Asthma

Rommel N. Tipones, MD,FPCCP,FPCP

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A chronic inflammatory disorder of the airways in which many cells and

cellular elements play a role. The chronic inflammation causes an
associated increase in airway hyperresponsiveness that leads to
recurrent episodes of wheezing, breathlessness, chest tightness, and
coughing, particularly at night or in the early morning. These episodes
are usually associated with widespread but variable airflow obstruction
that is often reversible either spontaneously or with treatment.

Asthma Prevalence

300 M people
10-12% of adults, 15% of children
occurs at all ages, peak at 3

2:1 M:F preponderance in childhood which equalizes by age 30

Atopy

single largest risk factor

allergic asthma
personal / family history
rhinitis, urticaria, eczema
positive wheal-and-flare skin reactions
increased levels of IgE in serum
positive response to provocation tests
Nonatopic: Intrinsic Asthma

most common stimuli for exacerbation

uncertain role in etiology

respiratory syncytial virus in infancy

Uncommon
Genetic Considerations

Poorly controlled disease

Frequent use of prn bronchodilator
Lack of steroid therapy
Hospital admissions

ENDOGENOUS FACTORS

ENVIRONMENTAL FACTORS

Genetic Predisposition

Indoor allergens

Atopy

Outdoor allergens

Airway hyperresponsiveness

Occupational sensitizers

Gender

Passive smoking

Ethnicity?

Respiratory infections
Obesity
Early viral infections

Notes:

Familial association
Polygenic
Gene interaction
Chromosome 5q polypmorphisms
TH2 cells, interleukins 4,5,9,13
Affects response to therapy

Inflammatory Mediator Soup in Asthma

Histamine
Acetylcholine
Bradykinin
Adenosine
PgD2
PgF2a
TxA2
Proteases
PAF
Leukotrienes
Cytokines

What then could be the mechanism of these changes?

Asthma is an extremely variable disease and the variability during
pregnancy is because the disease itself has a variable natural history.

This graph shows the variability of asthma symptoms and use of reliever
medication.

We see that the course of asthma is indeed punctuated by periods of

exacerbations requiring short course of corticosteroids, with periods of
worsening often obviated by continued suppression with maintenance
anti-inflammatory therapy.

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Infections

1/3 occur before age 40

Etiology / Risk FactorsPulmonary Pearls:

1/2 of cases before age 10

Asthma Deaths

Thus, it would seem that the course of asthma is pregnancy-specific.

Schatz et al in 1988 noted that 73 % of patients whose asthma changes

course during pregnancy revert to their pre-pregnancy status in the 3
months after delivery.

Environmental Factors

Hygiene hypothesis
Diet
Obesity
Air pollution
Allergens
Occupational exposures
Prematurity and low birth weight

Newly-Diagnosed Asthma
Low-power transmission EM. Bronchial biopsy specimen from an asthmatic
patients having asthma for less than a year.
E - damaged airway epithelium BM- thickened subepithelial basement
membrane
- eosinophilic inflammatory reaction in lamina propria with eosinophils
- lymphocytes
Effects of Inflammation

Airway epithelium

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Vascular responses
Mucus hypersecretion

Airway remodeling

Allergens

Exercise
Physical Factors
Food

pharmaceuticala agents
biologic enzymes
animal and insect dusts
secretions

metal salts
industrial chemicals/plastics
dyes
formaldehyde

Infections

most common stimuli for exacerbation

young children

respiratory syncytial virus

parainfluenza

older children & adults

Virus Infections
Pharmacologic Agents

wood and vegetable dusts

Low Molecular Weight

Airway smooth muscle

Neural effects

High Molecular Weight

Fibrosis

Asthma Triggers

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rhinovirus
influenza

Exercise

Attacks follow exertion

Higher ventilation
Lower heat content of air

Environment and Air Pollution

Occupational Factors
Hormonal Factors
Gastroesophageal Reflux
Emotional Stress

Stimuli That Incite Asthma

Allergens
Pharmacologic
Environment and Air Pollution
Occupational Factors
Infections
Exercise
Emotional Stress

Forms of Airflow Limitation

Pharmacologic

Aspirin
Coloring agents/Tartrazine
Beta-adrenergic antagonist/blockers
Sulfiting agents

Environmental & Air Pollution

Ozone

acute bronchoconstriction
swelling of the airway wall
chronic mucus plug formation
airway wall remodelling

Asthma symptoms
Inflammation
Airway hyperresponsiveness
Airway remodeling

Nitrogen dioxide
Sulfur dioxide

Occupational Exposure

Pulmonary Pearls:
Diagnosis of Asthma

Episodic or Intermittent Symptoms

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Usually triggered by exogenous factors

Typical atopic history

Family history of asthma
Positive response to bronchodilators
Must be differentiated from COPD
Not all that wheeze is asthma, not all asthma wheezes
Adult Onset Asthma is a reality

Diagnosing Asthma: Medical History

Symptoms

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Confirmatory Tests for Asthma

Spirometry
FEV1/FVC < 70% Obstructive Airways Disease
Acute Bronchodilator Response: > 12 % increase + absolute increase of 200
ml in FEV1 and/or FVC
Peak Flow Monitoring
Acute BD Response: > 15% increase in PEF
Diurnal variability > 10% (if no BD) or > 20% (if on BD)
Drop of >15% with 6-minute running/exercise
Bronchoprovocation Test
Methacholine/ Histamine Inhalation Challenge

Coughing

Helpful

Wheezing

Shortness of breath
Chest tightness

Patterns of symptoms
Severity
Family history

Diagnosing Asthma: Physical Examination

Sounds of wheezing during normal breathing

Hyperexpansion of the thorax
Increased nasal secretions or nasal polyps
Atopic dermatitis, eczema, or other allergic skin conditions

Positive wheal and flare reactions

Sputum and blood eosinophilia
Serum IgE measurements
Hyperinflation on chest radiograph

Who is unlikely to be an asthmatic?

A.
B.

18 y.o./F, on and off dyspnea and chest tightness for the past 10 years

C.
D.
E.

15 y.o. athlete who develops SOB after running

50 y.o./F, sole complaint of on and off cough for the past 2 years,
treated with various antibiotics
48 y.o. smoker with progressive SOB x 4 y and recent active hemoptysis
All can be considered asthmatics

Which statement about asthma diagnosis is correct?

Differential Diagnosis

Upper airway obstruction

Endobronchial disease
Acute left ventricular dysfunction
Recurrent pulmonary emboli
Chronic bronchitis

Diagnosis

Asthma can be diagnosed by taking the Hx and PE alone

The absence of wheezing during an attack means it is not due to asthma
The asthmatic who does not complain of SOB will have a normal PEFR
A drop in peak flow usually precedes the symptoms of an attack
All statements are correct

Elimination of the causative agent(s) from the environment of the allergic

individual is most successful!
Treatment

Lung function tests (spirometry)

Airway responsiveness
Hematologic tests
Imaging
Skin tests

Diagnosing Asthma: Spirometry

A.
B.
C.
D.
E.

Testing of lung function is another means of diagnosing asthma.

Spirometry

Measures rate at which lung volume is changing as a function of

time during breathing maneuvers

Simply put: measures lung volume and airflow from fully inflated
lungs

Current Asthma Medications

Relievers

Beta agonist
Short acting Theophylline
Anticholinergics

Controllers

Cromolyn Sodium
Nedocromil Na
Corticosteroids
Long Acting Theophylline
Long Acting Beta agonists

Anti-Leukotrienes

Medications to Treat Asthma: Quick Relief

Used in acute asthma episodes

Generally they are short-acting beta2-agonists

Adrenergic Stimulants

Catecholamines, resorcinols, saligenins

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Isoproterenol
B2 agonists

Tiotropium
Modest potency
Slow-acting (60 to 90 mins)
Muscarinic receptor antagonists
Prevent cholinergic nerve-induced

Terbutaline, fenoterol, albuterol

Side effects: tremors

Preferred route: Inhalation

Lasts 4 to 6 hours

Increased mucociliary clearance

Increased mucus secretion

glaucoma

Medium-potency bronchodilators
Decreased clearance

NO effect on chronic inflammation

Age, erythromycin, quinolones, allopurinol,cimetidine,

propranolol

Increased clearance

Inhaled route

Cigarettes, marijuana, phenobarbital, phenytoin,

hepatic microsomal enzyme inducers

Theophylline

Albuterol, salbutamol, terbutaline

LABAs: 12 hours duration, 2xday

Urinary retention

Theophylline

Decreased cough

Dry mouth

Methylxanthines

Inhibition of plasma exudation and airway edema

SABAs: 3-6 hours duration, rapid onset

Mucus secretion

Side effects

Clinical Use:

Bronchoconstriction

Less effective, only as add-on

Relaxation of airway smooth muscle

Inhibition of mast cell mediator release

Anti-inflammatory?

Ipratropium bromide

B2 Agonist Effects

Formoterol

Anticholinergics

Epinephrine

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Salmeterol, fomoterol

Long-acting compounds
Given once or twice daily
Side effects:

For control: ICS-LABA combination inhaler

Increased use of SABA- Asthma is not controlled!!!

Nausea, vomiting, anorexia, headache

Plasma levels> 30ug/ml

Cardiac arrhythmias, seizures

Side Effects

Muscle tremors

Theophylline: A New Look at an Old Cure

Fall in plasma potassium

As a bronchodilator: Weak

Tolerance

Palpitations

ICS prevent mast cell tolerance

Safety

LABA never without ICS

Adrenergic Stimulants
Long lasting ( 9 to 12 hours)

Down-regulation of receptors

Salmeterol (slow onset of action 30 mins)

phosphodiesterase inhibition, adenosine antagonism

Use as adjuvant therapy in moderate to severe asthma
esp. nocturnal symptoms

As a controller: New Anti - Inflammatory Properties

Eosinophil infiltration of airways

T - lymphocytes in alveolar epithelium mucociliary clearance

Alternative but not preferred controller in mild persistent asthma

Medications to Treat Asthma: Long-Term Control

Taken daily, over a long period of time

Used to reduced inflammation, relax airway muscles, and improve
symptoms and pulmonary function

Inhaled corticosteroids
Long acting beta2-agonists
Leukotriene modifiers

Glucocorticoids

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Combined Medications

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Inhaled steroid + long-acting B2 agonist

Budesonide + Formoterol
Fluticasone + Salmeterol

Most potent
Most effective anti-inflammatory agents
Systemic/oral for acute illness
Inhaled GCs for long-term control
Preferred drug for all levels of severity of persistent asthma
Emerging Role of the Anti-LTRs

Glucorticoids in Acute Illness

Not bronchodilators

DECREASED

cellularity usually resulting from decreases in eosinophils, mast

cells, and lymphocytes

dendritic cells and HLA-DR expression

thickness of basement membrane

cells expressing mRNA

symptoms
frequency and severity of exacerbations
oral steroid rescues
ER visits and hospitalization
relapse after an acute attack

IMPROVES

quality of life

Thrush and dysphonia

Adrenal suppression
Cataract
Decreased growth
Interference with bone metabolism
Purpura

Nedocromil sodium
Inhibit degranulation of mast cells
Atopic/Seasonal disease/ perennial airway stimulation
Block the acute obstructive effect of exposure to antigen

Anti-IgE: Omalizumab
Immunotherapy
Alternative therapies
Future therapies

Medications to Treat Asthma: Inhalers and Spacers

Health-care provider should evaluate inhaler technique at each

visit.

Medications to Treat Asthma: Inhalers and Spacers

Side Effects of Inhaled GCs

Cromolyn sodium

Inhalational is superior to oral therapy.

BHR
lung function

Specific Asthma Syndromes

Other Therapies

Clinical Effects of Inhaled Corticosteroids on Asthma

REDUCES

prn SABA use

Steroid Sparing

Mast Cell- Stabilizing Agents

cells expressing mRNA for IL-4 and IL-5

area of ciliated epithelium

Add-On

Effect

INCREASED

Second-Line Controller

Effects are not immediate (6 hours)

Effects of Corticosteroids on Histopathologic Characteristics in Asthma

Monotherapy as Alternative First-Line Controller

Spacers can help patients who have difficulty with technique and
can reduce potential side effects.

Medications to Treat Asthma: Nebulizers

Uses compressed air machine to deliver medicine as a mist

Good for small children or for severe asthma episodes

Levels of Asthma Control (GINA 2007)

Characteristic

Controlled (All
of the
following)

Partly controlled
(Any measure
present in any

Uncontrolled

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week)

Daytime
symptoms

None (Twice or
less/week)

> twice/week

Limitation of
Activities

None

Any

Nocturnal
symptoms/
awakening

None

Need for
reliever

None (Twice or
less/week)

> twice/week

Lung Function
(PEF or FEV1)

None

<80% predicted or
normal best

Exacerbations

None

One or more/year

Any

3 or more
partly
controlled
features
present in
any week

One in any
week

Exacerbation
Life-threatening? Level of Care?

PEFR or FEV1 should double after 1 hour if less than 20% of

glucocorticoids

PEFR falls by 20% of previous

PaCO2 is within normal or elevated
serial ABGs
ICU

Asthma control is

minimal/no daytime Sxs

minimal/ no nocturnal Sxs

Small Airways Disease

CURRENT FACTS ABOUT COPD

hMore prevalent than asthma, this debilitating disease affects about 30
million persons in US
hIn Philippines, it is estimated that 6.3% of adult population have COPD
iMirroring cigarette usage trends, COPD related mortality leveled off in men
during past 2 decades but increased markedly in women
hBecause advanced COPD leads to extensive use of health care resources,
national financial burden is substantial (in US exceeds $ 30 billion annually)

Note:
Although understanding of the specific etiology and pathophysiology of
chronic bronchitis has not advanced significantly, there is an increased
awareness of the impact that this inflammatory disease has on the patient's
well-being. Chronic bronchial disease eventually leads to more frequent and
more severe episodes of acute bacterial exacerbations.

Normal nonsmokers lose FEV1 at a rate of about 25 - 35 mL/yr

Among susceptible smokers the rate of FEV1 decline is about 90 mL per

year
hThe heavier the smoking, the steeper the decline in FEV1
hThe increased rate of decline moves toward normal soon after smoking
cessation
Other Risk Factors

Airway responsiveness
Respiratory infections ?
Occupational exposures ?
Ambient air pollution
Passive, or Second-Hand Smoking

infrequent attacks
minimal need for prn SABAs
no exercise/activity limitations
minimal/ no side effects from meds.
NO ER VISITS

Chronic Obstructive Pulmonary Disease

Chronic Bronchitis

Continuous nebulization

Danger Signs

Emphysema

B-agonists every 20 mins for 2 to 3 doses

predicted initially

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Chronic Airflow Obstruction

Emergency Situations

component is characterized by airflow limitation that is not fully

reversible. The airflow limitation is usually progressive and associated
with an abnormal inflammatory response of the lungs to noxious
particles or gases.

Chronic obstructive pulmonary disease(COPD) is a preventable and

treatable disease with some significant extrapulmonary effects that may
contribute to the severity in individual patients. Its pulmonary

Genetic Considerations

Alpha1-antitrypsin deficiency
Encoded by protease Inhibitor (PI) locus
S allele slightly reduced levels
Z allele markedly reduced levels
Caucasian populations
Piz individuals severe deficiency

Degree of
certainty
Certain

Environmental Factors

Congenital

Factors

Alpha1 antitrypsin
deficiency

Likely (burden of
proof good)

Cigarette smoking
Occupational exposure
(cadmium, silica)
Environmental pollution
Passive smoking

Possible

Adenovirus infection

Low birth weight

Airway
hyperresponsiveness
Genetic predisposition

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Pathogenesis of Emphysema

*Hyperinflation of the lungs in COPD occurs because of progressive

destruction of the alveoli, reduced expiratory flow rate, and the relatively
short time of exhalation that COPD patients experience because of
obstruction to airflow.
*Cholinergic tone contributes to reduced expiratory flow rate and inadequate
exhalation time.
*Other complications are the fact that chest wall recoil remains inward,
which results in a threshold load at the start of inspiration; and the flattened,
shortened diaphragm muscle, which leads to inefficiency in force generation.
*Patients work harder to breathe.
*The posteroanterior (PA) and lateral chest radiographs shown here illustrate
advanced findings of COPD and hyperinflation.
*Chest radiograph changes occur late. The expanded chest, retrosternal air
space, low and flat diaphragm, and decrease in peripheral vascularity
highlight the major radiographic findings. *Hyperinflation is readily apparent.
Gas Exchange

PaO2 remains normal until FEV1 is 50% of predicted

Elevated PaCO2 not expected until FEV1 is <25% predicted

Ventilatio-perfusion mismatching

Large Airways

airspaces

Cells release elastolytic proteinases which damage extracellular

matrix

Loss of matrix-cell attachment leads to apoptosis of structural cells

Ineffective repair of elastin result in airspace enlargement

Pathogenesis

Airflow limitation
Inflammation
Extracellular Matrix Proteolysis
Cell death
Ineffective repair

Symptoms
COUGH
DYSPNEA
SPUTUM

Mucous gland enlargement

Goblet cell hyperplasia
Cough and mucus
Squamous metaplasia of bronchi
Smooth muscle hypertrophy
Bronchial hyperreactivity

Small Airways

Chronic exposure to ETS lead to inflammatory cell recruitment in

Pulmonary hypertension, cor pulmonale, right ventricular failure

with chronic hypoxemia (<55mm Hg)

Goblet cell metaplasia

Replacement of surfactant-secreting Clara cells
Luminal narrowing

Just Short of Breath OR Could it Be COPD?

Do you cough several times most days?

Do you bring up phlegm or mucus most days?
Do you get out of breath more easily than others your age?
Are you older than 40 years?
Are you a current smoker or an exsmoker?

If you answered yes to three or more of these questions, ask your doctor if
you might have COPD and should have a simple breathing test. If COPD is
found early, there are steps you can take to prevent further lung damage and
make you feel better. - GOLD

Decreased alveolar attachments

Lung Parenchyma

Asthma or COPD?:
Role of Spirometry

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Laboratory Findings

ABGs
Oximetry
Hypoxemia
PaCO2> 45mmHg
Elevated Hematocrit
Right ventricular hypertrophy

Chest Radiography

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hThe overall approach to managing stable COPD should be characterized by a

stepwise increase in the treatment, depending on the severity of the disease.
hFor patients with COPD, health education can play a role in improving skills,
ability to cope with illness, and health status. It is effective in accomplishing
certain goals, including smoking cessation (Evidence A).
COPD:Pharmacotherapy

Bronchodilators
Anticholinergic agents
Beta agonists
Inhaled glucocorticoids
Oral glucocorticoids
Theophylline
Oxygen
Others

Bronchodilators
Inhalational is superior to oral therapy.
Bronchodilators in Stable COPD

Bullae

Bronchodilators are prescribed on an as-needed or on a regular

basis to prevent or reduce symptoms.

Regular treatment with long-acting inhaled bronchodilators is

more effective and convenient than treatment with short-acting
bronchodilators, but more expensive. Evidence A new

Combining bronchodilators may improve efficacy and decrease

the risk of side effects compared to increasing the dose of a single
bronchodilator.

Goals of COPD Management

Prevent disease progression
Relieved symptoms
Improved health status
Improved exercise tolerance
Prevent/treat exacerbations
Prevent/treat complications
Reduce mortality
Minimize side effects from treatment

Inhaled Corticosteroids

for symptomatic COPD patients with an FEV1 < 50% predicted

(Stages III & IV) and repeated exacerbations e.g. 3 in the last three
years (Evidence A was B)

COPD:Nonpharmacologic Tx

COPD:Treatment of Stable Phase

Interventions that influence natural history

Smoking cessation

Improve symptoms
Decrease frequency and severity of exacerbations

Pulmonary rehabilitation

Influenza, pneumococcal vaccine

Quality of life, dyspnea, exercise capacity

Less hospitalizations

Lung volume reduction surgery (LVRS)

Upper lobe predominant emphysema

Lung transplantation

This treatment has been shown to reduce the frequency of

Response of symptoms, cost, risks, and benefits of therapy

Smoking Cessation

General medical care

Oxygen therapy when chronically hypoxemic

Lung volume reduction surgery (selected)

Regular treatment with inhaled glucocorticosteroids is appropriate

Bupoprion
Nicotine Replacement

Manage Stable COPD

Key Points

exacerbations and improve health status (Evidence A new).

3 of these studies, glucocorticosteroid combined with a LABA was

more effective than the individual components

Oral Corticosteroids & Exercise

Chronic treatment with systemic glucocortico-steroids should be

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avoided because of an unfavorable benefit-to-risk ratio (Evidence

A).

All COPD-patients benefit from exercise training programs,

improving with respect to both exercise tolerance and symptoms
of dyspnea and fatigue (Evidence A).

Oxygen

Only therapy demonstrated to decrease mortality

Resting hypoxemia

With or without
symptoms

Inhaled Glucocortico-steroids if
significant symptoms and lung
function response

INTE Management of COPD: Severe

Characteristics
Recommended Treatment
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Bronchodilators (.)
CINEI 30% < FEV1 < 50%
(Regular Treatment)
I
Rehabilitation
predicted
With or without
Inhaled glucocortico-steroids if
symptoms

significant symptoms and lung

function response or if repeated
exacerbations

19 hrs > 12 hrs/day

Non-Pharmacologic Therapy

General Medical Care

Management of COPD: Very Severe

Characteristics

Influenza vaccine
Pneumococcal vaccine

Pulmonary Rehabilitation
Lung Volume Reduction Surgery
Lung Transplantation

FEV1/FVC < 70%

FEV1 < 30%
predicted or
presence of
respiratory
failure or right
heart failure

Length of Rehabilitation Program

The minimum length of an effective rehab program is 2 months; the longer
the program continues, the more effective the results (Evidence B)
Classification by Severity
Stage
I: Mild

Regular treatment with one or

more bronchodilators (.)

Inhaled glucocorticosteroids if
significant symptoms and lung
function response or if repeated
exacerbations

Treatment of complications

Consider surgical options

Rehabilitation
Long-term oxygen therapy if
respiratory failure

Characteristics

II: Moderate

III: Severe

IV: Very Severe

FEV1/FVC < 70%; FEV1 80%

predicted

Summary of Practical Treatment Guidelines for COPD

With or without chronic

symptoms (cough, sputum)

All patients

Smoking cessation

FEV1/FVC < 70%; 50% FEV1 <

80% predicted

Mild dyspnoea/rescue medication

With or without chronic

symptoms

Persistent/severe dyspnoea

FEV1/FVC < 70%; 30% FEV1 <

50% predicted

With or without chronic

symptoms

FEV1/FVC < 70%; FEV1 < 30%

predicted or FEV1< 50%
predicted plus chronic
respiratory failure

Long acting bronchodilators

Long-acting bronchodilator
Regular ipratropium + long acting beta2-agonist ?
plus high dose inhaled corticosteroid

Exacerbations of COPD

Increased dyspnea, cough, change in amount or character of

sputum
Moderate to severe airflow obstruction:

Management of COPD: Moderate

Characteristics

Recommended Treatment

FEV1/FVC < 70%

50% < FEV1< 80%

predicted

Bronchodilators (.) (Regular

Treatment)

Rehabilitation

Short-acting beta2-agonist

Recurrent exacerbations

Recommended Treatment

1 to 3 episodes/year (GOLD stages III, IV)

Assess severity
Identify precipitant
Institute therapy

International Consensus on Definition of COPD Exacerbation:

A sustained worsening of the condition, from the stable state and

beyond normal day-to-day variations

Acute in onset

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Mechanical Ventilatory Support

Necessitates a change in regular medication

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International Consensus on Staging of Severity of COPD Exacerbation

Mild = increased need for medication and which patients can manage
in their own normal environment

Moderate = increased need for medication and feel must seek

additional medical assistance

Noninvasive positive pressure ventilation(NIPPV)

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deterioration of condition, requiring hospitalization

Bacterial infections

No specific precipitant (20-35%)

Reduce frequency of exacerbations:
Inhaled glucocorticoids

Glucocorticoids

Life-threatening hypoxemia
Severe hypercapnia and/or acidosis
Mortality

60% for pxs >65 y.o. admitted to the ICU

Key Messages to Physicians & Public

Noninvasive (NIPPV), Invasive (intubation)

Broad spectrum antibiotics can reduce inflammatory response,

duration of symptoms and time to recovery of lung function initial
choice of older and less expensive antibiotic for 10-14 days is
reasonable
Oral corticosteroid (prednisolone 30 mg OD) for 2 weeks
Bronchodilators (inhaled anticholinergic + short acting beta agonist)
Methylxanthines are not beneficial and may be harmful in acute
exacerbations of COPD

MANAGEMENT OF ACUTE EXACERBATION

Long-term therapy and prevention aimed at decreasing frequency of
exacerbations, reducing ER visits and hospitalizations

17 30% for pxs requiring MV

Study on Physicians Awareness of COPD in Philippines (1997)

h Out of 237 physicians surveyed on a hypothetical case of COPD, only 137
(58%) gave a correct diagnosis of COPD
h Only 43/137 (31%) would use a spirometer to establish diagnosis of COPD

Mechanical ventilatory support

MANAGEMENT OF COPD EXACERBATION

Acute Event

Significant burns

Invasive Mechanical Ventilation

30 to 40mg oral prednisolone, 10-14 days

Oxygen (keep arterial saturation > 90%)

Extreme obesity

Antibiotics

Streptococcus pneumoniae,
Haemophilus influenzae, Moraxella catarrhalis

Craniofacial abnormalities/trauma

Inhaled B-agonist, anticholinergic

Copious secretions

Severe respiratory distress

Bronchodilators

Impaired mental status

Endotracheal tube

COPD Exacerbations: Interventions

Cardiovascular instability

Invasive Ventilation

Viral infections (1/3)

Contraindications:

Severe = patients or their caregivers recognize and/or rapid

Exacerbations:
Precipitating Causes

Respiratory failure

Bronchodilators (inhaled anticholinergic, long acting beta agonists) can

reduce incidence of exacerbations by 33% to 37%
hInhaled corticosteroids can reduce # of exacerbations in severe COPD
patients (FEV1 < 50% pred)
hMucolytic (N-acetylcysteine) and immunostimulatory agent OM-85 BV have
been shown to reduce # of exacerbations but need more evidence

Think COPD
Do spirometry
Reduce risk factors
Manage actively

COPD is preventable and treatable

TAKE HOME MESSAGE

COPD problem will worsen in the coming years in developing countries

like the Philippines (WHO)

COPD is a preventable and treatable disease

Physicians can make a difference in preventing the worsening of COPD
problem (with early detection and effective treatment)