and West Germany showed that
it is more in West Germany. Maybe because in East Germany the socioeconomic state is lower
and the family size is larger.

D- Occupational sensitizers:
With asthma of recent onset we should ask about occupation.
People working in Plastic factors or exposed to Isocyanates or other sensitizers are at risk.

E- Tobacco smoking:
There is a positive correlation between smoking and the prevalence of asthma, whether active
smoking or second-hand (passive) smoking or even mother smoke since there infants are more
likely to develop asthma.
Smokers have poor response to treatment.
Studies showed that environmental smoking is associated with increased asthma-like
symptoms.

F- Air pollution:
With sulphur dioxide, ozone and particulate matters. etc.

G- Diet:
Children who are breast fed are less likely to develop atopy and asthma in comparison to those
on formulas or cow's milk.
Increased anti oxidants (vegetables and fruits) might be protective.
n-6 PUFA( poly unsaturated fat ) present in margarine and vegetable oil increases the risk
While the 3-n PUFA present in fishy oil decreases it.

Pathogenesis

 This diagram shows a balance between Th1 & Th2 lymphocytes.

 Th2 lymphocytes directs atopic reaction through cytokines  interleukin 4 promote IgE
production and interleukin 5 which recruits & activates eosinophils so if inflammatory response
tend to be more toward Th2 lymphocytes you are more likely to develop allergic diseases
including asthma.

 allergens will be taken by APC-dendritic cells that will present antigens to Th2 cells, if Th2
lymphocytes are sensitized, they will produce interleukin 4 that promote IgE production and
interleukin 5 that recruits & activates eosinophils then activated eosinophils will produce
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eosinophil cationic proteins(ECP), major basic proteins (MBP) and peroxides (EPX) that some of
them cause epithelial destruction, others promote angiogenesis, also others cause smooth muscle
hypertrophy & mucus gland hyper secretion .

 So as we said there is an inflammation called chronic eosinophlilic bronchitis that is triggered by

the allergens, sensitizers, viruses and so on. If the inflammation is very severe the patients will
have symptoms all the time, if inflammation is mild or moderate they will have firstly airway
hyperresponsiveness, and they will show the symptoms whenever they are exposed to triggers,
allergens, exercise, cold air, SO2.etc or if they have viral infection like common cold.
 In very severe cases, asthma might behave like COPD leading to partially irreversible or
irreversible obstruction .Fortunately minority of pts have severe cases of asthma (5-10) %.

Picture A: shows normal airway where we have pseudostratified ciliated columnar epithelium with thin
symmetrical basement membrane.
Picture B: shows asthmatic airways where we have very thick basement membrane with increase numbers of
goblet cells & inflammatory cells mainly eosinophils; also we can see smooth muscle hypertrophy.
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Pathogenesis from Kumar & Clark's textbook:

The pathogenesis of asthma is complex. It involve number of cells , mediators, nerves, and vascular leakage
that can be activated by several different mechanisms of which exposure to allergen is among the most
significant.
Clinical severity and chronicity of asthma depend on the interplay between airway inflammation and
airway remodeling .

Airway inflammation :
The inflammatory component is driven by TH2 lymphocytes which facilitate IgE synthesis through IL-4 and
eosinophilic inflammation through IL-5. Several key cells are involved in the inflammatory response that
characterizes all types of asthma.
1. Mast cells
These are increased in the epithelium, smooth muscle, and mucus gland in asthma and release powerfully
performed and newly generated mediators that act on smooth muscle, small blood vessels, mucus secreting
cells and sensory nerves. These mediators include histamine, PGD2, LTC4 and its metabolites LTD4 and
LTE4  those cause immediate asthmatic reaction. Mast cells are inhibited by such drugs like sodium
chromoglicate and beta-2 agonist. Mast cells also release an array of cytokines, chemokines and growth
factors that contribute to the late asthmatic response and more chronic aspect of asthma.
2. Eosinophils
These cells are found in large numbers in the bronchial wall and secretions of asthmatics. These cells are
attracted by the eosinophilopoietic cytokines IL-3, IL-5, GM-CSF. Eosinophils when activated they release
LTC4, eosinophil cationic proteins (ECP), major basic proteins (MBP) and peroxides (EPX) that are toxic to
epithelium. Both the number and activity of eosinophils will be reduced by corticosteroids.
3. Dendritic cells and lymphocytes
These cells are abundant in the mucous membranes of the airways and alveoli. Dendritic cells have a role in
the initial uptake and presentation of allergen to lymphocytes. CD4+ has a role in cytokines production, those
cytokines plays a key part in migration and activation of mast cells (IL-3, IL-4, IL-9, IL-13) and eosinophils
(IL-3, IL-5, GM-CSF).

Airway remodeling :
A characteristic feature of chronic asthma is an alternation of structure and function of the formed elements of
the airways. Together, these structural changes interact with inflammatory cells and mediators to cause the
characteristic feature of asthma. Deposition of matrix proteins, swelling and cellular infiltration cause
expansion of the submucosa beneath the epithelium so that for a given degree of smooth muscle shortening
there's excess airway narrowing. Swellings outside the smooth muscle layer spread the retractile forces
exerted by the surrounding alveoli over a greater surface area so that the airway closes more easily. Several
factors contribute to these changes.
1. The epithelium
In asthma the epithelium is stressed and damaged with loss of ciliated columnar epithelium on the lumen.
Metaplasia occurs with a resultant increase in the number and activity of mucus-secreting goblet cells. Also
the epithelium is a major source of mediators, cytokines and growth factors that serve to enhance
inflammation and tissue remodeling. The damage make the epithelium more vulnerable to infection by
common respiratory viruses e.g. rhinovirus, coronavirus and to the effect of air pollution. There are also
increase (NO) production which indicates epithelial damage and activation.
2. Epithelial basement membrane
A pathognonomic feature of asthma is the deposition of repair collagen (type I, III, V) and proteoglycans
beneath the basement membrane. These, along with the deposition of other matrix proteins cause the
appearance of a thickened basement membrane observed by L.M.  these changes aid in cells movement,
prolong inflammatory cells survival and prime them for mediators' secretion.
3. Smooth muscles
A prominent feature of asthma is hyperplasia of the helical bands of airway smooth muscle. In addition to that
the smooth muscle alters in activity to contract more easily and stay contracted bcz of change in actin-myosin
cross link cycle. These changes allow asthmatic airways to contract too much and too easily.
4. Nerves
Neural reflexes both centrally and peripherally contribute to the irritability of asthmatic airways. Central
reflexes involve stimulation of nerve endings in the epithelium and submucosa with transmission of impulses
via spinal cord to the brain and then back to airways where release of acetylcholine from nerve endings
stimulate M3 receptors on smooth muscle causing contraction. Local reflexes involve the release of variety of
neuropeptides. Some of these are smooth muscle contractants (substance P, neurokinin A); some are
vasoconstrictors (Calcitonin gene-related peptide, CGRP); some are vasodilators (neuropeptides y, vasoactive
intestinal polypeptide)

Diagnosis
We depend mainly on history and physical examination, to a lesser extent on pulmonary function tests and
lab findings. Most of asthma cases are diagnosed by history & physical examination alone so if the patient
comes with typical symptoms of asthma especially if asthma is recurrent, the diagnosis can be made by
history & physical examination only.

1- History and physical examination

As in most diseases history and physical examination are very important. On taking history of an
asthmatic we have to concentrate on certain points; we ask about:
 Recurrent attacks of wheezing? Because asthma is an intermittent recurrent disease.
 Troublesome cough at night?
 Wheeze or cough after exercise? Usually those who have asthma develop SOB after exercise not
during it .while in COPD the opposite occurs.
 Wheeze or tightness after exposure to allergens or pollutants?
 Does the cold go to the chest or take more than 10 days to clear? In common cold it will stay
for 3-4 d and it will not affect the chest predominantly, in asthma cold is longstanding goes down
to the chest.
 Are symptoms improved by asthma treatment?

2- Pulmonary function tests

These are used to support the diagnosis but they are not a must for diagnosis because spirometry is not
available everywhere. If you have access, it is advisable to do spirometry for both diagnosis and follow
up.

A- Spirometry
 We measure the FEV1 (forced expiratory volume during the first second).
 We ask the patient to get a deep breath then blow as fast as hard as possible into the machine
and the amount of air that is expelled in the first second is the FEV1 and is normally >= 7080% of the vital capacity. I.e. FEV1/FVC ratio is >= 70-80%. Or >= 80%
 After administration of a bronchodilator (salbutamol) we repeat the test and we see how much
improvement in FEV1 (this is what we mean by reversibility = can be improved or reversed
by drugs) .IF there's FEV1 reversibility or improvement after giving bronchodilator by 12%
(or > 200 ml) from base line this indicates asthma.

B- Peak expiratory flow rate (PEFR)

 The subject is asked to take a full inspiration until total lung capacity achieved and then we ask
the pt to blow through the peak flow meter, which is held horizontally. This will give you a
record that is usually given in L/min or L/sec. The best of three tests is recorded.
 We ask the patient to measure his flow for diurnal variation "measure it in morning and
evening", normally in the morning the flow is less than the evening "thats why asthmatic
patient express symptoms in early morning" but the variation is less than 20% in normal
subject. If it is > 20 % with the presence of asthma symptoms this suggests asthma.
 improvement by 60ml (or 20% ) or diurnal variation of > 20% is suggestive for asthma
This is the peak flow device; there are
various devices with different shapes. All
what you need to do is to take deep breath
and blow in this machine and there's a scale
(L/sec or min). You can give it to the pt if
the pt has no symptoms at the time you
examine him, you ask the patient to record in
evening and morning (for diurnal variation)
and at time where he get symptoms.

C- Airway responsiveness
 Some difficult cases have symptoms of asthma but at time of examination they are normal with no
reversibility & normal by spirometry but they complain from asthma symptoms, for these pts we
can go and do for them Airway hyper responsiveness because this is a must in asthma to have
Airway hyper responsiveness.
Airway hyper responsiveness + symptoms = asthma even if the spirometry is normal
 We test for airway hyperresponsiveness by first measuring the FEV1, then we give histamine or
methacholine in a very low concentration and we start increasing the dose. FEV1 will decrease >
20% with a dose of histamine less than 8 milligrams.

The PC20 (Provocative Concentration): is the concentration that causes a 20% drop of
FEV1.
See that the higher the degree of AHR (airway hyperresponsiveness) the lesser the dose
needed to lower the FEV1.
All asthmatic patients have airway hyper responsiveness so there is a drop in FEV1 by >
20 % with less than 8 mg/ml of histamine or methacholine, because if you increase the
dose even in normal people this will cause drop so the cut point is less than 8 mg/ml.
Normally, we need 64 mg/ml to cause a drop in FEV1 whereas in mild asthma we need
less than 8 mg/ml, and as asthma become more severe fewer doses is needed.

This figure shows normal spirometry of

flow-volume curve.
We look for first three elements FVC,
FEV1, FEV1/FVC with a column of
predicted values so any reading between
80 120 % predicted is considered normal.
Here before giving bronchodilator:
FEV=3.11L=92% predicted,
FEV1=2.56L=90% predicted,
FEV1/FVC=82% predicted
After giving bronchodilator:
FEV=3.12L=92% predicted,
FEV1=2.57L=90% predicted,
FEV1/FVC=82 % predicted
 No change before & after "no
reversibility", all readings are normal and
above 80 %
 Normal subject, no asthma
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If you notice here

preFEV1 = 2.56L = 77%prdicted
postFEV1= 3.06 L= 92% predicted
 A change of 0.5L (> 200ml)
 A change of 20% (> 12%) from
baseline
This indicate asthma
Blue column = preFEV1 (before
bronchodilator), # 1
Red column = postFEV1 (after
bronchodilator), # 2
Note that red column is higher than blue
which
indicate
improvement
after
bronchodilator.

3- Laboratory tests
No need for them in most of the cases.

A. Chest XX-ray
Is done in a patient with exacerbation like those who came to ER with severe attacks and no response
to treatment to see whether he has pneumonia or pneumothorax (asthmatics are more likely to develop
pneumothorax) .X-ray is not to diagnose asthma but to see if there's complication or precipitating factors.

B. Blood tests
 Eosinophiles count:
In atopic asthma we can look for eosinophils count in the blood that is elevated in some but not all
asthmatic pts, whereas eosinophils count in airway are elevated all the times in all asthmatics, we look
for them by taking biopsy.
 IgE level :
In non-responding cases to classical treatment we may measure the IgE level and give anti-IgE
drugs.

C. Skin tests
Used to identify allergy in atopic asthma. We apply different allergens then we look for the allergic
reaction. Helpful in knowing what allergens should the patient avoid.

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Management of asthma
 Education and develop patient/doctor partnership.
Tell the patient that this is a chronic disease, a life long disease and there's treatment that relive
symptoms with normal life but with no cure; otherwise he will keep jumping between clinics.
 Identify and reduce exposure to risk factors.
From history and- as said -skin tests we can advise the patient to avoid exposure to allergens, not
to leave the house in certain times of the year or to change the job.
 Pharmacotherapy of asthma
Tell the patient that we have two types of treatment: Controllers and risk-medications (relievers).
And let your patient knows what is he going to benefit from each drug. Some patients will say I
don't like the brown or the red inhalers (steroids) because I don't feel any difference. Here you
have to tell the patient that he shouldn't expect effect before at least 3 to 4 weeks of usage.
You might see patients who are afraid of the steroids so explain to them that the amount of
steroids used in inhalers is far little to cause complications of systemic steroids.
Others may have phobia of inhalers in general. Talk to them about the advantages of inhalers;
lesser dose and access to target organ.
 Assess, treat, and monitor asthma

Pharmacotherapy of asthma
We have two groups, controllers "have anti inflammatory effects" and relievers

A. Controllers
1- Inhaled glucocorticoids.
The drugs used in Jordan are:
-Beclomethasone-CFC (chlorofluorocarbons) drawn from the markets bcz of its effect on ozone layer.
-Beclomethasone-HFA (hydro- flouro- alkane) the new one.
-Budesonide-DPI (dry powder inhaler).
-Fluticasone.
.
2- Long-acting inhaled 2-agonists
Although they are bronchodilators they have a controlling effect i.e. anti inflammatory effect.
These drugs must not be used alone; instead they are combined with steroids. Studies showed that giving
2-agonists with steroids is more effective than doubling the dose of steroids.
3- Leukotriene modifiers
Montelukast and zafirlukast are used.
4- Theophylline.
5- Cromones
Like sodium cromoglycate, may be used in children, not used in adult treatment, not effective, expensive,
inhaled glucocorticoids are superior to them.
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6- Anti-IgE
Very expensive (1000 JD a month). But may have a role in cases that are not controlled by common
asthma medications.
7- Systemic glucocorticoids
If the patient is on highest dose of inhaled steroid and dilator but still not improving he may need long
term systemic steroids.
 The last four are not a first line of treatment

B. Relievers
Relievers: given acutely at the moment of symptoms appearance
1- Rapid- acting 2-agonists
Were called short acting, but now we have drugs that are fast-long acting.
- Rapid-long acting: formoterol (works within minutes so used in high risk cases) & salmeterol (works
within 20 -60 min)
-Rapid-short acting: salbutamol
2- Anticholinergic
Like ipratropium
In those that can not tolerate b2-agonist because of tremor or palpitation.
We also use them in cases of acute severe asthma. In emergency room we combine ipratropium and
salbutamol. It was found that combining both is superior to use either one of them alone.
3- Systemic glucocorticoids
Used in acute severe and life threatening asthma.
4- Theophylline.
Rarely used.
This is Inhaler with aerosols inside
them.
Small, cheep, but difficult to be
used bcz it need synchronization
(firing and inhalation at the same
time).
Studies shows that 2/3 of pts can't
use it in right ways.

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This device is called Discuss

"not sure", this is powder based
device, there's powder inside
not aerosols, easy to use but it's
expensive

Inhaler with spacer device, for

those who can't synchronize
firing and inhalation.

Factors affecting compliance

 Route of drug administration (oral vs. inhaled)
Teach the patient how to use inhalers. The problem with inhalers is that they are difficult to use since
we need synchronization between firing and inhalation. With perfect use of the inhaler (10 -15%) of the
dose will reach the airways.
If it difficult to use as in children or elderly patients use the spacer, where there is no need for the
synchronization.
The patient should not stop the medication if he sees improvement of his case because asthma is an
intermittent disease and relapse of the symptoms does not occur immediately after stopping the
medications. As a result some patients may think they don't need the medications any longer .This is not
true.
 Complexity of drug regimen:
We need to simplify the treatment, make combination of drugs in one device, now drugs contain
steroids along with bronchodilators so it is less difficult.
 Side effects of medications
many patients are worried about side effects of steroid so we must ensure them that inhaler steroid
dont have side effects as much as systemic steroids (e.g. diabetes, H.T, HIRSUTISIM), also some of pts
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think that steroids have side effects on child development, in first two years there maybe some stunting in
growth by 1-2 cm but once they reach adulthood, they will be same height as they where before.
Tell the patient to rinse his mouth after steroids; otherwise he may get candidiasis, dysphonia and
vocal cord problems.
 Support of family and health care professionals.

Treatment of asthma
Treatment goals

Achieve and maintain control of symptoms

Maintain normal activity levels.

Maintain pulmonary function as close to normal as possible.

Prevent asthma exacerbations.

Avoid adverse effects from asthma medications.

Prevent asthma mortality.

Levels of Asthma control

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1. Controlled asthma
What do we mean by Controlled Asthma?
Nowadays we concentrate more on controlling asthma rather than classification into mild, moderate, severe
or very severe because asthma is dynamic not static disease  you might see pt that is fine today and after
week he presented with exacerbation.
1-Day time symptoms: none or twice /week.
2-No limitations of activity.
3-No nocturnal symptoms  if he wakes up complaining of symptoms even one time
monthly this is not controlled.
4-Need for reliever: None or twice/week.
5- Normal lung function.
6-No exacerbations.

2. Partly controlled asthma

In partly controlled asthma, in any given week we must see at least one of the characteristics of partly
controlled asthma shown above in table.

3. Uncontrolled asthma
To say this is uncontrolled asthma. At least three of the features of partly controlled asthma must be present in
any week

Our treatment based on the level of asthma control

If the patient has a controlled disease we have to continue the same treatment. If the patient has
uncontrolled disease we can step up his treatment "we have five steps of treatment". If the patient is
controlled for a long time we step down his treatment to keep him on a minimal effective dose of inhaled
corticosteroid that control his symptoms.

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Steps of treatment

These guidelines from the GINA guidelines which are the global initiative for the asthma management so its
done in all countries all over the world, the best choice is the low dose (ICS) plus the long acting if the
patients can offer or can pay for that ,if not you can go to the others.
 Step one: If the patient has an occasional symptoms (less than twice/week) and they are relieved by
2 agonist we dont need to give a controller medications (steps 2, 3, 4, 5), he can use the rapid acting
2 agonist on need.  This applied to all steps.
 Step two: if he has more symptoms, more than that we go to step two, we choose one of the
following  1) low dose inhaled corticosteroid (ICS) or 2) leukotriene modifier but the low dose
(ICS) is better. And those on green boxes in the table they have level A evidence (it means they are
preferable, they have been documented in randomized controlled studies). Again our monitor is how
much symptoms he has and how many times he used these two medications
 Step three: If he still has symptoms-more than twice /week-we go to step three, where we choose
one of the following  1)low dose (ICS) plus long acting 2 agonist which is better than the second
choice which is 2)medium or high-dose(ICS) or we can keep him on 3) low dose (ICS) plus
leukotriene modifier or 4)low dose (ICS) plus theophyllin, theophyllin actually we dont use it here
in Jordan in this step but in other countries they use it because theophyllin is very cheap while the long
acting and the inhaled steroid are cost .
 Step four : we give 1) medium or high dose (ICS) plus long acting 2 agonist, now if this doesn't
relieve the pt symptoms we add to him 2)leukotriene modifier (treatment will be 1+2) , if this also
doesnt give benefit we add 3)theophyllin (treatment will be1+2+3).
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 Step five: we dont have choices except oral glucocorticosteroids, which we try to avoid all the time
but unfortunately some patient probably (5%-10%) they required long term oral glucocorticosteroids
because they dont have other choice and should accept the complications of these drugs. Recently in
the last 4-5 years they produce anti-IgE treatment ,so those who have severe symptoms and they are
not controlled and the IgE level is high and they are atopic we can give him anti-IgE (monoclonal
antibodies directed to IgE)

Stepping Down Treatment

Review medications after 3-6 months of stability and if stable reduce medications by 25-50%
If the patient is controlled for three to six months we think of stepping down his treatment to decrease the
dose of (ICS) first. Later on we can decrease the dose of long acting 2 agonist. And remember we should
never treat the patient by long acting alone because there are studies show that there is some mortality if
asthmatics are using long acting alone without ICS (inhaled corticosteroid) while in combination there is no
definite increase in mortality .

Assessment in Emergency Department

According to the table:

Those who present to the ER with exacerbation we have to asses them quickly in the emergency
department according to the signs & symptoms.

Recently they have removed this mild exacerbation; they talked about the moderate and the severe
ones.
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From the way the patient is talking we can judge weather the asthma is mild, moderate or severe,
weather they can speak complete sentence or he is talking phrases or small words, weather he using
his accessory muscles by assessing the respiratory rate, put a pulse-oxy meter and see oxygen
saturation, according to that you classify the pt.

We have also to check the peak flow (PEFR), if the peak flow is > 70%  mild, if between 40%69% moderate, Less than 40% severe, Less than 25%  life threatening

Management of Acute Exacerbations

Those who came to the ER, the best assessment is to assess the patient after the first dose of nibulized
2 agonist bcz some pts might came with peak flow of less than 40%, with one nibulization this peak
flow become 80%, so the best assessment after you see the patient give him nibulized 2 agonist 5mg
dose, re-assess him again and see the response:
NOTE: for all these steps we give O2 supplementation.
If the peak flow jump above 70%  you can step up his treatment and rest the underlying
(precipitating) factor and send him home, but if he continues to have symptoms we add
ipratropium ( ipratropium + plus short acting 2) and there is evidence that ipratropium plus
short acting 2( salbutamol) nibulization is superior to salbutamol nibulization alone .
If he didnt respond after (2-3) doses of nebulizers  then probably we give him systemic
steroid either oral or parenteral (parenteral is superior to the oral, providing the patient isnt
vomiting and the GIT is normal), if he didnt respond then you can decide on admission of the
patient.
If the peak flow is less than 40%  combine short acting plus ipratropium plus systemic
steroid.
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 If its life threatening and the patient are drowsy, comatose, had bradychardia, low BP  you
have to admit him to the ICU, give him nibulized medication, we can give every 15min or we
give it as continuous medication, there is no much side effect the only side effects are the
tachycardia and tremor and these you can observe.

And if he didnt respond to all these  we can considered mechanical ventilation, put the
patient on ventilator until the asthma attack is over.

 Once you admitted the patient you continue do the nibulized medication, you continue do the systemic
steroids, the first thing to improve in these patient are the symptoms so they feel better although they still
wheezing, the second thing to improve are the signs (the wheeze will disappear but the peak flow will still
low).
On average pts with severe asthma attack admitted to hospital requires 7-10 days for the peak flow to be
normalized, so the last thing to be corrected is the beak flow.

When to Discharge Patient Home ?

Before discharging the patient from the hospital you have to keep him on home medications (the
medications you plan to give ) for 24 hours, home medication including: oral steroid, ICS, long acting 2
agonist, short acting 2 agonist. Keep him 24 hours, if the peak flow is stable (PEF > 70% of predicted or
personal best), then you can discharge him and you have to make early appointment in the clinic after two
weeks because they might relapse during that period.
Remember PEF variability is< 20%

 
 
Resources:
- doctor slides
- Kumar textbook
- ru2ia lecture

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