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Sarcoidosis
Sarcoidosisisamultisysteminflammatorydiseasemostcommonlyaffectingthelungs.
Otherorgansarelesscommonlyinvolvedandincludetheskin,lymphnodes,eyes,heart,andnervous
system.However,anyorganmaybeaffectedbysarcoidosis.
85
The cause of sarcoidosis has not been identified, but is likely the interaction of a number of
environmentalandhostgeneticfactors.
86
Sarcoidosistypicallyoccursinyoungadults.
It is more common in African Americans than in Caucasians (3–4 times higher incidence). African
Americans also present with earlier onset disease, and with a greater burden of extrapulmonary
disease.In addition,AfricanAmericanpatientshavehigherhospitalizationratesandhighermortality
rates(8–14timeshigher).
87
Inupto50%ofcases,sarcoidosismaybeasymptomaticanddetectedonincidentalchestimaging.
When symptomatic, patients often present with progressive dyspnea, nonproductive cough, or chest
pain.
Extrapulmonarymanifestationsofsarcoidosisinclude88:
Oculardiseasemayincludeuveitis,retinaldisease,conjunctivitis,andlachrymalglandinvolvement.
Skin disease may manifest with various rashes including erythema nodosum (raised, red, tender
nodulesonanterior legs) andlupus pernio (induratedplaques withassociateddiscolorationofthe
nose,cheeks,lips,andears).
Nervous system involvement can manifest as encephalopathy, granulomatous meningitis,
mononeuritismultiplex,orahostofotherneurologicanomalies.
Cardiac involvement may result in cardiomyopathy and heart failure, ventricular aneurysms,
arrhythmias, and sudden cardiac death.89 The heart may be the only organ involved in>20% of
cases.
Endocrineinvolvementcanmanifestashypercalcemiaandhypercalciuriasecondarytodysregulated
productionofcalcitriol.
90
Sarcoidosismayalsopresentwithtwowell-describedacuteclinicalsyndromes88:
Löfgren syndrome is characterized by arthritis, erythema nodosum, and bilateral hilar
lymphadenopathy.
86
Heerfordtsyndromepresentswitha combinationofuveitis, parotidgland swelling, fevers, andin
somecasesfacialpalsy.Itisalsoknownasuveoparotidfever.
CXRimaginginsarcoidosis maymanifestwithpulmonary opacities, thoracic lymphadenopathy, ora
combinationofboth.CXRisalsousedtostagethedisease(Table10-8).
TABLE10-8
SCADDINGSTAGINGOFSARCOIDOSIS
CXRFindings FrequencyatPresentation
(%)
Stage0:Normal 5–15
StageI:Hilarormediastinallymphadenopathy 25–65
StageII:Hilarormediastinallymphadenopathywithpulmonary
infiltrates
20–40
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StageIII:Pulmonaryinfiltrates 10–15
StageIV:End-stagefibrosis 5
AdaptedfromMallerV,KnipeH.Thoracicsarcoidosis(staging).AccessedMarch4,2021.http://radiopaedia.org/articles/thoracic-
sarcoidosis-staging?lang=us
On HRCT, parenchymal nodules appear in almost 80% of patients. They typically follow a
perilymphatic distribution andmay coalescence into larger opacities.86 Other findings may include
alveolaropacities,pulmonaryfibrosis,andairtrappingonexpiratoryimaging(Table10-6).
Laboratorytestingshouldbeobtained.Serumcalcium,urinecalcium,CBC,BMP,andLFTsshouldall
bechecked.Abnormalitiesinthesearenotdiagnostic ofsarcoidosisbutcanhelpdetermineextentof
diseaseandorganinvolvement.
Intheappropriateclinicalsetting,sarcoidosisisdiagnosedbythepresenceofnoncaseatinggranulomas
on biopsy samples of involved organs (commonlythe lung,lymphnodes, or skin).Thepresence of
granulomasinmorethanoneorgansystemispreferablewhenmakingthediagnosis.
90
Exclusionofotherdiseasesisobligatorywhendiagnosingsarcoidosis.90Excludinginfectiousdisease
is of particular importance, especially in patients who reside in areas with endemic fungal or
mycobacterialdisease,asthesecanmimicsarcoidosis.
Treatmentofsarcoidosis canbecomplicated,andreferral topulmonaryandotherspecialistsisoften
necessary.
Formilddisease,symptomsandradiographicchangesmayremitintheabsenceoftreatment.
In the setting of more symptomatic or progressive disease, corticosteroids are typically first-line
therapyandmanypatientscanbetreatedwithintermittentsteroidtherapyalone(Table10-7).
Patients with moreadvanced disease or those requiring longer-term steroid therapymay needtobe
transitionedtosteroid-sparingimmunosuppressionsuchasmethotrexateorazathioprine.
Tumor necrosis factor alpha antagonists are typically reserved for severe disease that progresses
despitetheaforementionedtherapies.
91
Prognosis is highly variable, ranging from indolent self-remitting disease to progressive fibrosis
requiring transplantation.Asabroadrule,acuteonsetdiseasetendstowardabetterprognosis,while
moreindolentonsetdiseasemaybecomeunremittinglyprogressive.
OrganizingPneumonia
OP is a nonspecific pulmonaryresponsetoinjurycharacterizedbyinflammationandproliferationof
granulationtissueinthealveoliandterminalbronchioles.
OPwaspreviouslyreferredtoasbronchiolitisobliteranswithOP.
OPmaybeeither:
Idiopathic,referredtoasCOP,andoneofthesubtypesofidiopathicinterstitialpneumonia,or
Secondary, and occur in association with CTDs, drug toxicity (e.g., amiodarone, checkpoint
inhibitors), infections,inhalational injury (e.g.,cocaine,industrialgasses),radiationtreatment,and
alongwithotherILDs(e.g.,vasculitis).
92
Patientsoften presentwithdyspnea,cough,fevers,malaise,fatigue,andweightlosslasting weeksto
months. Thesesymptoms maymimic pneumonia,anda frequentscenario is a patientpresenting with
multipleepisodesof“pneumonia”unresponsivetoantibioticstherapy.
On HRCT, OP manifests with multifocal patchy consolidation, often in a peripheral or
peribronchovasculardistribution.Theopacitiesmayaffectalllungzonesandwhenfollowedovertime
maybemigratory.92ThereversehalooratollsignisthoughttobeveryspecificforOPonHRCTbutis
notcommonlyseen(Table10-6).
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DiagnosisisoftensuggestedthroughacombinationofgoodhistorytakingandHRCTappearance.
PFTsarenonspecificandmaydemonstraterestriction.
BALisusefultoruleoutinfection.
Themethodoflungbiopsyiscontroversial.WhileTBBxmaymakethediagnosis,somefeelthatthey
maynotbesufficienttodetectsecondarycausesofOPduetothesmallsizeofthebiopsies.Assuch,
severalcentersrecommendVATSbiopsywhereOPissuspected.
64
Patientsnormallyhavegoodresponsetotreatmentwithsteroids.However,recurrenceiscommonand
long-termsteroidtherapyover3–6monthsisgenerallyrecommended.IfOPcontinueswithoutresponse
totreatmentorprogressestofibrosis,prognosisispoor.
Incasesassociatedwithotherdiseases(e.g.,vasculitis,CTD),treatmentisdirectedattheunderlying
cause.
Smoking-RelatedILD
CertainILDsmanifestalmostexclusivelyinsmokers.TheseincludeRB-ILD,DIP,andPLCH.
RESPIRATORYBRONCHIOLITISINTERSTITIALLUNGDISEASE
RB-ILDistypicallyassociatedwithheavysmoking(often30pack-yearsormore).
93
Itcommonlypresentsinthethirdtofifthdecadesoflife.
On HRCT, RB-ILD manifests with centrilobular ground-glass nodules, often with an upper lobe
predilection. In some cases, the nodules are more confluent and present as ground-glass opacities
(Table10-6).
Other changes related to smoking, such as emphysema and bronchial wall thickening, may also be
present.
94
Symptomsandradiographicfindingsoftenimprovewithsmokingcessation(Table10-7).
94
DESQUAMATIVEINTERSTITIALPNEUMONIA
DIPmayrepresentaspectrumofdiseasealongwithRB-ILD.
NinetypercentofpatientswithDIPareheavysmokers.
95
Theother 10%may haveCTD,HIV,or environmentalexposures. Acongenital form maybe seenin
children.
The predominant HRCTfinding in DIP is bilateral ground-glass opacity, which may be peripheral,
patchy, or diffuse in distribution. Itis classicallydescribed as triangular-shaped opacities radiating
fromthehilatotheperipheryofthelung;however,thisfindingisnotedinonlyaminorityofpatients
(Table10-6).
Smallcysticspacesoccasionallydevelopwithintheground-glassopacities.
Responsetosmokingcessationisfavorable,althoughsomepatientsmayrequirecorticosteroidtherapy
(Table10-7).
96
Thediseaseoccasionallypersistsdespitetherapy.
PULMONARYLANGERHANSCELLHISTIOCYTOSIS
Langerhanscellhistiocytosisisararedisorderofunknownetiology.
It results from abnormal clonal proliferation of Langerhans cells derived from bone marrow
precursors.
Multisystem involvement with extrapulmonary disease involving the skin, central nervous system,
skeleton, andotherorgans is commoninchildrenbutrare inadultswherediseaseis confinedtothe
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lungs.
97
PLCHpresentsinadultsmokersbetweentheagesof20and40yearswithcough,dyspnea,weightloss,
andoccasionallyspontaneouspneumothorax.
97
HRCTdemonstratesacombinationofnodulesandcysts.
63
Nodules tend to predominate in early disease. They range from few to innumerable in number and
typicallyhaveacentrilobulardistribution.Theymayhaveirregularmarginsandcavitatetoformcysts.
Cystic lung lesions predominate in later disease. The cysts are characterized by irregular/bizarre
marginsandhaveanupperlobepredominance,oftensparingthelungbases.Theycystsarecommonly
thinwalledbutmayoccasionallybeafewmillimetersthick.
UnliketypicalILDs,lungvolumesareoftenpreserved.
The primary therapy for PLCH is smoking cessation. Response to smoking cessation is considered
good,withupto50%ofpatientsdemonstratingimprovementorresolution.
98
Approximately20%ofpatientshavepersistent,progressivedisease.
Inthesepatients,atrailofsteroidtherapymaybeconsidered,butdataforthisarelacking.
In the most resistantforms of disease, chemotherapeutic agents including cladribineandvinblastine
havebeenusedwithvariablesuccess.
Some patients with PLCH have mutations in the mitogen-activated protein kinase pathway such as
BRAFV600E.Inthesepatients,targetedtherapywithvemurafenib(aBRAFkinaseinhibitor)hasbeen
used.
98
Pneumoconioses
Pneumoconioses are diseases ofthe lungparenchyma that result from exposureto airborne dustsor
fibersincludingasbestos,silica,beryllium,coal,tin,andothers.
99
Pneumoconiosis (with the exception of asbestosis) are characterized by upper lobe–predominant
nodularpatternsonCTthathavethepotentialtoconglomerateovertimetoformlargespaceoccupying
lesionsknownasprogressivemassivefibrosis.
ASBESTOS-INDUCEDLUNGDISEASE
Arises from exposure to asbestos, a substance historically used in construction, insulation, and
fireproofingmaterials.
HRCT findings may range from pleural thickening, pleural plaques (often with calcification),
subpleural banding (reticulation running parallel to the pleura), to parenchymal changes resembling
UIP. The presence of pleural plaques aids in differentiation from other ILDs, but asbestos-related
fibroticdiseasecanexistintheabsenceofpleuralmanifestations.
Treatmentfocusesonasbestosavoidanceandsupportivecare.
Prognosis is goodin mild disease, although the risk of lung cancer is significantlyincreased in the
settingofconcomitantcigaretteuse.
Exposuretoasbestosalsoincreasestheriskofdevelopingmesothelioma.
SILICOSIS
Silicosis results from exposure to crystalline silica, which is found in stone and sand. Foundry
workers,constructionworkers,sandblasters,andglassblowersareatincreasedrisk.
100
HRCT typically demonstrates small nodules in the upper and mid zones with hilar adenopathy in a
patternthatmayresemblethoseseeninsarcoidosis.Thisisknownassimplesilicosis.
Simplesilicosismayprogresstocomplicatedsilicosischaracterizedbycoalescenceofnodulesinthe
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perihilarareasofthelungtoformconglomeratemassesorareasofprogressivemassivefibrosis.
Treatment is supportive, although close monitoring for development of TB is warranted given the
increasedriskofTBinthesepatients.
101
An acute form of silicosis, also known as silicoproteinosis, has been described with episodes of
inhalation of high concentrations of silica. It appears as diffuse ground-glass opacities on CXR.
Mortalityishigh.
BERYLLIOSIS
Berylliosisiscausedbyexposuretoberylliumandberylliumcompounds.
102
Exposureoccursintheaerospaceindustry,atomicindustry,berylliummining,andfluorescentlightbulb
manufacturing.
Itisclinicallyindistinguishablefrompulmonarysarcoidosis.
COALWORKERS’PNEUMOCONIOSIS
Coals workers’ pneumoconiosis (CWP) is caused by inhalation of high carbon coal dust. It is
commonlyknownas“blacklungdisease.”
HRCT typically demonstrates small nodules in the upper and mid zones. This is known as simple
silicosis.
103
Simple CWP may progress to complicated CWP characterized by coalescence of nodules in the
perihilarareasofthelungtoformareasofprogressivemassivefibrosis.
Caplansyndrome,alsoknownasrheumatoidpneumoconiosis,isthepresenceofpulmonarynodulesin
the lungsofpatientsdiagnosed withrheumatoidarthritis whohavealsobeenexposedtocoaldust.It
hasalsobeendescribedinpatientswithrheumatoidarthritisexposedtosilica.
CysticLungDiseases
Cystic lung diseases are a heterogeneous group of disorders that include LAM, PLCH, BHD, LIP,
pulmonaryamyloidosis,andlightchaindepositiondisease.
These diseases are characterized by the presence of cysts on HRCT imaging. Cysts are air-filled
lucencies or low attenuation areas with thin (usually ≤2 mm) walls located within normal lung
parenchyma.
104
Thecystsrangefromfewtoinnumerableinnumber.
Cystsshouldnotbeconfusedwithemphysema,bullae,pneumatoceles,honeycombing,orcavitarylung
lesions.
Thelocationandthicknessofthecystwallscanbehelpfulfordiseasedifferentiation.
PLCH is generally characterized by upper lobe–predominant cysts with thicker and
irregular/bizarre-shapedwalls.
BHDdemonstrates larger-sized cystswitha peripheral andbasilar distribution, often abutting the
pleura.
LAM,LIP,andamyloidosismostoftenhavearandomdistributionofcysts.
105
Cystic lung diseases are associatedwith a high incidenceof pneumothoraxcompared tothegeneral
population,andpneumothoraxisacommonpresentingcomplaint.
LYMPHANGIOLEIOMYOMATOSIS
LAMisaprogressivecysticlungdiseaseseenalmostexclusivelyinwomenofchildbearingage.
LAM may develop sporadically or as part of tuberous sclerosis complex (TSC), a neurocutaneous
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multisystemdisordercharacterizedbymultiplebenignhamartomasoftheskin,brain,kidney,lung,and
otherorgans.
106
MenwithTSCmayalsodevelopLAM.
Most patients present with progressive dyspnea. Other presentations include pneumothorax, and
chylouspleuralandabdominaleffusions.
ThemostcommonextrapulmonarymanifestationsofLAMarerenalangiomyolipomas(AML)—benign
kidneytumorscontainingbloodvessels,smoothmuscle,andfattytissue.
107
LymphangioleiomyomasareanothercharacteristicfeatureofLAM.Theyarefluid-filledstructuresthat
canbeseenintheretroperitonealspace,pelvis,andmediastinum.
106
LAM is usually diagnosed based on a combination of clinical presentation and imaging findings
includingcysticlungdiseaseandrenalAMLs.
VEGF-Dlevelscanbetested,withlevels ≥800pg/mLreliablydistinguishingLAMfrom othercystic
lungdiseases.
62
Genetic testing for tuberous sclerosis (TSC1 and TSC2 gene mutations) can be undertaken where
clinicallyindicated.
Inrarecases,lungbiopsymaybeneededforhistopathologicconfirmation.
108
Thisis usuallypursued
via bronchoscopy and TBBx. Surgical biopsy is no longer commonly performed. Lesions will
demonstratecharacteristichumanmelanomablack45staining.
First-line therapy for pulmonary LAM currently is the mammalian target of rapamycin inhibitor,
sirolimus,whichhasbeenshowntoreducediseaseprogression.
109
Everolimushasbeenshowntobeeffectiveinpatientswhodonottoleratesirolimus.
110
Otherwise,supportivecare,includingoxygentherapy,avoidanceofactivitiesthatcouldplacepatients
athigherriskforpneumothorax,andpulmonaryrehabilitationaremainstaysoftherapy.
Insomecases,patientsmayrequireevaluationforlungtransplantation.
OTHERCYSTICLUNGDISEASES
PLCH:
PLCHisdescribedinthe“Smoking-relatedILD”section.
BHDsyndromeisararecauseofcysticdiseaseassociatedwithskinandrenalneoplasms.
111
ItistheresultofgermlinemutationsintheFLCNgene,whoseproductisfolliculin,aputativetumor
suppressorprotein.
PulmonarycystsinBHDareirregularlyshapedandcommonlylocalizedtothelungbases,oftenina
subpleurallocation.
112
BHDcanbediagnosedbasedonclinicalpresentationandmaybeconfirmedbyskinbiopsyshowing
fibrofolliculomas,askinhamartomacharacteristicofBHD.
GenetictestingforFLCNmutationcanalsobeperformed.
Treatmentissupportive,andprogressionisgenerallyslow.
107
Amyloidosis can be associated with cystic lung disease in the setting of underlying systemic
amyloidosis or maybe organ limited to the lungs (MALT lymphoma). It may also be seen inlongstandingCTDsormyeloma.
113
The cysts are variable insize and distribution. They may be associated with tracheal disease or
pulmonarynodules,whichoftencalcify.
Treatmentfocusesontheunderlyingcondition.
LIPisararedisease,usuallyassociatedwithCTDs(primarilySjögrensyndrome),lymphoproliferative
diseases(e.g.,lymphoma),andviralinfections(e.g.,HIV).Idiopathiccasesalsooccur.
114
Imaging demonstrates irregular cysts, multifocal ground-glass opacities, nodularity, and septal
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thickening.
Treatmentandprognosisarevariabledependingontheunderlyingcondition.
GeneralManagementConsiderations
All ILD patients should be monitored for the development of hypoxemic respiratory failure.
Supplementaloxygenationshouldbeprovidedtomaintainoxyhemoglobinsaturationbypulseoximetry
(SpO2)≥89%bothatrestandwithexertion(measuredby6MWtesting).
Smokingcessation/avoidanceshouldbestronglyencouraged.
Patientsshouldavoidoccupational/environmentaltriggersoftheirILD,ifidentified.
Pulmonaryrehabilitationtherapyshouldbeprescribedforallpatientsiftheymeeteligibilitycriteria.
Bone density assessment is recommended for patients receiving chronic systemic corticosteroid
therapy,alongwithperiodicreassessment(e.g.,every1–2years).
Pneumocystis jirovecii pneumonia prophylaxis should be considered in patients receiving chronic
steroidtherapy,
115
generallyatdosesof>15mgprednisonedaily.
Patientsonimmunosuppressivetherapyshouldhaveappropriatebloodwork(CBCand/orBMPand/or
LFT)monitoredperiodically.
Patientsshouldreceivevaccinationsagainstpneumococcusandinfluenza.
Patients withILDs should be considered for referral to centers with expertise in the diagnosis and
treatmentoftheseconditions,withconsiderationforparticipationinongoingclinicaltrials.
ILD increases the risk of PH.
116
Patients withdyspnea out of proportion to their parenchymal lung
diseaseorthosewithsymptomsofrightheartfailureshouldbescreenedwithTTE.Althoughtheuseof
pulmonary vasodilators in this population remains controversial, recent studies have shown
improvementinfunctionalstatuswithinhaledtreprostinil.
117
SeveralILDsareassociatedwithanincreasedincidenceofmalignancy.(e.g.,IPF,asbestosis).Rapid
weight loss or radiographic changes (e.g., new solitary nodules or persistent consolidation) should
raisesuspicionandpromptfurtherworkup.
Goalsofcareandexpectationsoftherapyshouldbemadecleartoallpatients.
Palliative care is anongoing partof disease managementinmanyILDs,andhospice care should be
discussedwithallpatientswithadvanceddiseasewhoarenottransplantcandidates.Opendiscussions
ofgoalsofcarearehelpfulinguidingmanagementofacuteexacerbationsandprogressivedisease.
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Hemoptysis
GENERALPRINCIPLES
Hemoptysisisthecoughingupofbloodorblood-stainedmucus.Itisasignofunderlyingpulmonary
pathology.Itcanbelifethreateningandrequiresrapididentification,workup,andtreatment.
Definition
Truehemoptysisisexpectorationofbloodfromthelowerrespiratorytractbelowtheglottis.
Massiveorlife-threateninghemoptysis:
Isusuallydefinedbyvolumeperunittime.
Itismostcommonlydefinedas>600mLofbloodexpectoratedper24hours.
119,120
Volumesof>100mL in24hours associatedwithgasexchangeabnormality,airwayobstruction, or
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hemodynamicinstabilityarealsoconsideredlifethreatening.
Classification
Clinically,hemoptysisisusuallyclassifiedasbeingmassive/lifethreateningornot(seeabove).Itmay
alsobeclassifiedbytheanatomiclocationofthebleeding.
Airway
Parenchyma
Vascular
Combination
Therearevariousotherclassificationsintheliteraturebasedonappearance,frequency,rate,volume,and
potentialforclinicalconsequencesofthehemoptysisthatmaysuggestanunderlyingetiologyorpredict
outcomeandthushelpguideindiagnosisandmanagement.However,considerableoverlapexistsinthe
clinicalpresentationbothwithinandbetweenetiologies.
Etiology
SeeTable10-9.
TABLE10-9
ETIOLOGYOFHEMOPTYSIS
Location Etiology
Airway Bronchitis,bronchiectasis,malignancy,foreignbody,trauma,pulmonary
endometriosis,andbroncholithiasis
Parenchymal Pneumonia,vasculitides,andpulmonaryhemorrhagesyndromes
(antineutrophilcytoplasmicantibody–positivevasculitis,Goodpasturesyndrome,
systemiclupuserythematosus,diffusealveolarhemorrhage,acuterespiratory
distresssyndrome)
Vascular Elevatedpulmonaryvenouspressure(LVfailure,mitralstenosis),pulmonary
embolism,arteriovenousmalformation,pulmonaryarterialtrauma(i.e.,
pulmonaryarterialcatheterballoonoverinflation),varices/aneurysms,
vasculitides,andpulmonaryhemorrhagesyndromes
Multiple
locations
Cavitarylungdisease(TB,aspergilloma,lungabscess),thrombocytopenia,
disseminatedintravascularcoagulation,anticoagulants,antiplatelets,cocaine
andotherinhaledagents,lungbiopsy,bronchovascularfistula,
bronchopulmonarysequestration,andDieulafoydisease
Other Upto50%.Favorableprognosis,ingeneral.Upto4%eventuallydiagnosed
withmalignancy3,
4
Epidemiology
Theincidenceofeachcauseofhemoptysisvariesconsiderably.Table10-10listssomeofthemost
commoncausesofhemoptysis.
121,122
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TABLE10-10
EPIDEMIOLOGYOFHEMOPTYSIS
Etiology Incidence(%)
Bronchitis 2–37
Bronchiectasis 1–37
TBandcavitarylungdisease 2–69
Malignancy 2–24
Pneumonia 1–16
Pulmonaryembolus 3
Pulmonaryedema 4
Idiopathic 2–50
Pathophysiology
Thesourceofhemoptysisdependsontheetiologyandlocationoftheunderlyingpathologicprocess.
Thepulmonaryarterialcirculationsupplies99%ofallbloodflowtothelungparenchymaunderlow
pressure. Disruption can result in minor hemoptysis or more life-threatening hemoptysis due to
processes such as vasculitis, diffuse alveolar hemorrhage, pulmonary embolism, acute respiratory
distress syndrome, arteriovenous malformation (AVM) rupture, pulmonary artery catheter trauma,
severemitralstenosis,LVfailure,orRasmussenaneurysm(pulmonaryarteryaneurysmassociatedwith
TB).
The bronchial arterial circulation arises from the aorta and intercostal arteries. It supplies high-
pressurebloodflowtothelungsbut accountsforonly1%ofpulmonarybloodflow.Disruptionbya
foreignbody,tumorinvasion,fungalinvasion,ordenudedairwaymucosa canresultinmassive, lifethreateninghemoptysis.Bleedingfromthebronchialcirculationmayaccountforupto88%ofallcases
ofmassivehemoptysis.
DIAGNOSIS
Identifyingandcorrectingtheunderlyingpathologicprocessisthebasisofdiagnosisandmanagementof
hemoptysis(Figure10-5).
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Figure10-5 Algorithm forevaluation of hemoptysis.ABG, arterial bloodgas; CBC,complete blood count; CMP, complete
metabolicpanel;EBUS,endobronchialultrasound;PT,prothrombintime;PTT,partialthromboplastin.(AdaptedfromEarwoodJS,
ThompsonTD.Hemoptysis:evaluationandmanagement.AmFamPhysician.2015;91:243-249.)
ClinicalPresentation
Hemoptysismaypresentinisolationoraccompanyothermanifestationsofanunderlyingdisorder(Table
10-9).Theappearance,timing,andvolumeofhemoptysiscanprovideimportantcluestonarrowingthe
differentialdiagnosis.
Appearance:Grossblood,blood-tingedsputum,blood-streaking,foamypinksputum
Timing:Firstepisode,recurrentepisodes,chronicsmallvolumes,acutelargevolumes
Volume:Minor,submassive,massive
HISTORY
Themostimportantfactstogatherincludevolume ofhemoptysis, patientage, smokinghistory,prior
lungdisease,previousmalignancy,riskfactorsforcoagulopathy,andpriorepisodesofhemoptysis.
Review of systems should focusonsymptoms suggesting cardiopulmonary disease, active infection,
underlyingmalignancy,andsystemicinflammatorydisorders.
PHYSICALEXAMINATION
Obtainingvitalsignsincludingoxygensaturationisthefirststepinpatientexamination.
Thereafter, one should pay attention to the patient’s general stateof health, lung examination noting
focal or diffusely abnormal findings such as bronchial breath sounds, crackles, stridor, and/or
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