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Chestwall:Hypoechoic,linearshadowsofsofttissuedensity.
Ribs:Hyperechoic,curvilinearstructureswithadeep,hypoechoic,posterioracousticshadow.
Pleura: Bright, hyperechoic, roughly horizontal line located approximately 0.5 cm below rib
shadows.
Diaphragm: Curvilinear, hyperechoic line that moves caudally with inspiration. In a seated
patient,itislocatedcaudadtotheninthrib.
Splenorenal and hepatorenal recesses: Should be confirmed before any procedure because its
curvilinearappearanceissimilartothatofthediaphragm.Identifiedbyvisualizationoftheliver
orspleenandthekidneycaudally.
Lung: Air-filled lung appears hyperechoic due to the poor echogenicity of air. Atelectatic or
consolidatedlungappearshypoechoicrelativetonormallung.
Sonographicartifactsandterminology:Anumberofsonographicartifactsarecausedbyair–tissue
interfaces,andpresenceorabsenceoftheseartifactsisindicativeofdisease.
76
Pleural line: Brightly echogenic, roughly horizontal line; caused by parietopulmonary interface
andindicatingthelungsurface.
A-lines: Brightly echogenic horizontal lines roughly parallel to the chest wall; caused by
reverberationsofthepleuralline.
B-lines: Also called “comet tails”; a grouping within one intercostal space is called “lung
rockets.” Hyperechoicline arisingperpendicularly from the pleural linethatextends across the
whole screen without fading, erasing A-lines; moves with lung slide. Caused by thickened
interlobularseptaorground-glassareas;isolatedB-linesareanormalvariant.SeeFigure8-5.
Figure8-5 Lung ultrasound.A-lines demonstrated onleftare equidistanthorizontal lines created by reflectionsof
thepleuralline.B-linesdemonstratedontherightarebrightverticallinesthatmovewiththepleuraandextendtothe
bottomofthescreenrepresentingthickenedfluid-filledinterlobularseptae.
Lung slide: “Twinkling” movement of the pleural line that occurs with the respiratory cycle;
causedbymovementofthelungalongthecraniocaudalaxisduringrespiration.InM-mode,lung
slideisvisualizedasthe“seashoresign,”withthechestwallgeneratingthe“waves,”theaerated
lungformingthe“sand,”andthepleurallineastheinterface.
Lungpulse:Pulsationofthepleurallineduetotransmissionoftheheartbeatthroughnoninflated
lung.
Ultrasonographyoflungpathology
Pleural effusion: A fluid collection bordered by the diaphragm, chest wall, and lung surface.
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Transudativeeffusionsaretypicallyanechoic;exudativeeffusionsmayhavesomeechogenicity.If
the effusion is loculated, septations—visualized as hyperechoic, weblike structures—may be
seen.Atelectaticlungmaybeseenintheeffusion.
Pneumothorax: Owing to air’s poor echogenicity, diagnosis of pneumothorax on ultrasound is
madebyartifactanalysis.
□ The presence of lung slide or lung pulse effectively rules out pneumothorax in the location
beinginvestigated.
□ Abolishment of lungslide hasa characteristic stratosphere sign inM-mode, withloss ofthe
“sand,”butisneithersufficientnorspecificfordiagnosisofpneumothorax.
□ Lungpointispathognomonicforpneumothoraxbuthaspoorsensitivity.Occursattheinterface
ofthepneumothorax andaeratedlung.Characterizedbyalternationbetweenabsentlungslide
andpresentlungslideorB-linesinonelocationwithrespirations.InM-mode,willtransition
betweenseashoresignandstratospheresign.
Pneumonia: Can only be visualized when the consolidation abuts the pleura. A heterogeneous,
hypoechoic area with irregular margins where aerated lung abuts the consolidated area. Air
bronchogramsshouldbeseentomakethediagnosisofpneumonia.
Pulmonaryedema:PresenceofmultipleB-lineswithinoneintercostalspace(“lungrockets”)may
indicatecardiogenicornoncardiogenicpulmonaryedema.CorrespondstotheKerleyB-linesseen
onchestradiograph.IsolatedB-linesareanormalvariant.
Abdominalultrasound:Abdominalultrasoundincriticalcareislimitedandintended toevaluatefor
intra-abdominalfluidandassesstheurinarytractandabdominalaorta.
Evaluatingforintra-abdominalfluid:Standardevaluationofthetraumapatientwhomayhaveintraabdominal bleeding includes the focused assessment with sonography for trauma (FAST)
examination.Thepatientisinthesupineposition,andfourviewsareobtained:
Hepatorenal space: Theprobeis placed ontherightinthe10thor11thintercostalspace at the
posterioraxillarylinewiththeorientationmarkpointedcephalad.
Pelvis: The probe is placed in the suprapubic area with the orientation mark in the 3-o’clock
position.
Perisplenicspace:Theprobeisplacedontheleftinthe10thor11thspaceatorslightlyposterior
totheposterioraxillarylinewiththeorientationmarkpointedcephalad.
Pericardialspace: Theprobeisplacedinthesubxiphoidpositionwith theorientationmarkerin
the3-o’clockposition.
Paracentesis:Paracentesisshouldbeperformedunderultrasoundguidancebecausethereisevidence
supporting adecreaseincomplications.Moredetails canbefoundintheWashingtonManual for
CriticalCare,SectionXIX.
Assessment of the urinary tract: Bedside ultrasonography can identify bladder distention or
hydronephrosis.
Bladder distention: Theprobe is placed inthesuprapubic positionwith the orientationmarker
pointed cephalad for longitudinal dimensions and in the 3-o’clock position for transverse
dimensions.
Hydronephrosis:Theprobeshouldbeplacedslightlycaudadtothelocationsusedforexamination
of the hepatorenal and perisplenic spaces in the FAST examination. Hydronephrosis is
characterizedbythinningoftherenalcortexasthecollectingsystemdilates.
Assessmentoftheabdominalaorta:Thegoalistovisualizetheentireabdominalaortatoensurethat
itsdiameterfromouterwalltoouterwallis<3cm. Theexaminationbeginscaudadtothexiphoid
process, with theprobe perpendicular to the abdominal wall andthe orientationmarker inthe3o’clockposition.
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Vasculardiagnosticultrasound:Bedsideultrasonographymaybeperformedtoevaluatefordeepvein
thrombosis when clinicallyindicated.Thetargetveinis visualizedinthetransverse plane.Avessel
with normal blood flow should appear internally anechoic and should be easily compressible.
Organized thrombus appears as a discrete, echogenic structure within the venous lumen. A very
recentlyformedthrombusmaybeanechoic,butthevesselwillbeincompressible.
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9
ObstructiveLungDisease
JamesG.Krings,LauraHalverson,RodrigoVazquezGuillamet,KaharuSumino
ChronicObstructivePulmonaryDisease
GENERALPRINCIPLES
Definition
Chronic obstructive pulmonary disease (COPD) is defined by the Global Initiative for Chronic
ObstructiveLungDisease(GOLD)asamostlypreventableandtreatabledisordercharacterizedbyan
expiratoryairflow limitationthat is notfullyreversible. Exposuretonoxious particles andgases,as
wellasabnormalitiesinlungdevelopment,predisposesindividualstothedevelopmentofCOPD.The
trajectoryofthediseaseisvariableandnotnecessarilyprogressive.
Recently,therehasbeenasuggestiontoexpandthediagnosticcriteriaofCOPDfromasinglemeasure
of lung function (expiratory airflow limitation) to include environmental exposure, symptoms, and
abnormalfindingsonCTscans.ThereisnowrecognitionthataCOPDdefinitionthatsolelyrelieson
lungfunctionmissespatientsintheearlystagesofthedisease.
TheairflowobstructioninCOPDiscausedbyemphysemaandairwaydisease.
Emphysemaisdefinedpathologicallyaspermanentenlargementofairspaces distaltotheterminal
bronchioleaccompaniedbydestructionofthealveolarwallsandtheabsenceofassociatedfibrosis.
However,fibrosiscancoexistwithemphysemaina syndrome calledcombinedpulmonaryfibrosis
andemphysema(CPFE).
TheairwaydiseaseinCOPDoccursprimarilyinsmallairways(i.e.,thosewithaninternaldiameter
of <2 mm). Chronic bronchitis is a common feature of COPD and is defined clinically as a
productive cough, on most days, for at least 3 consecutive months per year and for at least 2
consecutiveyears,andintheabsenceofotherlungdiseasesthatcouldaccountforthissymptom.
Emphysema and chronic bronchitis can be insidious and present in the absence of airflow
obstruction.Evenintheabsenceofairflowobstruction,COPDisstillassociatedwithadversehealth
outcomes.
Epidemiology
Although the true prevalence of COPD is difficult to determine, COPD is estimated to affect
approximately15millionpeopleintheUS.
PriortotheCOVID-19pandemic,COPDandotherchroniclowerrespiratorydiseasesrepresentedthe
thirdleadingcauseofdeathintheUS.1In2020,COVID-19wasthethirdleadingunderlyingcauseof
deathafterheartdiseaseandcancer,withCOPDandchroniclowerrespiratorydiseaserankingsixth.
ThemortalityrateforCOPDhassteadilyincreasedsince2012,andgloballytheburdenremainshigh.
TheWorldHealthOrganizationestimatedthatapproximately3.2milliondeathswerecausedbyCOPD
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in2015,accountingfor5%ofallworldwidedeathsthatyear.
COPD is protractedintime andis responsible for more years lived with disability (3.6%) than all
otherrespiratorydiseasescombined.
1
Etiology
MostcasesofCOPDareattributabletocigarettesmokingintheUS.
Environmentalandoccupationaldusts(e.g.,wood-burningstoves,fumes,gases,andchemicals)are
othercommoncausesofCOPDworldwide.Householdindoor airpollutionis a majorcauseoffatal
COPD,particularlyindevelopingcountriesandruralareas.
2
α1-Antitrypsin(A1AT)deficiencyisfoundin1%–2% ofCOPDpatients.Clinical characteristicsof
affected patients may include a minimal or nonexistent smoking history, early-onset COPD (e.g.,
younger than 45 years), a family history of lung disease, or lower lobe–predominant panacinar
emphysema.
Pathophysiology
The pathogenesis ofCOPD involves inflammation, immune reactions, imbalance of proteinases and
antiproteinases,turnoveroftheextracellularmatrix,oxidativestress,andapoptosis.
Pathologicfeaturesincludedestructionofalveolartissueandsmallairways,airwaywallinflammation,
edemaandfibrosis,andintraluminalmucus.
Pulmonaryfunctionchangesincludedecreasedmaximalexpiratoryairflow,hyperinflation,airtrapping,
andalveolargasexchangeabnormalities.
Anincreasedincidenceofosteoporosis,skeletalmuscledysfunction,andcoronaryarterydiseaseoccur
inCOPD,perhapsindicatingasystemiccomponentofinflammation.
3
Prevention
In Western countries, abstinence from smoking is the most effective measure for preventing
COPD.
Domestic biomass fuel smoke inhalation is responsible for COPD in nonsmoking patients in rural
settings and developing countries, who sometimes have comparatively low cigarette smoking rates.
Strategies aimed at improving access to cookstoves and cleaner fuel sources along with increased
ventilationareessentialinthesepopulations(e.g.,theGlobalAllianceforCleanCookstoveshasbeen
establishedforthispurpose).
InpatientswithCOPD,smokingcessationmayresultinareductionintherateoflungfunctiondecline
andimprovedsurvival.
4,5
Tobaccocessationattemptswarrantrepeatinguntilthepatientstopssmoking.Mostsmokersfailinitial
attempts at smokingcessation,andrelapsereflects the natureof thenicotinedependenceandnot the
failureofthepatientorthephysician.
Amultimodalityapproachisrecommendedtooptimizesmokingcessation.
Counseling on the preventable health risks of smoking, providing advice to stop smoking, and
encouragingfurtherattemptstostopsmokingevenafterpreviousfailures.
Providingsmokingcessationmaterialstopatients.
Prescribing pharmacotherapy (Table 9-1); providers should take every advantage to counsel and
providepharmacotherapy.
TABLE9-1
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PHARMACOTHERAPYFORSMOKINGCESSATION
Product Dosing SideEffects/Precautions
NicotineReplacementTherapy
a
Transdermal
patch
b
7,14,or21mg/24h
Usualregimen=21mg/d=6
wk,14mg/d×2wk,7mg/d×
2wk
Headache,insomnia,nightmares,nausea,
dizziness,blurredvision(appliestoallnicotine
products)
Chewing
gum,
lozenges
2–4mgq1–8h
Graduallytaperuse
Inhaler 10mg/cartridge(4mg
delivereddose)
6–16cartridges/d
Nasalspray 0.5mg/spray
1–2spraysineachnostrilq1h
NonnicotinePharmacotherapy
Bupropion
ER(Zyban)
150mg/d×3d,thenbid×7–
12wk
Start1wkbeforequitdate
Dizziness,headache,insomnia,nausea,
xerostomia,hypertension,seizure
Avoidmonoamineoxidaseinhibitors
Varenicline
(Chantix)
0.5mg/d×3d,bid×4days,
then1mgbid×12–24wk
Start1wkbeforequitdate
Nausea,vomiting,headache,insomnia,
abnormaldreams
Worseningofunderlyingpsychiatricillness
a
Combinationtherapyisoftenused.Along-actingproduct(e.g.,patch)isusedforbasalnicotinereplacement,withashort-
actingproduct(e.g.,inhalerorgum)usedforbreakthroughcravings.
b
Ifpatientsmokeslessthanahalfpackperday,startat14-mgdose.
SeealsoFioreMC,BakerTB.Clinicalpractice.Treatingsmokersinthehealthcaresetting.NEnglJMed.2011;365:12221231forstrategiesandapproach.
TheUSDepartmentofHealthandHumanServiceshasdevelopedatelephone-basedsupportsystem
(1-800-QUIT-NOW)withanInternetanalog(smokefree.gov).
DIAGNOSIS
ClinicalPresentation
HISTORY
Patientsareusuallyolderthan40yearsatdiagnosis.
Cliniciansshould obtainasmokinghistory andquantify exposure to environmental andoccupational
risk factors. A family history of COPD, maternal tobacco use during pregnancy, and secondhand
tobaccoexposurealsoincreasetheriskofdevelopingCOPD.
Common symptoms are dyspnea on exertion, cough, sputum production, and wheezing. Typically,
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dyspneaonexertionprogressesgraduallyoveryears.
Symptom presenceandseverity ofCOPDcanbecollectedusingstandardizedquestionnaireslikethe
COPDAssessmentTest(CAT)(Table9-2).
TABLE9-2
CHRONICOBSTRUCTIVEPULMONARYDISEASEASSESSMENTTOOL(CAT)
Inevercough. 1 2 3 4 5 Icoughallthetime.
Ihavenophlegmormucusinmychest. 1 2 3 4 5 Mychestiscompletelyfullofmucusor
phlegm.
Mychestdoesnotfeeltight. 1 2 3 4 5 Mychestfeelstight.
WhenIwalkupahilloroneflightof
stairs,Iamnotbreathless.
1 2 3 4 5 WhenIwalkupahilloroneflightof
stairs,Iamverybreathless.
Iamnotlimiteddoinganyactivitiesat
home.
1 2 3 4 5 Iamlimiteddoingactivitiesathome.
Iamconfidentleavingmyhomedespite
mylungcondition.
1 2 3 4 5 Iamnotatallconfidentleavingmy
homebecauseofmylungcondition.
Isleepsoundly. 1 2 3 4 5 Idonotsleepsoundlybecauseofmy
lungcondition.
Ihavelotsofenergy. 1 2 3 4 5 Ihavenoenergyatall.
Totalscoreissumofscoresfromindividualquestionscales.
FromJonesPW,HardingG,BerryP,etal.DevelopmentandfirstvalidationoftheCOPDAssessmentTest.EurRespirJ.
2009;34:648-654.ReproducedwithpermissionfromGlaxoSmithKline.GlaxoSmithKlineisthecopyrightowneroftheCOPD
AssessmentTest(CAT).However,thirdpartieswillbeallowedtousetheCATfreeofcharge.TheCATmustalwaysbeusedinits
entirety.ExceptforlimitedreformattingtheCATmaynotbemodifiedorcombinedwithotherinstrumentswithoutpriorwritten
approval.TheeightquestionsoftheCATmustappearverbatim,inorder,andtogetherastheyarepresentedandnotdividedon
separatepages.AlltrademarkandcopyrightinformationmustbemaintainedastheyappearonthebottomoftheCATandonall
copies.ThefinallayoutofthefinalauthorisedCATquestionnairemaydifferslightlybuttheitemwordingwillnotchange.TheCAT
scoreiscalculatedasthesumoftheresponsespresent.Ifmorethantworesponsesaremissing,ascorecannotbecalculated;
whenoneortwoitemsaremissingtheirscorescanbesettotheaverageofthenon-missingitemscores.
Overlap with asthma, obstructive sleep apnea (OSA), bronchiectasis, and interstitial lung disease
(ILD)exists.
Beyondcoexistencewithotherrespiratorydisease,patientswithCOPDfrequentlyhavecomorbidities
that impactquality of life and prognosis. Osteoporosis, anxiety, depression, cardiovascular disease,
tobacco related malignancies, malnutrition,anddiabetes are all more common than expected among
patientswithCOPD.Symptomsrelatedtocomorbiditiesshouldbeinvestigated.
3
Asthediseaseadvances,cause-specificmortalityforpatientswithCOPD shiftsfromcardiovascular
diseaseandmalignanciesintheearlystagestorespiratoryfailure.Bothsevereairflowobstructionand
ahighfrequencyofexacerbationsincreasethelikelihoodofarespiratorydeath.
6
Disease severity should be stablished using multidimensional tools such as the Body mass index,
airflowObstruction,Dyspnea,andExercisecapacity(BODE)index(Table9-3).TheBODEindexhas
beenvalidatedas a moreaccuratepredictor of COPDmortality thanforced expiratoryvolume in 1
second(FEV1)alone.
7,8
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