COPD is a common lung disease characterized by airflow limitation caused by exposure to noxious particles. It includes chronic bronchitis and emphysema. Globally, COPD affects over 300 million people and causes over 3 million deaths annually. The major risk factor is tobacco smoking. Symptoms include dyspnea, cough, and sputum production. Exacerbations are defined as worsening of symptoms and require treatments like bronchodilators, antibiotics, corticosteroids, and sometimes noninvasive ventilation. Management involves smoking cessation, vaccinations, pulmonary rehabilitation, and surgery in severe cases.

1. DR.BIPUL THAKUR
KMCTH

2. Definition
• 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.

3. COPD includes
• 1. Chronic bronchitis:
is defines as chronic productive cough onmost days for at least 3
consecutive months in 2 successive years.
• 2.Emphysema:
is defined as dilatation and destruction of air spaces distal to
terminal bronchioles without obvious fibrosis.

4. EPIDEMIOLOGY
• Prevalence directly related to tobacco smoking and use of biomass fuel in
low and middle income countries.
• Current estimates suggest that 80 million people worldwide
suffer from moderate to severe disease.
• A/c to BOLD and other large scale epidemiological studies, it is estimated
that no. of COPD cases was 384M in 2010 with global prevalence of 11.7%
• Globally around 3 million deaths occur annually
• With increasing prevalence and ageing , COPD prevalence expected to rise
over next 40 years and by 2060 there may be 5.4 million deaths annually.

5. RISK FACTORS

8. Clinical features:
• Dyspnea:
- Progressive over time
- Characteristically worse with exercise
- Persistent
• Cough:
- May be Intermittent or may be unproductive
- Recurrent Wheeze
• Chronic Sputum production:
- May be dry or productive
- Usually mucoid in nature
- Mucopurulent during acute exacerbation

9. Physical signs:
• Inspection:
- Barrel-shaped chest ,
- Accessory respiratory muscle participate ,Prolonged
expiration during quiet breathing. Expiration through
pursed lips
- Paradoxical retraction of the lower interspaces during
inspiration (ie, hoover's sign)
- Tripod Position

11. Tripod Position
• Patients with end-stage COPD
may adopt positions that relieve
dyspnea, such as leaning forward
with arms outstretched and
weight supported on the palms or
elbows.

12. • Palpation:
- Decreased vocal fremitus
• Percussion :
- Hyper resonant
- Depressed diaphragm,
- Diminution of the area of absolute cardiac dullness.

13. • Auscultation:
- Vesicular with Prolonged expiration
- Reduced breath sounds
- The presence of wheezing during quiet breathing
- Crackle can be heard if infection exist.

17. • The presence of a post-
bronchodilator FEV1/FVC <
0.70 confirms the presence
of persistent airflow
limitation and thus of
COPD.

22. • ABG: pH<7.3- sign of acute respiratory compromise
Type II RF: Chronic Bronchitis
Type I RF: Emphysema
• CBC: Polycythemia
Hematocrit>50
• Sputum examination:
Streptococcus pneumonia
Hemophilus influenzae
Moraxella catarrhalis
Klebsiella pneumonia

23. Chest x-ray-Chronic Bronchitis
• No apparent
abnormality
• Or thickened and
increased lung
markings are noted.
No apparent
abnormality
Or thickened and
increased lung
markings are noted.

24. Chest X-Ray -Emphysema
• Marked over inflation is noted
with flattened and low diaphragm
• Intercostal space becomes widen
• A horizontal
pattern of ribs
• A long thin
heart shadow
• Decreased markings of lung
peripheral vessels

25. CT(Computed tomography)
• Greater sensitivity and
specificity for emphysema
for evaluation of bullous
disease

27. © 2020 Global Initiative for Chronic Obstructive Lung Disease

28. • General: Exercise and management of Nutritional status
Weight loss if obese
• Reduce exposure to noxious agents:
1.Smoking cessation: aided by Bupropion(Noradrenergic
antidepressant), varenicline(Nicotinic receptor agonist antagonist)
2.Reduce Indoor and outdoor air pollution
3.Avoid dusty and smoke laden environment

37. Surgical Intervention
• Bulla: Bullectomy
• Lung volume reduction surgery
• Lung Transplantation

39. Acute exacerbation of COPD
• Is defined as any event in natural course of COPD characterized by a
change in patient’s baseline dyspnoea, cough and/or sputum that is
beyond normal day to day variations.
• Causes:
1.Infection
2.Air pollution
3.Cold

40. Management
• Initial treatment: 1. Position the patient up in bed
2. O2 therapy
3. If condition is not improving, intubation may be
required
• Bronchodilator: 1. SABA: Nebulized Salbutamol 2.5mg every 20 min
for initial 1-2 hr &/or
2. Short anticholinergic: Nebulized Ipratropium
bromide 0.5mg &/or
3. IV Aminophylline: Failure of above treatment
Loading dose:250mg IV in 20 min
Maintenance dose: 0.5-0.7mg/kg/hr
in 1 ltr of saline at 2.4ml/kg/hr

41. • Antibiotics:
1. Outpatient:
a. Doxycycline,cotrimoxazole or amoxiclav
b. Hospitalized pt >65 yrs: give one of the newer
FQs(Levoflox,Gemiflox,Moxiflox)
2. Hosptalized: IV anibiotics: Azithro or FQs or 3rd gen
Cephalosporins
3. Severe exacerbations: 3rd gen Cephalosporin + FQs or an
aminoglycoside
• Antibiotics should cover S. pneumoniae, H. influenza, Legionella sp.

42. • Steroids: Shortens recovery time, improve Lung function and hypoxia.
Hydrocortisone 200mg IV repea 6-8 hrly
or
Methyl prednisolone1-2mg/kg IV 6hrly not to exceed 125mg
: F/U with oral steroid: Presdnisolone 40-60mg/day in
tapering dose
• Monitoring
• Mgso4 IV single dose : 1.2-2gm infused over 20 min
• Diuretics: In pts with gross Rt. Ventricular failure

44. • NIPPV: 1.CPAP
2.BiPAP
MOA: 1. Prevents airways to collapse and air trapping
2. Reduces need for ET intubation