1. Airway Diseases
May 2013
Mekelle

2. Chronic Obstructive
Pulmonary Disease

3. COPD
Definition
 COPD- a disease state
characterized by airflow limitation
that is not fully reversible
 The airflow limitation is usually
progressive and associated with
an abnormal inflammatory
response of the lungs to noxious
particles or gases

4.  COPD includes
 Chronic bronchitis
 Emphysema
 Small airway disease
 COPD is the fourth leading cause
of death in the USA

5. Risk factors
 In the west
 Most important is cigarette smoking
 In developing countries
 Role of household fuels and indoor pollution have
important contribution.

6.  Occupational exposure
 Air Pollution
 Genetic- α-1 Antitrypsin Deficiency

7.  Regarding smoking
 The degree of damage to the lung (FEV loss) is
proportional to the amount of cigarettes smoked.
 Not all smokers develop COPD ( 15%) only; outlining
individual susceptibility
 Second hand (passive) smokers are also at risk

8.  Regarding asthma and COPD
 Dutch hypothesis – asthma and COPD are two diseases
in the same spectrum
 British hypothesis – different entities

10. Natural history
 Risk of mortality from COPD is closely associated with
reduced levels of FEV1
 FEV1 is a marker of obstruction

11.  Obstruction leads to hyperinflation.
 Hyperinflation leads to impaired diaphragmatic
function.

12. Pathology
 Cigarette smoke exposure may
affect the large airways, small
airways ( 2 mm diameter), and
alveolar space
 Large airway changes cause
cough and sputum (i.e. the
symptoms),
 small airways and alveolar

13.  Patterns
 Emphysema
 Defined in anatomic terms
 Destruction of the airways
 Pan or centri acinar pattern
 Chronic bronchitis
 Defined in clinical terms
 Based on symptoms

14. Diagnosis
 Consider COPD in any patient with combination of
these symptoms
 Dyspnea
 Chronic cough
 Chronic sputum production
 History of exposure to risk factors

15.  Physical examination is rarely
diagnostic in COPD
 Wheezes here and there

16.  With severe airflow obstruction-
 use of accessory muscles of respiration- tripod
position
 Cyanosis
 Systemic wasting
 Later on
 Signs of right sided heart failure
 Sometimes
 Features of systemic inflammation ( ischemic
heart disease osteoporosis ….), poor sleep

17. Laboratory findings
 CXR can be normal or some times shows some hyperinflation.
 Don’t rule out COPD b/c you have a normal CXR
 Pulm Function tests
 Low FEV1/FVC
 Low peak flow
 Some reversibility might be there in the obstruction

18.  Hct – for erythrocytosis
 ECG and Echo – for Cor pulmounale

19. Stage of COPD
 We use spirometric parameters
 GOLD staging

20. Management plan has four components
 Assess and monitor disease
 Reduce risk factors
 Manage stable COPD
 Manage exacerbations

21. Assess and monitor
 Stage of the disease
 Use spirometry and clinical features

22.  Risk factor reduction
 Smoking cessation

23. Stable COPD
 Bronchodilators – anticholinergics, beta agonist
 Inhaled corticosteroids- for patients with frequent
exacerbations
 Vaccination- influenza and pnuemococcal
 Non pharmacotherapies- pulmonary rehabilitation,
lung volume reduction surgery, lung transplantation

24. Treatment of exacerbations
 Exacerbations are a prominent
feature of the natural history of
COPD
 The frequency of exacerbations
increases as airflow obstruction
increases
 Exacerbations are commonly
considered to be episodes of
increased dyspnea and cough
and change in the amount and

25. Treatment includes-
 Bronchodilators
 Antibiotics
 Glucocorticoids
 Oxygen therapy
 Mechanical ventilation

26.  Home O2 therapy for resting and nocturnal
hypoxemia
 Lung volume reduction surgery

28. Asthma

29. Asthma
 Asthma is a syndrome characterized by
airflow obstruction that varies markedly,
both spontaneously and with treatment
 Narrowing of the airways is usually
reversible, but in some patients with
chronic asthma there may be an
element of irreversible airflow obstruction

30. Prevalence
 ~10–12% of adults and 15% of children affected by the
disease
 can present at any age
 peak age is 3 years

31.  Children with asthma – the asthma can subside as
they grow older.
 Adults with asthma-rarely so
 The severity of asthma does not vary significantly
within a given patient

32. Etiology
 Asthma is a heterogeneous disease with interplay
between genetic and environmental factors

33. Genetic predisposition suggested by-
 familial association of asthma
 high degree of concordance for asthma in identical
twins
The severity of asthma is also genetically determined
Environmental factors-in early life determine which
atopic individuals become asthmatic

34.  Atopy is the major risk factor for
asthma
 Allergic rhinitis and atopic dermatitis
 Allergens
 House dust mite

35.  Intrinsic Asthma or nonatopic asthma-~10% have
negative skin test to common inhalant allergens and
normal serum concentrations of IgE
 Usual adult onset

36. Pathogenesis
 Asthma is associated with a
specific chronic inflammation of
the mucosa of the lower airways
 The degree of inflammation is
poorly related to disease severity
and may be found in atopic
patients without asthma

37. Clinical features
 Wheezing,
 dyspnea, and
 Cough
These are variable, both spontaneously and with therapy
 Symptoms may be worse at night
 Typical physical signs are inspiratory, and to a great extent
expiratory, rhonchi throughout the chest

38.  Physical signs
 wheezes

39. Diagnosis
 Simple spirometry confirms airflow
limitation with
 a reduced FEV1,
 FEV1/FVC ratio,
 PEF
 Reversibility is demonstrated by a
>12% or 200 mL increase in FEV1 15
min after an inhaled short-acting
beta 2-agonist or, in some patients,
by a 2- to 4-week trial of oral

40.  Aims of treatment
 For the patient to have
 No or minimal symptoms esp. nocturnal
 No emergency OPD visits
 No frequent use of salbutamol
 No limitation of activity

41. Treatment
Two groups of drugs are used
 Bronchodilators
 beta 2-adrenergic agonists,
 anticholinergics, and
 theophylline
 Controllers
 Glucocorticoids
 Antileukotriens
 Cromones
 antiIGE
 Immunotherapy

42. Management of chronic asthma
 Avoid triggers
 Pharmacotherapy –stepwise
therapy
 Patient education
Goals
 Reduce impairment

43. Treatment of chronic
asthma
First try to determine severity.
This can be done by looking at
 Reported symptoms over the previous two to four weeks
 Night symptoms
 Current level of lung function (FEV1 and FEV1/FVC values)
 Number of exacerbations requiring oral glucocorticoids per
year
 Emergency visits

44.  Then stratify your patient by the severity to either
 Intermittent
 Mild persistent
 Moderate persistent
 Severe persistent
 Then institute therapy by the level of severity

46. Adjusting therapy
 Assess the status of the patient after 2-4 weeks of
therapy.
 If improving step down the treatment
 If not step up the ladder.

48. Management of acute severe asthma
 The best strategy for management of acute exacerbations of
asthma is early recognition and intervention, before attacks become
severe and potentially life threatening
 Treatment starts with assessment of severity of attack

49.  Look for simple clinical severity indicators
 Degree of dyspnea
 Can the patient finish a sentence?
 Degree of desaturation?
 Paradoxic breathing, accessory muscles
 Mental status
 Silent chest
 Level of V/S derangement

50. Provide
High flow oxygen therapy to keep
oxygen saturation >90%
High dose inhaled short acting beta
agonists are the main stay of therapy
(nebulized or via metered dose
inhaler)
Add inhaled anticholinergics if no

51.  Start systemic glucocorticoids if there is not an immediate and
marked response to the inhaled short-acting beta agonists
 Slow infusion of aminophylline may be effective in patients not
responding to high dose bronchodilators
 Make frequent (every one to two hours) objective assessments of the
response to therapy until definite, sustained improvement is
documented

52.  For patients with respiratory failure, it is necessary to intubate and
institute ventilation
 Consider antibiotics if signs of pneumonia

53. Refractory asthma
 A small proportion of patients (~5%
of asthmatics) are difficult to
control despite maximal inhaled
therapy
 Some of these patients will require
maintenance treatment with oral
corticosteroids
 The most common reason for poor
control of asthma is