Transcript COPD by Dr Sarma - drsarma.in

CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
Dr.Sarma RVSN, M.D., M.Sc (Canada)
Consultant in Medicine and Chest,
President IMA – Tiruvallur Branch
JN Road, Jayanagar, Tiruvallur, TN
+91 98940 60593, (4116) 260593
Dr.Sarma@works
1
GOLD
GLOBAL INITIATIVE
FOR CHRONIC
OBSTRUCTIVE
LUNG
DISEASE
NHLBI AND WHO COLLABORATIVE INITIATIVE
Dr.Sarma@works
2
WORLD COPD DAY
November 19, EVERY YEAR
Raising COPD Awareness Worldwide
Dr.Sarma@works
3
RELEVANCE
1. COPD is very
common
2. COPD is often covert
3. COPD is treatable
4. Culprit is smoking
5. Symptoms + DD
Use spirometry
6. GP must know to Dx.
Tests, Rx. and refer
7. New advances in Rx.
Dr.Sarma@works
PURPOSE OF THIS TALK
Present the
Global strategy
for the Diagnosis,
Management and
Prevention of COPD
(updated Nov 2004)
BASED ON THE GOLD, NICE
NAEPP, CDC, BTS,
GUIDELINES
4
DEFINITIONS
Dr.Sarma@works
5
CONTENTS
DEFINITION OF COPD
1. Definition - Key points
1. It is chronic
2. Epidemiology
2. It is progressive
3. Risk factors
3. Mostly fixed airway obstruction
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Antismoking strateg.
4. Non reversible by bronchodilators
5. Exposure to noxious agent is a must
6. Chronic obstructive lung disease (COLD)
8. Management Guide
7. Chronic obstru. airways disease (COAD)
9. Drug delivery options
8. Two entities in COPD – namely
10.Rehabilitation, Exace.
Dr.Sarma@works
1. Chronic Bronchitis 2. Emphysema
6
2. EMPHYSEMA
1. CHRONIC BRONCHITIS
1. Alveolar wall
destruction
1. Productive cough
2. Irreversible
enlargement of
the air spaces
3. In each of 2 consecutive years
3. Distal to the terminal
bronchioles
4. Without evidence
of fibrosis
Dr.Sarma@works
2. For a period of 3 months
4. Absence of any other identifiable
cause of excessive sputum production
5. Airflow limitation that is not fully reversible
6. Abnormal inflammatory response to
noxious agent - like smoking
7
CONTENTS
DEFINITION OF COPD
1. Definition - Key points
ROAD – Recurrent Obstructive Airways Disease
2. Epidemiology
• Bronchial Asthma
3. Risk factors
• Seasonal, Recurrent
4. Pathogenesis –Pathol
• Sensitizing Agent, Other Atopic disorders
5. Clinical features
• Reversible obstruction, Inflammation
6. Diagnosis, Spirometry
COLD – Irreversible, Chronic, Noxious agent
7. Stop smoking strateg.
• Chronic Bronchitis
8. Management Guide
• Emphysema
9. Drug delivery options
• Combination of both
10.Rehabilitation, Exace.
Dr.Sarma@works
8
OBSTRUCTIVE LUNG DISEASES
ASTHMA
EMPHYSEMA
CHRONIC
BRONCHITIS
FULL
NONE
REVERSIBILITY OF AIR WAY OBSTRUTION
ASTHMA
Dr.Sarma@works
COPD
9
EPIDEMIOLGY
OF COPD
Dr.Sarma@works
10
CONTENTS
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
KEY POINTS
• Underestimated, often covert
• It is not diagnosed until clinically overt
• By that time it is moderately advanced.
5. Clinical features
• The global burden of COPD will increase
6. Diagnosis, Spirometry
• Toll from ↑ tobacco use in alarming
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
Dr.Sarma@works
11
MORTALITY
Cause
Deaths
CHD
724,269
Cancer
534,947
CVA
158,060
COPD
114,318
BURDEN OF ILLNESS
• COPD is the 4th leading cause of
death (next to IHD, Cancer, CVA).
• In 2000, the WHO estimated 2.74
million COPD deaths worldwide.
• In 1990, COPD was ranked 12th
among the burden of diseases
Accidents
94,828
• By 2020 it is projected to rank 5th.
Diabetes
64,574
• Often, COPD is covert
Dr.Sarma@works
12
MORTALITY
TRENDS 1965 - 2000
Cause
% Change
COPD PREVALENCE 2000


CHD
- 59%
Cancer
- 64%



CVA
COPD
- 39%
+ 163%



Accident
+ 32%
All other
- 7%
Dr.Sarma@works

Established Market Economies
Formerly Socialist Economies
India
China
Other Asia and Islands
Sub-Saharan Africa
Latin America and Caribbean
Middle Eastern Crescent
World
6.98
7.35
4.38
26.20
2.89
4.41
3.36
2.69
9.34
*From Murray & Lopez, 2001
13
MORBIDITY
Year
Consultations
WHAT IS WRONG ?
• Cigarette smoking is the primary cause.
• USA - 47.2 million smoke, ♂ 28%, ♀ 23%
1980
6.1 million
1985
7.4 million
1990
10.1 million
• Many countries, rates are ↑ alarmingly.
1995
11.8 million
2000
13.9 million
• In India, 4,00,000 premature deaths
annually to use of biomass fuels, like
cow dung cakes, open fires
2010
Dr.Sarma@works
↑↑↑↑
• WHO estimates 1.1 B smokers in world.
• This increases to 1.6 billion by 2025.
• Indoor air pollution, Industrial pollution
are the major risk factors in our country.
14
SMOKING - THE CULPRIT
Dr.Sarma@works
15
MOST IMP RISK
RISK FACTORS FOR COPD
• Host Factors
– Genes (alpha1- anti-trypsin↓)
– Hyper responsiveness
– Lung growth, low BW, Age
• Exposure
– Tobacco smoke,
– Bio mass fuel smoke, open fires
– Occupational dusts and chemicals
– Chronic uncontrolled asthma
– Infections, overcrowding, damp
– Low socioeconomic status
– Low dietary vegetable and fruit intake
Dr.Sarma@works
16
WOMEN SMOKERS
PASSIVE SMOKERS
Dr.Sarma@works
17
INTENSE CAUSE FOR CONCERN ?
COLLEGE STUDENTS
TENDER AGE GROUPS
Dr.Sarma@works
18
COPD NH – EFFECT OF SMOKING
Mortality among women smokers is on the rise globally
Dr.Sarma@works
19
PATHOGENESIS
PATOLOGY
Dr.Sarma@works
AND
20
CONTENTS
PATHOGENESIS
1. Definition - Key points
NOXIOUS AGENT
(tobacco smoke, pollutants,
occupational exposures
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
Genetic factors
5. Clinical features
6. Diagnosis, Spirometry
Respiratory
infection
7. Stop smoking strateg.
Others
8. Management Guide
9. Drug delivery options
COPD
10.Rehabilitation, Exace.
Dr.Sarma@works
21
PATHOGENESIS
1. Definition -key
points
2. Burden of COPD
3. Classification
4. Risk factors
5. Pathogenesis,
6. Pathophysiology,
7. Management
8. Future research
Dr.Sarma@works
22
PATHOGENESIS
1. Definition -key
points
2. Burden of COPD
3. Classification
ATOPY
4. Risk factors
5. Pathogenesis,
6. Pathophysiology,
7. Management
8. Future research
Dr.Sarma@works
23
SHIFT IN THE DELICATE BALANCE
Nutrophil elastase
Alpha 1 Anti-trypsin
Cathepsisns
SLP 1, Elastin, TIMPs
MMP-1, MMP- 9, MMP – 12
Granzymes
Perforins
PROTEASES
ANTI PROTEASES
COPD
Dr.Sarma@works
24
CONTENTS
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
10.Rehabilitation, Exace.
Dr.Sarma@works
PATHOLOGY
• Irreversible – COPD – Why ?
– Fibrosis and narrowing of the airways
– Loss of elastic recoil due to alveolar
destruction
– Destruction of alveolar support that
maintains patency of small airways
• Reversible – Bronchial Asthma
– Accumulation of inflammatory cells,
mucus, and exudates in bronchi
– Smooth muscle contraction in peripheral
and central airways
– Dynamic hyperinflation during exercise
25
PATHOLOGY in COPD
COPD
1. Mucus gland hypertrophy
2. Smooth muscle hypertrophy
3. Goblet cell hyperplasia
Normal bronchial architecture
Dr.Sarma@works
4. Inflammatory infiltrate
5. Excessive mucus
6. Squamous metaplasia
26
DISSECTING MICROSCOPIC APPEARENCE
Normal parenchymal
architecture
Dr.Sarma@works
Emphysematous
Lung architecture
27
PATHOLOGY – COPD
ASTHMA
1. Eosinophilic inflamm.
2. CD4, Th2 Lymphocyte
3. Mast cells
4. Tissue destruct. less
5. Mainly allergic inflam.
6. Inflam. Mediators
LT D4
IL 4
IL 5
Dr.Sarma@works
1.
2.
3.
4.
5.
6.
7.
Neutrophilic inflammation
Macrophages and CD8 T cells ↑
Altered protease/antiprotiase balance
Tissue destruction progressive
Alpha1 AT↓- Young age emphysema
Goblet cell size and number ↑ in CB
Inflammatory mediators
LT B4
IL 8
TNF-α
28
PULMONARY HYPERTENSION IN COPD
1. Duplication of elastic lamina
2. Medial hypertrophy - PH
Normal Pulmonary Artery
Dr.Sarma@works
29
CLINICAL FEATURES
Dr.Sarma@works
30
EMPHYSEMA
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Severe dyspnea
Cough after dyspnea
Scant sputum
Less frequent infections
Terminal RF
PaCO2 35-40 mmHg
PaO2 65-75 mmHg
Hematocrit 35-45%
DLCO is decreased
Cor pulmonale rare.
Dr.Sarma@works
CHRONIC BRONCHITIS
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Mild dyspnea
Cough before dyspnea starts
Copious, purulent sputum
More frequent infections
Repeated resp. insufficiency
PaCO2 50-60 mmHg
PaO2 45-60 mmHg
Hematocrit 50-60%
DLCO is not that much ↓
Cor pulmonale common
31
EMPHYSEMA
CHRONIC BRONCHITIS
PINK PUFFER
BLUE BLOTTER
Dr.Sarma@works
32
ALPHA1 ANTITRYPSIN ↓
EMPHYSEMA
Specific circumstances of Alpha 1- AT↓include.
Dr.Sarma@works
•
Emphysema in a young individual (< 35)
•
Without obvious risk factors (smoking etc)
•
Necrotizing panniculitis, Systemic vasculitis
•
Anti-neutrophil cytoplasmic antibody (ANCA)
•
Cirrhosis of liver, Hepatocellular carcinoma
•
Bronchiectasis of undetermined etiology
•
Otherwise unexplained liver disease, or a
•
Family history of any one of these conditions
•
Especially siblings of PI*ZZ individuals.
•
Only 2% of COPD is alpha 1- AT ↓
33
A1AT LEVELS
ALPHA1 ANTITRYPSIN ↓
1. MM – A1AT 100%
2. MS – A1AT 75%
3. SS – A1AT 55%
4. MZ – A1AT 55%
5. SZ – A1AT 40%
6. ZZ – A1AT 8%
Dr.Sarma@works
34
SPIROMETRY
1. Decreased FEV1
2. Decreased FVC
3. FEV1 < 80%
4. FEV1 ÷ FVC < 70%
5. Post bronchodilator –
no change in FEV1
6. PEF is decreased
7. FET – is prolonged
8. V Max - decreased
Dr.Sarma@works
CLINICAL SIGNS
1.
2.
3.
4.
5.
6.
7.
8.
Physical exam may be negative
Hyper-inflated chest, Barrel chest
Wheeze or quite breathing
Pursed lip / accessory muscles resp.
Peripheral edema
Cyanosis, ↑ JVP
Cachexia
Cough, wheeze, dyspnea, sputum
35
MRC DYSPNOEA SCALE
ABOUT
SMOKING
1. No of cigarettes / day
2. No of smoker years
3. Age at starting
4. Time of
1st
cigarette
5. Desire to quit
Grade Degree of breathlessness - related activity
0
No breathlessness except on
strenuous exercise
1
Short of breath when walking uphill or
while hurrying to catch a bus or train
2
Walks slower than contemporaries or
has to stop for breath while walking alone
3
Stops for breath on walking 100 m or
after 2 or 3 minutes continuously
4
Too breathless to leave house or
breathless while dressing
6. Barriers to quit
7. Passive smoking
8. Occupational expo.
9. Domestic pollution
Dr.Sarma@works
36
OXYGEN COST DIAGRAM
OCCUPATIONAL
1. Coal mining
2. Cotton dust
3. Cement dust
4. Oil fumes
5. Cadmium fumes
6. Grain dust –
0
10
Rice millers
Grain handlers
Flour millers
Dr.Sarma@works
37
‘SUPPORT’
STUDY
1. Hypercapnic RF pts.
2. 1029 patients studied
3. 89% survived acute
hospitalization for RF
4. Only 51% are alive at
2 years of follow-up
5. Prognostic factors are
• Severity of RF
• Low BMI
• Older age
• Low PaO2/FIO2
Dr.Sarma@works
PROGNOSTIC FACTORS
Several factors affect survival in COPD.
• Age
• Smoking status
• Pulmonary artery pressure
• Resting heart rate
• Airway responsiveness
• Hypoxemia
• Most importantly the level of FEV1
• Use of long term oxygen therapy
38
WHY D.D
WITH ASTHMA
?
1. Different etiology
Clinical
COPD
ASTHMA
2. Different prognosis
Smoker
Nearly all
May or may not be
3. Different therapy
Age < 35
Rare
Nearly all
4. Different response
to therapy
Sputum
Productive
Mucoid or none
Dyspnea
Persistent
Episodic
Course
Progressive
Variable, static
Bronchiectasis- CSLD
Spirometry
Obstructive
Normal or Obstru.
Bronchogenic Ca.
Reversibility
Change < 15% Change > 15%
5. DD includes
Bronchial Asthma
DIFF. Dx. of COPD & ASTHMA
Most IMP Rx. IBD (Ipa+Salm) ICS
Anti leukotrn. Not useful
Dr.Sarma@works
Useful ad on Rx.
39
COPD IMAGES
Dr.Sarma@works
40
CHEST SKIAGRAMS
OF EMPHYSEMA
Dr.Sarma@works
41
V- P MISMATCH
NUCLEOTIDE IMAGING
Dr.Sarma@works
42
CHEST SKIAGRAM OF
CHRONIC BRONCHITIS
Dr.Sarma@works
43
CHEST LATERAL VIEW
CHRONIC BRONCHITIS
Dr.Sarma@works
44
HRCT – NORMAL CHEST
Dr.Sarma@works
45
HRCT – EMPHYSEMA
Dr.Sarma@works
46
HRCT – EMPHYSEMA
Dr.Sarma@works
47
ASSESSMENT
OF STABLE
COPD
Dr.Sarma@works
48
Rx. OBJECTIVES
MANAGEMENT OF COPD
1. Prevent disease
progression
1. Assess and monitor disease
2. Relieve symptoms
2. Reduce risk factors
3. Improve exercise
tolerance
3. Manage stable COPD
4. Improve health status

Education
5. Prevent and treat
exacerbations

Pharmacologic

Non-pharmacologic
6. Prevent and treat
complications
7. Reduce mortality
4. Manage exacerbations
8. Minimize side effects
from treatment
Dr.Sarma@works
49
MANAGEMENT
1. Definition - Key points
2. Epidemiology
3. Risk factors
ASSESSMENT OF COPD
Diagnosis of COPD is based on
1. H/o exposure to noxious agent
4. Pathogenesis –Pathol
2. Presence of Air flow limitation
5. Clinical features
3. Non-reversibility of the limitation
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
4. Chronic productive cough
5. Copious sputum, Dyspnea +/-
9. Drug delivery options
10.Rehabilitation, Exace.
Dr.Sarma@works
50
ASSESSMENT OF COPD
1. Assess and monitor
disease
Age 35 +
SYMPTOMS
2. Reduce risk
factors
EXPOSURE
3. Manage stable COPD
4. Education
COUGH
SPUTUM
5. Pharmacologic
SMOKING
+ or -
DYSPNEA
6. Non-pharmacologic
More than
7. Manage
one month
exacerbations
OCCUPATION
INDOOR /
OUTDOOR
Air Pollution
SPIROMETRY IS A MUST
Dr.Sarma@works
51
MANAGEMENT
ASSESSMENT OF COPD
1. Definition - Key points
Diagnosis of COPD
2. Epidemiology
• Spirometry is the Gold Standard
3. Risk factors
• Every COPD suspect must get
spirometry test done
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
• Like ECG, Spirometry is essential
• Arterial blood gas tensions are
needed if the FEV1 < 40%
• Respiratory failure, Corpulmonale
10.Rehabilitation, Exace.
Dr.Sarma@works
52
TESTS
1. Definition - Key points
2. Epidemiology
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
OTHER INVESTIGATIONS
1. Serial spirometry tests
2. Pulse Oximetry
3. Alpha1 Anti-trypsin levels
4. TLCO
5. HRCT
7. Stop smoking strateg.
6. ECG
8. Management Guide
7. ECHO
9. Drug delivery options
8. Sputum culture
10.Rehabilitation, Exace.
Dr.Sarma@works
53
SPIROMETRY
NORMAL AND COPD
0
FEV1
Normal
COPD
1
Liter
2
FVC
FEV1/ FVC
4.150
5.200
80 %
2.350
3.900
60 %
FEV1
3
COPD
4
FVC
FEV1
Normal
5
1
Dr.Sarma@works
2
3
FVC
4
5
6 Seconds
54
REVERSIBILITY
PROTOCOL
1. Definition - Key points
2. Epidemiology
WITH BRONCHODILATOR
1.
2.
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
3.
4.
5.
6.
Patient must be clinically stable
Patient should avoid
Short acting βagonists for 6 hours
Long acting βagonists for 12 hours
SR Theophylline for 24 hours
Baseline spirometry
Nebulize Salbuamol 2.5 mg + Ipatropium
500mg for 15 minutes with Nacl
Wait for 30 minutes
Repeat spirometry
9. Drug delivery options
10.Rehabilitation, Exace.
Dr.Sarma@works
55
REVERSIBILITY
PROTOCOL
WITH STEROIDS
1. Definition - Key points
1.
Spirometry before and after steroid
2. Epidemiology
2.
Two weeks treatment with 30 mg
Prednisolone daily or
3.
Six weeks treatment with 800 mcg to 1000
mcg of inhaled betamethasone/day
4.
Results to be interpreted.
3. Risk factors
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
9. Drug delivery options
Look for steroid contraindications
This predicts the COPD group who will benefit
from inhaled or systemic steroids
10.Rehabilitation, Exace.
Dr.Sarma@works
56
TESTING
WHAT IS REVERSIBILITY ?
1. Definition - Key points
Criteria for reversibility of obstruction
2. Epidemiology
• Spirometry is the Gold Standard
3. Risk factors
• Every COPD suspect must get spirometry
test done and reversibility assessed
4. Pathogenesis –Pathol
5. Clinical features
6. Diagnosis, Spirometry
7. Stop smoking strateg.
8. Management Guide
• Post bronchodilator FEV1 must show
increase of at least 200 ml ↑
• And the increase should be at least
15% of the baseline FEV1 value
9. Drug delivery options
10.Rehabilitation, Exace.
Dr.Sarma@works
57
FACTORS
SEVERITY OF COPD
1. Severity of symptoms
2. Stages of COPD
3. Frequency and severity
of exacerbations
4. Presence of
complications of COPD
5. Presence of respiratory
insufficiency
6. Co-morbidity
7. General health status
8. Number of medications
needed to manage the
disease
STAGES OF COPD
 Stage 0
Normal spirometry but with
(At risk)
chronic sym. – sputum, dyspnea
 Stage 1
FEV1 > 80%
Mild
FEV1 ÷ FVC is < 70%
 Stage 2
FEV1 < 80% but > 50%
Moderate FEV1 ÷ FVC is < 60%
 Stage 3
FEV1 < 50% but > 30%
Severe
FEV1 ÷ FVC is < 40%
 Stage 4
FEV1 < 30%
V. severe FEV1 ÷ FVC is < 30%
Dr.Sarma@works
58
RISK REDUCTION
STRATEGIES
Dr.Sarma@works
59
NO
TOMORROW!
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
IF ONE QUITS SMOKING
1. Treatment starts with reducing
risks – pack years concept*
2. Studies have shown that with
smoking cessation
•
The rate of decline in lung
function slows
•
There will be definite clinical
improvement in symptoms
5. Pharmacologic
6. Non-pharmacologic
7. Manage
exacerbations
* Packets per day x Years of smoking = Pack Years
Dr.Sarma@works
60
5 RELAPSE
TRIGGERS
RISK FACTORS REDUCTION
5. Withdrawal
1. ↓Exposure to smoking, noxious agn
4. Boredom
2. Emotional upset and
stress
2. Smoking cessation is the single most
effective - and cost effective intervention to reduce the risk of
developing COPD
1. Alcohol abuse !
3. It stops progression of COPD
3. Sense of deprivation
or depression
One devil replaced
by another devil
Dr.Sarma@works
61
DRUG TO QUIT
?
NICOTINE REPLACEMENTS
1. Antidepressant Bupropion
• Helpful for physical withdrawal symptoms
2. In psychological
dependence on
nicotine
• Costs the same as daily smoking habit
3. Useful in individuals
with or at risk for
depression–
4. Contraindicated in
drug interactions or
seizure disorder
Dr.Sarma@works
• Can be dosed according to degree of use
• Most products of NRT - cautious use in
cardiac patients
• Bupropion may be alternative to NRT
• Nicotex or Smoquit SR 150 b.i.d
• Patch is more constant level, sprays &
inhaler a more rapid effect
62
COPD MANAGEMENT
LATEST GUIDELINES
Dr.Sarma@works
63
MANAGEMENT
GOALS OF MANAGEMENT
1. Stable COPD
• Prevent disease progression
2. Exacerbations
• Relieve symptoms
3. Respiratory failure
4. Cardiac failure
• Improve exercise tolerance
• Improve health status
• Prevent and treat complications
• Prevent and treat exacerbations
• Reduce mortality
Dr.Sarma@works
64
HOW TO
ASSESS?
OUTCOME MEASURES
1. Assess and monitor
disease
1. Spirometric assessment
2. Reduce risk factors
2. Walking distance
3. Manage stable COPD
3. Dyspnea indices
4. Education
5. Pharmacologic
4. Symptom scores
6. Non-pharmacologic
5. Exacerbation rates
7. Manage
exacerbations
Dr.Sarma@works
65
BRONCHODILATORS
1. Assess and monitor
disease
MANAGEMENT - IBD
• IBD are the main stay
2. Reduce risk factors
• As when needed basis
3. Manage stable COPD
• The main drugs are
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage
exacerbations
Dr.Sarma@works
– β2 - Agonists (Salbutamol group)
– Anticholinergics (Ipatropium group)
– Their combination
– ?? Theophylline
66
MANAGEMENT
1. Assess and monitor
disease
2. Reduce risk factors
BUT UNFORTUNATELY
1.
IBD do not alter the pathology
2.
Drug Rx. is to improve
symptoms and ↓complications.
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
3.
But stopping smoking will halt
COPD
7. Manage
exacerbations
Dr.Sarma@works
67
THE RULES
MANAGEMENT RULES
1. Assess and monitor
disease
1.
NO systemic steroids in stable COPD
2.
Inhalation treatment is BEST
2. Reduce risk factors
3.
Salmeterol is the FIRST choice
3. Manage stable COPD
4.
Ipatropium is the SECOND choice
4. Education
5.
Salbutamol for short bursts
6.
Inhaled steroids THIRD choice
7.
Combination Ipa + Salmet inhalers beneficial
8.
Oral β2 Agonists FOURTH choice
9.
Theophyllins ? role – LA preps. No injectables
5. Pharmacologic
6. Non-pharmacologic
7. Manage
exacerbations
Dr.Sarma@works
10. Oxygen therapy for exacerbations and RF
68
BRONCHO
DILATORS
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Manage
exacerbations
Dr.Sarma@works
IS IT A PARADOX ?
• Bronchodilators in COPD have been
shown to be ineffective in modifying the
long-term decline in lung function which is
the hallmark of this disease (Class 1).
• There will be no ↑ in FEV1 or FEV1 ÷ FVC
• But, ↑ in exercise capacity demonstrated.
Ipratropium and Salmeterol have been
shown to improve COPD clinical status
69
SYNERGISM
IPATROPIUM
Dr.Sarma@works
BRONCHODILATION
SABA and LABA
70
ß AGONISTS
1. Selective ß agonists
2. Short acting drugs
3. Long acting drugs
4. Oral medication
5. Inhaled form
Dr.Sarma@works
BRONCHODILATORS
1. Direct action on the beta2 receptors in the
bronchial smooth muscle – relaxation
2. Salbutamol most widely used
3. In COPD 1 mg is the maximum dose
4. Short acting – every 4 to 6 hours
5. Salmeterol is long acting – 12 hours
6. Slow onset, dose 50 μg b.i.d
7. Formoterol still longer -12 μg b.i.d
8. Side effects – tremors, tachycardia etc.,
71
ANTI ACH
BRONCHODILATORS
1. Anti-cholinergics
1. ↑ Cholinergic drive is in the bronchii
2. Short acting drugs
2.
Anti-cholinergics ↓resting bronchial tone
3. Long acting drugs
3.
Three muscarinic receptors M1, M2, M3
4. Inhaled forms
4.
5. Combination with
beta agonists
Ipatropium, Oxitropium – onset slower than
ß agonists – but more effective
5.
Sustained broncho-dilatation – up to 8 h
6.
Have influence on sleep quality in COPD
7.
Ipatropium optimal dose 80 μg as inhaler
8.
Tiotropium – selective to M1, M3 receptors
9.
It is long acting – once a day – dose 40 μg
Dr.Sarma@works
72
ORAL
STEROIDS
CORTICOSTEROIDS
1. Asthmatic component
Inhaled Glucocorticoids
2. Quick recovery from
acute exacerbations
•
•
•
3. Delays next exacerb.
4. Only small number of
patients sustained
improvement
•
•
5. Similar to asthmatics
6. Significant risk of side
effects
•
•
Dr.Sarma@works
In stage I and II COPD – no role to play
Betamethasone, Budisonide, Fluticasone
Inhaled steroids are preferable and they
reduce the # of episodes of exacerbation
To be used in stage III and stage IV COPD
They are useful in short bursts in acute
exacerbations
In people with significant asthma component
they are found useful
No role for long acting steroid injections
73
THEOPHYLLIN
E
BRONCHODILATORS
1. Deriphyllin group
1.
Assumed to relax the airway smooth muscle
2. Nausea, tachycardia
2.
At therapeutic concentration NO direct action
on the bronchial smooth muscle
3.
Toxicity – Many drug interactions
4.
Low therapeutic index - Poor safety window
5. Smokers have higher
theophylline toxicity
5.
Need to monitor blood levels frequently
6.
Adverse effects on liver and in elderly
6. Already tachycardiac
7.
Their use is at best questionable
7. Only oral - if at all
8.
Never injectable – in may countries banned
9.
SR prep has some add on value
3. Fatal arrhythmias
4. Interactions with
drugs - Macrolides
Dr.Sarma@works
74
INHALED Rx.
MANAGEMENT
1. Assess and monitor
disease
• IBD is the preferred drugs
2. Reduce risk factors
• LABA + Tiotropium is best
3. Manage stable COPD
• LABA + TIO + ICS for Stage III, IV
4. Education
5. Pharmacologic
6. Non-pharmacologic
• Combination is better than increasing
individual drugs
7. Manage
exacerbations
Dr.Sarma@works
75
NO SYSTEMIC
STEROIDS
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
MANAGEMENT
• No systemic steroids because of
• unfavorable benefit-to-risk ratio
• Exercise training programs,
4. Education
• LTOT > 15 hours per day for RF
5. Pharmacologic
• LTOT increases survival
6. Non-pharmacologic
7. Manage
exacerbations
Dr.Sarma@works
76
MANGEMENT
AS PER STAGING
Dr.Sarma@works
77
AT RISK
MANAGEMENT - STAGE 0
1. Chronic symptoms
• Avoidance of risk factors
2. Cough
• Stop smoking
3. Phlegm
4. Dyspnea
5. H/o smoking
• Influenza vaccine
• Regular follow up spirometry
6. Spirometry Normal
Dr.Sarma@works
78
MILD COPD
MANAGEMENT – STAGE I
1. Chronic symptoms
• Avoidance of risk factors
2. Cough
• Stop smoking
3. Phlegm
4. Dyspnea
• Influenza vaccine
5. H/o smoking
• Regular follow up spirometry +
6. Spirometry abnormal
• SABA + IPATROP
7. FEV1 > 80% but
• Inhaled route
8. FEV1 / FVC < 70%
Dr.Sarma@works
79
MANAGEMENT – STAGE II
MODERATE
COPD
1. Chronic symptoms
2. Cough
3. Phlegm
4. Dyspnea
5. H/o smoking
6. Spirometry abnormal
7. FEV1 < 80% but > 50%
•
•
•
•
•
•
•
Avoidance of risk factors
Stop smoking
Influenza vaccine
Regular follow up spirometry
SABA + IPA inhalations +
LABA or TIOTROP or BOTH in inhaled
Pulmonary Rehabilitation
8. FEV1 / FVC < 60%
Dr.Sarma@works
80
SEVERE COPD
MANAGEMENT – STAGE III
1. Chronic symptoms
• Avoidance of risk factors
2. Cough
• Stop smoking
3. Phlegm
• Influenza vaccine
4. Dyspnea
• Regular follow up spirometry
5. H/o smoking
• SABA + IPA inhalations +
6. Spirometry abnormal
7. FEV1 < 50% but > 30%
8. FEV1 / FVC < 40%
• LABA or TIOTROP or BOTH inhaled
• Pulmonary Rehabilitation
• ICS – Budesonide
• LTOT at least 15 hours per day
Dr.Sarma@works
81
MANAGEMENT – STAGE IV
V. SEVERE
COPD
1. Chronic symptoms
2. Cough
3. Phlegm
4. Dyspnea
5. H/o smoking
6. Spirometry abnormal
7. FEV1 < 30%
8. FEV1 / FVC < 30%
9. Chronic Resp. Failure
Dr.Sarma@works
•
•
•
•
•
•
•
•
•
•
•
Avoidance of risk factors
Stop smoking
Influenza vaccine
Regular follow up spirometry
SABA + IPA inhalations +
LABA or TIOTROP or BOTH inhaled
Pulmonary Rehabilitation
ICS – Budesonide
LTOT at least 15 hours per day
Oral steroids in short bursts
Surgical treatments
82
DRUG DELIVERY
SYSTEMS - OPTIONS
Dr.Sarma@works
83
DRUG
DELIVERY
DRUG DELIVERY - OPTIONS
1. Dexterity
• MDI – Metered Dose Inhalers
2. Hand grip strength
• Rotahalers, Diskhalers
3. Co-ordination
• Spacehalers
4. Severity of COPD
• Nebulizers
5. Educational level
• Oxygen mixed delivery
6. Age of the patient
• Oral tablets, syrups ??
7. Ability to inhale
and synchronize
• Parenteral – I.M or I.V use ????
Dr.Sarma@works
84
NEBULISED THERAPY
1.
2.
3.
4.
5.
Severe breathlessness despite using inhalers
Assessment should be done for improvement
Choice between a facemask or mouth piece
Equipment servicing and support are essential
Dosage 0.5 ml of Ipatropium +
0.5 ml of Salbutamol + 5 ml of NaCl (not DW)
6. If decided to use ICS (FEV1 < 50%) –
0.5 ml of Budusonide is added to the above
6. 15 minutes and slow or moderate flow rate
7. Can be repeated 2 to 3 times a day – Mouth Wash
Dr.Sarma@works
85
EDUCATION AND
REHABILITATION
Dr.Sarma@works
86
REHABILITATION
For the lungs to get more air
PURSED-LIP BREATHING
(like breathing out slowly into a straw)
INHALE
Dr.Sarma@works
EXHALE
87
REHABILITATION
For the lungs to get more air
DIAPHRAGMATIC BREATHING
1. Sit comfortably and
relax your shoulders.
Sit comfortably and
relax your shoulders
Note:
2. Put one hand on your 3. Then push in your
abdomen. Now inhale
abdominal muscles and
slowly through your
breathe out using the
nose. (Push your
pursed-lip technique.
abdomen out while you
(You should feel your
Putbreathe
one hand
Then pushgoindown)
your abdominal
in)on your abdomen.abdomen
Now inhale slowly through your muscles and breathe out
nose. (Push
your abdomen
therest.
pursed-lip technique
• Repeat the above maneuver
three times
and thenout
takeusing
a little
whilemany
you breathe
• This exercise can be done
times ain)
day.
Dr.Sarma@works
88
HEALTH EDUCATION – TEAM WORK
Dr.Sarma@works
89
EXACERBATIONS
RESP. FAILURE
Dr.Sarma@works
90
OXIGENERATO
R
MANAGEMENT – REFERRAL
• Diagnosis uncertain
• Disproportionate symptoms
• Persistent symptoms
• Development of lung cancer
• Pulmonary rehabilitation
• Nebulizer assessment
• Oxygen assessment
Dr.Sarma@works
91
WHEN
SUSPECT?
1. ↑ in symptoms
2. ↑ in sp purulence
3. ↑ in sp volume
4. Fever, chills
5. Ankle edema
6. Cyanosis
7. ↓ Consciousness
Dr.Sarma@works
D.D. of EXACERBATIONS
1.
2.
3.
4.
5.
6.
Pulmonary embolism
Pneumothorax – rupture of bullae
Myocardial infarction
Left ventricular failure
Acute pneumonia
Bronchogenic carcinoma
92
WHAT EXTRA ?
1. Oxygen therapy
MANAGE EXACERBATIONS
2. NIPPV mostly or
1. Exacerbations of symptoms requiring
Rx. are important clinically in COPD.
3. Macha. Ventilation
2.
4. Ipatropium inhalation
5. SA - Beta agonists
6. No theophylline group
7. Narrow spectrum
antibiotics – 2 wks
8. Oral steroids for 2 wk
9. Diuretics may help
Dr.Sarma@works
The most common causes of exacerbation are
Infection of the bronchial tree and
Air pollution and ↑ in smoking
In 35% of cases cause is not known
3. Systemic corticosteroids – oral better
4. Antibiotics in short bursts – what to give
5. NIPPV – Non invasive intermittent
positive pressure ventilation - Home
93
INDICATIONS
1. FEV1 < 30% must
2. Consider if < 50%
3. PaO2 < 90%
4. PaCO2 > 60%
5. Cyanosis
6. ↑ JVP, Pedal edema
7. Pulmonary HT
8. Polycythemia
Dr.Sarma@works
LONG TERM OXYGEN THERAPY
•
•
•
•
•
•
Pulse oximetry to know PaO2
Arterial blood gas saturation monthly
Review LTOT every year
Oxygen concentrators - oxygen cylinders
Fire warning – smoking
Ambulatory oxygen therapy – O2 cylinders,
liquid oxygen
• SBOT - Short burst OT – Exacerbations.
• NIPPV in patients with ↓respiratory drive
94
FEATURES
1. Increasing dyspnea
2. Peripheral oedema
3. ↑ venous pressure
4. Parasternal heave
5. Loud pulmonary
second heart sound
CORPULMONALE
•
•
•
•
•
•
LTOT
Diuretics, Sodium restriction
ACEi
Alpha blockers
Digoxin
Heart failure management
6. ECG changes of RVH
and PH
7. Echo evidence
Dr.Sarma@works
95
RESP. FAILURE
1. Assess and monitor
disease
2. Reduce risk factors
3. Manage stable COPD
4. Education
5. Pharmacologic
6. Non-pharmacologic
7. Management of
exacerbations
Dr.Sarma@works
RESPIRATORY FAILURE
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Pulmonary hypertension
Right ventricular hypertrophy
Right ventricular diastolic dys. function
Right ventricular systolic dysfunction
Corpulmonale – Right heart failure
Acute respiratory insufficiency
Life threatening respiratory failure
Hypercapnia, Severe hypoxia
Intubation and IPPV
Managing RVF and RF – ICU care
96
SURGERY
1. Bullectomy
2. LVRS - Lung volume
reduction surgery
3. Single lung transplant
Dr.Sarma@works
LUNG RESECTION
1.
2.
3.
4.
5.
6.
7.
8.
Increasing dyspnea
Single large emphysematous bulla
Severe - FEV1 < 35% but > 20%
Upper lobe emphysema
PaCo2 not more than 55%
TLCO must be at least 20%
Age less than 65
Severe pulmonary hypertension
97
WHAT NOT !
1. No Anti-tussives
2. Mucolytics ??
3. No prophylactic
antibiotics
4. No long term
antibiotics
5. No systemic steroids
6. No narcotics
7. No vigorous exercise
8. No with holding the
benefits of Oxygen
Dr.Sarma@works
WHAT ELSE WE CAN GIVE
• Pneumococcal vaccine may be given
• Early initiation of O2 shown to ↑ survival
• Prolonged use of inhaled steroids –
long acting better – 2 weeks duration
• Alpha1 anti-trypsin (Prolastin, Aralast)
• Antibiotics in short bursts for exacerbations
• N-Acetyl cysteine (NAC) is shown useful
• Immuno-modulators are under trial
• Calcium and vitamin D supplementation
98
COPD - FUTURE DEVELOPMENTS
Dr.Sarma@works
99
NEXT DECADE
1. COPD will increase
2. Mortality will increase
3. Dx. facilities increase
4. Quit smoking a must
5. Industrial pollution ↑
6. Newer drugs
7. New drug delivery
8. Oxygen Therapy ↑
Dr.Sarma@works
FUTURE DEVELOPMENTS
•
•
•
•
•
•
•
•
•
Emphasis on early diagnosis
Effective anti smoking services
COPD will be primary care issue by GP
New drug development for COPD perse
Tiotropium takes a center stage
New M1 and M3 blockers are in line
PDE4 inhibitors – for bronchodilatation
Drugs to ↓Neutrophilic inflammation
Mediator antagonists - ↓inflammation
100
TAKE HOME MESSAGES
•
•
•
•
•
•
•
•
•
COPD is no more a specialists concern – it is ours !
It is alarmingly increasing – It is preventable
Please differentiate Asthma and COPD
Use spirometry, peak flow meter - just as ECG
Don’t embark on Deri + Bet iv for all breathlessness
Don’t use Theophylline as far as possible
Inhalation therapy is the best – Drug delivery choices
Don’t spare any body from early oxygen therapy
And finally, motivate smokers to quit smoking
Dr.Sarma@works
101
SELF SCREENING
Dr.Sarma@works
102
Could it be COPD?
Do you know what COPD is ? This chronic lung disease is a major cause of illness.
Many people have it and yet don’t know it.
If you answer these questions, it will help you find out if you could have COPD.
1. Do you cough several times most days?
Yes ___ No ___
2. Do you bring up phlegm or mucus most days?
Yes ___ No ___
3. Do you get out of breath more easily than others your age?
Yes ___ No ___
4. Are you older than 40 years?
Yes ___ No ___
5. Are you a current smoker or an ex-smoker?
Yes ___ No ___
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.
Take time to think about your lungs……Learn about COPD!
Dr.Sarma@works
103
ASTHMA V/s COPD
Take HOME GUIDE
Dr.Sarma@works
104
ASTHMA V/s COPD
ASTHMA
COPD
Sensitizing trigger needed
Chronic exposure -Noxious
Innate Atopy is essential
Any body may be effected
No noxious external agent
Smoking is the noxious ag.
ETIOLOGICAL BASIS
Dr.Sarma@works
105
ASTHMA V/s COPD
ASTHMA
COPD
Primarily Allergic Inflamm.
Destructive Inflammation
Secondary bronchospasm
Primary ↑ in bronchial tone
Small airways - bronchioles Disease of alveloli, bronchi
No destruction or fibrosis
Alveolar destruc. Br fibrosis
PATHOLOGY
Dr.Sarma@works
106
ASTHMA V/s COPD
ASTHMA
COPD
Recurrent allergic inflamm.
Progressive destr. inflamm.
Airway remodeling occurs
Emphysema, Bronchial fibr.
↑↑ IgE + other atopic disea. ↑ Proteases, ↓in antiprote.
CD4 T, Mast cells, Eosino
CD 8 T, MF, Neutrophils
LT D4, IL 4, IL 5, - Th2
LT B4, IL 8, TNF-α
PATHOGENESIS
Dr.Sarma@works
107
ASTHMA V/s COPD
ASTHMA
COPD
Young subjects, any age
Age always > 35 yrs, smoke
Episodic, recurrent, normal
Chronic, progressive, Exaca
Sputum mucoid or none
Sputum purulent & copious
Episodic dyspnea – moder.
Progressive dyspn, Hr. Gr.
Seasonal symptoms
Perennial symptoms
Dr.Sarma@works
CLINICAL FEATURES
108
ASTHMA V/s COPD
ASTHMA
COPD
Normal or obstructive
Always obstructive pattern
FEV1 < 80% but > 60%
FEV1 < 70% may be < 40%
FEV1 ÷ FVC < 70%
FEV1 ÷ FVC < 60%
Reversible - > 15 % ↑
Irreversible - < 15 % ↑
Resp. failure rare
Resp. failure,Corpulmonale
Dr.Sarma@works
SPIROMETRY
109
ASTHMA V/s COPD. - Rx.
ASTHMA
COPD
Relievers and Preventers
Quitting of smoking crucial
ICS are the main stay
LABA + Antibiotics – Ac. exa
SABA for acute attacks
SABA not much, ICS useful
Ipatropium add on only
Ipatrop., Tiotrop. are first line
LTA are very useful
LTA have no role at all
Mast cell stabilizers useful
Cromolyn, Ketotifen no use
LTOT not needed mostly
LTOT must in stage III and IV
Oral steroids have little role
Oral steroids in stage III & IV
SR Theophylline?? some role SR Theophylline contraindic.
Dr.Sarma@works
Treatment
110
“The old order changeth
yielding place to new;
Lest, one good custom
should corrupt the world.”
Tennyson Sir Lord, Alfred
This is most pertinent today to Asthma
and COPD
Holm and Harris & NEJM
Dr.Sarma@works
111
PREVENT COPD
Dr.Sarma@works
112
THE DEADLIEST DEVIL
Dr.Sarma@works
113
SURE TO GRAVE
Dr.Sarma@works
114
AND FINALLY
Tell me what harm smoking
does not cause ??
Dr.Sarma@works
115
TELL ME THE
ORGAN SPARED
1. The Heart
2. Blood vessels
3. Metabolic effects
4. Lungs
5. Nervous system
6. G I tract
7. Bones
8. Fetus in utero
9. The psyche
10.The Purse
Dr.Sarma@works
PROVEN DISASTERS
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
IHD, MI, ↑ Restenosis
Atherosclerosis – PVD, IR, ↑ DM
Oxidation of LDL, ↑ LDL, ↓ HDL, ↑ TG
COPD, Lung Cancer
Tremors, Peripheral neuritis
APD, NUD, Oro-pharyngeal Cancers
Osteoporosis
Poor fetal development
Nicotine dependence
Wasteful expenditure
116
The Onus here is on us
Most of these effects have dose-response relationship.
Most of them are reversible if smoking is stopped early.
Reducing the # reduces the risk – inverse response.
If we are a smoker, let us quit smoking – set an example.
Let us motivate every month at least one person to quit.
What right we have, to make others passive smokers?
Dr.Sarma@works
117
Pledge to stop smoking
Dr.Sarma@works
118
WHAT CAN WE DO ??
Dr.Sarma@works
119
MY SINS
IF CARE NOT TO DO
THESE – THEN ALL
If, in patients I treat, I have
• Not controlled his DM
• Not evaluated for IHD
• Not kept BP to goal
• Not controlled lipids
• Not advised the obese
• Not persuaded a smoker
• Not prevented OS
• Not health educated and
PUNYAS
I have not updated my K
Not shared what I have
Dr.Sarma@works
SINS
120
MY GAINS
HAVE NO MEANING &
ARE MERELY FUTILE
1. My possessions
2. My positions
3. My achievements
4. My abilities
5. My privileges
6. My prayers
7. My visits to temples
8. My scriptural K
9. My rituals
PUNYAS
SINS
Dr.Sarma@works
121
REMEMBER, WE ARE BLESSED
WITH THE OPPORTUNITY
Dr.Sarma@works
122
Om Asatho maa sad gamaya
Om Tamaso maa jyothir gamaya
Om Mrityor maa amritam gamaya
Om Sarveshaam swasthir bhavathu
Om Sarveshaam shaantir bhavathu
Om Shaantihi Shaantihi Shaantihi ||
Dr.Sarma@works
123
Important Announcement
A CD format of today’s presentation is ready
1. COPD, Asthma and basics of spirometry
In addition it, also contains
2. ECG workshop presented earlier
3. Guidelines on Hypertension treatment
This can be used in Computer & DVD player
Dr.Sarma@works
124
Resources for
COPD and Asthma
1. ACCP
www.chestnet.org
2. ATS
www.thoracic.org
3. BTS
www.brit-thoracic.org.uk
4. COPD profess. www.copdprofessional.com
5. GOLD
www.goldcopd.com
6. NICE
www.nice.uk.org
7. Chest Net
www.chestnet.net
8. CDC
www.cdc.nih.gov
9. NAEPP
www.naepp.nhlbi.org
10.COPD
Rapid series by ELSEVIER
Dr.Sarma@works
125
PLEASE CONTACT US
Dr.Sarma RVSN, M.D., M.Sc (Canada)
JN Road, Jayanagar, Tiruvallur, TN
+91 98940 60593, (4116) 260593
Dr. Kumaran.M, B.Sc., M.B.B.S.,
10 North Raja St, Tiruvallur, TN
+91 98941 10450, (4116) 260288
WE WILL MEET AGAIN SOON
Dr.Sarma@works
126
NANRI,
VANAKKAM
Dr.Sarma@works
127