肺部HRCT基础解读
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Secondarylobule
Knowledge of the lung anatomy is essential
forunderstandingHRCT.
The secondary lobule is the basic anatomic
unitofpulmonarystructureandfunction.
Interpretation of interstitial lung diseases is
based on the type of involvement of the
secondarylobule.
Itisthesmallestlungunitthatissurrounded
byconnectivetissuesepta.
Itmeasures about12 cmand ismade upof
515pulmonaryacini,thatcontainthealveoli
forgasexchange.
The secondary lobule is supplied by a small
bronchiole(terminalbronchiole)inthecenter,
thatisparallelledbythecentrilobularartery.
Pulmonary veins and lymphatics run in the
peripheryof thelobulewithintheinterlobular
septa.
Under normal conditions only a few of these
verythinseptawillbeseen.
There are two lymphatic systems: a central
network,thatrunsalongthe bronchovascular
bundletowardsthecentreofthelobuleanda
peripheral network, that is located within the
interlobular septa and along the pleural
linings.
PublicationdateDecember24,2006
Inthisarticleapracticalapproachisgivenfor
theinterpretationofHRCTexaminations
Wewilldiscussthefollowingsubjects:
Anatomyofthesecondarylobule
BasicHRCTpatterns
Distributionofabnormalities
Differentialdiagnosisofinterstitiallung
diseases
by Robin Smithuis, Otto van Delden and
CorneliaSchaeferProkop
LungHRCTBasicInterpretation
RobinSmithuis,OttovanDeldenandCorneliaSchaeferProkop
RadiologyDepartmentoftheRijnlandHospital,LeiderdorpandtheAcademicalMedicalCentre,
Amsterdam,theNetherlands
Secondarylobule
Secundarylobules.Thecentrilobularartery(in
blue:oxygenpoorblood)andtheterminal
bronchioleruninthecenter.Lymphaticsandveins
(inred:oxygenrichblood)runwithinthe
interlobularsepta
Centrilobulararea isthecentral part ofthe
secundarylobule.
Itisusuallythesiteofdiseases,thatenterthe
lung through the airways ( i.e.
hypersensitivity pneumonitis, respiratory
bronchiolitis,centrilobularemphysema).
Perilymphatic areais the peripheral part of
thesecundarylobule.
It is usually the site of diseases, that are
locatedinthelymphaticsofintheinterlobular
septa ( i.e. sarcoid, lymphangitic
carcinomatosis,pulmonaryedema).
Thesediseasesareusuallyalsolocatedinthe
central network of lymphatics that surround
thebronchovascularbundle.
BasicInterpretation
A structured approach to interpretation of
HRCTinvolvesthefollowingquestions:
WhatisthedominantHRpattern:
reticular
nodular
highattenuation(groundglass,
consolidation)
lowattenuation(emphysema,
cystic)
Whereisitlocatedwithinthesecondary
lobule(centrilobular,perilymphaticor
random)
Isthereanupperversuslowerzoneora
centralversusperipheralpredominance
Arethereadditionalfindings(pleural
fluid,lymphadenopathy,traction
bronchiectasis).
These morphologic findings have to be
combined with the history of the patient and
importantclinicalfindings.
When we study patients with HRCT, we have
to realize that we are looking at a selected
groupofpatients.
Common diseases like pneumonias,
pulmonary emboli, cardiogenic edema and
lungcarcinomaarealreadyruledout.
So uncommon diseases like Sarcoidosis,
Hypersensitivity pneumonitis, Langerhans cell
histiocytosis, Lymphangitic carcinomatosis,
UsualInterstitialPneumonitis(UIP)andmany
others become regular HRCT diagnoses and
canberealAuntMinnies.
Centrilobularareainblue(left)andperilymphatic
areainyellow(right)
TypicalUIPwithhoneycombingandtraction
bronchiectasisinapatientwithidiopathic
pulmonaryfibrosis(IPF)
In the reticular pattern there are too many
lines, either as a result of thickening of the
interlobular septa or as a result of fibrosis as
inhoneycombing.
Septalthickening
Thickening of the lung interstitium by fluid,
fibroustissue,orinfiltrationbycellsresultsin
a pattern of reticular opacities due to
thickeningoftheinterlobularsepta.
Although thickening of the interlobular septa
is relatively common in patients with
interstitial lung disease, it is uncommon as a
predominant finding and has a limited
differentialdiagnosis(Table).
Smooth septal thickening is usually seen in
interstitial pulmonary edema (Kerley B lines
on chest film); lymphangitic spread of
carcinoma or lymphoma and alveolar
proteinosis.
Nodular or irregular septal thickening occurs
in lymphangitic spread of carcinoma or
lymphoma;sarcoidosisandsilicosis.
On the left we see focal irregular septal
thickeningintherightupperlobeinapatient
withaknownmalignancy.
This finding is typical for lymphangitic
carcinomatosis.
There are also additional findings, that
support this diagnosis like mediastinal lymph
nodes and a nodular lesion in the left lung,
thatprobablyrepresentsametastasis.
Pulmonary lymphangitic carcinomatosis
(PLC)
In 50% of patients the septal thickening is
focalorunilateral.
This finding is helpful in distinguishing PLC
from other causes of interlobular septal
thickening like Sarcoidosis or cardiogenic
pulmonaryedema.
Hilar lymphadenopathy is visible in 50% and
usuallythereisahistoryof(adeno)carcinoma.
Identicalfindingscanbeseeninpatientswith
LymphomaandinchildrenwithHIVinfection,
who develop Lymphocytic interstitial
pneumonitis (LIP), a rare benign infiltrative
lymphocyticdisease.
Reticularpattern
Focalseptalthickeninginlymphangitic
carcinomatosis
OntheleftapatientwhohadaCTtoruleout
pulmonaryembolism.
There is a combination of smooth septal
thickening and groundglass opacity with a
gravitationaldistribution.
The diagnosis based on this CT was
cardiogenicpulmonaryedema.
Cardiogenic pulmonary edema generally
results in a combination of septal thickening
andgroundglassopacity.
There is a tendency for hydrostatic edema to
showaperihilarandgravitationaldistribution.
Thickening of the peribronchovascular
interstitium, which is called peribronchial
cuffing, and fissural thickening are also
common.
Common additional findings are an enlarged
heartandpleuralfluid.
Usually these patient are not imaged with
HRCT as the diagnosis is readily made based
on clinical and radiographic findings, but
sometimes unsuspected hydrostatic
pulmonaryedemaisfound.
On the left a patient with both septal
thickening and ground glass opacity in a
patchydistribution.
Somelobulesareaffectedandothersarenot.
This combination of findings is called 'crazy
paving'.
Crazy paving was thought to be specific for
alveolarproteinosis,butisalsoseeninmany
other diseases such as pneumocystis carinii
pneumonia, bronchoalveolar carcinoma,
sarcoidosis, nonspecific interstitial pneumonia
(NSIP), organizing pneumonia (COP), adult
respiratory distress syndrome and pulmonary
hemorrhage.
Alveolar proteinosis is a rare diffuse lung
disease of unknown etiology characterized by
alveolar and interstitial accumulation of a
periodic acidSchiff (PAS) stainpositive
phospholipoproteinderivedfromsurfactant.
Septalthickeningandgroundglassopacitywitha
gravitationaldistributioninapatientwith
cardiogenicpulmonaryedema.
Alveolarproteinosis
Honeycombing represents the second
reticularpatternrecognizableonHRCT.
Because of the cystic appearance,
honeycombingisalsodiscussedinthechapter
discussingthelowattenuationpattern.
Pathologically, honeycombing is defined by
the presence of small cystic spaces lined by
bronchiolar epithelium with thickened walls
composedofdensefibroustissue.
Honeycombing is the typical feature of usual
interstitialpneumonia(UIP).
ThedistributionofnodulesshownonHRCTis
the most important factor in making an
accuratediagnosisinthenodularpattern.
In most cases small nodules can be placed
into one of three categories: perilymphatic,
centrilobularorrandomdistribution.
Randomreferstonopreferenceforaspecific
locationinthesecondarylobule.
Perilymphaticdistribution
In patients with a perilymphatic distribution,
nodules are seen in relation to pleural
surfaces, interlobular septa and the
peribronchovascularinterstitium.
Nodules are almost always visible in a
subpleural location, particularly in relation to
thefissures.
Centrilobulardistribution
Incertaindiseases,nodulesarelimitedtothe
centrilobularregion.
Unlike perilymphatic and random nodules,
centrilobular nodules spare the pleural
surfaces.
The most peripheral nodules are centered 5
10mmfromfissuresorthepleuralsurface.
Randomdistribution
Nodularpattern
HoneycombinginapatientwithUIP
Nodules are randomly distributed relative to
structuresofthelungandsecondarylobule.
Nodules can usually be seen to involve the
pleural surfaces and fissures, but lack the
subpleural predominance often seen in
patientswithaperilymphaticdistribution.
Algorithmfornodularpattern
The algorithm to distinguish perilymphatic,
random and centrilobular nodules is the
following:
Lookforthepresenceofpleuralnodules.
Theseareofteneasiesttoseealongthe
fissures.
Ifpleuralnodulesareabsentorfewin
number,thedistributionislikely
centrilobular.
Ifpleuralnodulesarevisible,thepattern
iseitherrandom(miliary)or
perilymphatic.
Iftherearepleuralnodulesandalso
nodulesalongthecentral
bronchovascularinterstitiumandalong
interlobularsepta,youaredealingwitha
periplymphaticdistribution.
Ifthenodulesarediffuseanduniformly
distributed,itislikelyarandom
distribution.
Perilymphaticdistribution
Perilymphatic nodules are most commonly
seeninsarcoidosis.
They also occur in silicosis, coalworker's
pneumoconiosis and lymphangitic spread of
carcinoma.
Notice the overlap in differential diagnosis of
perilymphatic nodules and the nodular septal
thickeninginthereticularpattern.
Sometimesthetermreticulonodularisused.
On the left a typical case of perilymphatic
distribution of nodules in a patient with
sarcoidosis.
Notice the nodules along the fissures
indicating a perilymphatic distribution (red
arrows).
Alwayslookcarefullyforthesenodulesinthe
subpleural region and along the fissures,
because this finding is very specific for
sarcoidosis.
Typically in sarcoidosis is an upper lobe and
perihilar predominance and in this case we
seethe majorityofnoduleslocatedalongthe
bronchovascularbundle(yellowarrow).
Sarcoidosis
Ontheleftanothertypicalcaseofsarcoidosis.
Inadditiontotheperilymphaticnodules,there
are multiple enlarged lymph nodes, which is
alsotypicalforsarcoidosis.
In end stage sarcoidosis we will see fibrosis,
which is also predominantly located in the
upperlobesandperihilar.
Centrilobulardistribution
Centrilobularnodulesareseenin:
Hypersensitivitypneumonitis
Respiratorybronchiolitisinsmokers
infectiousairwaysdiseases
(endobronchialspreadoftuberculosisor
nontuberculousmycobacteria,
bronchopneumonia)
Uncommoninbronchioloalveolar
carcinoma,pulmonaryedema,vasculitis
In many cases centrilobular nodules are of
groundglassdensityandilldefined(figure).
Theyarecalledacinairnodules.
Treeinbud
In centrilobular nodules the recognition of
'treeinbud' is of value for narrowing the
differentialdiagnosis.
Treeinbud describes the appearance of an
irregular and often nodular branching
structure, most easily identified in the lung
periphery.
Itrepresentsdilated andimpacted(mucus or
pusfilled)centrilobularbronchioles.
Treeinbud almost always indicates the
presenceof:
Endobronchialspreadofinfection(TB,
MAC,anybacterialbronchopneumonia)
Airwaydiseaseassociatedwithinfection
(cysticfibrosis,bronchiectasis)
lessoften,anairwaydiseaseassociated
primarilywithmucusretention(allergic
bronchopulmonaryaspergillosis,
asthma).
Sarcoidosis
Illdefinedcentrilobularnodulesofgroundglass
densityinapatientwithhypersensitivity
pneumonitis
Ontheleftatreeinbudisseen.
In the proper clinical setting suspect active
endobronchialspreadofTB.
In most patients with active tuberculosis, the
HRCTshowsevidenceofbronchogenicspread
of disease even before bacteriologic results
areavailable(6).
Langerhanscellhistiocytosisisan uncommon
disease characterised by multiple cysts in
patientswithnicotineabuse.
In a very early stage, these patients show
only nodules, that later on cavitate and
becomecysts(figure).
Asinallsmokingrelateddiseases,thereisan
upperlobepredominance.
Randomdistribution
Ontheleftapatientwithrandomnodulesasa
resultofmiliaryTB.
The random distribution is a result of the
hematogenousspreadoftheinfection.
Smallrandomnodulesareseenin:
Hematogenousmetastases
Miliarytuberculosis
Miliaryfungalinfections
Sarcoidosismaymimickthispattern,
whenveryextensive
Langerhanscellhistiocytosis(early
nodularstage)
Sarcoidosis usually has a perilymphatic
distribution, but when it is very extensive, it
spreads along the bronchovascular bundle to
the periphery of the lung and may reach the
centrilobulararea.
HighAttenuationpattern
TypicalTreeinbudappearanceinapatientwith
activeTB.
Randomdistributionofnodulesinmiliary
tuberculosis
Langerhanscellhistiocytosis:earlynodularstage
beforethetypicalcystsappear.
Increased lung attenuation is called ground
glassopacity(GGO)ifthereisahazyincrease
in lung opacity without obscuration of
underlying vessels and is called consolidation
if the increase in lung opacity obscures the
vessels.
In both ground glass and consolidation the
increase in lung density is the result of
replacementofairinthealveolibyfluid,cells
orfibrosis.
In GGO the density of the intrabronchial air
appears darker as the air in the surrounding
alveoli.
Thisiscalledthe'darkbronchus'sign
In consolidation, there is exclusively air left
intrabronchial.
Thisiscalledthe'airbronchogram'.
Groundglassopacity
Groundglassopacity(GGO)represents:
Fillingofthealveolarspaceswithpus,
edema,hemorrhage,inflammationor
tumorcells.
Thickeningoftheinterstitiumoralveolar
wallsbelowthespatialresolutionofthe
HRCTasseeninfibrosis.
So groundglass opacification may either be
the result of air space disease (filling of the
alveoli) or interstitial lung disease (i.e.
fibrosis).
The location of the abnormalities in ground
glasspatterncanbehelpfull:
Upperzonepredominance:Respiratory
bronchiolitis,PCP.
Lowerzonepredominance:UIP,NSIP,
DIP.
Centrilobulardistribution:
Hypersensitivitypneumonitis,
Respiratorybronchiolitis
Darkbronchussigningroundglassopacity.
Completeobscurationofvesselsinconsolidation.
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属性:25 页
大小:6.44MB
格式:PDF
时间:2025-04-23
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