Editorials Stuart
A.
Groskin,
MD
Emphysema: or Just a Lot To
learn
how
must learn diagnosis scheme Charcot]
we we
do
we
name
W. Smith]
(1)
physema
ous
(2-5).
Much
confusion
of
emphysema
the
arises
from
as clinias emvery
pervades
obvi-
discussions three
corn-
The first misconception originates from the definition of emphysema. Although emphysema is considered part of the spectrum of chronic obstructive pulmonary diseases, expiratory air-flow obstruction is not rnon
misconceptions.
invariably
present
physema.
Expiratory
in
patients
with
em-
air-flow obstruction is neither mentioned in the definition of emphysema nor is it formally required in the diagnosis of emphysema. Emphysema is a pathologic entity that is defined in strictly morphologic terms as the abnormal, irreversible dilatation of terminal air spaces with or without accompanying destruction of alveolar
Until
walls
(6).
the diagnosis of emall but the pathologist because emphysema is, by definition, an abnormality of lung structure, not function, and is diagnosed on the basis of anatomic alterations instead of physiologic abnormalities or clinical sympphysema
toms.
recently, eluded
Definitions
Index terms: high-resolution pulmonary, Radiology
not
withstanding,
em-
Computed tomography (CT), ‘ Editorials #{149}Emphysema, 60.751 #{149}Lung, CT, 60.1211 1992;
183:319-320
From the Department of Radiology, State University of New York Health Science Center at Syracuse, 750 E Adams St, Syracuse, NY 13210. Received March 3, 1992; accepted March 4. Address reprint requests to the author. RSNA, 1992 See also the article by Gurney et al (pp 457463) in this issue. I
expiratory
disease
process.
As
the word “emphysema” eral pathologic observation; imply
of
that
symptomatic
specific
them.
have engendered much anatomic, physiologic, and radiologic controversy
diagnosed only with clinically
sig-
air-flow
obstruction. The second common misconception about emphysema is that it is a single,
we know
EW entities
cal,
nificant
Martin
the things necessarily
Fiction, Air?’ physema is usually when it is associated
one it. The in the
[Jean
name not
because
[Homer
F
disease,
to recognize best trump
of treatment. (1)
Though know, them
to treat
how is the
Fact, offlot
either
a specific
noted
refers
which air
are spaces
associated only,
dial
above,
to a genit does not
dysfunctional
state or a specific pathogenetic nism. Spencer (6) describes anatomic types of emphysema, with and
mecha12 different five of dilatation
seven
of
of which
are
associated with air-space dilatation and alveolar-wall destruction. Some of these forms of emphysema have a clear-cut genetic basis, while others do not. Some
are clearly
related
to cigarette
while others are not. physema frequently significant disability, not. The
third
physema ratory
air-flow
the
airways both
about
the
etiology
obstruction
cur in patients with neither contraction nor
smoking,
that
emphysema. of smooth
em-
the anatomic patient
of mu-
obstruct
air
flow
in
patients with other types of obstructive airways disease, figure prominently in the pathologic or clinical picture of emphysema, some other mechanism of obstruction must be postulated. It was logical, convenient, and tidy to try to find a way to link alveolar-wall destruction, the constant and required morphologic abnormality that defines emphysema, to the air-flow obstruction seen in patients with emphysema. The loss of elastic recoil of the lung and the concomitant loss of radial traction on the small airways seemed likely to provide this link. The intrinsic tendency of the elastic tissue in the alveolar walls to recoil when stretched is the major motivational force for expiratory air flow. Since the connective tissue of the alveolar walls is directly connected to the axial connective tissue surrounding the small airways, the elastic recoil of the alveolar walls also exerts radial traction on small, compliant
airways,
during expiration, trathoracic pressure compress
Destruction
and
pulling
them
open
when positive inwould otherwise
collapse
of alveolar
them.
walls
of radial
may
oc-
should
Both
of these
losses
could
traction
apparently
play
supporting, not starring, roles in this “mortality” play (2). Once we have corrected our misconceptions about emphysema, we are free to ask three questions: (a) Why doesn’t
of expiSince muscle in
hypersecretion
of which
traction.
and should decrease the rate of expiratory air flow. Unfortunately, attempts to directly correlate the extent of alveolarwall destruction with the severity of expiratory air-flow obstruction in patients with emphysema have, at best, met with incomplete success (7-10). Patients with severe emphysema may have few symptoms and little evidence of expiratory air-flow obstruction, while patients with minimal or moderate grades of emphysema may have significant, disabling pulmonary dysfunction. The loss of elastic recoil and the reduc-
tion
types of emclinically others do
misconception
concerns
cus,
Some produce while
reduce the intrinsic elastic recoil of the lung and should also increase the dynamic compression and obstruction of small airways because of the loss of ra-
tent tion
extent
correlate
of emphysema
precisely
of measurable in that patient,
in a
with
pulmonary
the
ex-
dysfunc-
(b) what noninvabe used to most easily and diagnose emphysema, and
sive test can most reliably (c) is there any reason to diagnose anatomically apparent but clinically asymptomatic emphysema? Although it is convenient and cornfortable to think of emphysema as a distinct, discrete entity, it is now widely
recognized ever, exists
that emphysema rarely, if clinically in a pure form. In-
flammation
and fibrosis of small airways bronchiolitis) are found in most patients with emphysema who have verifiable expiratory air-flow obstruction. The extent of these lesions and the severity of the narrowing of the (respiratory
airways
ter,
but
ity
of
extent
that
still
they
produce
correlate
imperfectly,
air-flow
with
obstruction
the
than
of the emphysematous
bet-
sever-
does
the
changes
(7-9).
We will likely match
between
of emphysema lion computed or diagnosed
never the
achieve
presence
a perfect and
extent
detected on high-resolutomographic (CT) scans in surgical or postmortem
lung specimens and measurements expiratory air-flow obstruction,
in most patients, alveolar-wall tion is not the only morphologic
of because
destrucabnor319
mality producing High-resolution
cannot extent
air-flow obstruction. CT has not and likely
be used to assess the degree and of concomitant narrowing of
small
airways.
Dr. Gurney possible
crepancies cabby
et al (11) propose
explanation
another
for apparent
between
dis-
the radiographi-
determined
extent
of emphysema
and physiologic measurements of expiratory air-flow obstruction. They observed that patients who had emphysematous
changes
lung
zones
expiratory
who
had
lung
zone.
primarily
in the
upper
usually had more normal air flow than did patients changes primarily in the lower Dr. Gurney
et al speculate
that because less ventilation normally takes place in the upper lung zones than in the lower lung zones, obstruction
of the
zone
airways
in the
is less likely
ically apparent struction. This cabby attractive
upper
to produce
lung
physiobog-
expiratory air-flow obproposal is physiobogiand benefits from the
generally
accepted
functional
“silent”
precedent zones,
of other where
sub-
stantiab pathologic abnormalities can exist without producing commensurate clinical or physiologic abnormalities. Numerous studies have demonstrated the spectacular capability of CT, particularly high-resolution CT, in the diagnosis of emphysema (12-15). High-
resolution
CT can reliably
physema
and
delineate
depict
em-
its extent
and
severity with accuracy and precision that rival those of direct pathologic amination. This capability is hardly prising.
High-resolution
CT is the
exsurubti-
mate noninvasive way to display the fine anatomic detail of the pulmonary parenchyma.
Although
rich anatomic the diagnosis
detail is of little help in of many pulmonary disor-
extraordinarily
dens, it is precisely what is required for diagnosing emphysema, since emphysema is a disease that is defined not by
the presence of a particular abnormal cellular infiltrate or specific biochemical or functional abnormality, but by an alteration of normal pulmonary structune. The marriage of high-resolution CT and emphysema is truly a match made in heaven. Is it worthwhile
nose
emphysema
tients?
I believe
question
to attempt
to diag-
in asymptomatic that
is a qualified
the
answer
“yes.”
pato this
The early
diagnosis of benign, nonprogressive, functionally insignificant forms of emphysema such as paracicatricial emphysema is, for the most part, unimportant.
On the other of progressive,
320
Radiology
#{149}
hand, the early diagnosis potentially debilitating
forms of emphysema such as centnlobubar emphysema associated with cigarette smoking or panacinar emphysema associated with alpha1-antitrypsin deficiency may have a significant clinical impact. Sequential high-resolution CT studies obtained in asymptomatic and symptomatic patients with potentially disabling forms of emphysema may allow us to learn more about the evolution and natural history of emphysema and provide us with a noninvasive means of measuring
disease
activity
and
response
to therapy. Also, although truly effective treatment for emphysema is still in the developmental stages, once such treatment becomes available, early diagnosis will presumably allow the institution of treatment at an earlier stage, before reversal of or compensation for extensive lung damage is necessary. Finally, if one picture is really worth a thousand words, a high-resolution CT image that graphically demonstrates the destruction of an asymptomatic smoker’s own lung tissue may provide an extremely persuasive argument for him or her to stop smoking. In conclusion, although the cellular and biochemical bases of emphysema are now being elucidated, we still do not truly understand many of the most basic
aspects
of this
disorder.
We
New CT task easier
and may allow us to evaluate the dynamic functional changes taking place in the airways and air spaces of these patients. The eminent pathologist Thurbbeck (2)
why
stated,
“It
so much
spent
trying
nary
function
is interesting
time
and
to
with
has been
tests
of pulmo-
lesions
.
.
The complexity are often not
of the properly
relarecog-
rateby predict some morphological sion. This is predictably the most sive fishing expedition since the
for Moby Dick” (2, pp 129-131). We should respond, “Whale Away
the
boats!”
beexpensearch
ho!
U
References 1. 2.
Strauss
MB.
Boston:
Little, Brown,
Familiar
medical
quotations.
1968; 86, 96.
Thurlbeck WM. Chronic air flow obstruction: correlation of structure and function. In: Petty TL, ed. Chronic obstructive pub-
monary disease. 2nd ed. New York: Dekker, 1985; 129-209. 3.
Bates
DV.
Respiratory
function
ease. 3rd ed. Philadelphia: 4.
172-187. Fraser RG,
Pare
Genereaux
GP.
JAP,
Pare
PD,
Diagnosis
Fraser
RS,
of
Saunders,
Marcus EB, Bulst AS, Maclean CJ, Yano K. Twenty-year trends in mortality from chronic obstructive pulmonary disease: the Honolulu Dis 1989;
6.
1989;
of diseases
the chest. 3rd ed. Philadelphia: 1990; 2087-2166. 5.
in dis-
Saunders,
Heart Program. 140:564-568.
Spencer
H.
Oxford:
Pergamon,
Pathology
Am
Rev
Respir
of the lung.
4th ed.
1985.
7. Silvers GW, MaiselJC, Mitchell
8.
9.
10.
RS.
Petty TL, Filley CF. Flow limitation during
forced expiration in excised human lungs. Appl Physiol 1974; 36:737-744. WrightJL, Lawson UM, Pare PD, Kennedy S, Wiggs B, Hogg JC. The detection of small airways disease. Am Rev Respir Dis 1984; 129:989-994. Hogg JC, Pare PD, Wright JL. Airways disease: evolution, pathology, and recognition. Med J Austrab 1985; 142:605-607. West WW, Nagal A, Hodgkin JE, Thurlbeck WM. The National Institutes of Health Intermittent Positive Breathing Trial-Pathobogy Studies. II. The diagnosis of em-
physema.
Am Rev Respir
Dis 1987; 135:
123-129. 11.
12.
Gurney JW, Jones KK, Robbins RA, et al. Regional distribution of emphysema: correlation of high-resolution CT with pulmonary function tests in unselected smokers. Radiology 1992; 183:457-463. Bergin C, Muller N, Nichols DM, et al. The diagnosis of emphysema: a computed
tomographic-pathologic correlation. Rev Respir Dis 1986; 133:541-545. 13.
Hruban RH, Meziane al. High-resolution
phy of inflation-fixed 14.
15.
Am
MA, Zerhouni EA, et computed tomogra-
lungs.
Am Rev Respir
Dis 1987; 138:935-940. Kuwano K, Matsuba K, Ikeda T, et al. The diagnosis of mild emphysema correlation of computed tomography and pathology scores. Am Rev Respir Dis 1990; 141:169178. Sanders C. The radiographic diagnosis of emphysema. Radiol Clin North Am 1991; 29:1019-1030.
ponder
effort
to correlate
.
nized and there are those even now who search for the Holy Grail of a test of pulmonary function that will accu-
cannot
adequately explain the etiology of the air-flow obstruction in patients with emphysema, nor do we understand the factors that determine an individual’s susceptibility to develop emphysema. Why all people who smoke two packages of cigarettes a day don’t develop emphysema remains a mystery. We should not be disappointed in our inability to exactly match the extent of emphysematous changes with the Severity of pulmonary function abnormalities in patients with emphysema; such a match is not possible, since other factors contribute to the physiologic dysfunction seen in these patients. This does not diminish or devalue the information provided with high-resolution CT and should encourage, not discourage, further efforts to document the sequence of morphologic changes in both the alveoli and the airways that charactenize evolving emphysema. techniques may make this
lungs. tionships
in the
May
1992
A.
Groskin,
MD
Emphysema: or Just a Lot To
learn
how
must learn diagnosis scheme Charcot]
we we
do
we
name
W. Smith]
(1)
physema
ous
(2-5).
Much
confusion
of
emphysema
the
arises
from
as clinias emvery
pervades
obvi-
discussions three
corn-
The first misconception originates from the definition of emphysema. Although emphysema is considered part of the spectrum of chronic obstructive pulmonary diseases, expiratory air-flow obstruction is not rnon
misconceptions.
invariably
present
physema.
Expiratory
in
patients
with
em-
air-flow obstruction is neither mentioned in the definition of emphysema nor is it formally required in the diagnosis of emphysema. Emphysema is a pathologic entity that is defined in strictly morphologic terms as the abnormal, irreversible dilatation of terminal air spaces with or without accompanying destruction of alveolar
Until
walls
(6).
the diagnosis of emall but the pathologist because emphysema is, by definition, an abnormality of lung structure, not function, and is diagnosed on the basis of anatomic alterations instead of physiologic abnormalities or clinical sympphysema
toms.
recently, eluded
Definitions
Index terms: high-resolution pulmonary, Radiology
not
withstanding,
em-
Computed tomography (CT), ‘ Editorials #{149}Emphysema, 60.751 #{149}Lung, CT, 60.1211 1992;
183:319-320
From the Department of Radiology, State University of New York Health Science Center at Syracuse, 750 E Adams St, Syracuse, NY 13210. Received March 3, 1992; accepted March 4. Address reprint requests to the author. RSNA, 1992 See also the article by Gurney et al (pp 457463) in this issue. I
expiratory
disease
process.
As
the word “emphysema” eral pathologic observation; imply
of
that
symptomatic
specific
them.
have engendered much anatomic, physiologic, and radiologic controversy
diagnosed only with clinically
sig-
air-flow
obstruction. The second common misconception about emphysema is that it is a single,
we know
EW entities
cal,
nificant
Martin
the things necessarily
Fiction, Air?’ physema is usually when it is associated
one it. The in the
[Jean
name not
because
[Homer
F
disease,
to recognize best trump
of treatment. (1)
Though know, them
to treat
how is the
Fact, offlot
either
a specific
noted
refers
which air
are spaces
associated only,
dial
above,
to a genit does not
dysfunctional
state or a specific pathogenetic nism. Spencer (6) describes anatomic types of emphysema, with and
mecha12 different five of dilatation
seven
of
of which
are
associated with air-space dilatation and alveolar-wall destruction. Some of these forms of emphysema have a clear-cut genetic basis, while others do not. Some
are clearly
related
to cigarette
while others are not. physema frequently significant disability, not. The
third
physema ratory
air-flow
the
airways both
about
the
etiology
obstruction
cur in patients with neither contraction nor
smoking,
that
emphysema. of smooth
em-
the anatomic patient
of mu-
obstruct
air
flow
in
patients with other types of obstructive airways disease, figure prominently in the pathologic or clinical picture of emphysema, some other mechanism of obstruction must be postulated. It was logical, convenient, and tidy to try to find a way to link alveolar-wall destruction, the constant and required morphologic abnormality that defines emphysema, to the air-flow obstruction seen in patients with emphysema. The loss of elastic recoil of the lung and the concomitant loss of radial traction on the small airways seemed likely to provide this link. The intrinsic tendency of the elastic tissue in the alveolar walls to recoil when stretched is the major motivational force for expiratory air flow. Since the connective tissue of the alveolar walls is directly connected to the axial connective tissue surrounding the small airways, the elastic recoil of the alveolar walls also exerts radial traction on small, compliant
airways,
during expiration, trathoracic pressure compress
Destruction
and
pulling
them
open
when positive inwould otherwise
collapse
of alveolar
them.
walls
of radial
may
oc-
should
Both
of these
losses
could
traction
apparently
play
supporting, not starring, roles in this “mortality” play (2). Once we have corrected our misconceptions about emphysema, we are free to ask three questions: (a) Why doesn’t
of expiSince muscle in
hypersecretion
of which
traction.
and should decrease the rate of expiratory air flow. Unfortunately, attempts to directly correlate the extent of alveolarwall destruction with the severity of expiratory air-flow obstruction in patients with emphysema have, at best, met with incomplete success (7-10). Patients with severe emphysema may have few symptoms and little evidence of expiratory air-flow obstruction, while patients with minimal or moderate grades of emphysema may have significant, disabling pulmonary dysfunction. The loss of elastic recoil and the reduc-
tion
types of emclinically others do
misconception
concerns
cus,
Some produce while
reduce the intrinsic elastic recoil of the lung and should also increase the dynamic compression and obstruction of small airways because of the loss of ra-
tent tion
extent
correlate
of emphysema
precisely
of measurable in that patient,
in a
with
pulmonary
the
ex-
dysfunc-
(b) what noninvabe used to most easily and diagnose emphysema, and
sive test can most reliably (c) is there any reason to diagnose anatomically apparent but clinically asymptomatic emphysema? Although it is convenient and cornfortable to think of emphysema as a distinct, discrete entity, it is now widely
recognized ever, exists
that emphysema rarely, if clinically in a pure form. In-
flammation
and fibrosis of small airways bronchiolitis) are found in most patients with emphysema who have verifiable expiratory air-flow obstruction. The extent of these lesions and the severity of the narrowing of the (respiratory
airways
ter,
but
ity
of
extent
that
still
they
produce
correlate
imperfectly,
air-flow
with
obstruction
the
than
of the emphysematous
bet-
sever-
does
the
changes
(7-9).
We will likely match
between
of emphysema lion computed or diagnosed
never the
achieve
presence
a perfect and
extent
detected on high-resolutomographic (CT) scans in surgical or postmortem
lung specimens and measurements expiratory air-flow obstruction,
in most patients, alveolar-wall tion is not the only morphologic
of because
destrucabnor319
mality producing High-resolution
cannot extent
air-flow obstruction. CT has not and likely
be used to assess the degree and of concomitant narrowing of
small
airways.
Dr. Gurney possible
crepancies cabby
et al (11) propose
explanation
another
for apparent
between
dis-
the radiographi-
determined
extent
of emphysema
and physiologic measurements of expiratory air-flow obstruction. They observed that patients who had emphysematous
changes
lung
zones
expiratory
who
had
lung
zone.
primarily
in the
upper
usually had more normal air flow than did patients changes primarily in the lower Dr. Gurney
et al speculate
that because less ventilation normally takes place in the upper lung zones than in the lower lung zones, obstruction
of the
zone
airways
in the
is less likely
ically apparent struction. This cabby attractive
upper
to produce
lung
physiobog-
expiratory air-flow obproposal is physiobogiand benefits from the
generally
accepted
functional
“silent”
precedent zones,
of other where
sub-
stantiab pathologic abnormalities can exist without producing commensurate clinical or physiologic abnormalities. Numerous studies have demonstrated the spectacular capability of CT, particularly high-resolution CT, in the diagnosis of emphysema (12-15). High-
resolution
CT can reliably
physema
and
delineate
depict
em-
its extent
and
severity with accuracy and precision that rival those of direct pathologic amination. This capability is hardly prising.
High-resolution
CT is the
exsurubti-
mate noninvasive way to display the fine anatomic detail of the pulmonary parenchyma.
Although
rich anatomic the diagnosis
detail is of little help in of many pulmonary disor-
extraordinarily
dens, it is precisely what is required for diagnosing emphysema, since emphysema is a disease that is defined not by
the presence of a particular abnormal cellular infiltrate or specific biochemical or functional abnormality, but by an alteration of normal pulmonary structune. The marriage of high-resolution CT and emphysema is truly a match made in heaven. Is it worthwhile
nose
emphysema
tients?
I believe
question
to attempt
to diag-
in asymptomatic that
is a qualified
the
answer
“yes.”
pato this
The early
diagnosis of benign, nonprogressive, functionally insignificant forms of emphysema such as paracicatricial emphysema is, for the most part, unimportant.
On the other of progressive,
320
Radiology
#{149}
hand, the early diagnosis potentially debilitating
forms of emphysema such as centnlobubar emphysema associated with cigarette smoking or panacinar emphysema associated with alpha1-antitrypsin deficiency may have a significant clinical impact. Sequential high-resolution CT studies obtained in asymptomatic and symptomatic patients with potentially disabling forms of emphysema may allow us to learn more about the evolution and natural history of emphysema and provide us with a noninvasive means of measuring
disease
activity
and
response
to therapy. Also, although truly effective treatment for emphysema is still in the developmental stages, once such treatment becomes available, early diagnosis will presumably allow the institution of treatment at an earlier stage, before reversal of or compensation for extensive lung damage is necessary. Finally, if one picture is really worth a thousand words, a high-resolution CT image that graphically demonstrates the destruction of an asymptomatic smoker’s own lung tissue may provide an extremely persuasive argument for him or her to stop smoking. In conclusion, although the cellular and biochemical bases of emphysema are now being elucidated, we still do not truly understand many of the most basic
aspects
of this
disorder.
We
New CT task easier
and may allow us to evaluate the dynamic functional changes taking place in the airways and air spaces of these patients. The eminent pathologist Thurbbeck (2)
why
stated,
“It
so much
spent
trying
nary
function
is interesting
time
and
to
with
has been
tests
of pulmo-
lesions
.
.
The complexity are often not
of the properly
relarecog-
rateby predict some morphological sion. This is predictably the most sive fishing expedition since the
for Moby Dick” (2, pp 129-131). We should respond, “Whale Away
the
boats!”
beexpensearch
ho!
U
References 1. 2.
Strauss
MB.
Boston:
Little, Brown,
Familiar
medical
quotations.
1968; 86, 96.
Thurlbeck WM. Chronic air flow obstruction: correlation of structure and function. In: Petty TL, ed. Chronic obstructive pub-
monary disease. 2nd ed. New York: Dekker, 1985; 129-209. 3.
Bates
DV.
Respiratory
function
ease. 3rd ed. Philadelphia: 4.
172-187. Fraser RG,
Pare
Genereaux
GP.
JAP,
Pare
PD,
Diagnosis
Fraser
RS,
of
Saunders,
Marcus EB, Bulst AS, Maclean CJ, Yano K. Twenty-year trends in mortality from chronic obstructive pulmonary disease: the Honolulu Dis 1989;
6.
1989;
of diseases
the chest. 3rd ed. Philadelphia: 1990; 2087-2166. 5.
in dis-
Saunders,
Heart Program. 140:564-568.
Spencer
H.
Oxford:
Pergamon,
Pathology
Am
Rev
Respir
of the lung.
4th ed.
1985.
7. Silvers GW, MaiselJC, Mitchell
8.
9.
10.
RS.
Petty TL, Filley CF. Flow limitation during
forced expiration in excised human lungs. Appl Physiol 1974; 36:737-744. WrightJL, Lawson UM, Pare PD, Kennedy S, Wiggs B, Hogg JC. The detection of small airways disease. Am Rev Respir Dis 1984; 129:989-994. Hogg JC, Pare PD, Wright JL. Airways disease: evolution, pathology, and recognition. Med J Austrab 1985; 142:605-607. West WW, Nagal A, Hodgkin JE, Thurlbeck WM. The National Institutes of Health Intermittent Positive Breathing Trial-Pathobogy Studies. II. The diagnosis of em-
physema.
Am Rev Respir
Dis 1987; 135:
123-129. 11.
12.
Gurney JW, Jones KK, Robbins RA, et al. Regional distribution of emphysema: correlation of high-resolution CT with pulmonary function tests in unselected smokers. Radiology 1992; 183:457-463. Bergin C, Muller N, Nichols DM, et al. The diagnosis of emphysema: a computed
tomographic-pathologic correlation. Rev Respir Dis 1986; 133:541-545. 13.
Hruban RH, Meziane al. High-resolution
phy of inflation-fixed 14.
15.
Am
MA, Zerhouni EA, et computed tomogra-
lungs.
Am Rev Respir
Dis 1987; 138:935-940. Kuwano K, Matsuba K, Ikeda T, et al. The diagnosis of mild emphysema correlation of computed tomography and pathology scores. Am Rev Respir Dis 1990; 141:169178. Sanders C. The radiographic diagnosis of emphysema. Radiol Clin North Am 1991; 29:1019-1030.
ponder
effort
to correlate
.
nized and there are those even now who search for the Holy Grail of a test of pulmonary function that will accu-
cannot
adequately explain the etiology of the air-flow obstruction in patients with emphysema, nor do we understand the factors that determine an individual’s susceptibility to develop emphysema. Why all people who smoke two packages of cigarettes a day don’t develop emphysema remains a mystery. We should not be disappointed in our inability to exactly match the extent of emphysematous changes with the Severity of pulmonary function abnormalities in patients with emphysema; such a match is not possible, since other factors contribute to the physiologic dysfunction seen in these patients. This does not diminish or devalue the information provided with high-resolution CT and should encourage, not discourage, further efforts to document the sequence of morphologic changes in both the alveoli and the airways that charactenize evolving emphysema. techniques may make this
lungs. tionships
in the
May
1992
