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167. SwensenSJ,ViggianoRW,MidthunDE,etal.LungnoduleenhancementatCT:multicenterstudy. Radiology.2000;214:73-80.
168. GouldMK,DoningtonJ,LynchWR,etal.Evaluationofindividualswithpulmonarynodules— whenisitlungcancer?Diagnosisandmanagementoflungcancer,3rded:AmericanCollegeof ChestPhysiciansevidence-basedclinicalpracticeguidelines.Chest.2013;143:e93s-e120s. doi:10.1378/chest.12-2351
169. MacMahonH,NaidichDP,GooJM,etal.Guidelinesformanagementofincidentalpulmonary nodulesdetectedonCTimages:fromtheFleischnerSociety2017.Radiology.2017;284:228-243.
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173. LightRW.Anewclassificationofparapneumoniceffusionsandempyema.Chest.1995;108:299-
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174. LightRW,GirardWM,JenkinsonSG,GeorgeRB.Parapneumoniceffusions.AmJMed. 1980;69:507-512.
175. MillerAC,HarveyJE.Guidelinesforthemanagementofspontaneouspneumothorax.Standardsof careCommittee,BritishThoracicSociety.BMJ.1993;307:114-116.
176. FraserRS.Pneumothorax.In:FraserRG,PareAJ,eds.FraserandPare’sDiagnosisofDiseases oftheChest.4thed.WBSaunders;1999:2781-2794.
177. JantzMA,PiersonDJ.Pneumothoraxandbarotraumas.ClinChestMed.1994;15:75-91.
178. BoylanA,BroaddusVC.Tumorsofthepleura.In:MasonRJ,MurrayJF,NadelJA,Broaddus VC,eds.MurrayandNadel’sTextbookofRespiratoryMedicine.4thed.ElsevierHealth Sciences;2005:1989-2010.
179. FerrerJS,MuñozXG,OrriolsRM,etal.Evolutionofidiopathicpleuraleffusion:aprospective, long-termfollow-upstudy.Chest.1996;109:1508-1513.
180. AlmoosaKF,McCormackFX,SahnSA.Pleuraldiseaseinlymphangioleiomyomatosis.Clin ChestMed.2006;27:355-368.
181. HeffnerJE,BrownLK,BarbieriCA.Diagnosticvalueofteststhatdiscriminatebetween exudativeandtransudativepleuraleffusions.Chest.1997;111:970-980.
182. SahnSA,HeffnerJE.Spontaneouspneumothorax.NEnglJMed.2000;342:868-874.
183. SahnSA.Stateoftheart.Thepleura.AmRevRespirDis.1988;138:184-234.
184. LightRW.Clinicalmanifestationsandusefultests.In:LightRW,ed.PleuralDiseases.4thed. LippincottWilliamsandWilkins;2001:42-86.
185. LeeYCG,LightRW.Futuredirections.In:LightRW,LeeYCG,eds.TextbookofPleural Diseases.HodderArnold;2003:536-541.
186. LightRW,MacgregorMI,LuchsingerPC,BallWCJr.Pleuraleffusions:thediagnosticseparation oftransudatesandexudates.AnnInternMed.1972;77:507-513.
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187. SolookiM.Diagnosticyieldofcytologyinmalignantpleuraleffusion:impactofvolumeand repeatedthoracentesis.EurRespJ.2011;38:p3550.
188. KennedyL,SahnSA.Noninvasiveevaluationofthepatientwithapleuraleffusion.ChestSurg ClinNAm.1994;4:451-465.
189. WoodringJH.Recognitionofpleuraleffusiononsupineradiographs:howmuchfluidisrequired? AmJRoentgenol.1984;142:59-64.
190. ChenA,MassoniJ,JungD,CrippinJ.Indwellingtunneledpleuralcathetersforthemanagement ofhepatichydrothorax:apilotstudy.AnnAmThoracSoc.2016;13:862-866.
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192. HeffnerJE,KleinJS.Recentadvancesinthediagnosisandmanagementofmalignantpleural effusions.MayoClinProc.2008;83:235-250.
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11
AllergyandImmunology
JenniferM.Monroy,DayneVoelker
AdverseDrugReactions
GENERALPRINCIPLES
Definition
Anadversedrugreaction(ADR)isanundesiredpharmacologicalresponsethatoccurswhenadrug isgivenfortheappropriatepurpose. Theetiologyofadrugreactioncanbeimmunologic,toxic,oridiosyncraticinnature. Drugallergyisduetoanimmuneresponsethatismediatedbydrug-specificantibodyorTcells.
Classification
TypeAreactionsarepredictable,oftendosedependent,andrelatedtothepharmacokineticsofthedrug. They comprise up to 80% of all ADRs (e.g., hepatic failure due to overdose of acetaminophen, sedativesideeffectsofantihistamines,drug–druginteractions,andgastrointestinalbacterialalteration afterantibiotics). TypeBreactionsareunpredictableandarenotrelatedtothedoseorthedrug’spharmacokinetics.They accountfor10%–15%ofallADRs.
Immune-mediated adverse reactionscanbe from a varietyofmechanisms. They usually occuron reexposuretotheoffendingdrug. Nonimmunologic reactions (pseudoallergic or anaphylactoid) are caused by IgE-independent degranulationofmastcells.
Epidemiology
ADRsarereportedtoaccountfor10%–15%ofhospitalizedpatients.
1
MortalityfromADRsissignificantandrangesfrom0.14%to0.32%.
2
Lifetimeprevalenceofdrug-inducedanaphylaxisis0.05%–2%.1ThemostcommondrugscausingIgE­mediatedanaphylaxisarepenicillinsandanestheticagentsgivenduringtheperioperativeperiod.Drug­inducedanaphylaxisisseenpredominantlyinolderagegroup.
Etiology
β-Lactam antibiotics are the most common drug class allergy in United States, which includes penicillins, penicillin derivatives (ampicillin and amoxicillin), cephalosporins, monobactams, and carbapenems. Penicillin allergy is the most prevalent antibiotic allergy of this class. About 8% of patientsinhealthcarereporthaveapenicillinallergy.
3
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About 90% patients with history of penicillin allergy will be able to tolerate penicillins, as most patientsoutgrowtheirallergyovertime.4Giventhelowerlikelihoodofhavingtruepenicillinallergy, antimicrobialstewardshipprogramshavebeendevelopedtodecreaseuseofβ-lactamalternatives. Hospitalizedpatients with a historyof penicillinallergy havebeen shownto havea longer hospital stay with increased incidence of vancomycin-resistant Enterococcus, methicillin-resistant Staphylococcusaureus,andClostridioidesdifficileinfectionscomparedtopatientswithoutareported penicillinallergy.
5
Thechemicalstructureofpenicillinsresultsintheirhighimmunogenicitywithareactiveβ-lactamring thatcovalentlybindswithcarrierproteinstoformahapten,whichstimulatesanimmuneresponse.
Themajordeterminantofimmunogenicityofpenicillinisthebenzylpenicilloylformseenin93%of tissue-boundpenicillin. The minor antigenic determinants are all remaining penicillin conjugates. They comprise
benzylpenicillin,benzylpenicilloate,andbenzylpenilloate. The cross-reactivity between β-lactam antibiotics is variable and largely determined by their side­chainstructureattachedtotheβ-lactamring.
Risk of a cross-reaction between a penicillin and cephalosporin that do not share the sameside
chainis<2%.Cross-reactivitybetweenpenicillinandmonobactamsis0%,betweenpenicillinand
carbapenemsis<1%,andbetweencephalosporinsandcarbapenemsis<1%.
6
Patients with amoxicillin allergy should avoid cefadroxil, cefprozil, and cefatrizine as all these
drugssharesameR-groupsidechain.
The monobactam aztreonam does share an identical R1-group side chain as ceftazidime and is
cross-reactive.
Sulfonamideallergy
There is an increase in allergy to sulfonamides in patients with HIV compared to the general
population.Trimethoprim–sulfamethoxazolehypersensitivityoccursin60%ofHIV-positivepatients
comparedto5%ofHIV-negativepatients.
7
TypeIIgE-mediatedreactionstosulfonamidesarenotcommon.Themostfrequentlyseenreactionis
a maculopapular rash (T cell–mediated) that develops 7–12 days after initiating the drug. Other
reactionsincludeurticariaand,lesscommonly,anaphylaxis,Stevens–Johnsonsyndrome(SJS),and
toxic epidermal necrolysis (TEN). Cross-reactivity between antibiotic and nonantibiotic sulfa-
containing medications is low.8 Patients with sulfonamide antibiotic allergy were more likely to
reacttopenicillinthanasulfonamidenonantibiotic.
8
NSAIDs and aspirin can cause IgE-mediated urticaria, angioedema, and anaphylaxis. It can also exacerbateurticariainpatientswhohavechronic urticaria. Exacerbationofrespiratorysymptomsin patients with underlying asthma is referred to as aspirin-exacerbated respiratory disease (AERD). AERD is composedofa triad consisting of asthma,NSAIDsensitivity, andnasal polyposis. COX2 inhibitorsaregenerallysafetoadministerinthesepatients.Aspirindesensitizationfollowedbydaily aspirin therapy in AERD patients improves asthma exacerbations, oral steroid use, reduced nasal polyps,andsinusinfections.CertainasthmabiologicscanalsobeusedinpatientswithAERD.
Pathophysiology
TheimmunologicmechanismsfordrughypersensitivityaredemonstratedintheGellandCoombs classificationofhypersensitivity(Table11-1).
TABLE11-1
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