CHRONIC OBSTRUCTIVE

PULMONARY DISEASE
Dr Yuranga Weerakkody and Dr Mai-Lan Ho et al.
Chronic obstructive u!"on#r$
%ise#se &COPD' represents a spectrum
of obstructive airway diseases. It
includes two key components wic
are cronic broncitis - small airways
disease and empysema.
Ei%e"io!o($
!e most common cause as
istorically been" and unfortunately
continues to be" smoking. It takes
many years of smoking to develop
#$%D and as suc typically patients
are older adults. !ere are owever a
number of oter less common risk
factors & aetiologies" eac wit teir
own demograpics. !ey include'
cigarette smoking
industrial e(posure )e.g
mining*
cystic fibrosis
alpa-+ antitrypsin
deficiency ),,!
+
deficiency*
intravenous drug use
immune deficiency
syndromes
vasculitides and connective
tissue disorders
C!inic#! resent#tion
-ymptoms include dyspnea on
e(ertion" wee.ing" productive coug"
pursed-lip breating" and use of
accessory muscles. %atients wit
cronic broncitis are classically /blue
bloaters"/ wile tose wit empysema
are known as /pink puffers./ In
advanced cases" muscle wasting"
asteri(is" and periperal oedema may
be seen.
P#thoh$sio!o($
In contrast to astma" te istologic
canges of #$%D are irreversible and
gradually progress over time. In
cronic broncitis" tere is diffuse
yperplasia of mucous glands wit
associated ypersecretion and
broncial wall inflammation.
0mpysema involves te destruction
of alveolar septa and pulmonary
capillaries" leading to decreased elastic
recoil and resultant air trapping. !e
morpological subtypes of empysema
include centriacinar" wic is
associated wit smoking and spreads
periperally from broncioles1
panacinar" wic is seen in
omo.ygous ,,!
+
deficiency and
uniformly destroys alveoli1 and
paraseptal )distal acinar*" wic
involves te distal airways.
%ulmonary function testing )%2!*
reveals airflow obstruction" as
evidenced by an increased forced
e(piratory volume in + second to
forced vital capacity )203
+
&23#* ratio.
,dministration of broncodilators as
no effect" unlike te reversible
obstruction seen in astma.
Severit$ c!#ssi)ic#tion
!e global initiative for cronic
obstructive lung disease )4$LD*
staging system is a commonly used
severity staging system based on air
flow limitation. ,ccording to tis"
tere are 5 key stages.
st#(e I - mild - 203
+
6 789
of normal
st#(e II - moderate - 203
+
:
;8-<=9 of normal
st#(e III - severe - 203
+
:
>8-5=9 of normal
st#(e IV - very severe
- 203
+
? >89 of normal
or ? ;89 of normal wit
presence of cronic respiratory
failure present.
!e 203
+
'23# ratio sould be ? 8.<8
for all stages
!e 4$LD staging system may be
insensitive in early stages.
C!inic#! henot$es
-everal distinct clinical penotypes
ave been described
5"@"7
empysema predominant
airways predominant
o small airways
predominant
o large airways
predominant
mi(ed
R#%io(r#hic )e#tures
P!#in )i!"
2indings of cronic broncitis on chest
r#%io(r#h$ are nonspecific and
include increased broncovascular
markings and cardiomegaly.
0mpysema manifests as lung
yperinflation wit flattened
emidiapragms" a small eart" and
possible bullous canges. $n te
lateral radiograp" a /barrel cest/ wit
widened anterior-posterior diameter
may be visuali.ed. !e /saber-seat
tracea/ sign refers to marked coronal
narrowing of te intratoracic tracea
)frontal view* wit concomitant
sagittal widening )lateral view*.
CT
2indings of #$%D may be seen in a
variety of CT studies" e.g. contrast
enanced #!" #!%," staging #!
cest" HA#!.
In chronic bronchitis" broncial wall
tickening may be seen in addition to
enlarged vessels. Aepeated
inflammation can lead to scarring wit
broncovascular irregularity
and fibrosis.
Computed tomography (CT) scan in
patient with chronic bronchitis showing
thickening of the bronchial walls (red
arrows) and mucous within
the bronchi (yellow arrows).
E"h$se"# is diagnosed by alveolar
septal destruction and airspace
enlargement" wic may occur in a
variety of distributions. #entrilobular
empysema is predominantly seen in
te upper lobes wit panlobular
empysema predominating in te
lower lobes. %araseptal empysema
tends to occur near lung
fissures and pleura. 2ormation of giant
bullae may lead to compression
of mediastinal structures" wile rupture
of pleural blebsmay produce
spontaneous pneumotora( & pneumom
ediastinum.
Posterior-Anterior and Lateral Chest
adiograph !emonstrating "yperinflated
Lung with emphysema
"igh esolution Computed Tomography
(CT) of the Chest - !emonstrating se#ere
changes of upper lobe predominant
pulmonary emphysema.
Tre#t"ent #n% ro(nosis
!ere is currently no cure for #$%D"
but it is igly preventable and
treatable. Aisk factor reduction via
smoking cessation" occupational
ealt" and air pollution reduction
sould be instituted.
Management of stable #$%D involves
te use of broncodilators"
corticosteroids" and oter medications
)metyl(antines" leukotriene receptor
antagonists*" as well as supplemental
o(ygen and pulmonary reabilitation.
,cute e(acerbations are treated wit
ig-dose steroids" sort-acting
broncodilators and antibiotics if
indicated.