CHRONIC OBSTRUCTIVE PULMONARY DISEASE

A General Overview

ACADEMIC HALF DAY

DECEMBER 2, 2003

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

A General Overview

ACADEMIC HALF DAY

DECEMBER 2, 2003

COPD OUTLINE

• Facts• Definition• Pathophysiology• Diagnosis• Treatment

– Chronic disease– Acute exacerbations

• Prevention• Other issues

• Major cause of death and disability• 4th leading cause of death in men

– 5544 deaths in 1999

• 5th leading cause of death in women– 3974 deaths in 1999

• Mortality rates in women have increased by 53% and are still rising

COPDGENERAL FACTS

COPDGeneral Facts

• 7th most common cause of hospitalization in men , 8th in women (2001/2002)

• Risk of rehospitalization is approx 40%• Accounts for 14 MILLION physician visits/year

(US)• Health cost $1.67 BILLION/year (CAN)

– Does not include physician costs or community based programs

COPD FACTS

• 3.9% Canadians have COPD (466,812) ??

• UNDERESTIMATE– Self reported– Not diagnosed until late– More than 50% Canadians who have COPD

remain undiagnosed

COPDCTS Definition

• Respiratory disorder• Caused mostly by smoking (90% cases)• Characterized by:

– Progressive, partially reversible airway obstruction

– Systemic manifestations – Increasing severity of exacerbations

COPD – Pathophysiology

• Not completely understood• Cigarette smoke main trigger• Chronic inflammation of cells lining bronchial tree• Leads to airway narrowing

– Edema– Excess mucus production– Decreased ciliary function

COPD - Pathophysiology

• EXPIRATORY FLOW LIMITATION– Hallmark of COPD

• Compromises ability of pt to expel air

• Hyperinflation and air trapping occurs

• Rib cage reconfigures over time

• Ventilatory muscles adapt temporarily

COPD - Pathophysiology

• V/Q mismatch develops– Regional inequalities throughout the lungs

• O2 uptake and CO2 elimination impaired

• Vasoconstrictor effects of chronic hypoxia

• Pulmonary hypertension

• Right heart failure

COPD - Diagnosis

• Early stages of COPD are silent – therefore patients do not often present

• Patients often present when SOB starts to affect their QOL or more commonly during and acute exacerbation

• Dyspnea on mild exertion = 50% loss of lung capacity

• Family doctors usually experience patients early in the course of the disease

• We have the opportunity to make the most impact

COPD – DiagnosisHISTORY

• Common presentation is DYSPNEA– Patients often attribute to “getting older”

• Wheezy

• Chest tightness/pain

• Cough/Sputum production

• Baseline functional ability

HISTORY (continued)

• ROS:• fatigue, depression, insomnia, confusion• Cardiac risks• PMH: frequency and severity of exacerbations,

past treatments, other lung diseases• Med history and compliance/proper technique• SMOKING – pack years, # of quitting attempts

HISTORY (continued)

• Occupational exposure • Allergies• FHx :

– Alpha-1 antitrypsin deficiency– Chronic lung disease

• SHx: Social supports, impact on QOL

MRC Dyspnea Scale

• Grade 1 – breathlessness with strenuous exercise• Grade 2 – SOB when hurrying on the level or

walking up a slight hill• Grade 3 – walks slower than people of the same

age on the level OR stops for breath when walking at own pace on the level

• Grade 4 – stops for breath after walking 100 yards

MRC Dyspnea Scale

• Grade 5 – too breathless to leave the house when dressing

• Scale helps:

• To identify patients with poor QOL

• To provide prognostic information

• To stratify disease severity (with PFTs)– See handout

COPDPhysical Exam

• Important, but not usually diagnostic• Signs of airflow obstruction are usually not

present until SIGNIFICANT lung impairment is present

• Advanced disease – signs of lung hyperinflation, right heart failure, muscle wasting, clubbing

COPD - Investigations

• PULMONARY FUNCTION TESTS– The best objective measurement of pulmonary

impairment

– Necessary for establishing diagnosis

– Not good in the acute setting

– Very underutilized

– Sensitive to small changes in flow limitations

– Mass screening of smokers not recommended

SPIROMETRYWho to screen?

• Smokers or ex-smokers > 40 years of age

• Patients with persistent cough and sputum production

• Patients with persistent respiratory infections

• Patients with progressive activity-related SOB

Spirometry Diagnostic Criteria

• Postbronchodilator forced expiratory volume in 1 second (FEV1) of LESS than 80% of the predicted normal value

AND…

• Ratio of FEV1 to forced vital capacity (FVC) of less than 0.70

COPDOther Tests

• CXR – often required to R/O cormorbidities• High resolution CT – not routine• Arterial Blood Gas

– FEV1<40% predicted– often useful in acute setting

• Alpha1- antitrypsin deficiency screening– COPD in patient <45 years of age– strong Family History

MANAGEMENTCOPD

• Management:1) Smoking cessation2) Chronic stable patients3) Acute exacerbations

• EVEN IN SEVERE CASES OF COPD THERAPY IS POSSIBLE AND CAN IMPROVE QOL

SMOKING CESSATION

• The only intervention shown to slow the progression of COPD

• Small improvements in FEV1

• Eventually the rate of decline in lung function returns to the same level of a non-smoker

• Brief interventions are effective

Chronic Stable COPDTreatment

• Patient & Family education• Pharmacotherapy

– Bronchodilators– Steroids

• inhaled• oral

• Oxygen• Pulmonary Rehabilitation• Surgery

Pharmacotherapy

• BRONCHODILATORS

• The mainstay of drug therapy for COPD

• Decrease airway muscle tone

• Three types (short & long acting):– Anticholinergics (inhaled)– Beta-2 agonists (inhaled) – Methylxanthines (po)

BronchodilatorsShort Acting (SABD)

• Improve pulmonary function/SOB/exercise performance

• Do not affect QOL• Combination SABD’s (Beta-agonists and anti-

cholinergics) produce better bronchodilation• For patients with MILD symptoms

– SOB on exertion

BronchodialtorsLong Acting (LABD)

• For patients who still have symptoms on SABD’s (MODERATE disease)

• More sustained effect on PFT’s, chronic SOB and QOL

• Anticholinergic – Tiotropium (OD)• Beta-2 agonists – Fomoterol, Salmeterol

• Early evidence these may prolong time between exacerbations

Bronchodilators

• Moderate – severe COPD– Tiotropium (long-acting anticholinergic)– LABD– SABD prn– If still severe – may benefit from theophylline

• Weak bronchodialtor• Monitor levels• Interactions• Side effects

Steroids

• Inhaled and oral• Not recommended as first line therapy• No consistent effect on decreasing inflammation• Consider inhaled form in those with mod-severe

disease• Consider in those who have maximal

bronchodilator therapy

ORAL STEROIDS

• Long term oral steroids not recommended• High risk for

– Cataracts– Muscle weakness– Hypertension– Osteoporosis– Diabetes

OXYGEN

• Definite survival benefit in severe COPD

• Should be considered for patients with:

1. Severe hypoxemia (PaO2 < 55mmHg)

2. PaO2 <60 mmHg + bilateral ankle edema, cor pulmonale or Hct >50%

Don’t smoke with your oxygen on!!!

Pulmonary Rehabilitation

• Pts with COPD are often deconditioned

• Leads to muscle wasting – contributes to dyspnea

• Should encourage all pts to remain active

• Formal rehab programs improve QOL and dyspnea

SURGERY

• Volume reduction surgery

• Lung transplant

• Have been used for severe COPD

• No clear cut guidelines

Don’t forget

• Flu shot

• Pneumovax

• Vaccinations help prevent exacerbations!

Acute ExacerbationsCOPD

• “Sustained worsening of dyspnea, cough or sputum production leading to an increase in the use of maintenance medications and/or supplementation with additional medications”.

• Usually 2-3 per year – 50% not reported to physicians

• Most common cause of admissions, ER visits and death in COPDers.

Acute ExacerbationsCOPD

• CXR – not necessary for diagnosis but may be needed to R/O things that can cause AE– CHF, pneumonia, pneumothorax

• Spirometry not useful in acute setting• ABG – useful• Fever uncommon

• Consider pneumonia if present

Acute ExacerbationsManagement

• Oxygen

• Bronchodilators

• Steroids

• Antibiotics

• Non-invasive PPV

OXYGENAcute Exacerbations

• Excess O2 should be avoided

• However should not be withheld for fear of hypercapnea

• O2 to maintain PaO2 at approx 60 mmHg

• Difficult to make decisions regarding long term O2 during AE – 50% will no longer meet criteria for home O2 in 1 month

BronchodilatorsAcute Exacerbations

• No difference in efficacy between Beta2-agonists and anticholinergics

• Some benefit from combination• MDI’s vs nebulizers:

– No difference in pulmonary function outcome

• Don’t:– Start theophylline – Use long-acting agents

SteroidsAcute Exacerbations

• Oral definitely has a role• Faster recovery / shorter hospitalizations• May prolong time to next relapse• Exact dose?• 5-14 days recommended• Question of whether pts with mild disease benefit• ?health consequences of frequent short courses• Role of inhaled steroids in acute disease not well

defined

ANTIBIOTICSCOPD

• Approx 50% exacerbations due to infectious etiology

• Mostly bacterial

• Especially helpful in severe exacerbations

• Purulent sputum more likely to benefit

• Antibiotic resistance an issue

Common Bugs

• Mild-moderate exacerbations:• Streptococcus pneumonia• Haemophilus influenzae• Moraxella catarrhalis• Mycoplasma pneumoniae• Viruses• Severe exacerbations:• Pseudomonas sp.• Gm –ve enteric bacilli

Non Invasive Positive Pressure Ventilation

• For persistent acidosis despite adequate bronchodilators (ph<7.3)

• Decrease morbidity/mortality• Decreases the need for intubation/ventilation• Decreases length of ICU stay• Requires awake/alert/cooperative/hemo stable pt• If no improvement in 4 hours unlikely to benefit

Other Issues

• WHEN TO REFER TO SPECIALIST:• Diagnosis uncertain• Symptoms are severe• Symptoms do not correlate with PFT’s• Early onset• Accelerated loss of function (FEV1 decline

>80ml/year over 2-year period)• Consideration for surgery

End of life issues

• QOL of patients with COPD is often poor (especially end stage disease)

• Mortality during acute exacerbations 10-20%

• Discussions of end-of-life issues often occur late (and in the ICU)

• Recommend targeting patients with advanced disease & have survived ICU

COPDSUMMARY

• COPD is preventable and treatable

• Most not diagnosed until late – prevention is paramount

• Spirometry is indicated for target groups

• Smoking cessation is the only intervention shown to slow disease progression