Overview of COPD. Disease, Diagnosis and treatment

1. COPD
Disease, Diagnosis and Treatment

2. EPIDEMIOLOGY
• 4th
leading cause of death (Globally)
• 8th
leading cause of poor health (disability adjusted life years) -
Globally
• 5% of all global deaths in 2021 – 90% of COPD deaths below 70 yrs in
LMIC
• High income countries: 70% cases of COPD – secondary to tobacco
smoking
• LMIC:30-40% COPD cases secondary to smoking. In the remaining -
Household air pollution is a major risk factor

3. EPIDEMIOLOGY
PAKISTAN
• Current data suggests: Prevalence in > 40 yrs: 9-10 %
• BOLD epidemiologic study in 2010: 11.7%
• Meta analysis 2018: Pak has highest prevalence in EMRO region
• Increasing prevalence due to increasing smoking trends

4. INTRODUCTION
COPD is a common, preventable and treatable disease that is
characterized by persistent respiratory symptoms and airflow limitation
that is due to airway and/or alveolar abnormalities usually caused by
significant exposure to noxious particles or gases and influenced by
host factors including abnormal lung development.

5. RISK FACTORS
1. Smoking
2. Indoor and outdoor air pollution
3. Genetic predisposition
4. Infections
5. Socioeconomic status
6. Age
7. Gender

6. SMOKING- PASSIVE
Contribution of exposure to passive smoking
Prenatal exposure
• o Reduced lung development
• o Low birth weight
Childhood
• o Decreased lung growth
• Adulthood
• o Accelerated decline in lung function
• o Lung destruction
• o Impaired lung repair

7. SMOKING
• Smokers suffer an irreversible loss of 4.4-10.4 ml in FEV1 per pack year smoked
• Greater the total no of cigarettes – greater the risk of COPD development
• PACK YEARS
• Pack year = Number of cigarettes smoked per day x Number of years of
smoking/20
• Loose tobacco is quantified as tobacco smoked in “ounces per week”, which
can be converted Into pack years
• Pack years = Ounces of loose tobacco per week × 2/7 × number of years
smoked

8. SMOKING
FUN FACT
• 25-45% of COPD patients are life long non smokers.
• Less than 50% of heavy smokers DO NOT develop COPD

9. PATHOGENESIS
• In healthy individuals, the lung shows an inflammatory response to
noxious/irritant particles.
• In COPD this response is modified and pathological changes occur in
airways, the lung parenchyma and the pulmonary vasculature.
• Oxidative stress secondary to smoke
• Protease-Antiprotease imbalance: Inactivation of anti-proteinases
leading to destruction of connective tissue
• Predominance of anti inflammatory cells: macrophages, activated
neutrophils and lymphocytes, eosinophils in mixed COPD/Asthma pts

10. PATHOGENESIS
• CHRONIC BRONCHITIS
• Chronic cough and sputum for at least 3 months a year for 2
consecutive years.
• (it is now known that chronic bronchitis is a distinct entity that can
exist with or without airflow limitation)
• EMPHYSEMA
• Abnormal permanent enlargement of airspaces distal to the terminal
bronchioles accompanied by destruction of their walls

11. PATHOGENESIS
EMPHYSEMA: Alpha 1 anti tyrpsin deficiency

12. PATHOGENESIS

13. SYMPTOMS
• Dyspnea
• Cough and sputum
• Wheezing and chest tightness
• Atypical chest pain
• Fatigue
• Psychiatric morbidity esp depression
• Poor sleep quality
• Wt loss ( hall mark of severe disease, poor prognosis)

14. SYMPTOMS
DYSPNEA
• The hallmark of COPD is chronic progressive dyspnea.
• Major cause of disability and anxiety associated with the disease. The
breathlessness increases with exertion, and it is there all the time.
• It can be assessed by using modified Medical Research Council
(mMRC) Dyspnea Scale

15. SYMPTOMS

16. SYMPTOMS
COUGH AND SPUTUM
• Can be non productive. Worse in the morning. Small in amount and
whitish in color
• Copious amount of sputum: Underlying Broncheictasis possible
• Persistent purulent sputum: bacterial colonization of airways
(Pseudomonas common)
• Cough syncope, cough fractures of ribs may also occur

17. SIGNS
• Uniformly diminished breath sounds
• Prolonged expiratory phase of breathing
• Purse-lipped breathing
• Use of accessory muscles of breathing
• Barrel-shaped chest
• Horizontal ribs with prominent sterna angle and wide sub-costal angle
• Inspiratory tracheal tug
• Hoover’s sign – horizontal position of the diaphragm pulls in the lower ribs during inspiration
• Decreased hepatic and cardiac dullness on percussion
• Signs of pulmonary hypertension (RV heave, loud P2, gallop rhythm, pansystolic
murmur, pitting pedal edema)
• Tender pulsatile liver
• Prominent v wave of jugular venous pulse

18. SIGNS

19. SIGNS

20. DIAGNOSIS- INVESTIGATIONS
• Spirometry: Confirmation + Assessment of severity + Follow up
assessment
• CXR
• Six minute walk test
• Pulse oximetry
• ABGs
• CT CHEST
• CBC
• ECG

21. DIAGNOSIS- CXR
• It is useful in excluding other
diagnosis.
• Increase lung volumes
• Flattened diaphragm
• Tubular heart (narrowed and
more vertical cardiac silhouette)
• Hyperlucency of lung fields
• Bullae

22. DIAGNOSTIC TOOLS – ASSESSMENT OF
SEVERITY
The following aspects of the disease must be assessed separately.
• The presence and severity of spirometric abnormality
• Current severity of symptoms
• History of exacerbations and future risk
• Presence of co-morbidities

23. DIAGNOSTIC TOOLS – ASSESSMENT OF
SEVERITY
• Spirometric classification of severity of COPD
• mMRC Dyspnea scale
• Combined Assessment Test (CAT Score)
• ABCD TOOL

24. CURRENT SEVERITY OF SYMPTOMS
• Breathlessness being the cardinal symptom of the disease, one tool to
assess severity of symptoms is mMRC dyspnea scale.
• But as a matter of fact COPD impacts patients beyond just dyspnea.
So combined assessment test (CAT) can be used to measure health
status in COPD.

25. COMBINED ASSESSMENT TEST

26. COMBINED ASSESSMENT TEST

27. HISTORY OF EXACERBATION AND FUTURE
RISK
COPD exacerbation is defined as:
• “An acute worsening of respiratory symptoms that require additional
therapy.”

28. HISTORY OF EXACERBATION AND FUTURE
RISK
• In 1987 Anthonisen gave the classic definition
• Describing three levels of exacerbation based on patient’s
symptomatology.
• This is the criteria recommended to be used in describing the
exacerbations.
• It is used to decide the need ofantibiotic therapy.

29. HISTORY OF EXACERBATION AND FUTURE
RISK

30. HISTORY OF EXACERBATION AND FUTURE
RISK

31. HISTORY OF EXACERBATION AND FUTURE
RISK
PREDICTORS OF FUTURE EXACERBATIONS RISK
• Two or more exacerbations in the past year
• History of hospitalization due to COPD in the past year
• Severe COPD, equivalent to GOLD 3 or 4
• Increased blood eosinophil count
• Use of LABA alone
• Non compliance to treatment

32. ASSESSMENT OF COMORBIDS
COPD is a systemic disease. These conditions can increase the risk of
hospitalizations and mortality in COPD. So co-morbid illnesses should
be looked for and treated promptly.

33. ABCD TOOL
• The Global Initiative for Chronic Obstructive Lung Disease (GOLD)
ABCD assessment tool is used to classify COPD patients into four
groups (A, B, C, D) based on symptom burden, exacerbation risk and
spirometry to guide personalized treatment.
• It helps clinicians tailor therapy such as choosing long acting
bronchodilators for high risk patients (C/D)

34. ABCD TOOL
KEY COMPONENTS OF ABCD TOOL
• Symptoms: Assessed using the COPD Assessment Test (CAT) or modified Medical Research Council (mMRC)
scale.
• Exacerbation History: Frequency of exacerbations and hospitalizations in the past year.
Categories:
• Group A: Low symptom burden, low risk (0-1 moderate exacerbations, no hospitalizations).
• Group B: High symptom burden, low risk.
• Group C: Low symptom burden, high risk (≥ 2 moderate exacerbation or ≥ 1 hospitalizations).
• Group D: High symptom burden, high risk.
Transition to ABE: Newer guidelines have begun shifting to an "ABE" classification for better treatment targeting.

35. ABCD TOOL

36. ABE TOOL
KEY COMPONENTS OF ABE TOOL
• Symptoms: Assessed using the COPD Assessment Test (CAT) or modified Medical Research Council (mMRC)
scale.
• Exacerbation History: Frequency of exacerbations and hospitalizations in the past year.
CATEGORIES
• Group A: Low symptom burden, low risk (0-1 moderate exacerbations, no hospitalizations).
• Group B: High symptom burden, low risk.
• Group E: Any symptom level, high risk (≥ 2 moderate exacerbation or ≥ 1 hospitalizations).

37. GOLD ABE ASSESSMENT TOOL
E
A B
mMRC 0-1
CAT < 10
mMRC >/=2
CAT >/=10
SYMPTOMS
2 OR >2 MODERATE
EXACERBATIONS
1 OR >1 LEADING TO
HOSPITALIZATION
0-1 MODERATE
EXACERBATIONS (NOT
LEADING TO
HOSPITALIZATION
Spirometrically
confirmed diagnosis
Assessment of air flow
obstriction
Assessment of Sx/risk
of exacerbation
EXACERBATION Hx
(PER YEAR)

38. DIFFERENTIAL DIAGNOSIS
The main differential diagnosis includes:
• Asthma
• Bronchiectasis
• Tuberculosis and post-tuberculosis sequelae
• Heart failure
• Interstitial lung diseases
A careful history, clinical examination, and investigations can help rule out these
close mimics ofCOPD.

39. MANAGEMENT OF STABLE COPD
Bronchodilators are first line therapy for COPD.
Pharmacologic management can reduce symptoms, improve exercise
capacity, reduce the risk of exacerbations, improve overall health status
and reduce mortality.

40. MANAGEMENT OF STABLE COPD

41. MANAGEMENT OF STABLE COPD

42. MANAGEMENT OF STABLE COPD

43. MANAGEMENT OF STABLE COPD
KEY POINTS
• Choice of inhaler device should be tailored individually (depending on access, cost,
prescriber, patient’s preference and ability.
• Teach inhaler technique technique and recheck on each visit.
• Check inhaler technique and compliance before changing medicines.
• Inhaled bronchodilators are preferred over oral.
• Theophylline is not recommended unless other long acting treatment bronchodilators
are not available or are unaffordable.
• Long term monotherapy with ICS is not recommended.
• Long term therapy with OCS is not recommended.

44. MANAGEMENT OF COPD
EXACERBATION
Exacerbation severity is assessed by using Anthonisen criteria

45. MANAGEMENT OF COPD
EXACERBATION
Investigations that are needed include:
• Complete blood count
• Sputum gram stain and culture
• Sputum AFB smear and gene xpert
• Serum urea, creatinine and electrolytes
• Arterial blood gases
• Chest X-ray
• FEV1
• Peak expiratory flow rate
• Electrocardiogram

46. MANAGEMENT OF COPD
EXACERBATION

47. MANAGEMENT OF COPD
EXACERBATION
Treatment for AECOPD treated at home
• Add or increase dose of bronchodilator, metered dose inhalers are preferred with spacer
device. Dose of salbutamol is 2 puff hourly (100 mg/puff) then 3 – 4 hourly. Ipratropium
bromide 2 puff 4 hourly (20 – 40 mg) can be added.
• If response is not adequate add 200 – 400 mg twice daily of sustained release theophylline.
• Add antibiotic if any evidence of infection. Amoxicillin ± clavulanate can be a good first line
option. Other antimicrobials that can be used are respiratory quinolones and macrolides.
• Oral steroids are not recommended in mild exacerbations but can be prescribed for more
severe symptoms and the dose is 30mg/day for one week.

48. COPD MANAGEMENT
PHARMACOLOGIC AND NON PHARMACOLOGIC APPROACH

49. GOALS FOR TREATMENT OF STABLE COPD
REDUCE
SYMPTOMS
• Relieve Sx
• Improve exercise tolerance
• Improve health status
REDUCE
RISK
• Prevent disease progression
• Prevent and treat exacerbations
• Reduce mortality

50. MANAGEMENT OF COPD
DIAGNOSIS
-Sx
-RF
Spirometry
INITIAL ASSESSMENT
-FEV1 – GOLD 1-4
-Sx – CAT or mMRC (GOLD ABE)
-Exacerbation Hx (GOLD ABE)
-Smoking status
-Blood eosinophil count
-Comorbids
INITIAL MANAGEMENT
- Smoking cessation
- Vaccination
- Active lifestyle and exercise
- Initial pharmacotherapy
- Manage comorbids
- Self management education
-RF management
-Inhaler technique
-Written action plan
-SOB
REVIEW
- Sx (CAT or mMRC)
- Exacerbations
- Smoking status
- Exposure to other RF
- Inhaler technique adherence
- Physical activity and exercise
- Vaccination
- Management of comorbids
- Spirometry (atleast annually)
- Need for O2, NIV, palliative
approaches
- Self management skills
-SOB
-Written action plan
ADJUST
- Pharmacotherapy
- Non pharmacological
therapy

51. INITIAL PHARMACOTHERAPY
LABA+LAMA*
Consider LABA+LAMA+ICS* if blood eos >300
LABA +LAMA*
A bronchodilator
2 or >2 moderate
exacerbations
1 or >1 leading to
hospitalization
0 or 1 moderate
exacerbations (not
leading to
hospitalization)
mMRC 0-1, CAT <10 mMRC >2, CAT >10
GROUP E
GROUP A GROUP B
*Single inhaler therapy maybe more convenient and effective than multiple inhalers, single inhalers improve adherence to Rx
Exacerbations refer to no of exacerbations per year

52. MANAGEMENT CYCLE
REVIEW
- Sx
- SOB
- Exacerbations
ASSESS
- Inhaler technique and adherence
- Non pharmacologic approaches
(Including pul rehab and self
management education
ADJUST
- Escalate
- Switch inhaler device or molecules
- De-escalate

53. FOLLOW UP PHARMACOLOGIC TREATMENT
LAMA OR LABA
LAMA+LABA
- Consider switching to inhaler
device or molecules
- Implement or escalate non
pharma Rx
- Investigate and treat other
causes of dyspnea
LABA OR LAMA
LABA + LAMA
LABA + LAMA + ICS
Roflumilast Azithromycin Dupilumab
DYSPNEA EXACERBATIONS
Blood eos >300
If blood eos <300
Blood eos
<100
Blood eos
>100
Blood eos > 300
Consider de-escalation of ICS if pneumonia or other considerable side effects

54. MANAGEMENT OF PATIENTS CURRENTLY ON LABA + ICS
• * Pt previously had exacerbations and responded to LABA + ICS Rx
Pt currently on
LABA + ICS
No relevant
exacerbation Hx
Consider changing to
LABA + LAMA
Consider escalating to
LABA + LAMA + ICS
-No current exacerbation
-Previous positive Rx
response*
Current exacerbation
Low Sx
load
High Sx
load
Blood
eosinophil
>100
Blood
eosinophil
<100
Continue
Rx

55. FACTORS TO CONSIDER WHEN INITIATING ICS
- Hx of hospitalization for exacerbations of COPD
- 2 or >2 moderate exacerbations of COPD per year
- Blood eosinophils 300 or > 300
- Hx of or concomitant Asthma
- 1 moderate exacerbation of COPD per year
- Blood eosinophils 100 to < 300
- Repeated pneumonia event
- Blood eosinophils < 100
- Hx of mycobacterial infection
STRONGLY
FAVOUR USE
FAVOURS USE
AGAINST USE
Factors to consider when adding ICS to long acting bronchodilators

56. GLUCOCORTICOIDS IN COPD
• Oral steroids should be avoided if possible in stable COPD.
• Systemic steroids may be used for short-term treatment (7-14 days)
during exacerbations.
• Inhaled corticosteroids (ICS) have modest bronchodilator effect. They
reduce exacerbation severity and frequency.

57. GLUCOCORTICOIDS IN COPD

58. ADVERSE EFFECTS OF GLUCOCORTICOIDS
• Increased risk of osteoporosis
• Cataract
• adrenal suppression
• Hypertension
• Diabetes
• Obesity
• Skin thinning
• Muscle de-conditioning
• Reactivation of tuberculosis

59. OTHER DRUGS TO AUGMENT COPD
TREATMENT
Antibiotics
• Azithromycin 250 mg/day or 500 mg three times per week for 1 year
may reduce exacerbation risk.
• Clarithromycin 250mg /day in advanced copd having bronchiectasis.
Mucolytics
• Carbocysteine and N-acetylcysteine can be used, they may reduce
exacerbations.
Antitussives
• No definite role is described for use of antitussives in COPD.

60. MAINTENANCE MEDICATION IN COPD

61. MAINTENANCE MEDICATION IN COPD

62. MAINTENANCE MEDICATION IN COPD

63. NON PHARMACOLOGIC MANAGEMENT OF
COPD
• Smoking prevention and cessation
• Control of occupational and indoor pollution
• Pulmonary rehabilitation: Exercise training, nutritional counseling,
disease education
• Vaccination: PCV (>65 yrs) and Influenza (All patients with COPD)
• Oxygen Therapy
• Non Invasive Ventilation: BiPAP

64. Smoking prevention and cessation
Smoking cessation is the single most effective way to reduce the risk of developing COPD and stop its
progression. Even a brief, three minute period of counseling to urge a smoker to quit can be effective. This
should be done for every smoker at each visit.
The five As for counseling regarding smoking cessation

65. Smoking prevention and cessation
• There is a misperception of using chewable tobacco (like snuff:
naswar) or ecigarettes to help in quit attempts.
• These are not recommended and should be discouraged.

66. Control of occupational and indoor pollution
• Indoor pollution due to burning of wood and coal to keep houses
warm in winter and use of biomass fuel in stoves should be minimized
and measures should be taken to reduce exposure as by cooking in
open air rather than a closed kitchen, having separate cooking area,
making chimneys etc.
• Exposure to irritant particles and gases should also be avoided at
work place.

67. Pulmonary rehabilitation
The main goals of pulmonary rehabilitation are to increase over all
resources of the patient, to reduce handicap caused by illness or
disability and to allow integration of patient in society. This can be done
by:
• Exercise training
• Nutritional counseling
• Education

68. Exercise training
• In patients with mild to moderate COPD, suitable exercises are
walking, cycling and swimming.
• Daily exercise should be done for about 30 minutes, it may be divided
into 2 – 3 phases or till the patient gets out of breath.
• In severe COPD, it should be done to improve strength and
endurance of muscles. This should involve respiratory, abdominal,
back, head, neck and limbs to improve quality of life.

69. Nutritional counseling
• Low BMI is an independent risk factor for mortality in COPD patients.
• Increased calorie intake should be accompanied by regimens with
anabolic action.
• On the other side obese individuals have greater levels of
breathlessness and impairment of activity.
• Well-balanced diet is recommended.

70. Education
• Educate regarding disease, its progressive nature, smoking cessation,
drug treatment and how to manage exacerbations.