Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4693_Библиотеки_им_академика_М_И_Перельмана
.pdf
million adults.
14
This temporal classificationsystemsays very little aboutthe etiology of CRS, which
remainsidiopathicintheoverwhelmingmajorityofcases.Averysmallfraction,however,areassociated
with systemic diseases such as Wegener granulomatosis, sarcoidosis, or cystic fibrosis, and these are
beyondthescopeofthischapter.
Rhinosinusitis is defined according to the Rhino sinusitis Task Force (RTF)
15
and the European
PositionPaperonRhinosinusitisandNasalPolyps(EPOS)guidelinedocuments.
13
Intermsofsymptoms,
diagnosis requires at least two symptoms of nasal obstruction/blockage/congestion, purulent nasal
discharge(anteriororposterior),facialpain/pressure,andhyposmia.TheEPOSguidelines(Table7.3)
goonestepfurtherandstipulatethat at leastonesymptommustbe obstruction/blockage/congestionor
nasaldischarge.TheguidelinesforthediagnosisofCRSincludebothsubjectiveandobjectivecriteria.
Althoughthesensitivityofsymptomsishigh,thespecificityislow.Positivecomputedtomography(CT)
scanswithLund–Mackayscores(Table7.4)of4ormorearefoundinonly20to36%ofpatientsmeeting
symptom criteria for CRS.
16–18
Therefore, thediagnosis of CRS should be accompanied byobjective
evidence inthe form of endoscopic or radiographic correlation.Specifically, endoscopic evidence of
CRS may take the form of middle meatal edema, polyps, or purulence. CT evidence of CRS is
characterizedbyair–fluidlevels,thickenedmucosa,orpolyps,withinthesinuses.TheseobjectiveCTor
endoscopic findings are important as they typically divide CRS into two broad subtypes: chronic
rhinosinusitiswithoutnasalpolyps(CRSsNP)andchronicrhinosinusitiswithnasalpolyps(CRSwNP),
whichwillbediscussedinmoredetailbelow.
Table 7.1Classificationofrhinitis
Infectious Noninfe ctious
Inflammatory
•Acuteviralrhinitis •Allergicrhinitis
•Acutebacterialrhinitis
•Occupational(synonym:work-relatedrhinitis;eitheran
allergicreactionoranirritantresponse[toxicrhinitis])
•Primaryatrophicrhinitis(attributedtoinfection
withKlebsiellaozaenae)
•Drug-inducedrhinitis(e.g.,aspirin-exacerbatedrespiratory
disease)
•Secondaryatrophicrhinitis
b
(e.g.,total
turbinectomy;superinfectionisuniformlypresent)
•NARES
a
•Hyperplasticadenoids
•Idiopathicrhinitis(e.g.,duetolocalimmunological
inflammation)
Noninflammatory
•Idiopathicrhinitis(e.g.,parasympathetic/sympathetic
dysregulation)
•Druginduced(e.g.,sideeffectsofACEinhibitorsor
reserpine)
•Hormonalrhinitis(e.g.,duringlasttrimesterofpregnancy)
•Emotionalrhinitis(e.g.,stressorsexualarousal)
•Food-inducedrhinitis(gustatoryrhinitis;e.g.,“hotfood”
stimulationofnervefibers)
•Cocainesniffing
a
Nonallergicrhinitiswitheosinophiliasyndrome.
b
Relatedtogranulomatousdiseases(e.g.,sarcoid,leprosy,rhinoscleroma).
ACE,angiotensin-convertingenzyme.
Table 7.2Differentialdiagnosisofrhinitis
Anatomicalfactors
Inflammatoryconditions
•Chronicrhinosinusitiswithorwithoutnasalpolyps
•Septaldeviation
•Turbinatehyperplasia
•Choanalatresia
Tumors
Benign(e.g.,invertingpapilloma,fibroma,neurilemoma,ossifyingfibroma,osteoma)
Malignant(e.g.,squamouscellcarcinoma,adenocarcinoma,lymphoma,melanoma,
esthesioneuroblastoma)
Granulomas
•Vasculitidae(Wegenergranulomatosis,Churg–
Strausssyndrome)
•Sarcoidosis
•Infectious
•Malignant—midlinedestructivegranuloma
Pseudotumors
•Adenoidalhyperplasia,mucoceles
Geneticdise ase
•Ciliarydefects
•Cysticfibrosis
Others
•Cerebrospinalrhinorrhea
•Foreignbodies
Even though the clinical pictures of rhinitis and rhinosinusitis are merging, the diseases will be
discussed separatelywithin this chaptertocover different time courses, etiologies, and therapyofthe
olfactorydisorder.
AcuteViralRhinitis—AcuteBacterialRhinosinusitis
ClincalCourse
Acute viral rhinitis (common cold) is defined as a as sudden onset, acute inflammation of the upper
airwaylastinglessthan10days.
6
Commoninitialsymptoms/signsareburningsensationslocatedinthe
noseornasopharynx,consistentwithanunderlyingviralinfection.Thecardinalsymptomsofacuteviral
rhinitisare nasal obstruction/blockage, nasal discharge (anterior/postnasaldrip),hyposmiaor anosmia,
and,dependingontheclinicalcourse,generalsymptoms.Thenasalsymptom–signcomplexforrhinovirus
andinfluenzaoccurswithin3daysafterexposure;thatforrespiratorysyncytialviruses(RSV)isdelayed
byasmuchas 7days.
7
Thesystemic symptomsoffever,headache, malaise, myalgia,andanorexiaare
relatedtotheeffectsofcytokinesreleasedfromimmunecells,andtheseresponsesdeveloprapidlyinthe
firstdaysofinfectionwhen the virus is detected bythe immunesystem.Thelocal symptoms of nasal
congestion and rhinorrhea are dependent on the generation of inflammatory mediators such as
prostaglandinsandbradykinin.
19
Headacheandpurulentsecretionindicatebacterialrhinosinusitis.
Table 7.3DefinitionofrhinosinusitisaccordingtotheEPOS(EuropeanPositionPaperonRhinosinusitisandNasalPolyps)guidelines
Inflammationofthenoseandtheparanasalsinusescharacterizedbytwoormoresymptoms,oneofwhichshouldbeeithernasal
blockage/obstruction/congestionornasaldischarge(anterior/posteriornasaldrip):
±facialpain/pressure
±reductionorlossofsmell
AND/EITHER
Endoscopicsignof:
•Polypsand/or
•Mucopurulentdischargeprimarilyfrommiddlemeatusand/oredema/mucosalobstructionprimarilyinmiddlemeatus
AND/OR
Computedtomographychanges
•Mucosalchangeswithintheosteomeatalcomplexand/orsinuses
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Chronicrhinosinusitiswithorwithoutnasalpolypsisdefinedas:
Presenceoftwoormoresymptomsoneofwhichshouldbeeithernasalblockage/obstruction/congestionornasaldischarge
(anterior/posteriornasaldrip):
±facialpain/pressure
±reductionorlossofsmell
for>12weeks
Table 7.4Lund–Mackayscore(computedtomographyscoringsystem)
Sinus syste m Left Right
Maxillary(0,1,2)
Anteriorethmoids(0,1,2)
Posteriorethmoids(0,1,2)
Sphenoid(0,1,2)
Frontal(0,1,2)
Osteomeatalcomplex(0or2
a
)
Totalpoints
0,noabnormalities;1,partialopacification;2,totalopacification.
Maximumscore:12/side
a
0,notoccluded;2,occluded
Pathophysiology
Acute viral rhinitis/rhinosinusitis is an inflammatory process of the nose and the paranasal sinuses,
causedmostlybyinfectionwithrhinoviruses,RSV,adenoviruses,influenzaviruses,parainfluenzaviruses,
coronaviruses, and others.
7,20
The viral infection frequently begins inthe nasal/nasopharygeal mucosa
and,upondetectionbythehost,invokestwointeractiveandtemporallyoverlappingdefensesystems:A
generalized, innate immune response and a virus-specific, adaptive immune response. Both systems
includeinflammatorypathwaysthatfacilitateandactivelyrecruitantiviralproteinsandeffectorcellsto
thesiteofinfection.
7
Rhinovirusesaccountfor30to50%ofallcolds,andcoronavirusesarethesecond
most common agent, accounting for 10 to 15% of colds.
19
These infections do not usually cause a
substantial destruction of olfactory epithelium. Nasal obstruction due to mucosal swelling with
hypersecretionispartlyresponsibleforthetypicaltemporaryolfactorydisorderthataccompaniesthese
viral URTIs. Nasal congestion in viral rhinitis is caused by the dilation of large veins in the nasal
epithelium(venoussinuses)inresponsetothegenerationofvasodilatormediatorsofinflammationsuch
asbradykinin,andswellingofmucousmembranesthatblockodortransporttowardtheolfactorymucosa.
The nasal dischargeassociated withviral rhinitis is a complex mix ofelements derived from glands,
goblet cells, plasma cells, and plasma exudates from capillaries, with the relative contributions from
thesedifferentsourcesvaryingwiththetimecourseoftheinfectionandtheseverityoftheinflammatory
response.
19
Moreover, numerous proinflammatory cytokines/chemokines and other mediators (e.g.,
histamine,leukotrienes,prostaglandins)havebeenreportedtobeinvolvedintheinflammatoryregulation
ofviralrhinitisandmightcontributetotheolfactorydisorder.However,appropriatestudiessupporting
thishypothesisarelacking.
If the clinical course is prolonged (more than 7 to 10 days) or complicated (e.g., purulent nasal
secretion), bacterial superinfectionshouldbe assumed.Some ofthe mainpathogensare Streptococcus
pneumoniaeorpyogenes,Haemophilusinfluenzae,Staphylococcusaureus,orMoraxellacatarrhalis.
21
Overall, however, only ~1% of viral respiratory infections lead to acute bacterial rhinosinusitis.
13
Pathologically,swellingofthenasalmucosapromotesblockadeoftheosteomeatalcomplexinthemiddle
meatus, followed by subsequent impairment of ventilation and drainage of the sinuses, and bacterial
superinfection.Other nonswellinginduced mechanisms,such as enhancedbacterial adhesion during the
viral replication phase, also promote superinfection (e.g., between influenza A virus infections and
streptococci).
Attheinitialinflammatoryphasethereisoverexpressionofinterleukin-6(IL-6),IL-8,andintercellular
adhesion molecule(ICAM).Apossiblesourceofthesecytokinesand ICAMisairwayepithelialcells.
The CXC-chemokine IL-8 has potent chemotactic properties for neutrophils, which are capable of
releasingproteasesandcytokines(e.g.,IL-8,tumornecrosisfactorα)aseffectorcellsinARS.
13
These
proinflammatorymediatorsalsoactivateT-helper(T
h
)cells,andmediatethemigrationofmacrophages
intotheinflamedtissue.IL-1β,IL-12,andotherproinflammatorycytokinesareupregulatedtoinitiateand
maintain cellular defense. As theseinflammatoryprocesses involve theolfactory epithelium,olfactory
disorders associated with ARS may also be a result of infiltration of the olfactory epithelium with
inflammatory cells, of interaction with the involved inflammatory mediators, or of a direct infection-
relatedfunctionalimpairment(e.g.,virulencefactorsorimmunomodulatorybacterialproducts).
OlfactoryDysfunction
Olfactorydysfunctionistemporaryandmildormoderateinmostpatientswithacuteviralrhinitisoracute
bacterial rhinosinusitis (ABRS), and typically olfactory function mirrors the clinical course of the
respiratorydisease. Akerlundetal
9
studied olfactorythresholdsandnasal mucosalchangesinpatients
with experimentallyinduced common colds. They found that individuals with an induced coronavirus
229E rhinitis had impaired olfaction and that the change in smelling ability correlated to the nasal
congestionbutnottothenasaldischarge.Hummeletal
22
foundthefollowingeffectsonolfactionafterthe
onsetofviralrhinitis:atransientincreaseinolfactorythreshold;adecreaseofodorintensityrating;anda
decrease in the N1 peak of chemosensoryevent-related potential (CSERP)amplitudeto olfactory and
trigeminalstimuli.Theyalsostudiedtheeffectofnasaldecongestionwithoxymetazolineduringthecold
andreportedthatN1CSERPamplitudes toolfactorystimuli—butnotolfactorythresholdsortrigeminal
CSERP—exhibited a significant increase. Hummel et al
22
concluded from this observation that viral
rhinitis has a small effect on olfactory function that may be independent of nasal congestion. To
summarize,itappearsthatthetemporaryolfactorydysfunctionassociatedwithviralrhinitisresultsmainly
from conductive causes owing to nasal blockage, but an inflammatory interaction with the olfactory
epitheliumorcentral olfactorystructures also appears possible. The endonasal regions that havebeen
showntoinfluencetheolfactoryperformancearedepictedinFig.7.1.
Treatment
Temporaryhyposmiaoranosmia,occurringduringacuteviralinfectionoftheupperrespiratorytract,is
thoughtnottorequirespecifictherapy.Usually,viralrhinitisistreatedsymptomaticallywithdrugssuch
as topical antihistamines, topical anticholinergic drops, decongestants, and antiphlogistic drugs.
However,theireffectsonolfactoryfunctionremainunclear.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Fig. 7.1 Endonasal regions that influence olfactory performance (indicated in orange). (From Hummel T, Welge-Lüssen A. Riech- und
Schmeckstorungen:Physiologie,PathophysiologieundTherapeutischeAnsatze.Stuttgart:Thieme;2005.)
ABRS resolves withoutantibiotic treatment in most cases. Antibiotic or anti-inflammatory therapy
should be considered in patients suffering from repeated severe episodes of ABRS with significant
prolongedolfactorydysfunction.Antibiotictherapyshouldtargetthemainpathogens.First-linetherapyat
mostcentersisusuallyamoxicillin,oramacrolideantibioticinpatientsallergictopenicillin,becauseof
the low cost,easeofadministration,andlowtoxicity oftheseagents.Ifpatientsfail torespond tothe
initialcourseoftreatment,analternativeantibacterialagentshouldbeconsidered.Ideally,anasalswab
testshouldbeconductedbeforeinitiatinganalternativeregimen.
Decongestants, mucolytic agents, and nasal or oral steroids are in widespread use is adjuvant
therapies. While the evidence for treatment with decongestants and mucolytics mainly results from
clinical experience, several studies have documented positive effects of flunisolide, budesonide, and
mometasoneonABRSsymptoms.Iflocaldecongestantsareused,theyshouldbeplacedoncottonasso-
called high inlay in the middle meatus.
13
The efficacy of antibiotics or adjuvant drugs on olfactory
disordersinABRShasnotbeensystematicallyevaluated.
AllergicRhinitis
ClincalCourse
ARisasymptomaticnasalhypersensitivityreactioncausedbyallergen-inducedimmunoglobulinE(IgE)-
mediatedinflammationofthemucousmembrane.
6
According to the World Health Organization (WHO), AR is subdivided, based on the duration of
symptoms,into“intermittent”(symptomson<4daysperweekoron<4weeksperyear)and“persistent”
(symptomson>4daysperweekandon>4weeksperyear).
6,23
Theseverityofsymptomsinuntreated
patients should be quantified, according to the Allergic Rhinitis and its Impact on Asthma (ARIA)
guidelines, as “mild” (mild symptoms, no impact on social life, school, and work) or “moderate to
severe”(severesymptoms,restrictionoflifequality,school,andwork).ThesymptomsofARarecaused
by the interaction of inflammatory mediators with glandular, vascular, or neurogenic structures of the
nose.Nasalsecretionsresultfromanincreaseofplasmaexudatesorsecretionsofsubmucosalglandsand
goblet cells, triggered by parasympathetic innervations or by increased transmitter release (e.g.,
vasoactiveintestinalpeptide,themainsourcemaybealsoT
h
2lymphocytes).Sneezingisaconsequence
of trigeminal nerve fiber stimulation by histamine, bradykinin, or various neuropeptides. Acute nasal
blockageiscausedbydilationandfillingofvenoussinusoidstriggeredbyparasympathetictransmitters.
Thelong-termdecreaseinnasalbreathingisthoughttoresultfromthickeningofthevascularconnective
tissue due to infiltration with inflammatory cells, organized edema, and fibrosis. However, airway
remodelingappearstobelessextensiveinthenasalmucosathaninthebronchialmucosa.
8,23
Pathophysiology
TheimmuneresponseinARinvolvesthereleaseofinflammatorymediatorsaswellastheactivationand
recruitment of cells to the nasal mucosa. In AR, different stages of the disease can be distinguished.
Duringsensitization,antigen-presentingcellsplayacrucialrole.Dendriticcellstakeuptheallergenand
migratetothemucosa-associatedlymphoidtissueandnecklymphnodes,wheretheyprimenaïveCD4+
T-lymphocytes (T
h
0 cells) that bear receptors for the specific antigen. The nasal mucosa in AR is
characterizedbythepresenceofahighpercentageofactivatedT
h
2cellsreleasingIL-4,IL-5,andIL-13.
IL-4 andIL-13thenactonB-cells topromote productionofantigen-specific IgE antibodies. Allergen-
specific IgE becomes fixed tohighaffinity IgE receptors (FcεRI)onthe membranes of mast cells and
basophils.Mastcellsarenotonlyeffectorcellsoftheimmediatephaseresponse,butalsoplayarolein
ongoing allergic inflammation. Eosinophils are both increased in numbers and activated in the nasal
mucosa of symptomatic allergic patients. T-cells, macrophages, fibroblasts, and other cells are also
present.Oncethepatientissensitizedtothespecificallergen,subsequentexposureleadstoacascadeof
events that resultinthe symptoms of AR. Theallergic response can be divided intotwo phases: The
immediateresponse(withinminutes afterallergen exposure)andthe late-phaseresponse(4 to8hours
afterallergenexposure).
23
OlfactoryDysfunction
Olfactorydysfunctionhasbeenreportedin~23to88%ofpatientswithAR.
24,25
InAR,thereisusuallya
temporaryquantitative olfactory dysfunctionwith periodsofreducedor abrogated olfactory sensitivity
duringallergenexposure.
26
Insubjectswithgrasspollenallergies,performanceinolfactoryidentification
and discrimination tests is not different from nonallergic controls if tested out of the season, but a
significantdecreaseinodorthresholdandodoridentificationhasbeenreportedfromtheseventhdayof
theallergyseasoninuntreatedpatients.
27
InpersistentAR,patientshaveamorestable,moderatelossof
smell,withahigherimpairmentinthosewithself-reportedhyposmiaandmoderate-to-severerhinitis.
28
Patients with dust mite rhinitis performed worse than healthy controls in odor identification, odor
threshold,andodordiscriminationtestingduringthewinterseason,whenhighallergenexposuremaybe
expected.
25
There are three reasonsforolfactory disorderinAR: (1) Conductive olfactory dysfunction(dueto
swelling of nasal mucous membranes or massive hypersecretion); (2) changes in olfactory mucus
(qualitativeorquantitative);and(3)directeffectsofmucosalinflammationon theolfactorycleft.With
few exceptions (e.g., upregulation of eosinophil cationic protein), the interactions between
immunoinflammatory or neurogenic mediators and the olfactory epithelium are widely unknown in
AR.
23,27,29
Infiltrationoftheolfactorycleftmucosawitheosinophilshasbeendescribedinhumanswith
seasonalAR,
29
andasignificantrelationshipbetweenolfactorythresholdandeosinophillevelsinblood
andnasaldischargehasbeenreported.
30
Itisthereforethoughtthatthemostimportantcausesofolfactory
dysfunctioninAR are infiltration byinflammatorycells andupregulationof immunological mediators,
alteringthefunctionofneurogenicolfactorystructures.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Treatment
Althoughthegeneralconsensusisthatallergenavoidanceshouldleadtoanimprovementinsymptoms,a
systematic review ofdust miteallergen avoidancehas shownthat single measures arenot effectivein
reducingsymptomsofAR.Theroleofallergenavoidancefortheimprovementofolfactorydisordersis
notyetclear.
13,23
Topicalsteroidshavebeenusedsuccessfullytoimproveodorthreshold,odoridentification,andodor
discrimination.
26,29
Topical steroids are superior to antihistamines intreatment of nasal congestion in
seasonalAR,andparticularlyinthe improvement ofolfactoryfunction.
31
However,usingconventional
dropsorspraydevices,mostofthedrugisdepositedintheanteriorthirdofthenasalcavity,andhasno
directeffectontheolfactoryregion.
32,33
Toachievebetterdepositionofthedrugatorneartheolfactory
cleft,nasal drops canbe administered in theso-called head-down-forward position,
33
or sprays with
prolongedapplicatorsorcannulaeshouldbeused(Fig.7.2).
34
Fig.7.2ashowsareshapedspraycannula
(for Xylocaine®pump spray, AstraZeneca GmbH,Wedel, Germany) on a self-made budesonide pump
spray. Fig. 7.2bdepictsthecannulainsertedintherightnasalcavitydirectly below theolfactory cleft.
Patients can be trained with video endoscopy to locate the head of the spray cannula correctly.
Additionally,oralsteroidscanbeusedintherapy-refractoryrhinitis,especiallyasaso-calledshort-term
oral steroid trial insevere cases. The short-term administrationoftopical decongestants may provide
additiveeffectsasatrailblazerforotheranti-inflammatorydrugsinpatientswithseverenasalblockage.
Leukotrienereceptorantagonistsplaynoroletodayinthetreatmentofsinonasalolfactorydisorders.
Specificimmunotherapy(SIT)addressesthecauseofallergicdiseasesandshould be usedearlyin the
course of the disease when indicated.
6,23
The effect of SIT on olfactory dysfunction has not been
systematicallyevaluated.Surgicalinterventionmaybeusedtoimproveseverenasalobstruction(e.g.,in
patientswithmassiveseptaldeviationorturbinatehyperplasia).
6,23
Otherformsofrhinitisareclassifiedasidiopathicrhinitis(IR),whichisanumbrellatermsuggested
by theARIA–WHO Working Group for rhinitis with an unknown pathogenesis.
6,8,23
Olfactoryfunction
wasreportedlypoorerin“nonallergicrhinitis”patientsthaninseasonalorperennialARpatients.
35,36
The
poorly understood pathophysiology of IR does not currently allow a precise hypothesis for sinonasal
olfactory disorders. However, it is likely that the modified release of neurotransmitters in neurogenic
inflammation affectstheolfactoryandtrigeminalsystemsinIR.
37
Treatment consistsoftopical steroids
(budesonide400or800mg/d,orfluticasone200or 400 mg/d) or topicalantihistamine(azelastine1.1
mg/d).
8
Nonallergic rhinitis with eosinophilia syndrome is characterized by the presence of nasal
eosinophilia(nasalcytologyanalysisshowinggreaterthan20%eosinophils)andperennialsymptomsof
sneezing,itching,andrhinorrheaintheabsenceofdemonstrableallergy.
6
Anosmiaisaprominentfeature
notsharedwithAR.Treatmentconsistsmainlyofintranasalcorticosteroidswithorwithouttheaddition
ofsecond-generationantihistaminesorleukotrienereceptorantagonistsasanadjuvant.
38
Fig.7.2a,bAdministrationofnasalspraytotheolfactorycleft.
aSelf-madespraydevicewithlongcannula.
bEndoscopicviewintotherightnasalcavity:thespraycannulaislocateddirectlybelowtheolfactorycleft.
AtrophicRhinitis
Primary atrophic rhinitis is characterized by progressive atrophy of the nasal mucosa and underlying
bone.Ciliatedepitheliumisreplacedbystratifiedsquamousepithelium.Thenasalcavityiswidenedand
isfilledwithstinkingcruststhatareblackordarkgreenanddry.Ithasbeenattributedtoinfectionwith
Klebsiella ozaenae, although its role as a primary pathogen has notbeen determined.
6
The condition
produces nasal obstruction, a persistent hyposmia or anosmia, and an unpleasant odor. It must be
distinguished from secondary atrophic rhinitis, which is associated with specific conditions such as
syphilis, lupus, leprosy, rhinoscleroma, granulomatous disease, excessive nasal surgery, and radiation
therapy.
6,39,40
Thesensorylossofatrophicrhinitismayberelatedtoatrophyofnervesinthenasalcavity.
Treatmentofatrophicrhinitiscanbeeithermedicalorsurgical,includingnasalirrigationwithsaline,
localantibiotics,ornarrowingofnasalcavitiesby,forexample,medialdisplacementofthelateralwall
ofthenose.
39,40
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
ChronicRhinosinusitis
ClinicalCourse
According to the definition, symptoms of rhinosinusitis include facial pain and pressure, nasal
obstruction,drainage,andhyposmia.WhileviralURTIshaveanestablishedalthoughunknownincidence
ofolfactoryloss (seeChapter 8),neitherARSnorRARShavea significantassociationwitholfactory
loss. CRS,onthe otherhand, isassociatedwith olfactory deficits,but literatureontheoutcomeofits
treatmenthasfocusedonreliefofobstructionandpain/pressuresymptomswithrelativelylittledataon
eithertheincidenceofsmelllossinCRSorimprovementposttreatment.Morerecentstudies,whichhave
focused on this issue, demonstrated that olfactory dysfunction occurs in over 60% of patients with
CRS,
2,41
even though 8 to 25% of these patients are not aware of their olfactory deficit.
42,43
Nasal
polyposis, asthma,acetylsalicylic acidintolerance,andrevisionsurgeryareriskfactorsforhyposmia
andanosmiainpatientswithCRS.
1,44
Furthermore,thedegreeofolfactorydysfunctioncorrelateswiththe
burdenofinflammatorydiseaseonendoscopyandCT.Thediagnosis,asmentionedintheintroduction,is
made according to RTF
15
and EPOS guidelines,
13
the latter of which also distinguishes acute from
recurrentandchronicrhinosinusitis.Endoscopically,twodifferentforms,CRSsNPandCRSwNP,canbe
distinguished.Theetiologyofbothformsremainsunclearandsignificantoverlapcanexist,buttheycan
bedistinguishedtoadegreebythepatternofinflammationandclinicalcourse.Specifically,CRSwNPis
associatedwithaT
h
2patternofinflammationandmore pronouncedsymptomsofobstructionandsmell
lossthanCRSsNP.CRSsNPexhibitsaT
h
1patternofinflammationandmorepronouncedcomplaintsof
drainage andfacial pressure.
45
While both forms can cause smell loss, the presence of nasal polyps
carriesanoddsratioof2.38forriskofhyposmia.
1
Pathophysiology
BiopsyoftheolfactorymucosademonstratesinflammatorychangesinCRS,suggestingthatdirectdamage
tothereceptorepitheliumcontributestoolfactorydysfunctioninCRSpatients(Fig.7.3).Moreover,there
appears tobeacorrelationbetweentheintensityoftheinflammationintheolfactorymucosaonbiopsy
andthepresenceofolfactorydysfunction.
46,47
Morerecently,Yeeetalidentifiedthreepatternsofmucosal
change associated with CRS.
48
While many patients demonstrated normal olfactory neuroepithelium,
severaldistincthistologicalpatternsweredescribed,apparentlyreflectinglocalpathological responses
tovariousdegreesofchronicinflammation.Thegobletcellhyperplasia pattern ischaracterizedbythe
presenceofgobletcells intermixedwith olfactorysupportingcells with preservationoftheunderlying
neuronallayers withinthe olfactory epithelium.Undernormal circumstances, gobletcellsare typically
found in the respiratory epithelium only, and not the olfactory epithelium. The squamous metaplasia
pattern is characterized by a change of the apical layers to thick squamous layers extending into the
olfactory epithelium. Severe squamous metaplasia is characterized by sloughing of apical layers with
transformationintoacontinuoussquamouslayer.Thispatternisalsocharacterizedbyhyperproliferation
of basal layers. The squamous change has been hypothesized to be a protective response to injury,
irritation,andchronicinflammation,butthismayactuallyinhibitrecoveryofsensoryepithelium.Finally,
theerosivepattern canrangefrom mildlossofapical celllayersandsome supportingcells,tosevere
erosionwithpreservationofonlyafewlayersofbasalcells,tocompleteerosionwithexposedbasement
membrane.This pattern is presumed to resultfrom the local activity ofdegradative enzymes released
frominflammatorycells,renderingtheepitheliumvulnerabletomechanicalstressesandsloughing.Itis
postulatedthatthesepatternsrepresentaspectrumofdiseaseintensity.Givenadecreasingprevalenceof
eosinophils, macrophages, and neutrophils from erosion, to squamous metaplasia, to goblet cell
hyperplasia, itispossible thatthismay representa sequenceofdamagefollowedbyrepair.However,
whether this representsanorderlyprogressionofchangeremainsunclear.Lastly,itshould bebornein
mind that olfactory mucus has vastlydifferent ion concentrations from surrounding respiratory mucus.
Maintenance of this ionic milieu is critical for olfactory transduction along the apical surface of the
sensoryepithelium.
49,50
Althoughthistopichasnotbeenproperlystudied,chronicinflammationislikely
toaltertheseconcentrationswithsecondary,negativeeffectsonolfaction.Mostlikely,olfactorydeficits
inpatientswithCRSarethesummationofdiminishedairflow,damagetotheepithelium,andalterations
tothelocalionicmicroenvironment.
Fig.7.3 Highpowerhematoxylinandeosin–stainedolfactorymucosain chronic rhinosinusitis.Note thepresence ofinflammatoryinfiltrate
withintheolfactoryepithelium.N,olfactorynervebundles;L,lymphocyticinfiltrate.
MedicalTreatment
The medical treatment ofCRS depends onits pheno type. For CRSsNP,treatment should include oral
antibiotictherapyformorethan2weeksaswellasintranasalsteroidsandnasalsalinedouches.There
arenocleardataontheefficacyoforalsteroids,buttheyareincludedinguidelinerecommendationsin
some countries (e.g., Germany), and they are commonly prescribed for unresponsive patients, in
particularthosewithsignificantconcomitantAR.Theuseoforalprednisone,inadditiontoantibiotics,is
particularlycommoninpatientswithCRSsNPwhopresentwithsignificantolfactorydeficits.Thechoice
ofantibioticshouldbedirectedagainstorganismsisolatedonculturewhenpossible,but,whenpurulent
secretionsarenotidentified,abroadspectrumantibioticwithcoverageforgram-positive,gram-negative,
andsomeanaerobiccoverageshouldbeinitiated.
51
CRSwNP is typically more responsive to corticosteroid treatment, and current recommendations
includetheuseofsteroids(bothoralandintranasal)aswellasnasalsalinedouches.Steroidtherapyhas
beenshowntoreverseolfactorydysfunction,althougheffectstendtobeincompleteandtransient.Seiden
andDuncanperformedaretrospectivestudyofpatientswithhyposmia/anosmiaasaprimarysymptom.
52
Aftera“pulsedose”oforalsteroids,theyfoundthat83%(30/36)improved,whileonly25%(13/52)of
those treated with topical steroids noticed improvement. Complete failure to respond to oral
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Соседние файлы в папке Библиотека им академика М.И. Перельмана