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‫بسم هللا الرحمن الرحیم‬
‫‪COPD‬‬
‫‪Dr.Cheraghvandi‬‬
Chronic Obstructive Pulmonary
Disease (COPD): definition
• GOLD (Global Initiative on Chronic Obstructive
Lung Disease) definition:
COPD is a progressive but preventable chronic
disease most frequently caused by smoking
COPD is characterized by:
- a progressive airflow limitation, which is not fully
reversible
- a rapid decline in lung function
- a local and systemic inflammatory process not
responsive to corticosteroids
Close to the Beltway but a World Apart
COPD
• Chronic obstructive pulmonary disease is
a slowly progressive disease that is
characterized by a gradual loss of lung
function
• COPD includes chronic bronchitis, chronic
obstructive bronchitis, or emphysema, or
combinations of these conditions
Asthma
• Asthma is a chronic
inflammatory
pulmonary disorder
that is characterized
by reversible
obstruction of the
airways
Chronic Bronchitis
• Inflammation of the main
airway passages
(bronchi) to the lungs,
which results in the
production of excess
mucous, a reduction in
the amount of airflow in
and out of the lungs, and
shortness of breath
Chronic bronchitis
•
•
•
•
Increase in the number of mucous cells
Large amount of sputum
Diffusion normal
Hypercarbia due to deceased alveolar
ventilation
Emphysema
• A respiratory disease
characterized by
breathlessness
brought on by the
enlargement, or overinflation of, the air
sacs (alveoli) in the
lungs
Emphysema
• What is it?
• Destruction of alveolar walls-- below the
bronchioles
• Decreases surface area
• Decreases area available for exchange
• Increase resistance to pulmonary blood
flow
Emphysema cont...
•
•
•
•
•
•
•
Can lead to pulmonary hypertension
Cor pulmonale = right heart failure
Lungs can not recoil and air is trapped
Residual lung capacity increases
PO2 decreases over time
Increased RBC
Polycythemia-- high hematocrit
Emphysema cont...
•
•
•
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•
PCO2 increased
Hypoxic drive
Causes
Complications of disease
Pneumonia
URI
Dysrhythmias
cancer
Emphysema cont...
•
•
•
•
Home drugs
Bronchodilators
Steroids
Later-- oxygen
Emphysema cont..
•
•
•
•
•
•
Assessment
Weight loss-- thin
Dyspnea esp on exertion
Cough only in AM
Barrel chest
Tachypnea
Emphysema cont..
•
•
•
•
Pink puffers
Enlarged accessory muscles
Clubbing of fingers
Pursed lips-- prolonged expiration-- active
now
• Wheezing or rhonchi may or may not be
present
Chronic bronchitis
•
•
•
•
•
Assessment
Overweight
Blue bloaters
Rhonchi
RHF-- JVD, pedal edema
Epidemiology
• 20.3 million Americans report having
asthma
• 5,000 deaths annually from asthma
• 12.1 million Americans reported being
diagnosed with COPD
• 119,000 deaths annually from COPD
• COPD is the 4th leading cause of death in
the U.S.
Wayne McLaren…Former Marlboro
Man
Age 30…a robust
young man
Age 51…riding
into the sunset
% Change in Age Adjusted Death Rate
US 1965-1998…gotta die of something
US Leading Causes of Death 2001
The Real Story
Etiology
• Cause of asthma is unknown but many factors play a
part:
– Genetic factors: Asthma tends to run in the family
– Environmental factors: pollen, dust, mold, tobacco
smoke
– Occupational exposure: chemicals and gases
• Smoking is the leading cause of COPD followed by
occupational exposures
Clinical Features of Asthmatic
Patients
• General: intermittent wheezing, coughing,
and breathlessness
• During an attack: decreased peak flow,
tachypnea, use of accessory muscles to
breathe, hyperinflation or barrel chest, and
prolonged inspiration
Clinical Features of COPD Patients
• Mild COPD: no abnormal signs, smokers cough,
little or no breathlessness
• Moderate COPD: breathlessness with/without
wheezing, cough with/without sputum
• Severe COPD: breathlessness on any
exertion/at rest, wheeze and cough prominent,
lung inflation usual, cyanosis, peripheral edema,
and polycythemia in advanced disease
Diagnosis
• Spirometry
– Breathing test which measures the amount and rate at which air
can pass through the airways
• Bronchodilator Reversibility Testing
– Relaxing tightened muscles around the airways and opening up
airways quickly to ease breathing
• Other pulmonary function testing
– Diffusion capacity
• Chest X-ray
• Arterial Blood Gas
– Shows oxygen level in blood
Medical Management of Asthmatic
Patient
• Limit exposure triggering agents
• Medications such as: inhaled
corticosteroids, inhaled beta2 adrenergic
agonist, and cromolyn sodium
Medical Management of COPD
Patient
• Smoking cessation and elimination of
environmental pollutants
• Palliative measure such as regular
exercise, good nutrition, flu and
pneumonia vaccines
• Bronchodilators, corticosteroids,
anticholinergics, and NSAIDs
Dental Management of COPD
Patient
•
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Review history for concurrent heart disease
Avoid treatment if upper respiratory tract infection is present
Treat in upright position
Avoid rubber dam in severe cases
Use pulse oximetry (if pulse ox <91%, use low flow 2-3L/min)
Avoid Nitrous oxide/oxygen in severe cases
Avoid barbiturates, narcotics, antihistamines, and
anticholinergics
• If patient is on steroid regimen, supplement as needed
• Drug interactions with COPD medication
Other Sad Facts
• Direct Cost 2002- 18 Billion
• Indirect Costs- 14 Billion
• In US 47 million still smoke
– 28% males
– 23% females
• WHO: 1 billion smokers worldwide…to
increase to 1.6 billion 2025. Increasing in
lower income areas
Objectives of COPD Management
• Prevent Progression
• Relieve symptoms
• Improve exercise tolerance and general
health status
• Prevent and treat exacerbations and
complications
• Minimize treatment side effects
Pathophysiology Simplified
Bad Genes
Breathe Noxious Crap
COPD
THE Guideline
• Global Initiative for Chronic Obstructive
Lung Disease (GOLD), World Health
Organization (WHO), National Heart, Lung
and Blood Institute (NHLBI)
4 Keys to Management
• Assess and Monitor Disease
• Reduce Risk Factors
• Manage Stable COPD
– Education
– Med management
– Non med management
• Treat exacerbations
Assess and Monitor Disease
Classification of COPD
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•
Stage 0
Stage I
Stage II
Stage III
Stage IV
At Risk
Mild COPD
Moderate COPD
Severe COPD
Very Severe COPD
Stage 0
At Risk
• Normal spirometry
• +/- Chronic symptoms (cough, sputum,
production)
Stage I
Mild COPD
• FEV1/FVC <70%
• FEV1 >80% predicted
• With or without chronic symptoms (cough,
sputum production)
Stage II
Moderate COPD
• FEV1/FVC <70%
• 50% <FEV1 <80% predicted
• With or without chronic symptoms (cough,
sputum production)
Stage III
Severe COPD
• FEV1/FVC <70%
• 30% <FEV1 <50% predicted
• With or without chronic symptoms (cough,
sputum production)
Stage IV
Very Severe COPD
• FEV1/FVC <70%
• FEV1 <30% predicted or FEV1 <50%
predicted plus chronic respiratory failure
GOLD Guideline in Japan
Assess: Who Has Early Stages
And Who Do You Test?
• Test patients with:
– chronic cough and sputum
– exposure to risk factors
– even if no dyspnea
• Early Stage:
– airflow limitation that is not fully reversible
– with or without the presence of symptoms
Assess for COPD:
A Common Story
• Cough
– intermittent or daily
– present throughout day- seldom only nocturnal
• Sputum
– Any pattern of chronic sputum production
• Dyspnea
– Progressive and Persistent
– "increased effort to breathe" "heaviness" "air hunger"
or "gasping"
– Worse on exercise
– Worse during respiratory infections
• Exposure to risk factors
– Tobacco smoke
– Occupational dusts and chemicals
– Smoke from home cooking and heating fuels
Assess:
Spirometry to Diagnose
 FEV1/FVC <70% and a postbronchodilator
FEV1 <80% predicted confirms the presence
of airflow limitation that is not fully reversible.
 Must have access to spirometry
Assess: Medical History in Those
With Established Disease
• Exacerbations or hospitalizations?
• Comorbidities that contribute to restriction of
activity
• Appropriateness of current medical treatments
• Impact of disease on patient's life
– limitation of activity
– missed work and economic impact
– effect on family routines
– depression or anxiety
• Social and family support
• Possibilities for reducing risk factors, esp smoking
Assess:
Physical Examination
• Rarely diagnostic in COPD
• Physical signs of airflow limitation
– rarely present until significant impairment of
lung function
– low sensitivity and specificity
Assess:
Measure Airflow Limitation
• Patients with COPD typically show a
decrease in both FEV1 and FVC
• Postbronchodilator FEV1 <80% predicted
+ FEV1/FVC <70% confirms the presence
of airflow limitation that is not fully
reversible
• FEV1/FVC <70% is an early sign of airflow
limitation in patients whose FEV1 remains
normal (>80% predicted).
Assess: Additional Investigations
> Stage II: Moderate COPD
• Bronchodilator reversibility testing
–
–
–
–
rule out asthma
establish best attainable lung function
gauge a patient's prognosis
guide treatment decisions
• Chest x-ray
– seldom diagnostic unless obvious bullous disease
– valuable in excluding alternative diagnoses
– CT not routinely recommended
Assess: Additional Investigations
> Stage II: Moderate COPD
• Arterial blood gas measurement
– In advanced COPD: FEV1 <40% predicted or signs
suggestive of respiratory failure or right heart failure
– central cyanosis, ankle swelling, JVD
– Respiratory failure
• PaO2 < 60 mm Hg +/- PaCO2 >50 mm Hg
• Alpha-1 antitrypsin deficiency screening
– COPD at a young age
– strong family history of the disease
Differential Diagnosis
• A major differential diagnosis is asthma
• In some patients with chronic asthma, a
clear distinction from COPD is not possible
• In these cases, current management is
similar to that of asthma
• Other potential diagnoses are usually
easier to distinguish from COPD
COPD
•
•
•
•
•
Onset in mid-life
Symptoms slowly progressive
Long smoking history
Dyspnea during exercise
Largely irreversible airflow limitation
Asthma
•
•
•
•
Onset early in life (often childhood)
Symptoms vary from day to day
Symptoms at night/early morning
Allergy, rhinitis, and/or eczema also
present
• Family history of asthma
• Largely reversible airflow limitation
Congestive Heart Failure
• Fine basilar crackles on auscultation
• Chest x-ray shows dilated heart,
pulmonary edema
• PFTs indicate restriction- not obstruction
• BNP can help
Other Diff Dx to Consider
• Bronchiectasis
– Large volumes of purulent sputum
– bacterial infection
– CXR/CT shows bronchial dilation, bronchial
wall thickening
• TB
– History with the usual suspects
• BOO and BOOP
– nonsmokers
– environmental exposures
– CT on expiration shows hypodense areas
Monitoring: This is a progressive
disease
• Lung function worsens over time- even with best
care
• Monitor symptoms and objective measures of airflow
limitation to determine when to adjust therapy
• Spirometry should be performed if there is a
substantial increase in symptoms or a complication
• ABG should be considered in all patients with an
FEV1 <40% predicted or clinical signs of respiratory
failure or right heart failure (JVD/edema)
Reduce Risk Factors
Reduce Risk Factors:
Key Points
• Reducting exposure to tobacco smoke,
occupational dusts, and chemicals, and indoor
and outdoor air pollutants
• Smoking cessation is the single
most effective -- and cost-effective
-- intervention to reduce the risk of
developing COPD and stop its
progression (Evidence A)
Reduce Risk Factors:
Key Points
• Brief tobacco dependence treatment is
effective (Evidence A)
• Every tobacco user should be offered at
this treatment at every visit
• Three types of counseling are especially
effective: practical counseling, social
support as part of treatment, and social
support arranged outside of treatment
(Evidence A)
Reduce Risk Factors:
Key Points
• There are effective pharmacotherapies for
tobacco dependence (Evidence A)
• Add meds to counseling if necessary
• Progression of many occupationally
induced respiratory disorders can be
reduced or controlled by reducing inhaled
particles and gases (Evidence B)
Maybe This
Would be
Better Than
Drugs
Manage Stable COPD
Key Points 1
• Stepwise increase in treatment based on disease
severity
• 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).
• None of the existing medications for COPD
affects long-term decline in lung function that is
the hallmark of this disease (Evidence A)
• Pharmacotherapy for COPD is used to decrease
symptoms and/or complications
Therapy by Stage- Pretty Simple
Manage Stable COPD
Key Points 2
• Bronchodilators central to symptom management
(Evidence A)
• PRN or regular basis to reduce symptoms
• Use beta2-agonist, anticholinergic, theophylline,
or a combination of one or more of these drugs
(Evidence A)
• Regular treatment with LABs is slightly more
effective and convenient than with SABs, but
more expensive (Evidence A)
• TECHNIQUE IS KEY
• MDI BETTER THAN NEB IF USED CORRECTLY
Manage Stable COPD
Key Points 3
• Add inhaled steroids to bronchodilators for
symptomatic COPD patients with an FEV1
<50% predicted (Stage III: Severe COPD
and Stage IV Very Severe COPD) and
repeated exacerbations (Evidence A)
• Avoid chronic treatment with systemic
steroids - unfavorable benefit-to-risk ratio
(Evidence A
Manage Stable COPD
Key Points 3
• The long-term O2 with chronic respiratory failure
increases survival (Evidence A)
• Improves exercise tolerance
• If hypercapnic titrate SpO2 to 88-90%
• Walk your clinic patients if RA SpO2 OK
Manage Stable COPD
Key Points 4
• All COPD patients benefit from exercise
training program
• Improves both exercise tolerance and
symptoms of dyspnea and fatigue
(Evidence A)
Medications
Bronchodilators
Beta2-agonists
• Short-acting
– Fenoterol
– Salbutamol (albuterol)
– Terbutaline
• Long-acting
– Formoterol
– Salmeterol
Bronchodilators
Anticholinergics
• Mode of Action
– Cholinergic tone is only reversible component of COPD
– Normal airway have small degree of vagal cholinergic
tone
• Short-acting
– Ipratropium bromide
– Oxitropium bromide
• Long-acting
– Tiotropium
BronchodilatorsCombos and Methylxanthines
• Combination beta2-agonists plus
anticholinergic in one inhaler
– Fenoterol/Ipratropium
– Salbutamol/Ipratropium
• Methylxanthines
– Aminophylline (slow release preparations)
– Theophylline (slow release preparations)
– RARELY OF SIGNIFICNAT BENEFIT
– LEVEL 8-12 mcg/ml
Other Med Adjuncts?
• Influenza vaccines significantly reduce serious
illness and death (Evidence A)
• Pneumococcal vaccine –OK to use but data
lacking (Evidence B)
• Antibiotics: other than treating infectious
exacerbations- not recommended (Evidence A)
• Mucolytic Agents: a few patients with viscous
sputum may benefit but the widespread use
cannot be recommended (Evidence D)
• Antitussives: Cough, a troublesome symptom
in COPD, has a protective role. Regular use of
antitussives contraindicated (Evidence D)
• Narcotics: The use of PO and IV opioids
effective for dyspnea in advanced disease
Therapy by Stage- Pretty Simple
• “Make everything
as simple as
possible, but not
one bit simpler”
Einstein
Manage Exacerbations
• Do you admit? You and your patient
decide….little guidance in the literature
Manage Exacerbations 1
• Infection of tracheobronchial tree and air
pollution are most common causes
• Cause of about 1/3 of severe
exacerbations cannot be identified
Manage Exacerbations 2
 (Evidence A) treatment
 Inhaled bronchodilators (beta2-agonists
and/or anticholinergics)
 Systemic, preferably oral, glucocorticosteroids
 (Evidence B) Antibiotic treatment if signs of
airway infection
 increased volume/change of color of
sputum
 fever
 O2 of course….but caution with retainers
 Little evidence for Methyxanthines
Manage Exacerbations 3
 Noninvasive intermittent positive pressure
ventilation (NIPPV) improves blood gases and
pH, reduces in-hospital mortality, decreases
the need for invasive mechanical ventilation
and intubation, and decreases the length of
hospital stay (Evidence A)
 BIPAP is Best!
• Set FiO2, inspiratory (IPAP) and expiratory
(EPAP)
• Difference between IPAP and EPAP
augments tidal volume and improves
minute ventilation
• CO2 gets blown off
Best References
• Stoller J. Acute Exacerbations of COPD,
NEJM Mar 28, 2002
• Sutherland E. Management of COPD,
NEJM June 24, 2004
• GOLD (Global Initiative for Chronic
Obstructive Lung Disease) Executive
Summary www.goldcopd.org
• New….TORCH NEJM Feb 22, 2007
Questions?
COPD - Pathogenesis
Tobacco Smoke
Host factors
Chronic Inflammation*
Anti-oxidants
Anti-proteinases
Oxidative Stress
Proteinases
Repair Mechanisms
Emphysema
Chronic Bronchitis
*CD8+ T-lymphocytes
Macrophages
Neutrophils
IL-8 and TNF
COPD Therapy
Prolong Life
Smoking Cessation
Oxygen
Reduce exacerbations
Pulmonary
Rehabilitation
• LVRS (selected
patients)
• Lung Transplantation
•
•
•
•
Symptomatic
• MDI Therapy
– SA beta-2 agonists
– LA beta-2 agonists
– SA and LA
Anticholinergics
• Theophylline
• Corticosteroids
(inhaled or oral)
• Combination
Preparations
– SABA and anticholinergic
– LABA and corticosteroids
Management of COPD
Stage 0: At Risk
Characteristics
Treatment
• Risk factors
•Chronic symptoms
- cough
- sputum
• No spirometric
abnormalities
Recommended
•Adjust risk factors
•Immunizations
Management of COPD
Stage I: Mild COPD
Characteristics
Treatment
• FEV1/FVC < 70 %
• FEV1 > 80 %
predicted
• With or without
symptoms
Recommended
• Short-acting
bronchodilator as
needed
Management of COPD
Stage II: Moderate COPD
Characteristics
Treatment
•FEV1/FVC < 70%
•50% < FEV1< 80%
predicted
•With or without symptoms
Recommended
•Treatment with one or
more long-acting
bronchodilators
•Rehabilitation
Management of COPD
Stage III: Severe COPD
Characteristics
Treatment
•FEV1/FVC < 70%
•30% < FEV1 < 50%
predicted
•With or without symptoms
Recommended
•Treatment with one
or more long-acting
bronchodilators
•Rehabilitation
•Inhaled glucocorticosteroids if repeated
exacerbations
(>3/year)
Management of COPD
Stage IV: Very Severe
COPD
Characteristics
Treatment
•FEV1/FVC < 70%
•FEV1 < 30% predicted
or presence of
respiratory failure or
right heart failure
Recommended
•Treatment with one or more
long-acting bronchodilators
•Inhaled glucocorticosteroids if
repeated exacerbations
(>3/year)
•Treatment of complications
•Rehabilitation
•Long-term oxygen therapy if
respiratory failure
•Consider surgical options
Bronchodilator Therapy
Some General Principles
• Inhaled therapy (with spacer) preferred
• Long-acting preparations more convenient
• Combined preparations improve effectiveness
and decrease risk of side effects
– Ipratroprium-albuterol
– Fluticasone-salmeterol
– Budesonide-formoterol
• MDI almost always as effective as nebulizers (in
equal doses)
Effectiveness of
BronchodilatorTherapy?
• FEV1 does not always correlate with
symptoms
– Concept of “dynamic hyperinflation” in
COPD
• Quality of life issues are important
– Chronic fatigue
– Depression
– Physical immobility
– Dyspnea
COPD - Surgical Options
• Giant Bullous Disease
– Consider bullectomy if see normal lung compression
• Lung Volume Reduction Surgery*
– FEV1 (<20% pred) plus diffuse emphysema or
Dlco<20% pred = high risk of surgical death
– Upper lobe emphysema and low exercise capacity =
decreased mortality, increased exercise and QOL
• Lung Transplantation
– FEV1<25% predicted, younger patient
– 3-5 year mortality 55%
*NETT Research Group. N Eng J Med 348:2059, 2003
COPD Exacerbation
Definition Elements
• Worsening dyspnea
• Increased sputum
purulence
• Increase in sputum
volume
Severity
• Severe - all 3
elements
• Moderate - 2
elements
• Mild - 1 element
plus:
Modified from Anthonisen et al. Ann Int Med 106:196, 1987
• URI in past 5
days
• Fever without
apparent cause
• Increased
wheezing or
cough
• Increase (+20%)
COPD Exacerbation
Pathophysiology - Current Hypothesis
Chronic Inflammation
Viral
Infection
Unknown
20%
25%
Bacterial
Infection
50%
Acute
Inflammation
Exacerbation
Air
Pollution
5%
Therapy of COPD
Exacerbation
Guidelines
Variable
Diagnostic
ACCP-ACP
CXR for admissions
GOLD
CXR, EKG, ABG,
sputum culture, lytes,
cbc
Bronchodila Ipratroprium, add B2
tors
agonist. No
methylxanthine
B2 agonist, add
ipratroprium. Yes
methylxanthine
Delivery
system
None preferred
Not discussed
Antibiotics
Yes, in selected
(severe). Duration
Ann Int Med 134:595, 2001
unclear
Yes, with purulence,
Rx local sensitivities
http:/www.goldcopd.com
COPD Exacerbation
Effects on Lung Function Decline
Infrequent
Frequent
• 109 pts (mean FEV1 =
1.0 L over 4 years
• Frequent
exacerbators:
– faster decline in PEFR
and FEV1
– more chronic
symptoms (dyspnea,
wheeze)
– no differences in PaO2
or PaCO2
Conclusion:
Frequent exacerbations
accelerate decline in
lung function
Donaldson et al. Thorax 57:847, 2002
Therapy of COPD
Exacerbation
Guidelines
Variabl ACCP-ACP
e
GOLD
Steroids
Yes, for up to
two weeks
Yes, oral or IV for 10-14 days
Oxygen
Yes
Yes - target PaO2 60 torr or
Sat of 90% with ABG check
Chest PT
No
Maybe - for atelectasis or
sputum control
Mucokinet No
ics
Ann Int Med 134:595, 2001
Not discussed
http:/www.goldcopd.com
Therapy of COPD
Exacerbation
Guidelines
Variable
Mechanical
Ventilation
ACCP-ACP
GOLD
Yes - use NIPPV in Yes if ≥2 of:
severe
Severe dyspnea,
exacerbation
access. muscle or
paradox, pH <7.35
and PCO2 >45,
RR>25
LMWH, fluids, diet
Other
Ann Int Med 134:595, 2001
http:/www.goldcopd.com
COPD Therapy - New
Horizons
• Newer anti-inflammatory agents
– Matrix metalloproteinase inhibitors
– Specific phosphodiesterase (PDE4) inhibitors
• Cilomilast
• Rofumilast
• Piklanilast
• Anabolic steroids
• Repair agents
– Retinoic acid
• Long-acting anti-muscarinic agents
– tiotropium
Tiotropium
Specific M1 and M3 Muscarinic Blockade
• 470 patients - stable
COPD
• 3 month, randomized,
double blind, once daily
tiotropium vs. placebo
Conclusions:
Increased FEV1 and FVC
No tachyphylaxis
Decreased rescue
albuterol
Decreased wheezing,
SOB
Dry mouthCasaburi
in 9.3%
et al. CHEST 118:1294, 2000
Tiatroprium
Specific M1 and M3 Muscarinic Blockade
• 1207 patients, double
blind, randomized trial,
• qd tiotropium vs. bid
salmeterol vs. placebo
Conclusions: Tiotropium
Fewer exacerbations
Increased time to first exacerbation
Fewer admissions
Increased QOL
Brusasco et al. Thorax 58:399:2003
Lung Volumes in Obstructive Disease
TLC
Volume
Room to
Breathe
TLC
FRC
Room to
Breathe
FRC
RV
RV
Normal
COPD