CHRONIC OBSTRUCTIVE PULMONARY DISEASE

advertisement
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
By Dr Aguilera
Definition


In 2001, the Global Initiative for Chronic
Obstructive Lung Disease (GOLD) report was
developed to define COPD by an expert panel
which includes the National Heart, Lung and
Blood Institute and the World Health
Organization.
COPD is “A disease state characterized by airflow
limitation that is not fully reversible; it is usually
both progressive and associated with an
abnormal inflammatory response of the lungs to
noxious particles or gases.”
Definition Cont’d


Previous Guidelines and Definitions
included Chronic bronchitis and
emphysema, but these are not included in
the current definition.
The GOLD report’s definition of COPD
regards chronic bronchitis, emphysema
and asthma as different aspects of the
disease that are not mutually exclusive.
Definition Cont’d

Chronic Bronchitis


Emphysema


Defined by the presence of chronic productive cough
for three months in each of two successive years in a
patient in whom other causes of cough are excluded
Is a pathological term describing the abnormal
permanent enlargement of airspaces distal to the
terminal bronchioles, accompanied by destruction of
their walls without obvious fibrosis.
Asthma

Chronic inflammatory disease of the airways with
bronchial hyper-responsiveness, reversible airway
obstruction, and respiratory symptoms. (See previous
lecture)
Pathophysiology

Bronchial inflammation

Caused by inflammatory cells (macrophages,
neutrophils and CD8 cytotoxic T cells) in a response
to noxious stimuli

release of enzymes (proteases)




these cause destruction of connective tissue in the airways and
alveolar walls.
Also stimulate mucus production by goblet cells
Different than what we see in Asthma (CD4 and
eosinophils)
Ciliary damage occurs directly by noxious stimuli
(tobacco, occupational dusts and chemicals, and
air pollution)
Pathophysiology Cont’d

Variability of Response to Noxious Stimuli

Genetics

imbalance of antiproteases



May explain why only approximately 15% of smokers
develop COPD
Alpha-1-antitrypsin deficiency
As a result, air trapping, collapse of alveoli
and inability to clear debris from the
airways occur, which manifest clinically as
the COPD syndrome.
Disease Interrelationships
Chronic bronchitis
Emphysema
1
COPD
2
5
3
4
8
7
6
10
9
Airflow
Obstruction
Asthma
Epidemiology


Approx 16 million people in U.S. have COPD
5th leading cause of death







In 2000: ED visits = 1.5 million
Hospitalizations = 726,000
Deaths = 119,000
Health care costs approx 15 billion/year
Tobacco smoking accounts for 80-90% of cases



4th in people > 45 yrs
Most deaths occur in people > 65 years
Only 15% of smokers develop COPD
Women are affected more than men with same tobacco exposure
Alpha-1-antitrypsin accounts for <.1% of cases



Homozygous (.02%) < Heterozygous (2-3%) - whites
When to test for serum levels? In pts with COPD at young age, particularly in
those with (+) FHx and no exposure to tobacco
Replace with alpha-1-proteinase inhibitor (Prolastin)
Diagnosis

History




Patients with COPD usually have been smoking at
least 20 pack years before symptoms develop.
Cough usually is the first symptom. This is followed
by sputum production and then shortness of breath
which worsen over time and may get worse with
exacerbations.
Wheezing may be present
Exposure to risk factors: tobacco, occupational dusts
and chemicals, air pollution
Diagnosis Cont’d

Physical Examination


Usually normal early in the course of the disease
Findings are variable as the disease progresses

Chest Signs



Prolonged expiration with/out wheeze; decreased breath
sounds; Crackles especially with exacerbations; Increased
anteroposterior diameter due to hyperinflation
Distant heart sounds
Extrathoracic Signs


Leaning forward to relieve dyspnea; weight loss, cyanosis
Manifestations of Cor Pulmonale
 Poor Px
Diagnosis cont’d

Pulmonary Function Test (PFT)/Spirometry

Gold standard for diagnosis COPD





FEV1/FVC ratio of < 70% defines the presence of obstructive
disease.
Cannot determine difference between COPD, chronic bronchitis or
emphysema
FEV1 is used to determine severity of disease
Peak Expiratory Flow Rate (PEFR) is used to monitor response to
therapy
Lung function should be measured with bronchodilator
evaluation. The absence of a significant response (>15%
increase in FEV1) on one test should not be the reason to hold
bronchodilator therapy.


If improvement >20% and FEV1 becomes normal = Asthma
If FEV1 increases but is still below normal = Mixed Asthma/COPD
Diagnosis Cont’d

Chest X-Ray (CXR)



Arterial Blood Gas (ABG)




Radiological changes don’t usually occur until COPD is advanced
(overdistention, bullae formation
Done to identify co-existing conditions
Used in most cases to determine if a patient requires oxygen
maintenance based on level of hypoxia
Usually done when FEV1 < 40%, and in those with signs of
respiratory failure (PO2<60 or PCO2>45) or right heart failure
Can also give information regarding CO2 levels
Complete Blood Count (CBC)

Can identify erythrocytosis/polycythemia as a result of chronic
hypoxemia and should be done in patients being considered for
O2 supplementation
Classification of COPD
(Remember FEV1/FVC is used in the Dx COPD!)
% Predicted FEV1
1995 ATS %
Predicted FEV1
80-100%
2001 GOLD Report
% Predicted FEV1
Symptoms
Stage 0: At risk, but
PFT’s are normal
FEV1/FVC > 70%
Cough and sputum
production may be
present
Stage I: Mild
> 80% predicted
Cough and sputum
production may be
present
50-80%
Stage I: Mild
50-80% predicted
Stage IIA: Moderate
50-80% predicted
Cough and sputum
and dyspnea may be
present
0-50%
Stage II: Moderate
35-50% predicted
Stage IIB: Moderate
30-50% predicted
Cough, sputum and
dyspnea with more
exacerbations
Stage III: Severe
<35% predicted
Stage III: Severe
< 30% predicted or
resp failure or RHF
Cough, sputum and
dyspnea with
frequent
exacerbations
Overall Treatment of COPD

1st Step is to establish a diagnosis



Spirometry in patients with Sx or RF
CXR to exclude other conditions
2nd Step is to Classify the stage of disease

Used to guide therapy


For example, Stage II requires smoking cessation, an ABG,
pharmacotx and consultation with a pulmonologist
3rd Step is to educate your patients


This is the key component
Main goals of treatment are to improve quality of life
and decrease mortality

Only 2 interventions decrease mortality: smoking cessation
and long term O2 supplementation
Overall Treatment Cont’d

4th Step is to begin Pharmacotherapy

Inhaled Bronchodilators



Improve symptoms and decrease airflow limitation
Albuterol 2 puffs Q6hrs/PRN
Ipratropium



Common problems




Usually first line therapy
Start with 2 puffs QID and may increase to 6 puffs TID
Inadequate education regarding meds and technique
Suboptimal dosing
Inadequate monitoring of response to treatment
The use of long acting beta agonists (Salmeterol and
Formoterol) in COPD is still in evolution.
Overall Treatment Cont’d

Inhaled Steroids



Do not affect the decline in FEV1, thus the severity
In mod-severe disease these meds showed a significant
decrease in the frequency of symptoms and exacerbations
Theophylline


GOLD report recommends against its use due to availability
of other drugs, high Sfx profile and drug interactions.
Does work for some patients



Keep levels between 8-12 mcg/ml
Monitor regularly
Be aware of drug interactions
Overall Treatment Cont’d

Oral Steroids

Long term use is not recommended




A beneficial response to a short course of an oral steroid
does not predict benefit from the chronic use of oral
steroids.
Long term disease effects are unknown.
Studies failed to show a difference in the # of
exacerbations, symptoms or spirometry results when
continuation vs withdrawal of prednisone was compared
If considering long term oral steroids for a patient
with severe disease, then use smallest dose
possible. Usually done in conjunction with
pulmonologist.
Overall Treatment Cont’d

5th step is to prevent and treat complications

Chronic Hypoxia



Consequences include dyspnea, impaired cognition, ischemic
CM, ploycythemia/ erythrocytosis with hyperviscosity
syndromes, and pulmonary HTN
Supplemental O2 can improve symptoms and prevent some
of these complications. In fact, life expectancy increases.
ABG evaluation at appropriate times

MediCare guidelines
 PaO2 < 55mmHg; POx < 88% for any patient
 PaO2 55-59mmHg; POx = 89% for those with chronic
hypoxic complications as listed above
Overall Treatment Cont’d

Immunizations
Annual influenza shots
 Polyvalent pneumococcal vaccine at time of
diagnosis and again in 5 years or at age 65,
whichever comes later.


Consultation with a specialist

Pulmonologist


Stage IIB and III
Surgeon

When considering lung volume reduction surgery or
transplantation
THE END
Download