AIRWAY DISEASES

By: Dr. Abiy W.

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Components of airway diseases
 BRONCHIAL ASTHMA

Def: Syndrome of intermittent reversible

airway obstruction manifested by paroxysms
of dyspnea, cough and wheezing.

Pathologic def: chronic inflammatory disease

of airway with increased responsiveness of
tracheobronchial trees to multiple stimuli.
Epidemiology
Asthma is one of the most common chronic
diseases globally and currently affects ~300
million people.
In developed, 10–12% of adults and 15% of
children affected by the disease.
In developing countries - prevalence of
asthma had been much lower, and there is a
rising incidence associated with increased
urbanization.
present at any age with a peak age of 3yrs
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In childhood, 2X M, than females but by adulthood
the sex ratio has equalized.
Adults with asthma, rarely become permanently
asymptomatic.
Major risk factors for asthma deaths are:
 poorly controlled disease with frequent
use of bronchodilator inhalers
 Lack of corticosteroid therapy
 previous admissions to hospital with
near-fatal asthma.

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CAUSES
• Heterogenous disease

• Genetic and environmental factors contribute to

initiation and continuance.
Risk factors and triggers in asthma
1) Atopy
is due to the genetically determined production of
specific IgE antibody
major risk factor for asthma, and
Patients with asthma commonly suffer from other
atopic diseases; allergic rhinitis (80% of asthmatic
patients), and atopic dermatitis (eczema).
may be found in 40–50% of the population in
wealthy countries, with only a proportion
becoming asthmatic
Allergens that lead to sensitization are usually
proteins that have protease activity

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2. Idiosynchriatic (Intrinsic Asthma / non atopic)
HX of allergy.
 later onset o≈ 10% asthmatics have normal
serum concentrations of IgE.
 negative skin tests to common inhalant
allergens
 No personal/family f disease (adult-onset asthma)
 commonly have concomitant nasal polyps
 may be aspirin-sensitive.
 usually have more severe, persistent asthma.

3. Mixed groups - both

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Pathogenesis
Asthma is associated with a specific chronic
inflammation of the mucosa of the lower
airways (trachea - terminal bronchioles)
The airway mucosa is infiltrated with activated
eosinophils and T-lymphocytes, and there is
activation of mucosal mast cells.
One of the main aims of treatment is to
reduce this inflammation.

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Pathology
 Thickening of the basement membrane due to
subepithelial collagen deposition; also the airway
wall itself may be thickened, edematous &
narrowed rarely fibrosis occurs.
 Hypertrophy and hyperplasia of airway smooth ms
 There is also vasodilatation and increased numbers
of blood vessels (angiogenesis).
 In fatal asthma, occlusion of the airway lumen by a
mucous plug, which composed of mucus secreted
from goblet cells and plasma proteins from leaky
bronchial vessels.

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 Muscles

Goblet cells Ciliated

cells

Bronchial glands

Cartilage

Bronchioles (section)
 Mucosal
edema

Mucus
Muscle contraction
secretion
increase

Asthma case
Mast Cells
important in initiating the acute
bronchoconstrictor responses
are localized to the airway smooth ms layer; not
found in patients with eosinophilic bronchitis.
• activated by allergens through an IgE-dependent
mechanism
• Mast cells release several bronchoconstrictor
mediators; prostaglandin D2, histamine, cysteinyl-
leukotrienes, cytokines, chemokines, growth factors,
and neurotrophins.

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Macrophages and Dendritic Cells
Release of certain pattern of cytokines
Dendritic cells are specialized macrophage-like
cells, which are the major antigen-presenting cells.

Eosinophils
Inhalation of Allergen results in a marked increase
in activated eosinophils in the airways.
Eosinophils - linked to AHR through the release of
basic proteins and oxygen-derived free radicals

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Other cells

T-lymphocytes: release cytokines, resulting in the

recruitment and survival of eosinophils and in the
maintenance of a mast cell population in the
airways.
 Structural cells of the airways, including
epithelial cells, fibroblasts and airway smooth ms
cells, are also an important source of inflammatory
mediators, in asthma.

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Inflammatory Mediators
such as histamine, PG, and cysteinyl-leukotrienes ;
contract airway smooth muscle
increase microvascular leakage
increase airway mucus secretion
attract other inflammatory cells.
Chemokines - attracting inflammatory cells from the
bronchial circulation into the airways.
Cytokines
(IL-4, IL-5, and IL-13) mediate allergic inflammation
proinflammatory cytokines;(TNF-alpha) and IL-1,
amplify the inflammatory response.
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 Nitric Oxide
 Produced by airway epithelial cells and
macrophages by NO-synthase.
Increased NO may contribute to the bronchial
vasodilation observed in asthma.

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Asthma Triggers
Exercise
 Exercise-induced asthma (EIA) typically begins
after exercise has ended and recovers spontaneously
in 30 min.
 EIA is worse in cold, dry climates than in hot,
humid conditions.
 more common in cross-country running in cold
weather & ice hockey than in swimming.
It may be prevented by prior administration of β2-
agonists and antileukotrienes, but is best prevented
by regular treatment with inhaled glucocorticoids.

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Pathophysiology
Limitation of airflow is mainly due to
bronchoconstriction, but airway edema, vascular
congestion, and luminal occlusion with exudate
may also contribute.
This results in a reduction in (FEV1), FEV1 /
forced vital capacity (FVC) ratio, and peak
expiratory flow (PEF), as well as an increase in
airway resistance.
Early closure of peripheral airway results in lung
hyperinflation (air trapping), and increased residual
volume, particularly during acute exacerbations.

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AHR (Airway Hyper Responsiveness) =
excessive bronchoconstrictor response to
multiple inhaled triggers
The increase in AHR is linked to the
frequency of asthma symptoms; thus, an
important aim of therapy is to reduce AHR.

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 Clinical features
• Disease Pattern
Episodic - acute exacerbations interspersed with
symptom-free periods
 Chronic - daily AW obstruction which may be
mild, moderate or severe ± superimposed acute
exacerbations
 Life-threatening -- slow-onset or fast-onset
(fatal within 2 hours)
Clinical features…
• Symptoms- Triad of dyspnea, cough, wheezing
• Wheezing is typical-expiratory/inspiratory
• Cough variant without wheezing
• Severe-only wheeze/ no adevential sound
• Sense of constriction in the chest
• Non productive cough - stringy mucus
• Tachypenia / tachycardia
• Barrel chest
• Atelectasis/spontaneous pneuomothorax/
pneumomediastinum
Clinical sign of severe asthma
• Unable to speak in full sentences
• RR > 25/min
• PR > 110/min
• Peak flow < 50% predicted best
• Accessory muscle use
Life threatening asthma
• Silent chest - no wheezing or air entry
• Cyanosis / feeble or no respiratory effort
• Pulsus paradoxus, bradycardia, hypotension
• Exhausted, confused or unconscious
Status asthmaticus
◦ Severe, life-threatening attack refractory to
usual treatment where patient poses risk for
respiratory failure.
Causes include
◦ Viral illnesses
◦ Ingestion of aspirin or other NSAIDs
◦ Environmental pollutants or allergen exposure
◦ Abrupt discontinuation of drug therapy
◦ Abuse of aerosol medication
◦ Ingestion of -adrenergic blockers
Diagnosis of asthma
Lung Function Tests
demonstrating reversibility of obstruction
Reversibility is demonstrated by a >12%
and 200-mL increase in FEV1 15 min after a
2 puffs inhaled short-acting β2-agonist
Simple spirometry confirms airflow
limitation with a reduced FEV1, FEV1/FVC
ratio, and PEF.

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 Cont…

• Sputum eosinophilia – suggests but non

specific
• Total serum IgE and specific IgE to inhaled
allergens [radioallergosorbent test (RAST)]
• CXR (hyperinflation) to rule out
pneumothorax in severe asthma
• Positive wheal and flare reaction to skin test
with various allergens
+++

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 DDx
Endobronchial obstruction with a FB, neoplasm =
Persistent wheezing in a specific area of the chest
LV failure = basilar crackles are present
Eosinophilic pneumonias and systemic vasculitis,
may be associated with wheezing.
Upper AW Obstruction – tumor, laryngeal edema
(stridor localized to large airways)
COPD - Sx show less variability, never completely
remit, and much less (no) reversibility to
bronchodilators.
* Approximately 10% of COPD patients have features of
asthma, respond to oral corticosteroids; probably have both
diseases concomitantly.
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 Management
Aims of Asthma Therapy
• Minimal chronic symptoms
• No emergency visits
• Minimal (ideally no) use of β 2-agonist
• No limitations on activities
• Minimal (no) adverse effects from medicine

• Pharmacologic Vs non pharmacologic

Management cont…
Allergen Avoidance
• Difficult, house dust /work place change, education
Patient education
• Basic facts about asthma
• Concept of “rescue” and “controllers” meds
• Environmental control
• Inhaler technique
• Concept of self management
 Desentization and immunotherapy
 Drug treatment    
Mgt asthma cont…

A. Quick relief “rescue” medication

B. long term “controller” medication

 Bronchodilator Therapies
Act primarily on airway smooth muscle to reverse
the bronchoconstriction of asthma.
Thus, bronchodilators are not sufficient to control
asthma in patients with persistent Sx
There are 3 classes:
β2-adrenergic agonists
Anticholinergics, and
Theophylline

*of these, β2-agonists are by far the most effective

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B2-Agonists
MOA
β2-Agonists activate β2-receptors
β2-receptors are coupled through a
stimulatory G protein to adenylyl cyclase,
resulting in increased intracellular cAMP,
which relaxes smooth-muscle cells and
inhibits certain inflammatory cells.
Additional effects:
inhibition of mast cell mediator release.
No effect on AHR.

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Clinical Use
SABAs, such as albuterol and terbutaline, have a
duration of action of 3–6 hours.
Used as needed for symptom relief.
Also prevent EIA if taken prior to exercise.
Used in high doses by nebulizer or via a
metered dose inhaler with a spacer.

• LABAs include salmeterol and formoterol, both

of which have a duration of action over 12 hours
and are given twice daily.

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 LABAs should not be given in the absence of
ICS therapy as they do not control the
underlying inflammation.
Better to use fixed combination inhalers that
contain a corticosteroid and a LABA, which
have proved to be highly effective in the
control of asthma.
Side effects
The most common are muscle tremor and
palpitations, commonly in elderly patients.

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 Anti-Cholinergics
M-receptor antagonists, such as
ipratropium bromide, prevent
bronchoconstriction and mucus secretion.
much less effective than β2-agonists, as they
inhibit only the cholinergic reflex component
of bronchoconstriction, whereas β2-agonists
prevent all bronchoconstrictor mechanisms.
therefore only used as an adjuvant in asthma that is
not controlled on other inhaled medications.
Slower onset of bronchodilation.
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Side effects
less side effects as there is little or no systemic
absorption.
The most common SEs are
Dry mouth; in elderly patients,
Urinary retention
Glaucoma

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Theophylline
Inexpensive
now fallen out of favor as side effects are common.
The bronchodilator effect is due to inhibition of
phosphodiesterases in airway smooth-muscle cells,
which increases cAMP.

Aminophylline - occasionally used (via slow

IV infusion) in patients with severe
exacerbations that are refractory to high-dose
SABAs.

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Side Effects

most common - nausea, vomiting, and

headaches - due to phosphodiesterase
inhibition.
Diuresis and palpitations may also occur, and
at high concentrations cardiac arrhythmias,
epileptic seizures, and death may occur
side effects are related to plasma
concentration

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 Controller Therapies
1. Inhaled Corticosteroids (ICS)
ICSs are by far the most effective
controllers for asthma, and their early use
has revolutionized asthma therapy.
2. Systemic steroids
3. Cromones
4. Omalizumab

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MOA
ICSs are the most effective anti-
inflammatory agents, reducing the number of
inflammatory cells and their activation in the
airways.
 ICSs reduce eosinophils in the airways and
sputum, and numbers of activated T
lymphocytes and surface mast cells in the
airway mucosa.

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uses
ICSs reduce AHR (airway HS reaction), but
maximal improvement may take several
months of therapy.
Early treatment with ICSs appears to
prevent irreversible changes in airway
function that occur with chronic asthma.
They suppress inflammation and symptoms
but do not cure the underlying condition.

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Side Effects
Local - hoarseness (dysphonia) and oral
candidiasis.
Which may be reduced with the use of a
large-volume spacer device or mouth wash

Have minimal systemic effects

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 Systemic Corticosteroids
 IV (hydrocortisone or methylprednisolone)
for the treatment of acute severe asthma.
A course of oral corticosteroids (usually
prednisolone 30–45 mg po/d for 5–10 days)
is used to treat acute exacerbations of asthma;
no tapering of the dose is needed.
 ≈ 1% of asthma patients may require
maintenance treatment with oral
corticosteroids; the lowest dose necessary to
maintain control needs to be determined
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Side effects
Truncal obesity, bruising, osteoporosis,
diabetes, HTN.
Gastric ulceration, proximal myopathy,
depression, and cataracts

*IM triamcinolone acetonide is a depot

preparation that is occasionally used in
noncompliant patients, but proximal
myopathy is a major problem with this
therapy.
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Cromones
Cromolyn sodium and nedocromil sodium:
asthma controller drugs - inhibit mast cell
and sensory nerve activation
Effective in blocking EIA, and allergen- and
sulfur dioxide-induced symptoms.
 little benefit in the long-term control of
asthma due to their short duration of action
(at least 4X daily by inhalation).
They are very safe.

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Steroid-Sparing Therapies
Methotrexate, cyclosporine,
azathioprine, and IV gamma globulin
have all been used as steroid-sparing
therapies, but none of these treatments
has any long-term benefit and each is
associated with a relatively high risk of
side effects.

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Anti-IgE Omalizumab
is a blocking antibody that neutralizes circulating
IgE without binding to cell-bound IgE; thus
inhibits IgE-mediated reactions.
can reduce the number of exacerbations in
patients with severe asthma and may improve
asthma control
very expensive and only used in those who have
a circulating IgE within a specified range.
usually given as SC injection every 2– 4 weeks
appears not to have significant side effects.

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 Management of Chronic Asthma
Triggers that worsen asthma control, such
as allergens or occupational agents, should
be avoided.

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Step wise therapy

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Stepwise Therapy
For patients with mild, intermittent
asthma, a SABA is all that is required
use of a reliever medication > 3X a
week indicates the need for regular
controller therapy, ICS given twice
daily.
If symptoms are not controlled, LABA
should be added

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In patients with severe asthma:
Low-dose oral theophylline is also helpful, and
when there is irreversible airway narrowing, the
long-acting anticholinergic ipratropium bromide
may be tried.
Maintenance treatment with an oral corticosteroid
may be needed, and the lowest dose that maintains
control should be used.
Once asthma is controlled, it is important to
slowly decrease therapy in order to find the optimal
dose to control symptoms.

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 Acute severe asthma
Increasing chest tightness, wheezing, and dyspnea
Patients may be so breathless that they are unable to
complete sentences, may become cyanotic.
Examination usually shows increased ventilation,
hyperinflation, and tachycardia.
There is a marked fall in spirometric values and PEF.
Arterial blood gases on air show hypoxia.
CXR is not usually informative, but may show
pneumonia or pneumothorax.

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Acute Severe Asthma: Treatment
A high concentration of oxygen should be
given to achieve oxygen saturation of > 90%
The mainstay of Rx is high doses of SABA.
An inhaled anti-cholinergic may be added if
there is non satisfactory response to SABA
 In patients who are refractory to inhaled
therapies, a slow infusion of aminophylline
may be effective -- monitor blood levels
MgSo4 given IV or by nebulizer has also been
shown to be effective when added to inhaled
SABA, but is not routinely recommended.
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-----acute severe asthma.

Prophylactic intubation may be indicated for

impending respiratory failure
Sedatives should never be given as they may
depress ventilation.
Antibiotics should not be used routinely
unless there are signs of pneumonia.

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 Refractory Asthma
(approximately 5% of asthmatics) are
difficult to control despite maximal inhaled
therapy.
Some of these patients will require
maintenance treatment with oral
corticosteroids.
In managing these patients, it is important
to investigate and correct any mechanisms
that may be aggravating asthma.

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Mechanisms
Noncompliance with medication, particularly ICS.
Exposure to high, ambient levels of allergens or
unidentified occupational agents.
Severe rhinosinusitis may make asthma more
difficult to control; upper airway disease
GERD common in asthmatics due to
bronchodilator treatment, but not significant factor
in worsening asthma.
Some have chronic infection with M. pneumoniae
or C. pneumoniae and benefit from macrolides Rx.

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-----refractory asthma, mechanisms

 Drugs such as β blockers, aspirin, and

other (COX) inhibitors may worsen asthma.
 Hypo / hyperthyroidism
Some patients with COPD may be
diagnosed as asthmatic and may show poor
response to corticosteroids and
bronchodilators,
but some patients with COPD also have
concomitant asthma.

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 Refractory Asthma: Treatment

Check compliance and the correct use of inhalers

 identify and eliminate any underlying triggers.
Low doses of theophylline may be helpful in some
patients
Most patients will require maintenance treatment
with oral corticosteroids.
In allergic asthma, omalizumab is effective,
particularly when there are frequent exacerbations.
A few patients may benefit from infusions of β2-
agonists

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 CHRONIC OBSTRUCTIVE
PULMUNARY DISEASE (COPD)
Definitions
• Preventable and treatable disease state
characterized by airflow limitation that is
not fully reversible.
• The airflow limitation is usually
progressive and is associated with abnormal
inflammatory response of the lungs to
noxious particles or gases, primarily caused
by cigarette smoking.
• Although COPD affects the lungs, it also
produces significant systemic consequences.
Epidemiology:

In USA, it is the 4th leading cause of death

and affects >10 million persons.

 Expected to be the 3rd leading cause of death

by 2020
Types of COPD
•Emphysema, chronic bronchitis, small
airways disease,
Emphysema is abnormal and
permanent enlargement of the airspaces
distal to the terminal bronchioles.
accompanied by destruction of the
airspace walls, without obvious
fibrosis.
 Chronic bronchitis

• is defined by a chronic productive cough for

3 months for 2 successive years in a patient
where other causes of chronic cough have
been excluded.
Chronic bronchitis and emphysema commonly
occur together.
Persons with chronic bronchitis, emphysema,
or both are not considered to have COPD if no
airflow obstruction
AIRFLOW OBSTRUCTION
COPDs
Risk factors
• Cigarette smoking – calculated by pack year (dose X
years)
• Airway responsiveness as in asthma (genetic
predisposition)
• Respiratory infections- childhood, recurrent
(initiate/exacerbate)
• Occupational exposure- dust (coal mine dust), gold,
↓FEV1
• Air pollution town > rural, ↑Women (exposure to
smoke produced by biomass combustion )
• +/- genetic or environmental + passive Smoking
Exposure
• Genetic –α1 antitrypsin deficiency (emphysema)
Pathophysiology
chronically reduced FEV1, ratio of FEV1/FVC
The reduced FEV1 in COPD seldom shows large
responses to inhaled bronchdilators
“Air trapping” (increased residual volume and
increased ratio of residual volume to TLC)
Hyperinflation- increased total lung capacity.
The PaO2 usually remains near normal until the FEV1 is
decreased to ~50% of predicted.
An elevation of PaCO2 is not expected until the FEV1 is
< 25% of predicted
 Corpulmonale and RV failure - occurs only when
FEV1 < 25% of predicted.
Pathology
 Large Airways
Cigarette smoking often results in mucous gland
enlargement and goblet cell hyperplasia.
Cough and mucus production
Bronchi also undergo squamous metaplasia;,
disrupts mucociliary clearance.
Patients may have smooth-muscle hypertrophy
and bronchial hyper-reactivity leading to airflow
limitation
Small Airways (2mm diameter)
Major site of increased resistance
Include goblet cell metaplasia and replacement of
surfactant-secreting cells with mucus-secreting &
infiltrating inflammatory cells.
Reduced surfactant may increase surface tension
 Smooth-muscle hypertrophy may also present.
Luminal narrowing by excess mucus, edema, and
cellular infiltration.
 Lung Parenchyma
Emphysema destructs gas-exchanging
airspaces, i.e., the respiratory
bronchioles, alveolar ducts, and alveoli.
Their walls become perforated and later
obliterated to become abnormal and
much larger airspaces.
 CLINICAL FEATURES

Insidious onset
The 3 most common Sx in COPD are cough,
sputum production, and exertional dyspnea
Activities that allow the patient to brace the
arms and use accessory muscles of
respiration are better tolerated.
Acute exacerbation - wheezing, cough with
purulent sputum, dyspnea, chest tightness.
Physical Findings
 In early stages, usually normal P/E.
 Current smokers - signs of active smoking, including an
odor of smoke or staining of fingernails.
 More severe disease - expiratory wheezing
 barrel chest and poor diaphragmatic excursion.
 If severe - use of accessory muscles
 Cyanosis, visible in the lips and nail beds.
 Weight loss.
 paradoxical inward movement of the rib cage with
inspiration
 Clubbing of the digits is not a sign of COPD
 Cor pulmonale
 Emphysema Chronic Bronchitis
• Slight Cough • Severe cough
• Blood gas values - NORMAL • Hypercapnia & Severe
• No cyanosis hypoxemia
• Lean forward to breathe easier • Cyanotic
• Diffusing capacity is low • History of recurrent
• Over-distension severe infections
• Pink puffers • Purulent sputum
• Blue bloaters
Laboratory Findings

The hallmark of COPD is airflow obstruction with

reduction in FEV1 and FEV1/FVC .
With worsening disease severity, lung volumes may
increase, resulting in an increase in TLC, functional
residual capacity, and residual volume.
Global Initiative for Lung Disease (GOLD)
 Radiographic studies:
Obvious bullae, paucity of parenchymal
markings, or hyperlucency suggest emphysema.
 Increased lung volumes and flattening of the
diaphragm suggest hyperinflation.
 CT scan:
current definitive test for emphysema.
Diagnosis
• Clinical- risk +lab.-px
◦ lab- ↓FEV1,↓FEV1/FVC → air flow obstruction
↑lung volume.
◦ ↓ diffusion capacity in emphysema
◦ ABG- not sensitive (a-b balance, Pco2, po2,pH)
◦ RVH (→sn of chronic hypoxemia)
◦ CXR- emphysema,(bullae, decreased paranchymal
markings, hyperlucency)
◦ CT – emphysema
◦ Serum α1AT < 50 year age
◦ ECHO
◦ Sputum - exacerbating infection
Diagnosis of COPD

EXPOSURE TO RISK
SYMPTOMS FACTORS
cough tobacco
sputum occupation
dyspnea indoor/outdoor pollution

SPIROMETRY
• For the diagnosis and assessment of COPD,
spirometry is the gold standard.
Spirometry: Normal Vs Patients with COPD
 DDx: COPD vs Asthma
COPD ASTHMA
 Onset in mid-life  Onset early in life (often

 Symptoms slowly childhood), Any age

progressive  Sx vary from day to day

 Dyspnoea during  Sx at night/early morning

exercise  Allergy, rhinitis, and/or

 Long smoking history eczema also present

 Largely irreversible  Family history of asthma

airflow limitation  Largely reversible

 Management
Smoking cessation
Oxygen therapy in chronically hypoxemic
patients
Lung volume reduction surgery in selected
patients with emphysema
The use of inhaled glucocorticoids may alter
mortality (but not lung function).
 All other current therapies are directed at
improving Sx and decreasing the frequency
and severity of exacerbations.
Smoking Cessation
Successfully stopping smoking
experienced a significant improvement in
the rate of decline in pulmonary function.
Thus, all patients with COPD should be
strongly urged to quit and educated about
the benefits of quitting.
Bronchodilators:
used for symptomatic benefit in COPD.
The inhaled route is preferred
Salmeterol, has benefits comparable to
ipratopium bromide
The addition of a β2 agonist to inhaled
anticholinergic therapy has been demonstrated
to provide incremental benefit.
Inhaled Glucocorticoids / IGC
Some analyses suggest that inhaled
glucocorticoids reduce exacerbation frequency
by ~25%.
recent studies suggests that they may also
reduce mortality by ~25%.
A trial of IGC should be considered in
patients with
- Frequent exacerbations ( 2 or more/ yr), and
- In patients who respond to inhaled
bronchodilators.
 Oral Glucocorticoids
chronic use for Rx of COPD is not
recommended because of an
unfavorable benefit/risk ratio.
Theophylline
produces modest improvements in
expiratory flow rates and vital capacity
and a slight improvement in arterial
O2 and CO2 levels in moderate to
severe COPD.
Oxygen
Supplemental O2 is the only pharmacologic therapy
demonstrated to decrease mortality in COPD.
Significant impact if resting O2 saturation <88% or
< 90% with signs of P. HTN or RV failure.

Other Agents
N-acetyl cysteine
- mucolytic and antioxidant properties.
IV alpha 1AT augmentation therapy
- available for individuals with severe α1AT deficiency
Pulmonary Rehabilitation & Patient Education

Includes exercise, education & psychological

support
Shown to:
Improve symptoms, exercise capacity
Reduce use of medical care
Reduce anxiety & depression
Non pharmacologic Therapies
Lung Volume Reduction Surgery (LVRS) for
emphysema:
Exclusion:
 significant pleural disease,
 pulmonary artery systolic pressure >45 mmHg
 CHF,
 severe comorbid conditions.
 FEV1 < 20% of predicted and either
 diffusely distributed emphysema on CT scan
 Patients with upper lobe–predominant emphysema
most likely benefit from LVRS.
Lung transplantation
Indication
Should be <65 years
Have severe disability despite maximal medical
therapy
Free of comorbid conditions such as liver, renal,
or cardiac disease.
 Exacerbations of COPD

Common in moderate to severe air flow obstruction.

Sx
Increased dyspnea and cough
Change in the amount and character of sputum.
They may or may not be accompanied by: fever,
myalgias, and sore throat.
Precipitating Causes
Bacterial infections play a role in many.
Viral respiratory infections ≈ 1/3rd of exacerbations
20–35%, no specific precipitant can be identified.
acute exacerbation….

Do CXR if:

Moderate or severe distress or
Those with focal findings
 Approximately 25% of x-rays will be
abnormal (usu. pneumonia and CHF)
Rx of acute exacerbations
Need for inpatient treatment if :
 Patients with respiratory acidosis and
hypercarbia,
Significant hypoxemia, or
Severe underlying disease or
Those whose living situation is not
conducive.
Bronchodilators

An inhaled agonist, often with the addition

of an anticholinergic agent.
Addition of theophylline to this regimen can
be considered
Frequency of administration depends on the
severity of the exacerbation.
Antibiotics
frequently implicated bacteria in COPD
exacerbations include :
St. pneumoniae,
H. influenzae, and
M. catarrhalis
Mycoplasma or Chlamydia pneumoniae
(5–10%) of exacerbations
Glucocorticoids
Among patients admitted to the hospital,
Reduce the length of stay,
hasten recovery, and
reduce the chance of subsequent
exacerbation or relapse up to 6 months.
*The GOLD guidelines recommend 30–40
mg of oral prednisolone for 10–14 days.
Oxygen
Supplemental O2 should be supplied to
keep arterial saturations 90%.
Mechanical ventilation via an endotracheal tube
is indicated for patients with
Severe respiratory distress despite initial
therapy,
Life-threatening hypoxemia,
Severe hypercapnia and/or acidosis,
Markedly impaired mental status,
Respiratory arrest,
Hemodynamic instability, or other
complications.
The mortality of patients requiring mechanical
ventilatory support is 17–30% .
CASE STUDY
Case study
• 72 years old male retired army officer
presented with wheezing, coughing with
excessive production of sputum sometimes
blood streaked. He smoked 80 pack years.
Recently lost significant weight and
worsening of SOB, had clubbing of fingers.
• Raised JVP, S3 gallop, basal rales
• Hepatomegaly, leg edema
• No other medical problem, don’t drink
Case study….

•What are the DDX/why?

•Appropriate management?
•What counseling should be given to the
patient?
DDX
• COPD: risk factor, cough, wheez

• Lung CA: risk factor, cough, weight loss,

clubbing

• IHD: risk factor, cough, wheez, shortness of

breath

• Corpulmonale: risk factor, hepatomegaly,

raised JVP, leg edema
Appropriate management
• Diagnosis
• Further detailed history (esp cardiac,
liver)
• Investigations- CXR, bronchoscope,
biopsy, ECG, ECHO,
• Treat appropriately according to the
diagnosis
Case study…
• Counseling to quiet smoking