c o p d by dr sarma

Dr.Sarma@works1

CHRONIC OBSTRUCTIVEPULMONARY 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

Consultant in Medicine and Chest,

President IMA – Tiruvallur Branch

+91 98940 60593, (4116) 260593

Dr.Sarma@works2

GOLDGOLDGLOBAL INITIATIVE

CHRONIC

OBSTRUCTIVE

DISEASENHLBI AND WHO COLLABORATIVE INITIATIVENHLBI AND WHO COLLABORATIVE INITIATIVE

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WORLD COPD DAYNovember 19, EVERY YEAR

Raising COPD Awareness WorldwideRaising COPD Awareness Worldwide

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PURPOSE OF THIS TALKRELEVANCE

Present the

Global strategy

for the Diagnosis,

Management and

Prevention of COPD

(updated Nov 2004)

BASED ON THE GOLD, NICE NAEPP, CDC, BTS,

GUIDELINES

BASED ON THE GOLD, NICE NAEPP, CDC, BTS,

GUIDELINES

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.

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DEFINITIONSDEFINITIONS

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DEFINITION OF COPDCONTENTS

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

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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1. CHRONIC BRONCHITIS2. EMPHYSEMA

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

1. Alveolar wall destruction

2. Irreversible enlargement of the air spaces

3. Distal to the terminal bronchioles

4. Without evidence of fibrosis

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DEFINITION OF COPDCONTENTS

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

2. Epidemiology

3. Risk factors

7. Stop smoking strateg.

8. Management Guide

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OBSTRUCTIVE LUNG DISEASES

ASTHMA COPD

REVERSIBILITY OF AIR WAY OBSTRUTION

FULL NONE

ASTHMA

EMPHYSEMA CHRONIC BRONCHITIS

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EPIDEMIOLGY OF COPD

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KEY POINTSCONTENTS

• 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

2. Epidemiology

3. Risk factors

8. Management Guide

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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

Cause Deaths

CHD 724,269

Cancer 534,947

CVA 158,060

COPD 114,318

Accidents 94,828

Diabetes 64,574

MORTALITY

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COPD PREVALENCE 2000

Cause % Change

CHD - 59%

Cancer - 64%

CVA - 39%

COPD + 163%

Accident + 32%

All other - 7%

MORTALITY TRENDS 1965 -

2000 Established Market Economies 6.98

Formerly Socialist Economies 7.35

India 4.38

China 26.20

Other Asia and Islands 2.89

Sub-Saharan Africa 4.41

Latin America and Caribbean 3.36

Middle Eastern Crescent 2.69

World 9.34

*From Murray & Lopez, 2001

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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.

• 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.

Year Consultations

1980 6.1 million

1985 7.4 million

1990 10.1 million

1995 11.8 million

2000 13.9 million

2010 ↑↑↑↑

MORBIDITY

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SMOKING - THE CULPRITSMOKING - THE CULPRIT

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RISK FACTORS FOR COPD MOST IMP RISK

• 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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TENDER AGE GROUPS

COLLEGE STUDENTS

INTENSE CAUSE FOR CONCERN ?

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COPD NH – EFFECT OF SMOKING

Mortality among women smokers is on the rise globally

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PATHOGENESIS AND PATOLOGY

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NOXIOUS AGENT(tobacco smoke, pollutants,

occupational exposures

PATHOGENESIS CONTENTS

Genetic factors

Respiratory infection

Others

2. Epidemiology

3. Risk factors

8. Management Guide

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1. Definition -key points

2. Burden of COPD

3. Classification

4. Risk factors

5. Pathogenesis,

6. Pathophysiology,

7. Management

8. Future research

PATHOGENESIS

INFLAMMATION

Small airway diseaseAirway inflammationAirway remodeling

Parenchymal destructionLoss of alveolar attachments

Decrease of elastic recoil

AIRFLOW LIMITATION

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1. Definition -key points

2. Burden of COPD

3. Classification

4. Risk factors

5. Pathogenesis,

6. Pathophysiology,

7. Management

8. Future research

PATHOGENESIS

ASTHMAASTHMASensitizing agent

COPDCOPDNoxious agent

Asthmatic airway inflammationCD4+ T-lymphocytes

Eosinophils

COPD airway inflammationCD8+ T-lymphocytes

MacrophagesNeutrophils

Airflow limitationCompletelyreversible

Completelyirreversible

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SHIFT IN THE DELICATE BALANCE

PROTEASES ANTI PROTEASES

Nutrophil elastase

Cathepsisns

MMP-1, MMP- 9, MMP – 12

Granzymes

Perforins

Alpha 1 Anti-trypsin

SLP 1, Elastin, TIMPs

COPDCOPD

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PATHOLOGY CONTENTS

• 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

2. Epidemiology

3. Risk factors

8. Management Guide

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PATHOLOGY in COPD

Normal bronchial architecture

1. Mucus gland hypertrophy

2. Smooth muscle hypertrophy

3. Goblet cell hyperplasia

4. Inflammatory infiltrate

5. Excessive mucus

6. Squamous metaplasia

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DISSECTING MICROSCOPIC APPEARENCE

Normal parenchymal architecture

Emphysematous Lung architecture

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PATHOLOGY – COPD ASTHMA

1. Neutrophilic inflammation2. Macrophages and CD8 T cells ↑3. Altered protease/antiprotiase balance4. Tissue destruction progressive5. Alpha1 AT↓- Young age emphysema6. Goblet cell size and number ↑ in CB7. Inflammatory mediators

LT B4IL 8TNF-α

1. Eosinophilic inflamm.

2. CD4, Th2 Lymphocyte

3. Mast cells

4. Tissue destruct. less

5. Mainly allergic inflam.

6. Inflam. Mediators

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PULMONARY HYPERTENSION IN COPD

Normal Pulmonary Artery

1. Duplication of elastic lamina

2. Medial hypertrophy - PH

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CLINICAL FEATURESCLINICAL FEATURES

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CHRONIC BRONCHITIS EMPHYSEMA

1. Mild dyspnea2. Cough before dyspnea starts3. Copious, purulent sputum4. More frequent infections5. Repeated resp. insufficiency6. PaCO2 50-60 mmHg

7. PaO2 45-60 mmHg

8. Hematocrit 50-60%9. DLCO is not that much ↓10. Cor pulmonale common

1. Severe dyspnea2. Cough after dyspnea 3. Scant sputum4. Less frequent infections5. Terminal RF

6. PaCO2 35-40 mmHg

7. PaO2 65-75 mmHg

8. Hematocrit 35-45%9. DLCO is decreased10. Cor pulmonale rare.

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CHRONIC BRONCHITIS EMPHYSEMA

BLUE BLOTTER PINK PUFFER

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ALPHA1 ANTITRYPSIN ↓ EMPHYSEMA

Specific circumstances of Alpha 1- AT↓include.

• 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 ↓

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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%

A1AT LEVELS

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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 SPIROMETRY

1. Physical exam may be negative 2. Hyper-inflated chest, Barrel chest3. Wheeze or quite breathing4. Pursed lip / accessory muscles resp.5. Peripheral edema6. Cyanosis, ↑ JVP7. Cachexia8. Cough, wheeze, dyspnea, sputum

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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

MRC DYSPNOEA SCALE ABOUT SMOKING

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

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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 OCCUPATIONAL

Sittin

Self w

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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 ‘SUPPORT’ STUDY

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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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 WHY D.D WITH

ASTHMA ? Clinical COPD ASTHMA

Smoker Nearly all May or may not be

Age < 35 Rare Nearly all

Sputum Productive Mucoid or none

Dyspnea Persistent Episodic

Course Progressive Variable, static

Spirometry Obstructive Normal or Obstru.

Reversibility Change < 15% Change > 15%

Most IMP Rx. IBD (Ipa+Salm) ICS

Anti leukotrn. Not useful Useful ad on Rx.

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COPD IMAGESCOPD 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 OF STABLE COPD

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1. Prevent disease progression

2. Relieve symptoms

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

MANAGEMENT OF COPD Rx. OBJECTIVES

1. Assess and monitor disease

2. Reduce risk factors

3. Manage stable COPD Education Pharmacologic Non-pharmacologic

4. Manage exacerbations

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ASSESSMENT OF COPD MANAGEMENT

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 +/-

2. Epidemiology

3. Risk factors

8. Management Guide

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3. Manage stable COPD

4. Education

5. Pharmacologic

6. Non-pharmacologic

ASSESSMENT OF COPD

SYMPTOMS EXPOSURE

SPUTUM

DYSPNEA

SMOKING

OCCUPATION

INDOOR / OUTDOOR

Air Pollution

SPIROMETRY IS A MUST

+ or -

More than one month

Age 35 +

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ASSESSMENT OF COPD MANAGEMENT

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

2. Epidemiology

3. Risk factors

8. Management Guide

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OTHER INVESTIGATIONS

1. Serial spirometry tests2. Pulse Oximetry3. Alpha1 Anti-trypsin levels

4. TLCO

5. HRCT6. ECG7. ECHO8. Sputum culture

2. Epidemiology

3. Risk factors

8. Management Guide

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NORMAL AND COPD SPIROMETRY

1 65432

Normal

4.150 80 %

60 %NormalCOPD

FVCFEV1 FVCFEV1/

Seconds

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WITH BRONCHODILATOR REVERSIBILITY PROTOCOL

1. Patient must be clinically stable

2. Patient should avoid

Short acting βagonists for 6 hours

Long acting βagonists for 12 hours

SR Theophylline for 24 hours

3. Baseline spirometry

4. Nebulize Salbuamol 2.5 mg + Ipatropium 500mg for 15 minutes with Nacl

5. Wait for 30 minutes

6. Repeat spirometry

2. Epidemiology

3. Risk factors

8. Management Guide

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WITH STEROIDS REVERSIBILITY PROTOCOL

1. Spirometry before and after steroid

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.

Look for steroid contraindications

This predicts the COPD group who will benefit

from inhaled or systemic steroids

2. Epidemiology

3. Risk factors

8. Management Guide

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WHAT IS REVERSIBILITY ? TESTING

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

2. Epidemiology

3. Risk factors

8. Management Guide

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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 FACTORS

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 REDUCTIONSTRATEGIES

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4. Education

5. Pharmacologic

IF ONE QUITS SMOKING NO TOMORROW!

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

* Packets per day x Years of smoking = Pack Years

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5. Withdrawal

4. Boredom

3. Sense of deprivation or depression

2. Emotional upset and stress

1. Alcohol abuse !

One devil replaced by another devil

5 RELAPSE TRIGGERS

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

RISK FACTORS REDUCTION

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1. Antidepressant - Bupropion

2. In psychological dependence on nicotine

3. Useful in individuals with or at risk for depression–

4. Contraindicated in drug interactions or seizure disorder

NICOTINE REPLACEMENTS DRUG TO QUIT ?

• 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 • Patch is more constant level, sprays &

inhaler a more rapid effect

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COPD MANAGEMENTLATEST GUIDELINESCOPD MANAGEMENTLATEST GUIDELINES

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MANAGEMENT

• Prevent disease progression

• Relieve symptoms

• Improve exercise tolerance

• Improve health status

• Prevent and treat complications

• Prevent and treat exacerbations

• Reduce mortality

1. Stable COPD

2. Exacerbations

3. Respiratory failure

4. Cardiac failure

GOALS OF MANAGEMENT

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HOW TO ASSESS?

1. Spirometric assessment

2. Walking distance

3. Dyspnea indices

4. Symptom scores

5. Exacerbation rates

4. Education

5. Pharmacologic

OUTCOME MEASURES

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BRONCHO- DILATORS

• IBD are the main stay

• As when needed basis

• The main drugs are

– β2 - Agonists (Salbutamol group)

– Anticholinergics (Ipatropium group)

– Their combination

– ?? Theophylline

4. Education

5. Pharmacologic

MANAGEMENT - IBD

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MANAGEMENT

1. IBD do not alter the pathology

2. Drug Rx. is to improve

symptoms and ↓complications.

3. But stopping smoking will halt

4. Education

5. Pharmacologic

BUT UNFORTUNATELY

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THE RULES

1. NO systemic steroids in stable COPD2. Inhalation treatment is BEST3. Salmeterol is the FIRST choice4. Ipatropium is the SECOND choice5. Salbutamol for short bursts6. Inhaled steroids THIRD choice7. Combination Ipa + Salmet inhalers beneficial8. Oral β2 Agonists FOURTH choice

9. Theophyllins ? role – LA preps. No injectables10. Oxygen therapy for exacerbations and RF

4. Education

5. Pharmacologic

MANAGEMENT RULES

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BRONCHO DILATORS

• 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

4. Education

5. Pharmacologic

IS IT A PARADOX ?

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SYNERGISM BRONCHODILATION

IPATROPIUM SABA and LABA

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ß AGONISTS

1. Direct action on the beta2 receptors in the bronchial smooth muscle – relaxation

2. Salbutamol most widely used3. In COPD 1 mg is the maximum dose4. Short acting – every 4 to 6 hours5. Salmeterol is long acting – 12 hours6. Slow onset, dose 50 μg b.i.d7. Formoterol still longer -12 μg b.i.d8. Side effects – tremors, tachycardia etc.,

1. Selective ß agonists

2. Short acting drugs

3. Long acting drugs

4. Oral medication

5. Inhaled form

BRONCHODILATORS

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ANTI ACH

1. ↑ Cholinergic drive is in the bronchii

2. Anti-cholinergics ↓resting bronchial tone

3. Three muscarinic receptors M1, M2, M3

4. 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

1. Anti-cholinergics

2. Short acting drugs

3. Long acting drugs

4. Inhaled forms

5. Combination with beta agonists

BRONCHODILATORS

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ORAL STEROIDS

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

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

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THEOPHYLLINE

1. Assumed to relax the airway smooth muscle

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. Need to monitor blood levels frequently

6. Adverse effects on liver and in elderly

7. Their use is at best questionable

8. Never injectable – in may countries banned

9. SR prep has some add on value

1. Deriphyllin group

2. Nausea, tachycardia

3. Fatal arrhythmias

4. Interactions with drugs - Macrolides

5. Smokers have higher theophylline toxicity

6. Already tachycardiac

7. Only oral - if at all

BRONCHODILATORS

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INHALED Rx.

• IBD is the preferred drugs

• LABA + Tiotropium is best

• LABA + TIO + ICS for Stage III, IV

• Combination is better than increasing individual drugs

4. Education

5. Pharmacologic

MANAGEMENT

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NO SYSTEMIC STEROIDS

• No systemic steroids because of • unfavorable benefit-to-risk ratio • Exercise training programs, • LTOT > 15 hours per day for RF• LTOT increases survival

4. Education

5. Pharmacologic

MANAGEMENT

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MANGEMENTAS PER STAGING

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AT RISK

• Avoidance of risk factors• Stop smoking• Influenza vaccine• Regular follow up spirometry

1. Chronic symptoms

2. Cough

3. Phlegm

4. Dyspnea

5. H/o smoking

6. Spirometry Normal

MANAGEMENT - STAGE 0

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MILD COPD

• Avoidance of risk factors• Stop smoking• Influenza vaccine• Regular follow up spirometry +• SABA + IPATROP• Inhaled route

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

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MODERATE COPD

• Avoidance of risk factors• Stop smoking• Influenza vaccine• Regular follow up spirometry• SABA + IPA inhalations +• LABA or TIOTROP or BOTH in inhaled• Pulmonary Rehabilitation

1. Chronic symptoms

2. Cough

3. Phlegm

4. Dyspnea

5. H/o smoking

7. FEV1 < 80% but > 50%

8. FEV1 / FVC < 60%

MANAGEMENT – STAGE II

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SEVERE COPD

• 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

1. Chronic symptoms

2. Cough

3. Phlegm

4. Dyspnea

5. H/o smoking

7. FEV1 < 50% but > 30%

8. FEV1 / FVC < 40%

MANAGEMENT – STAGE III

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V. SEVERE COPD

• 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

1. Chronic symptoms

2. Cough

3. Phlegm

4. Dyspnea

5. H/o smoking

7. FEV1 < 30%

8. FEV1 / FVC < 30%

9. Chronic Resp. Failure

MANAGEMENT – STAGE IV

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DRUG DELIVERYSYSTEMS - OPTIONS

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DRUG DELIVERY

• MDI – Metered Dose Inhalers• Rotahalers, Diskhalers• Spacehalers• Nebulizers• Oxygen mixed delivery• Oral tablets, syrups ??• Parenteral – I.M or I.V use ????

1. Dexterity

2. Hand grip strength

3. Co-ordination

4. Severity of COPD

5. Educational level

6. Age of the patient

7. Ability to inhale and synchronize

DRUG DELIVERY - OPTIONS

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NEBULISED THERAPY

1. Severe breathlessness despite using inhalers 2. Assessment should be done for improvement3. Choice between a facemask or mouth piece4. Equipment servicing and support are essential5. 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 above6. 15 minutes and slow or moderate flow rate7. Can be repeated 2 to 3 times a day – Mouth Wash

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EDUCATION ANDREHABILITATIONEDUCATION ANDREHABILITATION

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REHABILITATION

For the lungs to get more air

PURSED-LIP BREATHING(like breathing out slowly into a straw)

INHALE EXHALE

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1. Sit comfortably and relax your shoulders.

2. Put one hand on your abdomen. Now inhale slowly through your nose. (Push your abdomen out while you breathe in)

3. Then push in your abdominal muscles and breathe out using the pursed-lip technique. (You should feel your abdomen go down)

Note: • Repeat the above maneuver three times and then take a little rest.• This exercise can be done many times a day.

REHABILITATION

For the lungs to get more air

DIAPHRAGMATIC BREATHING

Sit comfortably and relax your shoulders

Put one hand on your abdomen. Now inhale slowly through your nose. (Push your abdomen out while you breathe in)

Then push in your abdominal muscles and breathe out using the pursed-lip technique

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HEALTH EDUCATION – TEAM WORK

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EXACERBATIONSRESP. FAILURE

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OXIGENERATOR

• Diagnosis uncertain• Disproportionate symptoms• Persistent symptoms• Development of lung cancer• Pulmonary rehabilitation• Nebulizer assessment• Oxygen assessment

MANAGEMENT – REFERRAL

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WHEN SUSPECT?

1. Pulmonary embolism2. Pneumothorax – rupture of bullae3. Myocardial infarction4. Left ventricular failure5. Acute pneumonia6. Bronchogenic carcinoma

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

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WHAT EXTRA ?

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 smokingIn 35% of cases cause is not known

3. Systemic corticosteroids – oral better4. Antibiotics in short bursts – what to give5. NIPPV – Non invasive intermittent

positive pressure ventilation - Home

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

8. Oral steroids for 2 wk

9. Diuretics may help

MANAGE EXACERBATIONS

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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

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

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CORPULMONALE

• LTOT• Diuretics, Sodium restriction• ACEi • Alpha blockers• Digoxin• Heart failure management

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

7. Echo evidence

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RESP. FAILURE

1. Pulmonary hypertension2. Right ventricular hypertrophy3. Right ventricular diastolic dys. function4. Right ventricular systolic dysfunction5. Corpulmonale – Right heart failure6. Acute respiratory insufficiency7. Life threatening respiratory failure8. Hypercapnia, Severe hypoxia9. Intubation and IPPV10. Managing RVF and RF – ICU care

4. Education

5. Pharmacologic

7. Management of exacerbations

RESPIRATORY FAILURE

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SURGERY

1. Increasing dyspnea2. Single large emphysematous bulla3. Severe - FEV1 < 35% but > 20%4. Upper lobe emphysema5. PaCo2 not more than 55%

6. TLCO must be at least 20%

7. Age less than 658. Severe pulmonary hypertension

1. Bullectomy

2. LVRS - Lung volume reduction surgery

3. Single lung transplant

LUNG RESECTION

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WHAT NOT !

• 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

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

WHAT ELSE WE CAN GIVE

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COPD - FUTURE DEVELOPMENTSCOPD - FUTURE DEVELOPMENTS

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NEXT DECADE

• 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

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

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• 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

TAKE HOME MESSAGES

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SELF SCREENINGSELF SCREENING

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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!

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!

Could it be COPD?Could it be COPD?

Dr.Sarma@works104

ASTHMA V/s COPDTake HOME GUIDEASTHMA V/s COPDTake HOME GUIDE

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ASTHMA V/s COPDASTHMA 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

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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

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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

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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

CLINICAL FEATURES

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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

SPIROMETRY

Dr.Sarma@works110Treatment

ASTHMA V/s COPD. - Rx.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@works111

“The old order changethyielding place to new;Lest, one good custom

should corrupt the world.”

“The old order changethyielding place to new;Lest, one good custom

should corrupt the world.”

This is most pertinent today to Asthma and COPD

Tennyson Sir Lord, AlfredTennyson Sir Lord, Alfred

Holm and Harris & NEJM

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PREVENT COPDPREVENT COPD

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THE DEADLIEST DEVILTHE DEADLIEST DEVIL

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SURE TO GRAVESURE TO GRAVE

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AND FINALLYAND FINALLY

Tell me what harm smoking

does not cause ??

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TELL ME THE ORGAN SPARED

1. IHD, MI, ↑ Restenosis2. Atherosclerosis – PVD, IR, ↑ DM3. Oxidation of LDL, ↑ LDL, ↓ HDL, ↑ TG4. COPD, Lung Cancer5. Tremors, Peripheral neuritis6. APD, NUD, Oro-pharyngeal Cancers7. Osteoporosis8. Poor fetal development9. Nicotine dependence10. Wasteful expenditure

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

PROVEN DISASTERS

Dr.Sarma@works117

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?

The Onus here is on usThe Onus here is on us

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Pledge to stop smokingPledge to stop smoking

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WHAT CAN WE DO ??WHAT CAN WE DO ??

120Dr.Sarma@works

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

MY SINS

PUNYAS

IF CARE NOT TO DO THESE – THEN ALL

121Dr.Sarma@works

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

MY GAINS HAVE NO MEANING & ARE MERELY FUTILE

PUNYAS

122 Dr.Sarma@works

REMEMBER, WE ARE BLESSED

WITH THE OPPORTUNITY

REMEMBER, WE ARE BLESSED

WITH THE OPPORTUNITY

Dr.Sarma@works123

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@works124

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

Important Announcement

Dr.Sarma@works125

1. ACCP www.chestnet.org2. ATS www.thoracic.org3. BTS www.brit-thoracic.org.uk4. COPD profess.

www.copdprofessional.com5. GOLD www.goldcopd.com6. NICE www.nice.uk.org7. Chest Net www.chestnet.net8. CDC www.cdc.nih.gov9. NAEPP www.naepp.nhlbi.org10.COPD Rapid series by ELSEVIER

Resources for COPD and Asthma

Dr.Sarma@works126

+91 98940 60593, (4116) 260593

PLEASE CONTACT US

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@works127

NANRI,

VANAKKAM

NANRI,

VANAKKAM

c o p d by dr sarma

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