1. CHRONICCHRONIC
OBSTRUCTIVEOBSTRUCTIVE
PULMONARY DISEASEPULMONARY DISEASE
Iman Galal, MDIman Galal, MD
Pulmonary Medicine DepartmentPulmonary Medicine Department
Ain Shams UniversityAin Shams University

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Contents of the Lecture:Contents of the Lecture:
EpidemiologyEpidemiology
DefinitionDefinition
Risk factorsRisk factors
PathogenesisPathogenesis
PathologyPathology
ClassificationClassification
ManagementManagement
COPD exacerbationsCOPD exacerbations

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Epidemiology:Epidemiology:
 Cigarette smoking is the primary cause of COPD.Cigarette smoking is the primary cause of COPD.
 The WHO estimates 1.3 billion smokers worldwide,The WHO estimates 1.3 billion smokers worldwide,
increasing to 2 billion by 2025.increasing to 2 billion by 2025.
 In 2000, the WHO estimated 2.74 million deathsIn 2000, the WHO estimated 2.74 million deaths
worldwide from COPD.worldwide from COPD.
 In 1990, COPD was rankedIn 1990, COPD was ranked 1212thth
as a burden of disease.as a burden of disease.
 After 25 years of smoking, at least 25% of smokers without
initial disease will have clinically significant COPD

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US Leading Causes of Death 2001US Leading Causes of Death 2001

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Chronic Obstructive Pulmonary Disease:Chronic Obstructive Pulmonary Disease:
Chronic Obstructive Pulmonary Disease (COPD) is aChronic Obstructive Pulmonary Disease (COPD) is a
preventablepreventable && treatabletreatable disease with some significantdisease with some significant
extrapulmonaryextrapulmonary effects that may contribute to the severityeffects that may contribute to the severity
in individual patients. Itsin individual patients. Its pulmonarypulmonary component iscomponent is
characterized bycharacterized by airflow limitationairflow limitation that isthat is not fullynot fully
reversible.reversible. The airflow limitation is usuallyThe airflow limitation is usually progressiveprogressive &&
associated with anassociated with an abnormal inflammatory responseabnormal inflammatory response ofof
the lung to noxious particles or gases.the lung to noxious particles or gases.
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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Emphysema:Emphysema:
 AbnormalAbnormal permanentpermanent enlargement of the airspaces distalenlargement of the airspaces distal
to the terminal bronchiole, accompanied by destruction ofto the terminal bronchiole, accompanied by destruction of
their walls without fibrosis.their walls without fibrosis.
 Types:Types:
(1)(1) Centrilobular (centriacinar)Centrilobular (centriacinar)
(2)(2) Panlobular (panacinar)Panlobular (panacinar)
(3)(3) Paraseptal (distal acinar)Paraseptal (distal acinar)
(4)(4) IrregularIrregular

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Chronic bronchitis:Chronic bronchitis:
 Presence ofPresence of chronic productive coughchronic productive cough forfor
3 months3 months in each ofin each of
2 successive years2 successive years in a patient in whomin a patient in whom otherother
causescauses ofof chronic coughchronic cough have beenhave been
excluded.excluded.

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Risk Factors:Risk Factors:
Genes
Exposure to particles
1. Tobacco smoke
2. Occupational dust, organic & inorganic
3. Indoor air pollution
4. Outdoor air pollution
Lung growth & development
Oxidative stress
Gender
Age
Respiratory infections
Previous TB
Socioeconomic status
Nutrition
Comorbidities

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Pathogenesis:Pathogenesis:
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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Pathogenesis:Pathogenesis:
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
InflammationInflammation
Small Airway DiseaseSmall Airway Disease
Airway inflammationAirway inflammation
Parenchymal DistructionParenchymal Distruction
Decrease elastic recoilDecrease elastic recoil
Loss of alveolar attachmentLoss of alveolar attachment
Airflow LimitationAirflow Limitation

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Overlap of Obstructive Lung DiseaseOverlap of Obstructive Lung Disease
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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Pathogenesis:Pathogenesis:
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
AsthmaAsthma
Asthmatic AirwayAsthmatic Airway
InflammationInflammation
CD4-T lymphocytesCD4-T lymphocytes
EosinophilsEosinophils
COPD AirwayCOPD Airway
InflammationInflammation
CD8-T lymphocytesCD8-T lymphocytes
MacrophagesMacrophages
NeutrophilsNeutrophils
Airflow LimitationAirflow Limitation
COPDCOPD
FullyFully
ReversibleReversible
Not FullyNot Fully
ReversibleReversible

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PathologyPathology
1.1.Mucus gland hypertrophyMucus gland hypertrophy
2.2.Smooth muscle hypertrophySmooth muscle hypertrophy
3.3.Goblet cell hyperplasiaGoblet cell hyperplasia
4.4.Inflammatory infiltrateInflammatory infiltrate
5.5.Excessive mucusExcessive mucus
6.6.Squamous metaplasiaSquamous metaplasia
Normal BronchialNormal Bronchial
ArchitectureArchitecture
COPDCOPD

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Healthy Respiratory MucosaHealthy Respiratory Mucosa
 This EM shows theThis EM shows the
respiratory mucosa in arespiratory mucosa in a
healthy state.healthy state.
 The cells are fully ciliated.The cells are fully ciliated.
 The cilia beat in a co-The cilia beat in a co-
ordinated fashion to moveordinated fashion to move
mucus out of the airwaysmucus out of the airways
(mucociliary transport).(mucociliary transport).
Scanning electron micrograph showing aScanning electron micrograph showing a
sheet of mucus being moved along by the ciliasheet of mucus being moved along by the cilia

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Damaged Respiratory MucosaDamaged Respiratory Mucosa
 Damage to the cilia & epitheliumDamage to the cilia & epithelium
occur as a result of diseaseoccur as a result of disease
processes in COPD. This can alsoprocesses in COPD. This can also
occur as a result of bacterialoccur as a result of bacterial
damage.damage.
 This slide shows the result ofThis slide shows the result of
bacterial infection stripping awaybacterial infection stripping away
the cilia from the mucosa.the cilia from the mucosa.
 The damage to the cilia meansThe damage to the cilia means
they are less effective in removingthey are less effective in removing
mucus from the airwaysmucus from the airways
Scanning electron micrograph showing cilialScanning electron micrograph showing cilial
and epithelial damage induced by bacteriaand epithelial damage induced by bacteria

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Centriacinar EmphysemaCentriacinar Emphysema
 Characterized by focal destruction limited to the respiratory bronchioles &Characterized by focal destruction limited to the respiratory bronchioles &
the central portions of acinus.the central portions of acinus.
 Is is associated with cigarette smoking & is most severe in the upper lobes.Is is associated with cigarette smoking & is most severe in the upper lobes.

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Panacinar EmphysemaPanacinar Emphysema
 It involves the entire alveolus distal to the terminal bronchiole.It involves the entire alveolus distal to the terminal bronchiole.
 It is most severe in the lower lung zones & generally develops in patientsIt is most severe in the lower lung zones & generally develops in patients
with homozygous alpha1-antitrypsin (AAT) deficiency.with homozygous alpha1-antitrypsin (AAT) deficiency.

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Distal acinar EmphysemaDistal acinar Emphysema
 Distal acinar emphysema orDistal acinar emphysema or
paraseptal emphysema, is theparaseptal emphysema, is the
least common form and involvesleast common form and involves
distal airway structures, alveolardistal airway structures, alveolar
ducts, and sacs.ducts, and sacs.
 This form of emphysema isThis form of emphysema is
localized to fibrous septa or tolocalized to fibrous septa or to
the pleura & leads to formationthe pleura & leads to formation
of bullae.of bullae.
 The apical bullae may causeThe apical bullae may cause
pneumothorax.pneumothorax.
 Paraseptal emphysema is notParaseptal emphysema is not
associated with airflowassociated with airflow
obstruction.obstruction.

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EmphysemaEmphysema

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EmphysemaEmphysema
EmphysemaEmphysemaNormal LungNormal Lung

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EmphysemaEmphysema
EmphysemaEmphysemaNormal LungNormal Lung

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Management of COPD:Management of COPD:
(1)(1) Assess and Monitor Disease.Assess and Monitor Disease.
(2)(2) Reduce Risk Factors.Reduce Risk Factors.
(3)(3) Manage Stable COPD.Manage Stable COPD.
(4)(4) Manage Exacerbations.Manage Exacerbations.

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A) Assess & Monitor of COPD:A) Assess & Monitor of COPD:
1) Assessment of symptoms:1) Assessment of symptoms:
 CoughCough
 DyspneaDyspnea
 Sputum productionSputum production
2) History taking:2) History taking:
 Exposure to risk factors e.g., smoking, occupational or environmental.Exposure to risk factors e.g., smoking, occupational or environmental.
 Pattern of symptom development.Pattern of symptom development.
 History of exacerbations or previous hospitalizationsHistory of exacerbations or previous hospitalizations
 Presence of comorbidities e.g., heart disease, malignancies & osteoporosisPresence of comorbidities e.g., heart disease, malignancies & osteoporosis
 Appropriateness of current medical treatments.Appropriateness of current medical treatments.
 Impact of disease on patients life, including limitation of activity, missed workImpact of disease on patients life, including limitation of activity, missed work
 Social and family support available to the patientSocial and family support available to the patient
 Possibilities for reducing risk factors, especially smoking cessationPossibilities for reducing risk factors, especially smoking cessation
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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MRC Dyspnea ScaleMRC Dyspnea Scale

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Chronic Cough with Normal CXRChronic Cough with Normal CXR
IntrathoracicIntrathoracic
 Chronic obstructive pulmonary diseaseChronic obstructive pulmonary disease
 Bronchial asthmaBronchial asthma
 Central bronchial carcinomaCentral bronchial carcinoma
 Endobronchial tuberculosisEndobronchial tuberculosis
 BronchiectasisBronchiectasis
 Left sided heart failureLeft sided heart failure
 Interstitial lung diseaseInterstitial lung disease
 Cystic fibrosisCystic fibrosis
ExtrathoracicExtrathoracic
 Postnasal dripPostnasal drip
 Gastroesophageal refluxGastroesophageal reflux
 Drug therapy (e.g., ACE inhibitors)Drug therapy (e.g., ACE inhibitors)
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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Systemic manifestations of COPD:Systemic manifestations of COPD:
 Skeletal muscle wastingSkeletal muscle wasting
 Cachexia: loss of fat-free massCachexia: loss of fat-free mass
 Lung cancer (SCLC & NSCLC)Lung cancer (SCLC & NSCLC)
 Pulmonary hypertensionPulmonary hypertension
 Ischaemic heart diseaseIschaemic heart disease
 Congestive cardiac failureCongestive cardiac failure
 OsteoporosisOsteoporosis
 Normocytic anaemiaNormocytic anaemia
 DiabetesDiabetes
 Metabolic syndromeMetabolic syndrome
 Obstructive sleep apneaObstructive sleep apnea
 DepressionDepression

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 Central cyanosisCentral cyanosis
 Hyperinflated chestHyperinflated chest
 Increased resting respiratory rate with shallow breathingIncreased resting respiratory rate with shallow breathing
 Pursed-lip breathingPursed-lip breathing
 Respiratory distressRespiratory distress
 Lower limb edemaLower limb edema
 Difficulty in detection of heart apexDifficulty in detection of heart apex
 Resonant bare area of the heartResonant bare area of the heart
 Downward displacement of the liverDownward displacement of the liver
 Distant breath soundsDistant breath sounds
 Wheezy chestWheezy chest
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
3) Physical Examination:3) Physical Examination:

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Hyperinflation in COPD:Hyperinflation in COPD:

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4) Spirometric Classification of COPD:4) Spirometric Classification of COPD:
Severity Based on Post-Bronchodilator FEV1Severity Based on Post-Bronchodilator FEV1
StageStage
Stage IStage I MildMild
FEV1/FVC < 0.70
FEV1 ≥ 80% predicted
Stage IIStage II ModerateModerate
FEV1/FVC < 0.70
50% ≤ FEV1 < 80% predicted
Stage IIIStage III SevereSevere
FEV1/FVC < 0.70
30% ≤ FEV1 < 50% predicted
Stage IVStage IV
VeryVery
SevereSevere
FEV1/FVC < 0.70
FEV1 < 30% predicted or FEV1 < 50% predicted
plus chronic respiratory failure
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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5) Bronchodilator Reversibility Testing:5) Bronchodilator Reversibility Testing:
PreparationPreparation
 Patients should be clinically stable & free from respiratory infection.Patients should be clinically stable & free from respiratory infection.
 Patients should not have taken inhaled short-acting bronchodilators in thePatients should not have taken inhaled short-acting bronchodilators in the
previous 6 hrs, long-acting bronchodilator in the previous 12 hrs, or sustainedprevious 6 hrs, long-acting bronchodilator in the previous 12 hrs, or sustained
release theophylline in the previous 24 hrs.release theophylline in the previous 24 hrs.
SpirometrySpirometry
 FEV1 should be measured before a bronchodilator is given.FEV1 should be measured before a bronchodilator is given.
 The bronchodilator should be given by metered dose inhaler through a spacerThe bronchodilator should be given by metered dose inhaler through a spacer
device or by nebulizer.device or by nebulizer.
 Possible dosage protocols are 400 gPossible dosage protocols are 400 g ββ2-agonist, up to 160 g anticholinergic, or2-agonist, up to 160 g anticholinergic, or
the two combined.the two combined.
 FEV1 should be measured again 10-15 minutes after a short-actingFEV1 should be measured again 10-15 minutes after a short-acting
bronchodilator is given; 30-45 minutes after the combination.bronchodilator is given; 30-45 minutes after the combination.
ResultsResults
 Increase in FEV1 both > 200 ml & 12% above pre-bronchodilator FEV1 isIncrease in FEV1 both > 200 ml & 12% above pre-bronchodilator FEV1 is
considered significant.considered significant.
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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6) Lung Volumes:6) Lung Volumes:
The three volumes most relevant to COPD are forced vital
capacity (FVC), residual volume (RV), & total lung capacity
(TLC).

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7) Exercise Testing:7) Exercise Testing:
Measurement COPD
VO2max Decreased
Anaerobic threshold Normal/decreased/indeterminate
Peak HR Decreased, Normal in mild
O2 pulse Normal or decreased
(VE/MVV) X 100 Increased
VE/VCO2 (at AT) Increased
VD/VT Increased
PaO2 Variable
P(A-a)O2 Variable, usually increased

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8) Arterial Blood Gases:8) Arterial Blood Gases:
 In advanced COPD, measurement of ABGs should be performed in stableIn advanced COPD, measurement of ABGs should be performed in stable
patients with FEV1 < 50% predicted or with clinical signs of respiratorypatients with FEV1 < 50% predicted or with clinical signs of respiratory
failure or right heart failure.failure or right heart failure.
 Changes in arterial blood gas tensions take time to occur. Thus, 20-30Changes in arterial blood gas tensions take time to occur. Thus, 20-30
minutes should pass before rechecking the gas tensions when the FIO2minutes should pass before rechecking the gas tensions when the FIO2
has been changed, e.g., during assessment for domiciliary oxygen therapy.has been changed, e.g., during assessment for domiciliary oxygen therapy.
 Adequate pressure must be applied at the arterial puncture site for atAdequate pressure must be applied at the arterial puncture site for at
least one minute, as failure to do so can lead to painful bruising.least one minute, as failure to do so can lead to painful bruising.
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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9) Chest X ray:9) Chest X ray:

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Differential Diagnosis of COPD:Differential Diagnosis of COPD:
DiagnosisDiagnosis Suggestive FeaturesSuggestive Features
COPDCOPD
Onset in mid-life.Onset in mid-life.
Symptoms slowly progressive.Symptoms slowly progressive.
Long history of tobacco smoking.Long history of tobacco smoking.
Dyspnea during exercise.Dyspnea during exercise.
Largely irreversible airflow limitation.Largely irreversible airflow limitation.
AsthmaAsthma
Onset early in life (often childhood).Onset early in life (often childhood).
Symptoms vary from day to day.Symptoms vary from day to day.
Symptoms at night/early morning.Symptoms at night/early morning.
Allergy, rhinitis, and/or eczema also present.Allergy, rhinitis, and/or eczema also present.
Family history of asthma.Family history of asthma.
Largely reversible airflow limitation.Largely reversible airflow limitation.
CongestiveCongestive
Heart FailureHeart Failure
Fine basilar crackles on auscultation.Fine basilar crackles on auscultation.
Chest X-ray shows dilated heart, pulmonary edemaChest X-ray shows dilated heart, pulmonary edema
Pulmonary function tests indicate volume restriction, not airflowPulmonary function tests indicate volume restriction, not airflow
limitation.limitation.
BronchiectasiBronchiectasi
ss
Onset all agesOnset all ages
Chest X-ray shows lung infiltrate.Chest X-ray shows lung infiltrate.
Microbiological confirmation.Microbiological confirmation.

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B) Reduce Risk Factors:B) Reduce Risk Factors:
1.1. SmokingSmoking
2.2. Occupational exposureOccupational exposure
3.3. Indoor/Outdoor air pollutionIndoor/Outdoor air pollution

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Smoking Cessation:Smoking Cessation:
ASK:ASK: Identify all tobacco users at every visit.Identify all tobacco users at every visit.
ADVISE:ADVISE: Strongly urge all tobacco users to quit.Strongly urge all tobacco users to quit.
ASSESS:ASSESS: Willingness to make a quit attempt.Willingness to make a quit attempt.
ASSIST:ASSIST: Aid the patient in quitting.Aid the patient in quitting.
ARRANGE:ARRANGE: Schedule follow-up contact.Schedule follow-up contact.

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COPD Risk & Smoking CessationCOPD Risk & Smoking Cessation
Adapted from Fletcher C et al. Br Med J. 1977;1:1645–1648.
Stopped smokingStopped smoking
at 45 (mild COPD)at 45 (mild COPD)
Stopped smokingStopped smoking
at 65 (severe COPD)at 65 (severe COPD)

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C) Manage Stable COPD:C) Manage Stable COPD:
 Pharmacological therapyPharmacological therapy
 Long-term oxygen therapyLong-term oxygen therapy
 Pulmonary rehabilitationPulmonary rehabilitation
 NutritionNutrition
 SurgerySurgery

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Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
C) Manage Stable COPDC) Manage Stable COPD::

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Pharmacological TherapyPharmacological Therapy::
 The medications for COPD currently available can reduce
or abolish symptoms, increase exercise capacity, reduce
the number and severity of exacerbations, and improve
health status.
 At present, no treatment has been shown to modify the
rate of decline in lung function.
 The inhaled route is preferred.

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Pharmacological TherapyPharmacological Therapy:: BronchodilatorsBronchodilators
 Three types of bronchodilators are available:Three types of bronchodilators are available:
1.1. β-agonistsβ-agonists
2.2. Anticholinergic drugsAnticholinergic drugs
3.3. Methylxanthines.Methylxanthines.
β-agonistsβ-agonists
 Salbutamol (Ventolin)Salbutamol (Ventolin)
 Sameterol (Servent)Sameterol (Servent)
 Formoterol (Foradil)Formoterol (Foradil)
 TerbutalinTerbutalin
AnticholinergicsAnticholinergics
 Ibrtropuim bromideIbrtropuim bromide
(Atrovent)(Atrovent)
 Tiotropuim bromideTiotropuim bromide
(Spiriva)(Spiriva)
MethylxanthineMethylxanthine
 AminophyllineAminophylline
(Uniphylline,(Uniphylline,
Quibron, Theo SR)Quibron, Theo SR)

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Pharmacological TherapyPharmacological Therapy:: Inhaled CorticosteroidsInhaled Corticosteroids
 Types of Inhaled Corticosteroids (ICS):Types of Inhaled Corticosteroids (ICS):
 Beclomethasone dipropionate (Clenil)Beclomethasone dipropionate (Clenil)
 Fluticasone propionate (Flexotide)Fluticasone propionate (Flexotide)
 Budesonide (Meflonide)Budesonide (Meflonide)
 Ciclesonide (Alvesco)Ciclesonide (Alvesco)

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Pharmacological TherapyPharmacological Therapy:: Aerosol TherapyAerosol Therapy
 Three types of bronchodilators are available:Three types of bronchodilators are available:
1.1. Meter dose inhalerMeter dose inhaler
2.2. DiskusDiskus
3.3. TubuhalerTubuhaler
4.4. AerolizerAerolizer
5.5. HandihalerHandihaler
6.6. NebulizerNebulizer

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Pharmacological TherapyPharmacological Therapy:: Aerosol TherapyAerosol Therapy

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C) Manage Stable COPD:C) Manage Stable COPD:
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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Long-term Oxygen Therapy:Long-term Oxygen Therapy:
 Long-term oxygen therapy (LTOT) improves survival,
exercise, sleep and cognitive performance.
 Physiological indications for oxygen include an arterial
oxygen tension (Pa,O2) <55 mmHg guided by ABGs.
 The therapeutic goal is to maintain Sa,O2 >90% during
rest, sleep and exertion.
 If oxygen was prescribed during an exacerbation, recheck
ABGs after 30–90 days.

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Long-term Oxygen Therapy:Long-term Oxygen Therapy:

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RehabilitationRehabilitation
For the lungs to get more airFor the lungs to get more air
PURSED-LIP BREATHINGPURSED-LIP BREATHING
(like breathing out slowly into a straw)(like breathing out slowly into a straw)
INHALEINHALE EXHALEEXHALE

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RehabilitationRehabilitation
Sit comfortablySit comfortably
&&
relax your shouldersrelax your shoulders
Put one hand on yourPut one hand on your
abdomen. Now inhaleabdomen. Now inhale
slowly through yourslowly through your
nose. (Push yournose. (Push your
abdomen out while youabdomen out while you
breathe in)breathe in)
Then push in yourThen push in your
abdominal musclesabdominal muscles
and breathe out usingand breathe out using
the pursed-lipthe pursed-lip
techniquetechnique
For the lungs to get more airFor the lungs to get more air
DIAPHRAGMATIC BREATHINGDIAPHRAGMATIC BREATHING

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Nutrition:Nutrition:
 Weight loss & depletion of fat-free mass (FFM) may be observed inWeight loss & depletion of fat-free mass (FFM) may be observed in
stable COPD patients.stable COPD patients.
 Being underweight is associated with an increased mortality risk.Being underweight is associated with an increased mortality risk.
 Criteria to define weight loss are:Criteria to define weight loss are:
Weight loss >10% in the past 6 months or >5% in the past month.Weight loss >10% in the past 6 months or >5% in the past month.
 Nutritional therapy may only be effective if combined with exercise orNutritional therapy may only be effective if combined with exercise or
other anabolic stimuli.other anabolic stimuli.
UnderweightUnderweight BMI <21 kgBMI <21 kg··mm-2-2
;age >50 yrs;age >50 yrs
Normal weightNormal weight BMI <21–25 kgBMI <21–25 kg··mm-2-2
OverweightOverweight BMI <30 kgBMI <30 kg··mm-2-2
ObeseObese BMIBMI ≥≥30 kg30 kg··mm-2-2

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Lung Volume Reduction In EmphysemaLung Volume Reduction In Emphysema
↓
↓
↑
↑
↑
↑
↓
↑ ↑
↓ ↓
↓

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What's a COPD Exacerbation?What's a COPD Exacerbation?
 An exacerbation of COPD is defined as an event in theAn exacerbation of COPD is defined as an event in the
natural course of the disease characterized by a change innatural course of the disease characterized by a change in
the patients baseline dyspnea, cough, and/or sputum that isthe patients baseline dyspnea, cough, and/or sputum that is
beyond normal day-to-day variations, is acute in onset, andbeyond normal day-to-day variations, is acute in onset, and
may warrant a change in regular medication in a patientmay warrant a change in regular medication in a patient
with underlying COPD.with underlying COPD.
Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.

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Anthonisen's Typing of COPD ExacerbationAnthonisen's Typing of COPD Exacerbation
Cardinal SignsCardinal Signs
Worsening dyspnea, increase in sputum volume & purulenceWorsening dyspnea, increase in sputum volume & purulence
Other SignsOther Signs
Upper respiratory tract infection in past 5 days, fever without otherUpper respiratory tract infection in past 5 days, fever without other
apparent cause, wheezing, increase cough & increase respiratoryapparent cause, wheezing, increase cough & increase respiratory
rate or heart rate by 20% above baselinerate or heart rate by 20% above baseline
All 3 cardinal symptomsAll 3 cardinal symptoms Type 1 (SEVERE)Type 1 (SEVERE)
2 of 3 cardinal symptoms2 of 3 cardinal symptoms Type 2 (MODERATE)Type 2 (MODERATE)
1 of 3 cardinal symptoms1 of 3 cardinal symptoms Type 3 (MILD)Type 3 (MILD)

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Causes of COPD ExacerbationsCauses of COPD Exacerbations

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D) Manage Exacerbations:D) Manage Exacerbations:
Assessment of COPD ExacerbationsAssessment of COPD Exacerbations
Medical HistoryMedical History
 Severity of FEV1Severity of FEV1
 Duration of worsening or newDuration of worsening or new
symptomssymptoms
 Number of previousNumber of previous
(exacerbations/hospitalizations)(exacerbations/hospitalizations)
 ComordibitiesComordibities
 Present treatment regimenPresent treatment regimen
Signs of SeveritySigns of Severity
 Use of accessory respiratoryUse of accessory respiratory
musclesmuscles
 Paradoxical chest wall movementsParadoxical chest wall movements
 Worsening or new central cyanosisWorsening or new central cyanosis
 Peripheral edemaPeripheral edema
 Hemodynamic instabilityHemodynamic instability
 Signs of right heart failureSigns of right heart failure
 Reduced alertnessReduced alertness

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Indications for Hospitalization in AECB:Indications for Hospitalization in AECB:
 Marked increase in symptoms, e.g. sudden development of restingMarked increase in symptoms, e.g. sudden development of resting
dyspnea.dyspnea.
 Severe underlying COPDSevere underlying COPD
 Onset of new physical signs (e.g., cyanosis, peripheral edema)Onset of new physical signs (e.g., cyanosis, peripheral edema)
 Failure of exacerbation to respond to initial medical managementFailure of exacerbation to respond to initial medical management
 Significant comorbidities.Significant comorbidities.
 Frequent exacerbations.Frequent exacerbations.
 Newly occurring arrhythmias.Newly occurring arrhythmias.
 Diagnostic uncertainty.Diagnostic uncertainty.
 Older age.Older age.
 Insufficient home support.Insufficient home support.

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Indications for ICU admission in AECB:Indications for ICU admission in AECB:
 Severe dyspnea that responds inadequately to initialSevere dyspnea that responds inadequately to initial
emergency therapy.emergency therapy.
 Changes in mental status (Confusion, lethargy, coma).Changes in mental status (Confusion, lethargy, coma).
 Persistent or worsening hypoxemia (PaO2<40 mmHg),Persistent or worsening hypoxemia (PaO2<40 mmHg),
and/or severe/worsening hypercapnia (PaCO2>60 mmHg),and/or severe/worsening hypercapnia (PaCO2>60 mmHg),
and/or severe/worsening acidosis (pH<7.25) despiteand/or severe/worsening acidosis (pH<7.25) despite
supplemental oxygen & non-invasive ventilation.supplemental oxygen & non-invasive ventilation.
 Need for invasive mechanical ventilation.Need for invasive mechanical ventilation.
 Hemodynamic instability – need for vasopressors.Hemodynamic instability – need for vasopressors.

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Management of COPD ExacerbationManagement of COPD Exacerbation

60. Thank YouThank You