This document discusses chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema. It covers the definition, causes, pathophysiology, clinical presentation, investigations, management, and complications of COPD. Key points include that COPD is characterized by irreversible airflow limitation caused by chronic bronchitis and emphysema. Cigarette smoking is the primary risk factor. Symptoms include cough, sputum production, and shortness of breath. Pulmonary function tests can confirm the diagnosis and assess severity. Chest imaging shows hyperinflation of the lungs in emphysema. Treatment involves smoking cessation, bronchodilators, corticosteroids, oxygen therapy, and surgery in severe cases

1. Shree b.m.patil medicalcollege,bijapur
Department of Radiology
PRESENTED BY-
-
Ravi Prakash

2. Chronic obstructive pulmonary
disease.
Disease state characterized by airflow
limitation that is not fully reversible.
A. Chronic bronchitis- a clinically defined
condition with chronic cough and phlegm.
B. Emphysema- an anatomically defined
condition characterized by destruction &
enlargement of lung alveoli.

3. Chronic bronchitis:-
condition associated with excessive
tracheobronchial mucus production
to cause cough with expectoration
for at least 3 month of year for
more than 2 year.
Aetiology-
 cigarette smoking
 air pollution
 occupational hazards -
cotton mill , coal mining , rubber
industry , gold mining
 familial factor
 genetic factor
 infection-by rhinovirus , strep

4. Pathophysiology-
 Hypertrophy & hyperplasia of mucus producing
gland
 Reduction in caliber of air passage

5. airflow obstruction

6. Clinical feature-
Cough
Sputum production
Exertional dyspnoea
Breathlessness relatively late onset
Percussion note- resonant over
lung field
Auscultation- vesicular breathing,
rhonchi, crepitation
Blue bloaters

7. Gold criteria-
GOLD
STAGE
SEVERITY SYMPTOM SPIROMETRY
0 At risk Chronic cough , sputum
production
normal
1 mild With or without chronic cough or
sputum production
FEV1/FVC<0.7
FEV1>=80%predi
cted
11 moderat
e
With or without chronic cough or
sputum production
FEV1/FVC<0.7
50%<=FEV1<80%
predicted
111 severe With or without chronic cough or
sputum production
FEV1/FVC<0.7
30%<=FEV1<50%
predicted
1V Very
severe
With or without chronic cough or
sputum production
FEV1/FVC<0.7
FEV1<=30%predi
cted
Or

8. Investigation-
PULMONARY FUNCTION TEST
FEV1-reduced
VC-reduced
RV-increased
TLC-increased
Gas transfer-decrease or normal
Arterial blood gas analysis-
pao2-decreased
Paco2-increased

9. Radiological studies-
CHEST X-RAY:-
a. Bronchial wall
thickening
b. Increase in lung
marking
c. Small,ill defined
opacity anywhere
in lung
d. Occasionally a
wide alteration in
lung marking may
be seen where the
normal vascular
pattern is partly

10. Linear shadow
Increase peribronchial marking
especially at the base due to
thickened bronchial &
peribronchial tissue

11. Bronchogram-
 dilatation of
bronchial gland
leading to irregular
out pouching from
bronchial lumen
mostly often seen in
wall of major bronchi.
 abrupt termination of
smaller branch of
bronchi with square
& truncated ending
 bronchiolar spasm
 increased secretion

12. Complication-
Mismatch of ventilation &
perfusion
Co2 narcosis Respiratory
failure
Hypoxaemia
hypercarbia
Pulmonary
vasoconstriction
Pulmonary
hypertension
Right ventricular
hypertrophy
Right
ventricular
failure
Increased
erythropoisis
Sec.
polycythe
mia
Desaturation
of Hb
cynaosis

13. Treatment-
1. general measure-
 Smoke caessation
 Regular exercise
 Weight loss
2.bronchodialator-
 Inhalation of b2 agonist-salbutamol 200mcg
Terbutalin 600mcg 6th
hourly
3.glucocorticoides-
 improve the gas exchange to some extent

14. 4.oxygen-
 Supplemental o2 by nasal catheter & through
face mask
 Mainly for exertional or nocturnal hypoxaemia
6.antibiotic-
If any infection is there-
Doxycycline,co-trimoxazole,amoxycillin-
clavulanate,gatifloxacin,iv azithromycin ,
ceftriaxone,cefotaxime
5.Others
 N-acetyl cysteine-mucolytic & antioxidant

15. Emphysema
Distension of air spaces
distal to terminal bronchiole
with destruction of the
alveolar septa.
Predisposing factors-
 smoking
 Environmental pollution
 Occupational exposure-cadmium,
furnace blower
 Alpha1antitrypsin deficiency

16. Type-
a. centriacinar- destruction & enlargement of
central & proximal part of respiratory
unit acinus.
Upper lobe and apices
Seen in male smokers
b.panacinar- uniform destruction & enlargement
of acinus
Mainly involve lower basal zone
Seen in alpha 1 antitrypsin def
patient
c.paraseptal- only distal acinus involve
Found near pleura

17. Type..

18. 1.compensatory-
 Normal lung tissue undergoes compensatory
mechanism for an extensive damage to other
lung or part of the same lung.
 Hyper resonant percussion note.
 Increase breath sound.
2.subcutaneous-
 seen in case of penetrating chest injury
 Rib fracture
 Intercostals tube introduction

19. 3.Mediastinal emphysema-
 Vertical translucent streak , separating & outlining
the soft tissue layers & structure of mediastinum.
 Air often separates the parietal pleura from the
mediastinum & pleura may then be visible as a
thin hair line running parallel to mediastinum.
 Air may be seen in neck also. Due to escape of air
rapidly into mediastinum after rupture of over
distended alveoli.
 On auscultation crunching sound heard.

20. Pathogenesis-
Cigarette
smoke
Inflammatory
cell
recruitment
neutrophil
macrophage
Serin
e
prote
inase
s
ECM
degradati
on, lung
tissue
destructio
n
Cyste
ine
protei
nases
Proteina
se
inhibitor
s

21. Clinical feature-
Progressive
Exertional
breathlessness
minimum
cough &
expectoratio
n
Weakness
lethargy
Weight
loss
anorexia

22. SIGN..
Inspection & palpation-
 Tachypnoeic
 Hypertrophy of accessory muscle of
respiration
 Purse lip breathing
 Chest bowel shaped
 AP diameter- increased
 AP:TD –altered(normal-5:7)
 Angle of Luis-prominent
 Sub costal angle widened(normal 70’)
 Apical impulse is usually invisible or
feeble.

23. Percussion-
 hyper resonant over lung field area
 cardiac dullness decreases
 liver dullness pushed down or absent if right
side involved
Auscultation-
 Breath sound –decreases
 Prolong expiration
 Pink puffers

24. Difference In chronic bronchitis &
emphysema.
feature chronic bronchitis emphysema
cough Before dyspnoea starts After dyspnoea starts
sputum Copious , purulent Scanty , mucoid
dyspnoea mild severe
cynosis present absent
infection common Less common
Chest x-ray Increased bronchovascular
marking , cardiomegaly
Feature of hyperinflation ,
bullae,tubular heart
Pulmonary
hypertension
Moderate to severe mild
Diffusing
capacity
normal decreased

25. Investigation-
PULMONARY FUNCTION TEST
FEV1 -decreases
VC -decreases
FEV1/VC -decreases
PEF -decreases
TLC -increases
RV -increases

26. CHEST X-RAY-
 Irregular area of
radiolucency related to
tissue loss
 Increase in retero
sternal air space

27. Alteration in vascular pattern
Presence of over inflation
Increased lung volume

29. Bullae-
 Multiple & small-
May be localized to a lobe
or may be B/L
Upper lobe more often
affected
 Giant bulla-
Rib interspaced is
widened in region of giant
bulla
Neighboring normal
tissue is compressed with
vessels crowded together

30. CT SCAN Finding:-
it permit the direct identification of destroyed lung
tissue with high precision.
It shows-
 Area of decreased attenuation without visible walls
 Pruning of pulmonary vessels
 Distortion of pulmonary vessels
 Decrease lung tissue gradient

31. Centrilobular-
lucent region initially
surrounded by normal
lung parenchyma but
become confluent
along with obliteration
of peripheral vascular
as disease progresses.
Panlobular-
Widespread area of
low attenuation usually
seen accompanied by
diffuse vascular
distortion.

32. Nuclear imaging-
 Functional evaluation of the lungs can be
carried out by using xenon-133 (133 Xe) lung
ventilation scintigraphy before and after lung-
volume–reduction surgery (LVRS) in patients with
pulmonary emphysema.
Xenon-133 washout curves during lung
scintigraphy exhibit a biphasic pattern:
(1) the first component corresponds to an initial
rapid phase in washout that reflects emptying
of the large airways, and
(2) the second component, reflects a slower
phase of washout that is attributed to gas
elimination in the small airways.

33. Complication-
pulmonary bullae
Significant Weight loss
Respiratory failure
Pulmonary hypertension-late
Right heart failure-late

34. Emphysema with chronic bronchitis-
Radiological finding--
 Decrease in size & no. Of small vascular marking
specially in middle & outer 1/3rd of lung
 Main pulmonary arteries are enlarged making hilar
shadow prominent
 May be barrel shaped chest with increase in AP
diameter & anterior bowing of sternum
 Ant mediastinal space is usually increased in depth

35.  Heart shadow is often long,narrow &
cardiothoracic ratio may change to 1:3 or 1:4.
 Lung fields are seen more translucent
 Increased vol of lung results in flattening of
contour of diaphragm
 Best seen in lateral projection & level is
lowered below the 11th rib.

36. Treatment-
cessation of smoking
Antibiotics
IV alpha1 AT therapy
Vaccination against
influenza & pneumococcal
Low dose benzodiazepine
i.e. alprazolam

37. Mechanical ventilatory support-
Noninvasive PPV-
paco2 more than 45 mmhg
Acidosis
Invasive PPV-
Severe respiratory distress
Severe acidosis
Severe hypoxia
NIPPV failure

38. Surgical-
A. bullectomy
B. Lung volume reduction surgery-
Not done if significant pleural disease
PASPmore than 45 mm mg
C.Lung transplantation-
Age should be less than 65 yrs
Free from liver cardiac renal disease

39. REFERENCES….
Harrison’s principles of internal medicine
Manual of practical medicine-R Alagappan
Fraser& pare’s diagnosis of diseases of chest
Roentgenlogic diagnosis bysaunder’s
CT & MRI imaging of whole body-Haaga,Tanzien,Gilkeson
Internet