COPD

• I have SOB X 3days• 62 yo/M with PMH COPD, HTN, DM-2,

PROSTATE CANCER, H/O CVA came with SOB X 3 days, productive sputum, whitish in color associated with chest pain which increases during inspiration.

• H/o of preceding common cold(URTI) but no h/o fever.

s

• Meds-metformin,lasix,nph-insulin,lisinopril,

• Atenolol,cardura, zocor, nexium.• Allergy-None• Smoking+• Etoh+ve• No drugs

• ER vitals-98/92/40//163/84—98%• Floor vitals-98/88/22//135/65—98%• Pt in mild distress• No JVD,No edema• Chest-Use of accessory muscles , B/L

diffuse wheezing,crepts+• CVS/PA/EXT-wnl

• CBC-WBC-11.4,H/H-13.9/42.1, PLT-316

• BMP-N/K-140/4.6,CL/HCO3-104/27• -BUN/CR-15/1, B.Sugar-122• LFT-3.5/6.7/18/20/0.4/113• CXR-Interstistial lung disease• Blood cx-p

Chronic Obstructive Pulmonary Disease (COPD)

Morning reportPGY-2Kanth, Rajan

Learning Objectives: To be able to…

• Conduct a relevant P.E. and interpret the findings in a patients with suspected COPD

• Identify medication and non-medication interventions for managing COPD

• Identify steps in the outpatient medical management for acute exacerbation of COPD and criteria for hospitalization

Overview

•Definition, epidemiology and pathophysiology

•Diagnsosis and Assessment (2 cases)

•Managemento Risk factor reductiono Stable chronic COPDo Acute exacerbations of COPD

Definition of COPD*

• COPD is a preventable and treatable chronic lung disease characterized by airflow limitation that is not fully reversible.

• The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung.

* Adapted from the Global Initiative for Chronic Obstructive Lung Disease 2007

Epidemiology of COPD • COPD is a leading cause of mortality

worldwide and projected to increase in the next several decades.

• COPD mortality trends generally track several decades behind smoking trends.

• In the US and Canada, COPD mortality for both men and women have been increasing.

• In the US in 2000, the number of COPD deaths was greater among women than men.

Percent Change from 1965 in Age-Adjusted Death Rates, U.S., 1965-1998

0

0.5

1.0

1.5

2.0

2.5

1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998

–59% –64%–35%

+163% –7%

CoronaryHeartDisease

Stroke Other CVD COPD All OtherCauses

Source: NHLBI/NIH/DHHS

COPD Mortality by Gender,U.S., 1980-2000

Number Deaths x 1000

Source: US Centers for Disease Control and Prevention, 2002 – cited in GOLD 2007

Risk Factors for COPD

Nutrition

Infections

Socio-economic status

Aging Populations

Pathophysiology of COPD

• Chronic inflammation, bronchial wall edema, mucous secretion, hyperinflation and air trapping

• Increase in proteinases compared to antiproteinases and in free radicals leading to parenchymal destruction

• Changes in pulmonary vasculature leading to ventilation-perfusion mismatching, pulmonary hypertension, cor pulmonale

LUNG INFLAMMATION

COPD PATHOLOGY

Oxidativestress Proteinases

Repair mechanisms

Anti-proteinasesAnti-oxidants

Host factorsAmplifying mechanisms

Cigarette smokeBiomass particlesParticulates

Source: GOLD 2007

Pathogenesis of COPD

Disrupted alveolar attachments

Inflammatory exudate in lumen

Peribronchial fibrosisLymphoid follicle

Thickened wall with inflammatory cells- macrophages, CD8+ cells, fibroblasts

Changes in Small Airways in COPD Patients

Source: COLD 2007

Alveolar wall destruction

Loss of elasticity

Destruction of pulmonarycapillary bed

↑ Inflammatory cellsmacrophages, CD8+ lymphocytes

Source: GOLD 2007

Changes in Lung Parenchyma in COPD

Chronic hypoxia

Pulmonary vasoconstriction

MuscularizationIntimal hyperplasiaFibrosisObliteration

Pulmonary hypertension

Cor pulmonale

Death

Edema

Pulmonary Hypertension in COPD

Source: GOLD 2007

Diagnosis and Assessment of COPD

Patient LG

• 54 year old man with a 80+ pack-year smoking history, presents with dyspnea while climbing stairs and an occasional, non-productive cough

•What would you look for/expect on exam?

Patient LG : Examination

• Diminished breath sounds on auscultation

• Forced expiratory time of >6 seconds

• Decreased I/E ratio• Increased thoracic circumference

and decreased change with respiration

• Increased resonance to percussion

Patient EC

• 62 year woman with 40 p-yr history presents with chronic cough for 3 months, productive of clear to light yellow phlegm

•What would you look for/expect on exam?

Patient EC

• Rhonchus breath sounds• 1+ ankle edema

Patients LG and EC

•What tests would you order?

Diagnosis and Assessment

• 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.

Spirometry: Normal and Patients with COPD

Classification of COPD Severityby Spirometry post

Bronchodilator*Stage I: Mild FEV1/FVC < 0.70 FEV1 > 80% predicted Stage II: Moderate FEV1/FVC < 0.7050% < FEV1 < 80% predicted

Stage III: Severe FEV1/FVC < 0.7030% < FEV1 < 50% predicted

Stage IV: Very Severe FEV1/FVC < 0.70FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure

* Adapted from the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2007

Patient LG : Test Results

• CXR – Hyperinflation and increased lucency

• FEV1/FEV=.55• FEV1=40%

Patient EC: Test Results

• CXR – peribronchial thickening• FEV1/FEV=.60• FEV1=55%

Patient LG

• 54 year old man with a 80+ pack-year smoking history, presents with dyspnea while gardening, occasional, non- productive cough

•What is his condition?

Patient EC

• 62 year woman with 40 p-yr history presents with chronic cough for 3 months, productive of clear to light yellow phlegm

•What is her condition?

Differential Diagnosis: COPD 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

Management of COPD

•Relieve symptoms •Prevent disease progression•Improve exercise tolerance•Improve health status•Prevent and treat complications•Prevent and treat exacerbations•Reduce mortality

GOALS of COPD MANAGEMENT

General Points

• Only smoking cessation and O2 therapy (when indicated) have been shown to prolong survival

• Other therapies aimed at relieving symptoms, improving quality of life, reducing exacerbations and need for hospitalizations

Risk Factor Reduction

• Smoking cessation (prolongs survival)

• Avoid exposure to second hand cigarette smoke

• Reduction of exposure to indoor and outdoor pollution

• Influenza vaccine• Pneumococcal vaccines

Brief Strategies to Help the Patient Willing to Quit Smoking

• ASK Systematically identify all tobacco users at every visit.

• ADVISE Strongly urge all tobacco users to quit. (even a brief (3-minute) period of counseling to quit results in smoking cessation in 5-10% of patients.)

• ASSESS Determine willingness to make a quit attempt (stages of change).

• ASSIST Aid the patient in quitting.• ARRANGE Schedule follow-up contact.

IV: Very SevereIII: SevereII: ModerateI: Mild

Therapy at Each Stage of COPD

• FEV1/FVC < 70%

• FEV1 > 80% predicted

• FEV1/FVC < 70%

• 50% < FEV1 < 80%

predicted

• FEV1/FVC < 70%

• 30% < FEV1 < 50% predicted

• FEV1/FVC < 70%

• FEV1 < 30% predicted

or FEV1 < 50% predicted plus chronic respiratory failure

Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation

Add inhaled glucocorticosteroids if repeated exacerbations

Active reduction of risk factor(s); influenza vaccinationAdd short-acting bronchodilator (when needed)

Add long term oxygen if chronic respiratory failure. Consider surgical treatments

Treatment of Stable COPD: Bronchodilators

• Bronchodilator medications are central to the symptomatic management of COPD (Evidence A).

• They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations.

• The principal bronchodilator treatments are ß2- agonists and anticholinergics used singly or in combination

• Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators

Treatment of Stable COPD: Inhaled Glucocorticoids

• Consider adding regular treatment with inhaled glucocorticosteroids to bronchodilator treatment is for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III and IV) and repeated exacerbations (Evidence A).

• An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than the individual components (Evidence A).

Treatment of Stable COPDOther Medications

• Chronic oral Prednisoneo Use in chronic COPD is controversial. No effect on

survival. May improve symptoms and reduce hospitalizations in some patients already at maximum treatment

• Mucolytics & Expectorants (SSKI, guafenesin)o Relives symptoms from copious, viscous

secretions• Oral Theophylline

o If inhalers not sufficiento Side effects common

Treatment of Stable COPD: Home Oxygen Therapy

• > 15 hours/day reduces mortality • Criteria for O2 therapy

o Pa O2 < 55 mm Hg (O2 saturation < 88%) at rest or during exercise or sleep or

o Pa O2 < 60 mm Hg and hematocrit >52%• Bipap when sleeping may provide

additional improvement

Treatment of Stable COPD:Pulmonary Rehabilitation and

Patient Education• Typically includes exercise,

education and psychological support • Shown to improve symptoms,

exercise capacity, reduce use of medical care, reduce anxiety and depression

Treatment of Stable COPD:Surgery

• Primarily for patients with emphysema

• Few RCTs, no evidence for improvement in mortality but can relieve symptoms

• Improves QOL and exercise capacity in patients with primarily upper lobe disease, low exercise capacity, and FEV1 between 20 and 30%

• Lung transplantation

Treatment of Acute Exacerbations of COPD

Acute Exacerbations of COPD

• The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified.

Outpatient Treatment of Acute Exacerbations: Bronchodilators

•Inhaled bronchodilators (particularly inhaled ß2-agonists with or without anticholinergics) are effective treatment for exacerbations of COPD (LOE: A).

Outpatient Treatment of Acute Exacerbations: Prednisone

•Oral prednisone is effective treatment for exacerbations of COPD (LOE: A).

Outpatient Treatment of COPD Exacerbation: Antibiotics

• Surprisingly little evidence of efficacy

• Typically use in patients with purulent sputum or other signs of infection

• Amoxicillin, doxycycline, azithromycin, trimethoprim-sulfa are reasonable first line choices

Indications for Hospital Admission of Patient with Acute

Exacerbation• Resting dyspnea after initial treatment• Lack of response to initial treatment• Significant co-morbid conditions)• Severe underlying COPD/prior ICU

ventilation for exacerbations• New physical signs (e.g., new peripheral

edema)• Diagnostic uncertainty• Insufficient home support

Inpatient Treatment of Acute Exacerbations

• Oxygen to keep O2 sat >90%• Nebulizer treatments with bronchodilators • Steroids (LOE A)

o (40 to 60 mg daily for 7 to 14 days, IV or PO)• Antibiotics (LOE B)–

o Typically ceftriaxzone (1 gram IV q 24 h) + doxycycline (100 mg po q 12 h) at SFGH

• Fluids

The End

Thank you