Transcript Obstructive Airway Disease

Obstructive Airway Disease
Dr. Khalid Al-Mobaireek
King Khalid University Hospital
Obstructive airway Disease:
• Obstructive diseases are worse during expiration in the thoracic cavity
– During inspiration, we have negative pleural pressure leading to airway expansion, and
with expiration the opposite happens leading to narrowing of the airways. Therefore,
obstructive diseases are worse on expiration.
• Reversible = Asthma
• Irreversible: Bronchiectasis because the membrane is destroyed therefore the
obstruction is permanent. They present with productive cough with high amount
of sputum that are more in the morning with clubbing (indicating pus formation).
• very important to know if its localized or systemic (diffuse)
– Localized: very important to know if its localized or systemic.
• Anatomical defect
– Airway: Internal, External,
– Parenchymal
– Examples: foreign body, a lymph node compressing the airway or vascular
problem compressing a segment, or a systemic disease starting as local.
– Diffuse:
• Aspiration
• Muco-ciliary clearance:
primary ciliary dyskinesia (PCD) is an autosomal recessive disease where
the ciliary function (clearance of mucous) is impaired and do not have
good coordination, with normal mucous secretions. They are at
increased risk of bronchiectasis. 50% have kartegner’s syndrome.
CF very thick and sticky secretions,, cilia and cough can not clear it out
it’s the worse than PCD
• Immune deficiency because of recurrent infections.
• Post-infectious: Pertussis, TB, adenovirus..
• Swallowing difficulties: Neuromuscular disease, GERD, and congenital
defects e.g. palate diseases or congenital defect in the cartilage, T-E
fistula. These can cause aspiration leading to bilateral bronchiectasis.
• Congenital bronchiatasis born with abnormal cartilage.
• Bronchiectasis:
CT is the diagnostic method of choice, characteristic finding is signet
ring appearance. Normally each bronchus is accompanied by a
vessel and shouldn’t exceed the vessel diameter. In
bronchiectasis, the diameter of the bronchus is larger than that
of the vessel. Tram line appearance (two airways running in
parallel lines) in cross section.
Definition of Asthma
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A chronic inflammatory disorder of the airways
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Many cells and cellular elements play a role
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Chronic inflammation is associated with airway
hyper-responsiveness to minor stimuli that leads
to recurrent episodes of wheezing,
breathlessness, chest tightness, and coughing
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Widespread, variable, and often reversible airflow
limitation recurrent disease.
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The commonest chronic disease in children.
Bronchospasm
Edema, Mucus
Hyper-responsiveness
INFLAMMATION!!!
(hallmark)
Asthma Inflammation: Cells and Mediators
Source: Peter J. Barnes, MD
Asthma Inflammation: Cells and Mediators
Source: Peter J. Barnes, MD
NORMAL
ASTHMA
AIR TRAPPING
INSP
EXP
Air trapping leads to enlargement of the alveoli, if these ruptured the air
will leak leading to pneumothorax and air under the skin (sub-cutaneous
emphysema).
In inspiration the airway pressure is negative and the outside pressure is
positive therefore the airway expands and dilate. The opposite happens
during expiration and the airways get narrowed.
If the obstruction was intra-thoracic, the obstruction will be more evident
during expiration (extra-luminal pressure higher than intra-luminal
pressure during expiration), because airway will be narrowed and the
pressure is positive inside the airway. While obstruction outside the
thoracic cavity will be more evident during inspiration (extra-luminal
pressure higher than intra-luminal pressure during inspiration e.g. vocal
cord paralysis). If the manifestations are present equally in both phases
think of sub-glottic stenosis.
Ventilation Perfusion (V/Q) Mismatch
There will be V/Q mismatch because the blood coming to the lung is not
being oxygenized due to obstruction.
Burden of Asthma
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Asthma is one of the most common chronic diseases worldwide
with an estimated 300 million affected individuals

Prevalence increasing in many countries, especially in children
almost 1 in 6 are affected.
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A major cause of school/work absence
Asthma Prevalence
Asthma Prevalence
Qaseem 13%
Khobar 6%
Riyadh 10 %
Jeddah 13%
Abha 17%
Factors that Influence Asthma
Development and Expression
Host Factors
 Genetic
- Atopy- hygiene hypothesis
(decreases the use of the
immune system (TH1) due
to excessive hygiene and
indoor life).
- Airway hyperresponsiveness
 Gender in children males
more common unlike
adults.
 Obesity
Environmental Factors
 Indoor allergens are biological
and not dose dependent.
 Outdoor allergens
 Occupational sensitizers (low
dose stimulate asthmatics
whereas high dose will stimulate
asthmatics and non-asthmatics
 Tobacco smoke
 Air Pollution
 Respiratory Infections
 Diet
Environmental Allergens and
Childhood Asthma
– Dust mites: fecal material are small enough
to pass through the covering of the pillow.
Treatment is by air-tight seal of sheets.
– Furry pets: isolate the patient from the pet
to assure the diagnosis.
– Molds
– Cockroaches:
– Cigarette Smoking: 1st hand, 2nd
hand, and 3rd hand from remnant on
furniture and from cars. Therefore, smoke in
an open space.
POLLENS
Management of Chronic Asthma
• Depends on
– Exacerbations and attacks.
– Exacerbations requiring steroids.
– Night symptoms: how many times you wake up
from sleep due to symptoms (if more than twice a
month, it is uncontrolled).
– Symptoms: cough, etc.
– Use of bronchodilators.
History
• Symptoms (cough, wheeze, SOB)
Wheeze: not every patient with a wheeze has asthma. A 2 or 3 months child who has
similar asthma symptoms you need to check for structural abnormality
compressing the airways as cystic disease.
Foreign body is suspected when the child presents with sudden acute cough and
wheeze worse in expiration, it needs index of suspicion, when you do CXR the
expiratory film will show failure of emptying in the obstructed side (one is larger
than the other but you won’t see the obstruction itself) the bronchoscopy is
diagnostic and therapeutic.
• Onset, duration, frequency and severity
• Activity and nocturnal exacerbation
• Previous therapy
• Triggers
• Other atopies
• Family history
• Environmental history, SMOKING
• Systemic review (widen your DDx)
Physical Examination
• Most important is growth parameter asthma usually
doesn’t impair growth if it did then think of another
diagnosis as cystic fibrosis or immunological problem
(immunodeficiency) .
• ENT part of respiratory problem because it is lined by
ciliary epithelium examine the ear if there was a ciliary
problem the ear will be effected.
• Features of atopy.
• Chest findings
• PEF
• Check for clubbing its present its unlikely asthma, think of
other suppurative diseases.
The diagnosis of asthma should depend on history and
examination.
Investigations
• Don’t usually need investigations, and is mainly
history and physical to role out other systemic
diseases.
• Pulmonary Function Test
• Chest X ray: not done except in the suspicion of
another disease or severe asthmatics.
• Allergy testing in some
• PFT is only complementary and is not done to
children less than six years.
Skin Testing
Differential Diagnosis
• Infections
• Congenital Heart Disease
• Foreign body are mostly food because they can’t grind due
to lack of molars and are not radio-opaque by CXR, but you
see its effect during expiration CXR will show and emptying
of one lung only. However, foreign body in the esophagus is
not food and tends to be radio-opaque.
• GERD
• Bronchopulmonary dysplasia
• Structural anomalies (any child with severe asthma at the
age of 3-4 months think of something else like structural
problems because asthma doesn’t start severe early in its
course.
Levels of Asthma Control
Characteristic
Controlled
(All of the following)
Partly controlled
(Any present in any week)
Daytime symptoms
None (2 or less / week)
More than
twice / week
Limitations of activities
None
Any
Nocturnal symptoms /
awakening
None
Any
Need for rescue /
“reliever” treatment
None (2 or less / week)
More than
twice / week
Lung function
(PEF or FEV1)
Normal
< 80% predicted or personal
best (if known) on any day
Exacerbation
(requirement of systemic
steroids)
None
One or more / year
Uncontrolled
3 or more features
of partly
controlled asthma
present in any
week
1 in any week
REDUCE
LEVEL OF CONTROL
TREATMENT OF ACTION
partly controlled
consider stepping up to
gain control
INCREASE
controlled
maintain and find lowest
controlling step
uncontrolled
exacerbation
step up until controlled
treat as exacerbation
REDUCE
INCREASE
TREATMENT STEPS
STEP
STEP
STEP
STEP
STEP
1
2
3
4
5
Treatment objectives
• Achieve and maintain control of symptoms
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Maintain normal activity levels, including exercise
Maintain pulmonary function as close to normal levels as possible
Prevent asthma exacerbations
Avoid adverse effects from asthma medications
Prevent asthma mortality
•
Because asthma is a chronic condition, it usually requires continuous
medical care
• The primary aim of treatment is control of asthma. According to the
GINA guidelines, control is defined in terms of absence of symptoms
(acute and chronic), need to use reliever therapy, lung function and
freedom from restrictions on physical activity
GINA Guidelines 2006
Pharmacological therapy
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Relievers
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Inhaled fast-acting 2agonists
Inhaled anticholinergics
Theophylline : not used
anymore as a relievers coz
very toxic and have a low
therapeutic index can lead to
seizures.
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Controllers
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Inhaled corticosteroids are good
because they are broad spectrum
affecting the different inflammatory
cells and mediators.
Inhaled long-acting
2agonists ( never used alone coz of
increase mortality must be
combined with corticosteroids)
Inhaled cromones not used any
more.
Oral anti-leukotrienes
(monateleucast singular)
Oral theophyllines
Oral corticosteroids
Why don’t patients comply
with treatment?
A common cause of non-controlled asthma is noncompliance. Therefore, before changing medication check
for compliance (60% are non-compliant)
Intentional
• Feel better
• Fear of side effects
• Don’t notice any benefit
• Fear of addiction
• Fear of being seen as an
invalid
• Too complex regimen
• Can’t afford medication
Unintentional
• Forget treatment
• Misunderstand regimen / lack
information
• Unable to use their inhaler
• Run out of medication
Cromolyn Sodium
• Non-steroidal antiinflammatory
• Weak action on Early and
late phases
• Slow onset of action
• If no response in 6 weeks
change to ICS
• Side effects: Irritation
Inhaled Corticosteroids
• Effective in most cases
• Safe especially at low doses
• The anti-inflammatory of choice in asthma (
drug of choice coz they are broad spectrum
so they target many cells and mediators)
Laitinen LA
Inhaled Steroids
Side Effects
• No systemic side effects with inhaled steroids , candida infection may
occur.
• Growth: No significant effect at low to moderate doses.
• Bones: not important
• HPA axis: No serious clinical effect (high doses)
• Alteration of glucose and lipid metabolism: Clinical significant is
unclear (high doses)
• Cataract: No increase risk
• Skin: Purpura, easily bruising, dermal thinning
• Local side effects
Assessment: History
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Symptoms
Previous attacks
Prior therapy
Triggers
Physical examination:
Signs of airway obstruction:
• Fragmented speech
• Unable to tolerate recumbent position prefer to sit in
order to use accessory muscles.
• Expiration > 4 seconds
• Tachycardia, tachypnea and hypotension
• Use of accessory muscles
• Pulsus paradoxus > 10 mmHg
• Silent hyper=inflated chest
• Air leak
• Wheezing is a poor sign of obstruction.
Physical examination:
Signs of tissue hypoxia:
• Cyanosis
• Cardiac arrhythmia and hypotension (due to
increase in thoracic pressure causing a
decrease in venous return and consequently
hypotension).
• Restlessness, confusion, drowsiness and
obtundation
Physical examination:
Signs of Respiratory muscles fatigue:
• Increase respiratory rate
• Respiratory alterans (alteration between
thoracic and abdominal muscles during
inspiration)
• Abdominal paradox (inward movement of the
abdomen during inspiration)
Investigations:
• Investigations do not help in acute asthma,
and blood gases are rarely done except in
severe cases
ONLY IN FEW CASES
• Peak expiratory flow rate
• Pulse oximetry
Only done in
• ABG ( its very painful)
severe cases
• CXR
• CBC will show leukocytosis because it’s an
inflammation.
Oxygen
• Hypoxemia is common
• It worsens airway hyperreactivity
• Monitor saturation
Inhaled β2 agonist
Every 20 minutes in the first hour (
6-8 puffs )
Assess after each nebulizer
-better than nebulizer because it’s
more localized, less side effects
and faster onset of action.
Steroids
• Do not wait for inhaled B2 agonist response,
start immediately on suspicion with oral
steroids because it takes 3-4 hours to work.
• If not responding to the β agonist
• If severe in the beginning
• If on PO prednisolone or high dose inhaled
steroids.
• Previous severe attacks
Ipratropium Bromide
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Anticholinergic is not routinely used
Anti-cholinergic
For severe cases
Along with β2 agonist
Response to the first hour
wait and observe for 1-2 hours and if he didn’t
respond then admit
POOR
Admit
Good
Discharge
Partial
Keep for 1-2 hours
Admit
Discharge
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Follow up
Give inhaled β2 agonist
Steroids
When to come back?
Turbohaler came in the last osce.