COPD by DR Sarma

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
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GOLD
GLOBAL INITIATIVE
FOR CHRONIC
OBSTRUCTIVE LUNG DISEASE
NHLBI AND WHO COLLABORATIVE INITIATIVE

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WORLD COPD DAY November 19, EVERY YEAR
Raising COPD Awareness Worldwide

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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
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
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7. New advances in Rx.
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DEFINITIONS
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CONTENTS
1. Definition - Key points 2. Epidemiology 3. Risk factors 4. Pathogenesis Pathol 5. Clinical features 6. Diagnosis, Spirometry 7. Antismoking strateg. 8. Management Guide 9. Drug delivery options 10.Rehabilitation, Exace.
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DEFINITION OF COPD
1. It is chronic
2. It is progressive 3. Mostly fixed airway obstruction
4. Non reversible by bronchodilators

5. Exposure to noxious agent is a must 6. Chronic obstructive lung disease (COLD)
7. Chronic obstru. airways disease (COAD)

8. Two entities in COPD namely 1. Chronic Bronchitis 2. Emphysema
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2. EMPHYSEMA
1. Alveolar wall destruction 2. Irreversible enlargement of the air spaces 3. Distal to the terminal bronchioles 4. Without evidence of fibrosis
1. CHRONIC BRONCHITIS
1. Productive cough
2. For a period of 3 months 3. In each of 2 consecutive years
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
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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.
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DEFINITION OF COPD
ROAD Recurrent Obstructive Airways Disease
Bronchial Asthma Seasonal, Recurrent Sensitizing Agent, Other Atopic disorders Reversible obstruction, Inflammation COLD Irreversible, Chronic, Noxious agent Chronic Bronchitis Emphysema Combination of both
OBSTRUCTIVE LUNG DISEASES

ASTHMA
EMPHYSEMA
CHRONIC BRONCHITIS
FULL
REVERSIBILITY OF AIR WAY OBSTRUTION
NONE
ASTHMA
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COPD
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EPIDEMIOLGY OF COPD
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CONTENTS
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KEY POINTS
Underestimated, often covert
It is not diagnosed until clinically overt By that time it is moderately advanced.
The global burden of COPD will increase

Toll from tobacco use in alarming
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MORTALITY
Cause CHD Cancer Deaths 724,269 534,947
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 By 2020 it is projected to rank 5th. Often, COPD is covert
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CVA
COPD Accidents Diabetes
158,060
114,318 94,828 64,574
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MORTALITY TRENDS 1965 - 2000 Cause CHD Cancer CVA % Change - 59% - 64% - 39%

COPD PREVALENCE 2000

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
COPD
Accident All other
+ 163%
+ 32% - 7%
*From Murray & Lopez, 2001
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MORBIDITY
Year 1980 1985 Consultations 6.1 million 7.4 million
WHAT IS WRONG ?
Cigarette smoking is the primary cause. USA - 47.2 million smoke, 28%, 23% WHO estimates 1.1 B smokers in world. This increases to 1.6 billion by 2025. Many countries, rates are alarmingly.
1990
1995 2000 2010
10.1 million
11.8 million 13.9 million
In India, 4,00,000 premature deaths annually to use of biomass fuels, like cow dung cakes, open fires
Indoor air pollution, Industrial pollution are the major risk factors in our country.
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SMOKING - THE CULPRIT
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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
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WOMEN SMOKERS
PASSIVE SMOKERS
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INTENSE CAUSE FOR CONCERN ?

COLLEGE STUDENTS
TENDER AGE GROUPS

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COPD NH EFFECT OF SMOKING
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Mortality among women smokers is on the rise globally
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PATHOGENESIS PATOLOGY
AND
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CONTENTS
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PATHOGENESIS
NOXIOUS AGENT (tobacco smoke, pollutants, occupational exposures
Genetic factors Respiratory infection Others
COPD
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PATHOGENESIS
1. Definition -key points 2. Burden of COPD
3. Classification
4. Risk factors 5. Pathogenesis,
6. Pathophysiology,
7. Management 8. Future research
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PATHOGENESIS
1. Definition -key points 2. Burden of COPD
ATOPY
3. Classification
4. Risk factors 5. Pathogenesis,
6. Pathophysiology,
7. Management 8. Future research
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SHIFT IN THE DELICATE BALANCE
Nutrophil elastase Cathepsisns MMP-1, MMP- 9, MMP 12 Granzymes
Alpha 1 Anti-trypsin SLP 1, Elastin, TIMPs
Perforins
PROTEASES
ANTI PROTEASES
COPD
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CONTENTS
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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
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PATHOLOGY in COPD
COPD
1. Mucus gland hypertrophy 2. Smooth muscle hypertrophy 3. Goblet cell hyperplasia
Normal bronchial architecture

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4. Inflammatory infiltrate 5. Excessive mucus
6. Squamous metaplasia
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DISSECTING MICROSCOPIC APPEARENCE
Normal parenchymal architecture Dr.Sarma@works
Emphysematous Lung architecture
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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
PATHOLOGY COPD
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-
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PULMONARY HYPERTENSION IN COPD

1. Duplication of elastic lamina 2. Medial hypertrophy - PH
Normal Pulmonary Artery

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CLINICAL FEATURES
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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.
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
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EMPHYSEMA
CHRONIC BRONCHITIS
PINK PUFFER
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BLUE BLOTTER
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EMPHYSEMA
ALPHA1 ANTITRYPSIN
Specific circumstances of Alpha 1- ATinclude. 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

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Family history of any one of these conditions

Especially siblings of PI*ZZ individuals. Only 2% of COPD is alpha 1- AT
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A1AT LEVELS
1. MM A1AT 100%
ALPHA1 ANTITRYPSIN
2. MS A1AT 75%
3. SS A1AT 55% 4. MZ A1AT 55% 5. SZ A1AT 40% 6. ZZ A1AT 8%
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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
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
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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 6. Barriers to quit 7. Passive smoking 8. Occupational expo. 9. Domestic pollution 0 1 2
MRC DYSPNOEA SCALE

Grade Degree of breathlessness - related activity No breathlessness except on strenuous exercise Short of breath when walking uphill or while hurrying to catch a bus or train Walks slower than contemporaries or has to stop for breath while walking alone
3
4
Stops for breath on walking 100 m or after 2 or 3 minutes continuously

Too breathless to leave house or breathless while dressing
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OCCUPATIONAL
1. Coal mining 2. Cotton dust 3. Cement dust 4. Oil fumes 5. Cadmium fumes 6. Grain dust Rice millers Grain handlers Flour millers
OXYGEN COST DIAGRAM
10
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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
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
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WHY D.D WITH ASTHMA ? 1. Different etiology

2. Different prognosis 3. Different therapy 4. Different response to therapy 5. DD includes Bronchial Asthma Bronchiectasis- CSLD Bronchogenic Ca.
DIFF. Dx. of COPD & ASTHMA

Clinical Smoker Age < 35 Sputum Dyspnea Course Spirometry COPD Nearly all Rare Productive Persistent Progressive Obstructive ASTHMA May or may not be Nearly all Mucoid or none Episodic Variable, static Normal or Obstru.
Reversibility
Change < 15% Change > 15%
Most IMP Rx. IBD (Ipa+Salm) ICS Anti leukotrn. Not useful
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Useful ad on Rx.
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COPD IMAGES
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CHEST SKIAGRAMS OF EMPHYSEMA
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V- P MISMATCH NUCLEOTIDE IMAGING
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CHEST SKIAGRAM OF CHRONIC BRONCHITIS
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CHEST LATERAL VIEW CHRONIC BRONCHITIS
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HRCT NORMAL CHEST
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HRCT EMPHYSEMA
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HRCT EMPHYSEMA
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ASSESSMENT
COPD
OF STABLE
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Rx. OBJECTIVES
1. Prevent disease progression 2. Relieve symptoms
MANAGEMENT OF COPD
1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD
3. Improve exercise tolerance

4. Improve health status 5. Prevent and treat exacerbations 6. Prevent and treat complications 7. Reduce mortality 8. Minimize side effects from treatment
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Education
Pharmacologic
Non-pharmacologic
4. Manage exacerbations
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MANAGEMENT
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ASSESSMENT OF COPD
Diagnosis of COPD is based on 1. H/o exposure to noxious agent 2. Presence of Air flow limitation 3. Non-reversibility of the limitation 4. Chronic productive cough 5. Copious sputum, Dyspnea +/-
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ASSESSMENT OF COPD
1. Assess and monitor disease
Age 35 +
SYMPTOMS 2. Reduce risk factors

3. Manage stable COPD 4. Education
EXPOSURE
SMOKING OCCUPATION INDOOR / OUTDOOR Air Pollution
COUGH
5. Pharmacologic
SPUTUM
+ or -
6. Non-pharmacologic
DYSPNEA
More than 7. Manage one month exacerbations

SPIROMETRY IS A MUST
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MANAGEMENT
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ASSESSMENT OF COPD
Diagnosis of COPD Spirometry is the Gold Standard Every COPD suspect must get spirometry test done Like ECG, Spirometry is essential Arterial blood gas tensions are needed if the FEV1 < 40% Respiratory failure, Corpulmonale
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TESTS
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OTHER INVESTIGATIONS 1. Serial spirometry tests 2. Pulse Oximetry 3. Alpha1 Anti-trypsin levels 4. TLCO
5. HRCT
6. ECG 7. ECHO
8. Sputum culture
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SPIROMETRY
0 1 2
NORMAL AND COPD

FEV1 FVC
5.200 3.900
FEV1/ FVC
80 % 60 %
Normal COPD
FEV1
4.150 2.350
Liter
COPD
4 5 1 2 FEV1 FVC
Normal
3 4
FVC 5 6 Seconds
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REVERSIBILITY PROTOCOL
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WITH BRONCHODILATOR
1. 2. Patient must be clinically stable Patient should avoid Short acting agonists for 6 hours Long acting agonists 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
3. 4. 5. 6.
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REVERSIBILITY PROTOCOL
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WITH STEROIDS
1. 2. 3. Spirometry before and after steroid Two weeks treatment with 30 mg Prednisolone daily or Six weeks treatment with 800 mcg to 1000 mcg of inhaled betamethasone/day
4.
Results to be interpreted.
Look for steroid contraindications This predicts the COPD group who will benefit
from inhaled or systemic steroids
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TESTING
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WHAT IS REVERSIBILITY ?
Criteria for reversibility of obstruction Spirometry is the Gold Standard Every COPD suspect must get spirometry test done and reversibility assessed Post bronchodilator FEV1 must show increase of at least 200 ml And the increase should be at least 15% of the baseline FEV1 value
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FACTORS
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
SEVERITY OF COPD
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%
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RISK REDUCTION STRATEGIES
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NO TOMORROW!
IF ONE QUITS SMOKING

1. Treatment starts with reducing risks pack years concept*
2. Reduce risk factors

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

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5 RELAPSE TRIGGERS
5. Withdrawal 4. Boredom 3. Sense of deprivation or depression 2. Emotional upset and stress 1. Alcohol abuse ! One devil replaced by another devil
RISK FACTORS REDUCTION

1. Exposure to smoking, noxious agn 2. Smoking cessation is the single most effective - and cost effective intervention to reduce the risk of developing COPD 3. It stops progression of COPD
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DRUG TO QUIT ?
1. Antidepressant Bupropion
NICOTINE REPLACEMENTS
Helpful for physical withdrawal symptoms Can be dosed according to degree of use Costs the same as daily smoking habit Most products of NRT - cautious use in cardiac patients Bupropion may be alternative to NRT Nicotex or Smoquit SR 150 b.i.d
2. In psychological dependence on nicotine

3. Useful in individuals with or at risk for depression 4. Contraindicated in drug interactions or seizure disorder
Patch is more constant level, sprays & inhaler a more rapid effect
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COPD MANAGEMENT LATEST GUIDELINES
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MANAGEMENT
1. Stable COPD 2. Exacerbations 3. Respiratory failure 4. Cardiac failure
GOALS OF MANAGEMENT
Prevent disease progression Relieve symptoms Improve exercise tolerance Improve health status
Prevent and treat complications

Prevent and treat exacerbations Reduce mortality
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HOW TO ASSESS?
OUTCOME MEASURES
1. Spirometric assessment

2. Walking distance
3. Dyspnea indices
5. Pharmacologic
4. Symptom scores
5. Exacerbation rates
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BRONCHODILATORS
MANAGEMENT - IBD IBD are the main stay As when needed basis The main drugs are 2 - Agonists (Salbutamol group) Anticholinergics (Ipatropium group) Their combination

5. Pharmacologic
?? Theophylline
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MANAGEMENT
BUT UNFORTUNATELY
1.
IBD do not alter the pathology

2.
3.
Drug Rx. is to improve

symptoms and complications. But stopping smoking will halt COPD
5. Pharmacologic
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THE RULES
1. Assess and monitor disease 1. 2.
MANAGEMENT RULES
NO systemic steroids in stable COPD Inhalation treatment is BEST

3.
4. 5.
Salmeterol is the FIRST choice

Ipatropium is the SECOND choice Salbutamol for short bursts
5. Pharmacologic
6.
7. 8. 9.
Inhaled steroids THIRD choice

Combination Ipa + Salmet inhalers beneficial Oral 2 Agonists FOURTH choice Theophyllins ? role LA preps. No injectables
10. Oxygen therapy for exacerbations and RF
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BRONCHO DILATORS
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

5. Pharmacologic
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SYNERGISM
BRONCHODILATION
IPATROPIUM
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SABA and LABA
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AGONISTS
1. Selective agonists 2. Short acting drugs 3. Long acting drugs 4. Oral medication 5. Inhaled form
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 g b.i.d 7. Formoterol still longer -12 g b.i.d 8. Side effects tremors, tachycardia etc.,
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ANTI ACH
1. Anti-cholinergics 2. Short acting drugs 3. Long acting drugs 4. Inhaled forms 5. Combination with beta agonists
BRONCHODILATORS
1. Cholinergic drive is in the bronchii 2. 3. 4. Anti-cholinergics resting bronchial tone Three muscarinic receptors M1, M2, M3 Ipatropium, Oxitropium onset slower than agonists but more effective
5.
6. 7.
Sustained broncho-dilatation up to 8 h
Have influence on sleep quality in COPD Ipatropium optimal dose 80 g as inhaler
8.
9.
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Tiotropium selective to M1, M3 receptors

It is long acting once a day dose 40 g
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ORAL STEROIDS
1. Asthmatic component 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
CORTICOSTEROIDS
Inhaled Glucocorticoids
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
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THEOPHYLLIN E
1. Deriphyllin group 2. Nausea, tachycardia 3. Fatal arrhythmias 4. Interactions with drugs - Macrolides
BRONCHODILATORS
1. 2. 3. 4. Assumed to relax the airway smooth muscle At therapeutic concentration NO direct action on the bronchial smooth muscle Toxicity Many drug interactions Low therapeutic index - Poor safety window
5. Smokers have higher theophylline toxicity

6. Already tachycardiac
5.
6. 7.
Need to monitor blood levels frequently

Adverse effects on liver and in elderly Their use is at best questionable
7. Only oral - if at all
8.
9.
Never injectable in may countries banned

SR prep has some add on value
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INHALED Rx.
MANAGEMENT IBD is the preferred drugs LABA + Tiotropium is best LABA + TIO + ICS for Stage III, IV Combination is better than increasing individual drugs

5. Pharmacologic
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NO SYSTEMIC STEROIDS
MANAGEMENT No systemic steroids because of unfavorable benefit-to-risk ratio Exercise training programs, LTOT > 15 hours per day for RF

5. Pharmacologic
LTOT increases survival
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MANGEMENT AS PER STAGING
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AT RISK
1. Chronic symptoms 2. Cough 3. Phlegm 4. Dyspnea 5. H/o smoking 6. Spirometry Normal
MANAGEMENT - STAGE 0
Avoidance of risk factors
Stop smoking
Influenza vaccine Regular follow up spirometry
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MILD COPD
1. Chronic symptoms 2. Cough 3. Phlegm 4. Dyspnea 5. H/o smoking 6. Spirometry abnormal 7. FEV1 > 80% but 8. FEV1 / FVC < 70%
MANAGEMENT STAGE I
Avoidance of risk factors
Stop smoking
Influenza vaccine Regular follow up spirometry +
SABA + IPATROP
Inhaled route
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MODERATE COPD
1. Chronic symptoms 2. Cough 3. Phlegm 4. Dyspnea 5. H/o smoking 6. Spirometry abnormal 7. FEV1 < 80% but > 50% 8. FEV1 / FVC < 60%
MANAGEMENT STAGE II
Avoidance of risk factors Stop smoking Influenza vaccine Regular follow up spirometry SABA + IPA inhalations + LABA or TIOTROP or BOTH in inhaled Pulmonary Rehabilitation
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SEVERE COPD
1. Chronic symptoms 2. Cough 3. Phlegm 4. Dyspnea 5. H/o smoking 6. Spirometry abnormal 7. FEV1 < 50% but > 30% 8. FEV1 / FVC < 40%
MANAGEMENT STAGE III

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
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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
MANAGEMENT STAGE IV
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
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DRUG DELIVERY SYSTEMS - OPTIONS
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DRUG DELIVERY
1. Dexterity 2. Hand grip strength 3. Co-ordination 4. Severity of COPD
DRUG DELIVERY - OPTIONS MDI Metered Dose Inhalers Rotahalers, Diskhalers Spacehalers Nebulizers
5. Educational level
6. Age of the patient 7. Ability to inhale and synchronize
Oxygen mixed delivery

Oral tablets, syrups ?? Parenteral I.M or I.V use ????
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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
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EDUCATION AND REHABILITATION
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REHABILITATION
For the lungs to get more air
PURSED-LIP BREATHING (like breathing out slowly into a straw)
INHALE
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EXHALE
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REHABILITATION
For the lungs to get more air
DIAPHRAGMATIC BREATHING
1. Sit comfortably and relax your shoulders.
Sit comfortably and relax your shoulders Note:
Now inhale slowly through your muscles and breathe out nose. (Push your abdomen out the pursed-lip technique Repeat the above maneuver three times and then takeusing a little rest. while you breathe This exercise can be done many times ain) day.
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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 Put one hand Then push indown) your abdominal breathe in)on your abdomen.abdomen go
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HEALTH EDUCATION TEAM WORK
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EXACERBATIONS RESP. FAILURE
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OXIGENERATO R
MANAGEMENT REFERRAL
Diagnosis uncertain
Disproportionate symptoms
Persistent symptoms Development of lung cancer
Pulmonary rehabilitation
Nebulizer assessment
Oxygen assessment
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WHEN SUSPECT?
1. in symptoms 2. in sp purulence 3. in sp volume 4. Fever, chills 5. Ankle edema 6. Cyanosis 7. Consciousness
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
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WHAT EXTRA ?
1. Oxygen therapy 2. NIPPV mostly or 3. Macha. Ventilation 4. Ipatropium inhalation 5. SA - Beta agonists 6. No theophylline group 7. Narrow spectrum antibiotics 2 wks
MANAGE EXACERBATIONS
1. Exacerbations of symptoms requiring Rx. are important clinically in COPD.
2. 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
8. Oral steroids for 2 wk

9. Diuretics may help
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3. Systemic corticosteroids oral better 4. Antibiotics in short bursts what to give 5. NIPPV Non invasive intermittent positive pressure ventilation - Home
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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
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
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FEATURES
1. Increasing dyspnea 2. Peripheral oedema 3. venous pressure 4. Parasternal heave 5. Loud pulmonary second heart sound 6. ECG changes of RVH and PH
CORPULMONALE
LTOT Diuretics, Sodium restriction ACEi Alpha blockers Digoxin Heart failure management
7. Echo evidence
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RESP. FAILURE
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
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5. Pharmacologic
6. Non-pharmacologic 7. Management of exacerbations
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SURGERY
1. Bullectomy 2. LVRS - Lung volume reduction surgery 3. Single lung transplant
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
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WHAT NOT !
1. No Anti-tussives 2. Mucolytics ?? 3. No prophylactic antibiotics 4. No long term antibiotics 5. No systemic steroids 6. No narcotics
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
7. No vigorous exercise
8. No with holding the benefits of Oxygen
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COPD - FUTURE DEVELOPMENTS
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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
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
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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 Dont embark on Deri + Bet iv for all breathlessness Dont use Theophylline as far as possible Inhalation therapy is the best Drug delivery choices Dont spare any body from early oxygen therapy And finally, motivate smokers to quit smoking
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SELF SCREENING
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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 dont 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? 2. Do you bring up phlegm or mucus most days? 3. Do you get out of breath more easily than others your age? 4. Are you older than 40 years? 5. Are you a current smoker or an ex-smoker? Yes ___ No ___ Yes ___ No ___ Yes ___ No ___ Yes ___ No ___ 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 lungsLearn about COPD!
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ASTHMA V/s COPD Take HOME GUIDE
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ASTHMA V/s COPD

ASTHMA
Sensitizing trigger needed Innate Atopy is essential No noxious external agent
COPD
Chronic exposure -Noxious Any body may be effected Smoking is the noxious ag.
ETIOLOGICAL BASIS
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ASTHMA V/s COPD

ASTHMA
Primarily Allergic Inflamm. Secondary bronchospasm
COPD
Destructive Inflammation Primary in bronchial tone
Small airways - bronchioles Disease of alveloli, bronchi No destruction or fibrosis Alveolar destruc. Br fibrosis
PATHOLOGY
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ASTHMA V/s COPD

ASTHMA
Recurrent allergic inflamm. Airway remodeling occurs CD4 T, Mast cells, Eosino LT D4, IL 4, IL 5, - Th2
COPD
Progressive destr. inflamm. Emphysema, Bronchial fibr. CD 8 T, MF, Neutrophils LT B4, IL 8, TNF-
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IgE + other atopic disea. Proteases, in antiprote.
PATHOGENESIS
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ASTHMA V/s COPD

ASTHMA
Young subjects, any age Episodic, recurrent, normal Sputum mucoid or none Episodic dyspnea moder. Seasonal symptoms
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COPD
Age always > 35 yrs, smoke Chronic, progressive, Exaca Sputum purulent & copious Progressive dyspn, Hr. Gr. Perennial symptoms
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CLINICAL FEATURES
ASTHMA V/s COPD

ASTHMA
Normal or obstructive
FEV1 < 80% but > 60% FEV1 FVC < 70% Reversible - > 15 %
COPD
Always obstructive pattern
FEV1 < 70% may be < 40% FEV1 FVC < 60% Irreversible - < 15 %
Resp. failure rare

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Resp. failure,Corpulmonale
SPIROMETRY
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ASTHMA V/s COPD. - Rx.

ASTHMA COPD
Relievers and Preventers
Quitting of smoking crucial
ICS are the main stay

SABA for acute attacks Ipatropium add on only LTA are very useful Mast cell stabilizers useful LTOT not needed mostly
LABA + Antibiotics Ac. exa

SABA not much, ICS useful Ipatrop., Tiotrop. are first line LTA have no role at all Cromolyn, Ketotifen no use LTOT must in stage III and IV
Oral steroids have little role

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Oral steroids in stage III & IV

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SR Theophylline?? some role SR Theophylline contraindic.
Treatment
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
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PREVENT COPD
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THE DEADLIEST DEVIL
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SURE TO GRAVE
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AND FINALLY
Tell me what harm smoking does not cause ??
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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
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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
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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?
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Pledge to stop smoking
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WHAT CAN WE DO ??
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MY SINS
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 I have not updated my K Not shared what I have Dr.Sarma@works
IF CARE NOT TO DO THESE THEN ALL
PUNYAS SINS
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MY GAINS
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
HAVE NO MEANING & ARE MERELY FUTILE
PUNYAS SINS
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REMEMBER, WE ARE BLESSED
WITH THE OPPORTUNITY
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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 ||
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Important Announcement A CD format of todays 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

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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
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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

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NANRI, VANAKKAM
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COPD by DR Sarma

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Dr.Sarma RVSN, M.D., M.Sc (Canada)

NHLBI AND WHO COLLABORATIVE INITIATIVE

WORLD COPD DAY November 19, EVERY YEAR

Raising COPD Awareness Worldwide

PURPOSE OF THIS TALK Present the Global strategy

for the Diagnosis,

7. New advances in Rx.

4. Non reversible by bronchodilators

7. Chronic obstru. airways disease (COAD)

4. Absence of any other identifiable cause of excessive sputum production

OBSTRUCTIVE LUNG DISEASES

The global burden of COPD will increase

In 2000, the WHO estimated 2.74 million COPD deaths worldwide.

COPD PREVALENCE 2000

*From Murray & Lopez, 2001

SMOKING - THE CULPRIT

MOST IMP RISK

RISK FACTORS FOR COPD

INTENSE CAUSE FOR CONCERN ?

TENDER AGE GROUPS

COPD NH EFFECT OF SMOKING

Mortality among women smokers is on the rise globally

SHIFT IN THE DELICATE BALANCE

Nutrophil elastase Cathepsisns MMP-1, MMP- 9, MMP 12 Granzymes

Alpha 1 Anti-trypsin SLP 1, Elastin, TIMPs

1. Mucus gland hypertrophy 2. Smooth muscle hypertrophy 3. Goblet cell hyperplasia

Normal bronchial architecture

4. Inflammatory infiltrate 5. Excessive mucus

DISSECTING MICROSCOPIC APPEARENCE

Normal parenchymal architecture Dr.Sarma@works

Emphysematous Lung architecture

PULMONARY HYPERTENSION IN COPD

Normal Pulmonary Artery

Cirrhosis of liver, Hepatocellular carcinoma

Family history of any one of these conditions

MRC DYSPNOEA SCALE

Stops for breath on walking 100 m or after 2 or 3 minutes continuously

OXYGEN COST DIAGRAM

WHY D.D WITH ASTHMA ? 1. Different etiology

DIFF. Dx. of COPD & ASTHMA

Change < 15% Change > 15%

CHEST SKIAGRAMS OF EMPHYSEMA

V- P MISMATCH NUCLEOTIDE IMAGING

CHEST SKIAGRAM OF CHRONIC BRONCHITIS

CHEST LATERAL VIEW CHRONIC BRONCHITIS

HRCT NORMAL CHEST

3. Improve exercise tolerance

SYMPTOMS 2. Reduce risk factors

More than 7. Manage one month exacerbations

NORMAL AND COPD

from inhaled or systemic steroids

RISK REDUCTION STRATEGIES

IF ONE QUITS SMOKING

2. Reduce risk factors

2. Studies have shown that with smoking cessation

* Packets per day x Years of smoking = Pack Years

RISK FACTORS REDUCTION

2. In psychological dependence on nicotine

COPD MANAGEMENT LATEST GUIDELINES

Prevent and treat complications

2. Reduce risk factors

2. Reduce risk factors