Chronic Obstructive Pulmonary Disease (COPD)

Omer Alamoudi, MD, FRCP,FCCP,FACP

Professor, consultant Pulmonologist

dramoudi@yahoo.com

COPD is a chronic obstructive pulmonary disease that is characterized by airflow limitation that is not fully reversible.

The airflow limitation is usually both progressive and associated with an abnormal inflammatory response

COPD is a preventable and treatable disease

Definition of COPD

Chronic Obstructive Pulmonary disease (COPD)

Chronic bronchitis Emphysema

COPD

DefinitionsChronic bronchitis: Cough and sputum

production for at least 3 months in each of two consecutive years in albescence of other endobronchial disease such as bronchiectasis

Emphysema: overinflation of the distal airspaces with destruction of alveolar septa

Prevalence of COPD worldwide and in KSA

Prevalence/Risk Factors

Prevalence/Risk Factors

Cigarette smoking is the primary cause of COPD.

Approximately 90% of COPD patients have a smoking history

The WHO estimates 1.1 billion smokers worldwide, increasing to 1.6 billion by 2025.

In low- and middle-income countries, rates are increasing at an alarming rate

Cigarette smoking is the primary cause of COPD.

Approximately 90% of COPD patients have a smoking history

The WHO estimates 1.1 billion smokers worldwide, increasing to 1.6 billion by 2025.

In low- and middle-income countries, rates are increasing at an alarming rate

• .

Cigarette Smoking

Smoking Prevalence Among Doctors

Country Male% Female%

UK 8 5

USA 9 7

Germany 9 6

Korea 4628

China 4235

S. Arabia 38 15

Global Burden of Disease (1990–2020)

Lower respiratory tract infections

1

Diarrhoeal diseases 2

Conditions during perinatal period

3

Unipolar major depression

4

Ischaemic heart disease 5

Cerebrovascular disease 6

Tuberculosis 7

Measles 8

Road traffic accidents 9

Congenital anomalies 10

Malaria 11

COPD 12

1 Ischaemic heart disease

2 Unipolar major depression

3 Road traffic accidents

4 Cerebrovascular disease

5 COPD

6 Lower respiratory tract infections

7 Tuberculosis

8 War

9 Diarrhoeal diseases

10 HIV

11 Conditions during perinatal period

12 Violence

1990 2020

COPD Prevalence in KSA

According to one report released by the executive office of the GCC Health Ministers Council, Saudi Arabia is the world’s fourth largest importer of cigarettes.

During the year of 2004, the kingdom imported 41,000 tons of tobacco at a value of SR 1.45 billion.

COPD Prevalence in KSA (Contd.)

Table 3. Ranking of the 10 most frequent diagnoses among hospitalized patients at KAUH

Diagnosis No %

Diabetes mellitus 570 10.5 Ischemic heart diseases 493 8.6 Bronchial asthma 311 5.8Chronic liver disease 293 5.4Congestive heart failure 203 3.8 Hypertension 153 2.8 Sickle cell anemia 141 2.6COPD 132 2.4Chronic renal failure 116 2.1Cerebrovascular accident 108 2.0

Risk Factors

Risk Factors for COPD

Host Factors

Genes (e.g. alpha1-antitrypsin deficiency)

Hyperresponsiveness

Exposure

Tobacco smoke

Occupational dusts and chemicals

Infections

Socioeconomic status

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Risk Factors for COPD

NutritionNutrition

InfectionsInfections

Socio-economic Socio-economic statusstatus

Aging PopulationsAging Populations

Pathogenesis of COPD

Pathogenesis of COPDPathogenesis of COPD

NOXIOUS AGENT(tobacco smoke, pollutants, occupational

agent)

COPD

Genetic factors

Respiratory infection

Other

LUNG INFLAMMATIONLUNG INFLAMMATION

COPD PATHOLOGYCOPD PATHOLOGY

OxidativeOxidativestressstress ProteinasesProteinases

Repair Repair mechanismsmechanisms

Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants

Host factorsAmplifying mechanisms

Cigarette smokeCigarette smokeBiomass particlesBiomass particles

ParticulatesParticulates

Source: Peter J. Barnes, MD Pathogenesis of

COPD

INFLAMMATION

Small airway diseaseAirway inflammationAirway remodeling

Parenchymal destructionLoss of alveolar attachments

Decrease of elastic recoil

AIRFLOW LIMITATION

Causes of Airflow Limitation

Irreversible

Fibrosis and narrowing of the airways

Loss of elastic recoil due to alveolar destruction

Destruction of alveolar support that maintains patency of small airways

Airway Pathology in COPD

Airway pathology in COPD

Airway pathology in COPD

Diagnosis of COPD

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Diagnosis of COPD

A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease.

The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible.

Comorbidities are common in COPD and should be actively identified.

SYMPTOMScoughcough

sputumsputumshortness of breathshortness of breath

EXPOSURE TO RISKFACTORS

tobaccotobaccooccupationoccupation

indoor/outdoor pollutionindoor/outdoor pollution

SPIROMETRYSPIROMETRY

Diagnosis of COPDDiagnosis of COPD

Diagnosis of COPD

SignsHands

Flapping tremor, dilated veins, collapsing pulse, warm hands (CO2 retention)

Cyanosis, clubbing of the finger (ca lung)

Chest (signs of hyperinflation)Barrel chest, use of accessory ms, decreased

expansion, absence cardiac dullness, tracheal tug

Hyperesonant on percussion

Diagnosis of COPD

Sign of pulmonary HTNIncreased JVP, left parasternal heave, Loud

P2, Hepatomegaly, Ascitis, lower limb edema

Fundus examinationPapilloedema

Extrapulmonary manifestationMs wasting

Signs of COPD

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Diagnosis of COPD: Spirometry

Spirometry should be performed after the administration of an adequate dose of a short-

acting inhaled bronchodilator to minimize variability.

A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible.

Diagnosis of COPD / Spirometry

Spirometry: Normal and Patients with COPD

Classification of COPD Severity by Spirometry

Stage I: Mild FEV1/FVC < 0.70

FEV1 > 80% predicted

Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted

Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted

Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or

FEV1 < 50% predicted plus chronic respiratory failure

The Effect of Smoking on Lung Function

Adapted from Fletcher & Peto 1977

FEV1 (% of value at age 25 y)

Stopped at 45

Age (y)

25 50 750

25

50

75

100 Never smoked or notsusceptible to smoking

Smoked regularly andsusceptible to its effects

DISABILITY

DEATH

Stopped at 65

Diagnosis of COPD/ chest X-ray

Diagnosis of COPD/ HRCT scan

Diagnosis of COPD

CBC WBC (increased with infection) Hb (secondary

Polycthemia)

ESR Increased with infection

malignancy

Diagnosis of AECOPD

Diagnosis of AECOPD

Diagnosis of AECOPD was based on ATS criteriaMajor

Increased dyspneaIncreased sputum productionPurulent sputum

MinorCough, wheeze, sore throat, and cold

and nasal discharge

Diagnosis of AECOPD/sputum culture

Pathogens isolated during exacerbationBacterial

Moraxella catarrhalisPseudomonasHaemophilus influenzae

ViralInfluenza

Atypical bacteriaMycoplasmaChlamydia

Differential Diagnosis Differential Diagnosis COPD VS Asthma COPD VS Asthma

Differential Diagnosis: Differential Diagnosis: COPD and AsthmaCOPD and Asthma

COPD ASTHMA

• Onset in mid-life

• Symptoms slowly progressive

• Long smoking history

• Dyspnea during exercise

• Largely irreversible airflow limitation

• Onset early in life (often childhood)

• Symptoms vary from day to day

• Symptoms at night/early morning

• Allergy, rhinitis, and/or eczema also present

• Family history of asthma

• Largely reversible airflow limitation

COPD and Co-Morbidities

COPD patients are at increased risk for:

• Myocardial infarction, angina

• Osteoporosis

• Respiratory infection

• Depression

• Diabetes

• Lung cancer

Chronic hypoxiaChronic hypoxia

Pulmonary vasoconstrictionPulmonary vasoconstriction

MuscularizationMuscularization

Intimal Intimal hyperplasiahyperplasia

FibrosisFibrosis

ObliterationObliteration

Pulmonary hypertensionPulmonary hypertension

Cor pulmonaleCor pulmonale

Death

EdemaEdema

Pulmonary Hypertension in COPD

Source: Peter J. Barnes, MD

Management of COPD and Exacerbation

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Management of COPD

Prevention

Smoking cessation: is the single most effective — and cost effective — intervention in most people to reduce the risk of developing COPD and stop its progression

Controlling pollution: Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD.

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Management of COPD Smoking cessation

Counseling delivered by physicians

Numerous effective pharmacotherapies for smoking cessation are available

Nicotine chewing gum, transcutaneous patches, nicotine inhalers or nasal spray

Buproprion (aminoketone) (reduce nicotine withdrawal symptoms) Epilepsy, tremor, insomnia, tachycardia

Nortiptyline

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Management of COPDBronchodilators

Anticholinergics

Ibratropium bromide (short acting)

Improve nocturnal O2 saturation

Improve quality of sleep

Doses: 40 ug 1 -2 puffs q6h

Mainly used during exacerbation and symptomatic patients

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Management of COPD Bronchodilators

Tiotropium bromide (long acting anticholinergic)

Once daily

No systemic cholinergic effect

M3 receptors antagonist

Dose: 18 ug/day

Used in combination with LAB ± ICS or alone in stable COPD

Decrease symptoms, improve exercise tolerance

Decrease exacerbation

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Management of COPD

Bronchodilators

ß2 -agonists (Salbutamol, Terbutaline)

Rapid relief of symptoms

Dose: 120 ug, 2 puffs q4 - 6h

Tachycardia, tremors

Methylxanthines (Theophylline)

week bronchodilator effect

Monitor serum level (55 -110 umol/l)

Hepatic disease, heart failure, drugs; erythromycin, ciprofloxacin increase serum level

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Management of COPDLong Acting Bronchodilators (LAB)

LAB is more effective and convenient than treatment with short-acting bronchodilators Salmeterol (50 ug) Formoterol (9 ug)Doses: q12h

It should be added with Ibratropium or tiotropium if further improvement in symptoms is required

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Management of COPD

Glucocorticosteroids

Long term use of ICS treatment is appropriate for:

● symptomatic COPD patients with an FEV1 < 50% predicted (stage 111,1V)

● repeated exacerbations ● Allergy

Budesonide 800 ucg BD Fluticasone 500 ucg BD

Chronic treatment with oral corticosteroids should be avoided because of an unfavorable benefit-to-risk ratio

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Management of COPD

Other Pharmacologic Treatments

Antibiotics: Only used to treat infectious exacerbations of COPD

Respiratory stimulants (improve ABG)

Doxapram

Almitrine

Mucolytic agents, Antitussives: Not recommended in stable COPD

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Management of COPDPharmacotherapy: Vaccines

Influenza vaccines can reduce serious illness and should be given yearly

Pneumococal polysaccharide vaccine may be given although there is no conclusive evidence to support is it use in COPD

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Management of COPD

Non-Pharmacologic Treatments

Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue

Oxygen Therapy: LTOT (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival

PO2: 55 mmHg or less

PO2: 59 mmHg + Polycythemia, Corpulmonale

Management of COPD

Surgical management BullectomyResection bulla allow expansion of the surrounding lung

tissue Lung Volume Reduction Surgery

FEV1 < 35% Lung transplant

Age <65FEV<35%Pao2<55mmHg, PaCO2 >55mmHgSecondary pulmonary HTN, absence of IHD

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Management COPD Exacerbations

Antibiotics 2nd generation cephalosporin Amoxicillin / clavulinate Quinolones

Inhaled bronchodilators, combination of Ibratropium B2 agonist

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Management COPD Exacerbations

Corticosteroid IV methyl prednisone Oral prednisoneShould be used in moderate to severe COPD

Hydration

Chest physiotherapy

Management COPD Exacerbations

Noninvasive mechanical ventilation

Decreases the need for endotracheal intubation

Mechanical ventilation

Deterioration of level of consciousness

PaO2 40 mmHg, pH < 7.25

Medications and education to help prevent future exacerbations should be considered as part of follow-up