COPD

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COPD

• (Bonus Lecture)Jim Pierce
• January 19, 2009

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COPD

• Chronic Obstructive Pulmonary Disease
• A group of diseases
• Intrathoracic Obstruction

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COPD
Asthma
Emphysema
Chronic Bronchitis
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COPD

• Clinical Diagnosis
• History
• Physical
• Physiologic Diagnosis
• Physiologic Testing
• Pathologic Diagnosis
• Anatomic Changes
• Pathologic (Histology) Changes

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COPD
Asthma
Emphysema
Physiologic Diagnosis
PathologicDiagnosis
Chronic Bronchitis
Clinical Diagnosis
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COPD

• Why are they grouped together?
• Intrathoracic Obstruction

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COPD

• Intrathoracic Obstruction
• Inspiration
• Transthoracic Pressure Gradient
• Airways Pulled Open
• Expiration
• Recoil or Transthoracic Gradient
• Airways Pushed Closed

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COPD

• Inspiration
• Relatively Normal Mechanics
• Expiration
• Abnormal Mechanics(Prolonged Expiratory Time)

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Hysteresis
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COPD

• Early
• Enough Expiratory Reserve
• Middle
• Expiratory Reserve Depleted
• Air Trapping
• Shift of Hysteresis Curve

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COPD
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COPD

• Late
• Expiratory Reserve Depleted
• Air Trapping causes Inefficiency
• Inefficiency so severe Active Exhalenecessary
  just to allow inhalation
• Increase in Work of Breathing

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COPD

• Very Late
• Air Trapping causes Inefficiency
• Air Trapping changes Diaphragmand Chest
  Dimensions
• Inefficiency so severe Active Exhalenecessary
  just to allow inhalation
• Dimensions Make Muscles functionSuboptimally Due
  to Angle and Length

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COPD

• Classic Description
• Barrel Chest
• Pursed Lip Breathing
• Shortness of Breath

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Barrel Chest
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Pursed Lip Breathing
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COPD

• Why does pursed lip breathing work?
• Fixed airway obstructioncauses air trapping
• Air trapping causesAirways to stay open

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COPD
Asthma
Emphysema
Physiologic Diagnosis
PathologicDiagnosis
Chronic Bronchitis
Clinical Diagnosis
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Chronic Bronchitis

• Clinical Diagnosis
• History
• Cough that leads to Sputum
• Almost Daily
• At least 3 months of year
• At least 2 years

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Asthma

• Physiologic Diagnosis
• Obstructive Physiologyon Pulmonary Function
  Tests
• Gets better with Smooth MuscleRelaxant
  (beta-adrenergic agonist)

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Asthma
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Emphysema

• Pathologic Diagnosis
• A Biopsy (or Autopsy)demonstrates destruction of
  alveoli and airway wallsleading to decreased
  elasticity

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Normal Lung versus Emphysema
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Normal Lung versus Emphysema
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COPD

• USA
• 14.2 Million People have COPD
• 12.5 Million Chronic Bronchitis
• 1.7 Million Emphysema
• Globally
• 9-10 of people 40 and older

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COPD

• Yearly Mortality, USA
• Males 50-80 200 per 100,000
• Females 50-80 80 per 100,000

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COPD

• The Truth
• No one has just one disease.
• There are components of
• Sputum Production and SOB
• Physiologic reversible obstruction
• Destruction of Lung Parenchyma

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COPD

• History
• Generally starts 40-50 yrs
• More frequently male
• Chronic Cough, worse in morning
• Sputum Clear or Carbonaceous
• 20 cigarettes a day for 20 years
• Shortness of breath, esp. on exertion

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COPD

• History
• Initially presents with either cough or acute
  illness (bronchitis/pneumonia)
• Over years, more frequent acute exacerbations /
  attacks
• By 60s, usually breathless on minimal exertion

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COPD

• Physical Exam
• Not very good at mild/moderatestage of illness
• VERY sensitive for severe illness
• Barrel Chest
• Weight loss
• Coughing
• Pursed Lip Breathing

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COPD

• Causes
• Smoking
• Air Pollution
• Airway Hyper-responsiveness
• Alpha1-Anti-Trypsin Deficiency

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Pathogenesis

• Inflammation
• Case 1
• Stimulus leads to local inflammatorymediators in
  airway
• Smooth Muscle responds to cytokines by increase
  in tone and reactivity
• This leads to chronic secretion stasis
• This leads to frequent acute attacks

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Pathogenesis

• Inflammation
• Case 2
• Stimulus leads to local inflammatorymediators in
  airway
• Smooth Muscle responds by hypertrophy and
  Connective tissue responds by Scar
• This leads to chronic secretion stasis
• This leads to frequent acute attacks

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Pathogenesis

• Inflammation
• Case 3
• Inflammatory mediators lead to mucus gland
  hypertrophy and increase in sputum
• This leads to sputum trapping and stasis, leading
  to more acute exacerbations

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Pathogenesis

• Inflammation
• Case 4
• Inflammatory mediators lead to an imbalance of
  proteinases (specifically MMP/TIMP imbalance)
• This leads to destruction of airway walls and
  pathophysiology of COPD

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Pathogenesis

• In all cases
• Chronic Inflammation withAcute Exacerbations
• Leads to some combination
• Secretions (Clinical)
• Airway Reactivity (Physiologic)
• Parenchymal Destruction (Pathologic)

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Diagnosis

• Threshold of DiagnosisMUST be related to therapy
• Examples
• Smoking Cessation
• Surgery

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Diagnosis

• History
• Physical
• Chest XRay / CT scan
• Arterial Blood Gas
• Pulmonary Function Tests
• Autopsy

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CXR
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CT Scan
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Pulmonary Function Tests
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Therapy

• Smoking Cessation
• Pulmonary Rehabilitation
• Medication
• Surgery

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Therapy

• Oxygen
• Bronchodilators (Beta-Agonist)
• Anticholinergic
• Anti-inflammatory
• Topical Steriod
• Oral/IV Steroid
• Anti-Leukotrienes
• Mucolytic
• Anti-Allergy
• Antibiotics

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Surgery

• Lung Volume Reduction Surgery
• NETT Trial

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NETT

• National Emphysema Treatment Trial
• 1996 Participating Centers announced
• 1997 Screening for entry begins
• July 2002 Recruitment Ends

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NETT

• After recruitment, patients
• Underwent exercise testing, pulmonary function
  testing, and radiography.
• Met with a Pulmonologist, Cardiologist, and
  Thoracic Surgeon
• Completed a 6-10 week courseof lung mechanical
  physiotherapy
• Exercise Protocol and Classes
• Oxygen and Medication Adjustment
• Perioperative Teaching
• Randomized to Bilateral LVRSversus continuing
  physiotherapy

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NETT

• Inclusion Criteria
• Diagnosis of Emphysema
• Met Radiologic and PFT criteria
• Accepted by all Physicians
• Severe Impact on Function

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NETT

• Exclusion Criteria
• Active smoker (within 4 months)
• Unstable angina or cardiac arrhythmia
• Heart attack within 6 months
• Had certain thoracic or cardiac surgeries or had
  another disease that was likely to interfere with
  participation in the trial or to reduce survival.

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NETT

• Medical Arm
• Continued Physiotherapy andOxygen/Medication
  managementby Center Pulmonologists
• Surgical Arm
• Bilateral LVRS
• Open (median sternotomy)and Thoracoscopic both
  allowed

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NETT

• 3777 people evaluated
• 1218 individuals selected
• 608 assigned surgery
• 610 assigned medical therapy only
• 95 received treatment as directed
• 99 surviving participants followup

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NETT

• Interim Outcomes
• May 2001
• Homogenous Disease identifiedas having less post
  operative benefit
• Severe Emphysema with Homogenous Disease noted to
  have increased risk of death
• Interim results published in NEJM
• Inclusion criteria adjusted

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NETT

• Final Outcomes
• Overall Long-term Mortality identical between
  Surgical and Medical arms
• 3 month Mortality 7.9 in surgery arm
• 3 month Mortality 1.3 in medical arm

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NETT

• Mostly upper-lobe emphysema
• With low exercise capacity
• More likely to live longer after LVRS
• More likely to function better after LVRS than
  after medical treatment
• With high exercise capacity
• No difference in survival between the LVRS and
  Medical participants
• Surgical group more likely to function better
  than medical group

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NETT

• Mostly non upper-lobe emphysema
• With low exercise capacity
• Similar survival and exercise ability after LVRS
  as after medical treatment
• Had less shortness of breath.
• With high exercise capacity
• Had poorer survival after LVRS than after medical
  treatment
• Both LVRS and Medical participants had similar
  low chance of functioning better

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NETT

• Identified and supported viaLevel One evidence
• Subset of Patients benefiting from surgery
• Subset of Patients harmed by surgery
• Efficacy of Medical Therapy

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Thanks!