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Prof E M Irusen, PhD Respiratory Division, Department of Internal Medicine, University of Stellenbosch & Tygerberg Academic Hospital President: SA Thoracic Society The New SA COPD Guideline (2011) A Critique

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Page 1: The New SA COPD Guideline (2011) A Critique - CRITICAL …old.criticalcare.org.za/images/presentations/Prof E M Irusen.pdf · The New SA COPD Guideline (2011) A Critique The best

Prof E M Irusen, PhDRespiratory Division, Department of Internal Medicine,

University of Stellenbosch

& Tygerberg Academic Hospital

President: SA Thoracic Society

The New SA COPD Guideline (2011)

A Critique

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The New SA COPD Guideline (2011)

A Critique

The best international guideline of all

(unbiased opinion)

Guidelines for the management of COPD-2011 (SATS Update)

SAMJ Jan 2011:101; 63-73.

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Key Message 1

Smoking is the major cause of COPD, but exposure to biomass fuels and tuberculosis are important additional factors

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Key Message 1

Caution in SA

Issues of lung development-background of deprivation

Concern –infectious aetiology (TB, HIV[ART])

Inclusion in clinical trials of non-smoking COPD- diff pathogenesis & pathology

- natural history

- complicate outcome analyses

(or extrapolating from existing data)

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Key Message 2

Spirometry is essential for the diagnosis and staging of COPD

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Lung Function (i)

Diagnosis of COPD: fixed ratio FEV1/FVC<0.7

Debate in current literature: LLN better

LLN-from epidemiology

- do not know if clinical diagnosis based on fixed ratio is different to one based on LLN.

Decreased fixed ratio more frequent in elderly and less so for younger subjects

Fixed ratio: simple, established (NB Guide!)

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Lung Function (ii)

Bronchodilator responsiveness (BDR)

Part of inclusion & exclusion criteria for COPD and asthma

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“Fixed Airways Obstruction”

Misconception: Reversibility Criteria of ATS define disease

BDR criteria (< 12%, 200ml):

Sensitivity of 55% for COPD

Post BD FEV1 < 80 % predicted

& FEV1/FVC ratio < 70%:

100% sensitive but 38% specific

•EM Irusen, DC Richter et al. Diagnostic value of post bronchodilator pulmonary

function testing to distinguish between stable, moderate to severe COPD and

asthma. Int J COPD 2008; 3(4): 693–699.

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Lung Function (iii)

Differentiating asthma from COPD impt

“splitter”

Natural history, expectations of therapy and package of care different

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Staging of COPD 2011

Stage 1

Mild

Stage 2

Moderate

Stage 3

Severe

Stage 4

Very severe

FEV 1After

bronchodilator

≥80% 50 - 80% 30 - 50% <30%

*or respiratory

failure

Dyspnoea MRC 2 MRC 3 - 4 MRC 5 MRC 5

6MWD >600 m 200 - 600 m <200 m

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Staging

Almost exclusively on severity of airflow limitation

Attempt to appreciate complexity: BODE

Composite score may fail to appreciate constituents

DOSE

Dyspnoea FEV1 Smoking Exacerb

2 3 3 2 10

1 2 1 6 10

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Staging

Natural history of COPD seen as the natural history of FEV1 decline

Change in FEV1- poor marker of development or progression of emphysema

Early pathological change in COPD not captured by spirometry

(cf asthma: clinical features + exacerb)

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Key Message 3

COPD is either undiagnosed or diagnosed too late so limiting the benefit of therapeutic interventions; performing spirometry in at-risk individuals will help establish an early diagnosis

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Key Message 4

Oral Corticosteroids are no longer recommended for maintenance treatment of COPD

Key Message 5 A therapeutic trial of oral corticosteroids to distinguish corticosteroid responders from non-responders is no longer recommended

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Key Message 6

Primary & secondary prevention are the most cost-effective strategies in COPD.

Bronchodilators are the mainstay of therapy

Key Message 7 Inhaled corticosteroids are recommended in

patients with frequent exacerbations and have a synergistic effect with bronchodilators in improving lung function, quality of life and exacerbation frequency

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Exacerbators

ECLIPSE

Presence or absence of exacerbator phenotype

Exac-known to influence course, major cost-driver

Better phenotypic guide- improved therapeutic decisions

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Stage 1:

Mild

Stage 2:

ModerateStage 3: Severe Stage 4: Very severe

Active reduction of risk factors (smoking cessation, influenza vaccination) and

rehabilitation

Add bronchodilators (short-acting beta-2 agonists or short-acting anticholinergic or

both) as needed or regularly and/or oral theophylline

Add regular treatment with long-acting anticholinergic or long-

acting beta-2 agonist or both

Add inhaled glucocorticosteroids especially for frequent

exacerbations (>2/yr)

Add long-term oxygen therapy if chronic

respiratory failure

Therapy at each stage of COPD

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Choice of therapy

LAMA LABA LABA/ICS

Choice based on cost

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When & how to start treatment

Current guides: maximal therapy for very severe disease

Trials: many severe subjects had stable disease

Mild/moderate may have more severe active disease (activity vs severity)

Are we intervening too late?

Mild vs early disease=not necessarily synonymous

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Conclusion

Heterogeneity of COPD in SA context

New biomarkers/imaging-improved understanding of therapeutic interventions

Current controversies and future perspectives in COPD

Alvar Agusti , Jørgen Vestbo AJRCCM epub June 16, 2011 as

doi:10.1164/rccm.201103-0405PP

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