chronic obstructive pulmonary disease (copd) omer alamoudi, md, frcp,fccp,facp professor, consultant...
TRANSCRIPT
Chronic Obstructive Pulmonary Disease (COPD)
Omer Alamoudi, MD, FRCP,FCCP,FACP
Professor, consultant Pulmonologist
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
15
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
25
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
32
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
50
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.
51
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
52
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
53
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
54
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
55
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
56
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
57
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
58
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
59
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
61
Management COPD Exacerbations
Antibiotics 2nd generation cephalosporin Amoxicillin / clavulinate Quinolones
Inhaled bronchodilators, combination of Ibratropium B2 agonist
62
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