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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
kartegners syndrome.
CF very thick and sticky secretions,, cilia and cough can not clear it
out its 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 shouldnt
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
A chronic inflammatory disorder of the airways
Many cells and cellular elements play a role
Chronic inflammation is associated with airway
hyper-responsiveness to minor stimuli that leads
to recurrent episodes of wheezing,
breathlessness, chest tightness, and coughing
Widespread, variable, and often reversible airflow
limitation recurrent disease.
The commonest chronic disease in children.
Bronchospasm
Edema, Mucus

Hyper-responsiveness

INFLAMMATION!!!
(hallmark)
Asthma Inflammation: Cells and
Mediators

Source: Peter J. Barnes,


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

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.
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 Environmental Factors
Genetic Indoor allergens are biological

- Atopy- hygiene hypothesis and not dose dependent.


(decreases the use of the Outdoor allergens

immune system (TH1) due Occupational sensitizers (low

to excessive hygiene and dose stimulate asthmatics


indoor life). whereas high dose will stimulate
asthmatics and non-asthmatics
- Airway hyper- Tobacco smoke
responsiveness Air Pollution
Gender in children males Respiratory Infections
more common unlike Diet
adults.
Obesity
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 wont 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 doesnt 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

Dont 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 cant
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 doesnt
start severe early in its course.
Levels of Asthma
Control
Controlled Partly controlled
Characteristic (Any present in any week)
Uncontrolled
(All of the following)

More than
Daytime symptoms None (2 or less / week)
twice / week

Limitations of activities None Any


3 or more features
Nocturnal symptoms / of partly
None Any controlled asthma
awakening
present in any
week
Need for rescue / More than
None (2 or less / week)
reliever treatment twice / week

Lung function < 80% predicted or personal


(PEF or FEV1) Normal
best (if known) on any day

Exacerbation
(requirement of systemic None One or more / year 1 in any week
steroids)
REDUCE
LEVEL OF CONTROL TREATMENT OF ACTION
maintain and find lowest
controlled controlling step

consider stepping up to
partly controlled gain control

INCREASE
uncontrolled step up until controlled

exacerbation 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
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
Relievers Controllers
Inhaled fast-acting 2- Inhaled corticosteroids are good
agonists because they are broad spectrum
affecting the different inflammatory
Inhaled anticholinergics
cells and mediators.
Theophylline : not used Inhaled long-acting 2 -
anymore as a relievers coz
very toxic and have a low agonists ( never used alone coz of
therapeutic index can lead increase mortality must be
to seizures. combined with corticosteroids)
Inhaled cromones not used any
more.
Oral anti-leukotrienes
(monateleucast singular)
Oral theophyllines
Oral corticosteroids
Why dont patients comply
with treatment?
A common cause of non-controlled asthma is non-
compliance. Therefore, before changing medication check
for compliance (60% are non-compliant)
Intentional Unintentional
Feel better Forget treatment
Fear of side effects Misunderstand regimen / lack
information
Dont notice any benefit
Unable to use their inhaler
Fear of addiction
Run out of medication
Fear of being seen as an
invalid
Too complex regimen
Cant afford medication
Cromolyn Sodium

Non-steroidal anti-
inflammatory
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
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
Peak expiratory flow rate ONLY IN FEW CASES
Pulse oximetry
ABG ( its very painful)
Only done in
CXR severe cases
CBC will show leukocytosis because its
an inflammation.
Oxygen
Hypoxemia is common
It worsens airway hyperreactivity
Monitor saturation
Inhaled 2 agonist
Every 20 minutes in the
first hour ( 6-8 puffs )
Assess after each nebulizer
-better than nebulizer
because its 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 agonist
If severe in the beginning
If on PO prednisolone or high dose
inhaled steroids.
Previous severe attacks
Ipratropium Bromide
Anticholinergic is not routinely used
Anti-cholinergic
For severe cases
Along with 2 agonist
Response to the first hour
wait and observe for 1-2 hours
and if he didnt respond then
admit

Good POOR
Discharge Admit

Partial
Keep for 1-2 hours
Admit
Discharge

Follow up
Give inhaled 2 agonist
Steroids
When to come back?
Turbohaler came in the last osce.