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corticosteroidswitheventransientimprovementshouldsuggestthepossibilityofadditionalcontributions
to olfactory loss beyond nasal polyposis. The use of antibiotics is not currently in the guideline
recommendationsforCRSwNP,althoughVanZeleetalrecentlyconductedadouble-blind,randomized,
placebo-controlled trial where patients with recurrent polyposis after surgery or massive polyposis
receivedplacebo (n=19),methylprednisolonetaper(n = 14),or doxycycline(n = 14)for20 days.
53
Theyfoundthatdoxycyclineprovidedlastingreductioninpolypsizeandreductioninpostnasaldripfor
the duration of the 12-week study period. Unfortunately, doxycycline did not provide any significant
change in smell loss. Methylprednisolone provided a more dramatic improvement initially, but these
changes—includingreducedhyposmia—returned tobaselinelevelswithin 1to2 months.
53
It hastobe
keptinmindthatonlysubjectiveratingswereobtained.Theseareknowntoberatherunreliableandtend
toreflectnasalbreathingratherthanmeasuredolfactoryfunction.
54
Oral antihistaminemayalsobebeneficialinallergic patientspostoperatively topreventrecurrence,
buthasnoimpactonpolypsizeandnodocumentedeffectonhyposmia.Oralleukotrieneantagonistsmay
havesomebenefitin thetreatmentofpolyps.Parnesand Chumafollowedanuncontrolledcohortof36
patients withCRSwNP whowere givenzafirlukast or zileutonin additiontostandard medical therapy
over a mean of 7.4 months.
55
Twenty-four patients noticed some symptomatic improvement including
rated,butnotmeasured,olfactoryacuity.However,thisiswithintherangeofexpectedimprovementfrom
standard medical therapy, making it difficult to attribute the change to the addition of leukotriene
antagonists. Prospective randomized controlled trials are needed. These medications are not currently
recommendedasastandardpartoftherapy.
If patients improve with medical therapy, maintenance regimens including intranasal steroids are
prescribed,butlongstandingimprovement,particularlyinolfactoryloss,canbeproblematic.
56
Patients
with either form of CRS who fail to improve with medical therapy, or require high-dose oral
corticosteroidstocontrolsymptoms,maybecandidatesforsurgicaltherapy.ApreoperativeCTshouldbe
obtained to facilitate surgical planning and to confirm the diagnosis (if not already identified via
endoscopy).
SurgicalTreatmentofChronicRhinosinusitis
In cases of medical failure, endoscopic sinus surgery(ESS) is the current gold standard approach to
addressing CRS symptoms, including hyposmia. An attempt should be made to address the affected
sinuses conservatively, without disruption of other sinus mucosa or outflow tracts.
57,58
As mentioned
earlier,CRSwNPhasamuchhigherincidenceofassociatedsmelllossthanCRSsNPandcasesofmore
severe olfactory deficits are only rarely the result of CRSsNP alone. Surgical goals are potentially
different for the two phenotypes as CRSsNP is widely believed to be related to mechanical outflow
obstruction at the osteomeatal complex, while CRSwNP probably reflects a more primary mucosal
inflammatoryprocess,developingindependentlyofventilationstatus.Assuch,newer,minimallyinvasive
balloon dilatational techniques, which are fundamentally geared toward establishing sinus ventilation
alone,maynotbeadequateformanagementofCRSwNP.Actualstudiesofballoondilatationaloneforthe
managementofCRSwNParelacking,however.StandardESSventilatesthesinuscavitiesandremoves
inflamed sinonasal tissue (including polyps), reducing the inflammatory burden as well as improving
airflowtotheolfactorycleft.Postoperatively,intranasalsteroidshaveincreasedaccesstothenasaland
olfactorymucosa,presumablyenhancingefficacy.ThelimitationofESSforthemanagementofCRSwNP
ispolyprecurrence.Studiesindicatethataround20%ofpatientswillrequirerepeatESSwithin5years
tomaintain symptomcontrol.
59
Moreover, hyposmia maybe the most difficultsymptom to control, as
smell loss is often the first sign of polyp regrowth. Hence, a combination of intermittent oral
corticosteroid bursts may be required post ESS to maintain olfactory sensationat normal levels. The
clinician must weigh the long-term side effects of this regimen versus quality of life issues in the
individual patient. Several studies have specifically focused on sinus surgery to maintain olfactory
sensationinCRSwNP.Jafeketal
60
firstreportedtwopatientswhohadnasalpolypsandanosmia.Both
patientshadundergonepolypectomyandsufferedrecurrenceoftheirpolyps.Followingrevisionsurgery,
both patientsremainedanosmic, ultimatelynecessitating oral corticosteroid regimensto maintainlong-
termimprovementofanosmia.Therequirementforcombinedtreatment(surgeryandcorticosteroids)was
thefirstsuggestionthatolfactorylossinCRSwNPwasmorecomplexthansimplemechanicalblockageof
airflowtothe olfactorycleft.Morerecently,Stevensstudied24patientswhohadpolypswith anosmia
andunderwentsinussurgery.
61
Halfofthepatientsremainedanosmicaftersurgeryandwereunresponsive
tonasalsteroids,butmostofthesepatients’senseofsmellwasrestoredwithoralsteroids.Inthisseries,
thepatientswhohadimprovementand thosewho didnot weresimilar,allhaving preoperative diffuse
sinonasalpolyposis. Theeffectivenessoforal corticosteroids inrestoring olfactory function reinforced
the work of Jafek's group, suggesting a direct effect on the olfactoryneuroepithelium. Further studies
focusingprimarilyonsurgicaleffectshavealsodocumentedimprovementinolfaction,albeitincomplete.
Lund andScadding
62
in a series of 50 patients followed over a mean of 2.3 years, found significant
improvementofvisualanalogandUniversityofPennsylvaniaSmellIdentificationTest(UPSIT)scores;
however the average UPSIT score of 25 remained in the markedly hyposmic range. Klimek et al
63
evaluated 31 patients with hyposmia and CRSwP immediately prior to surgery and at six times
postoperatively. They foundthat improvementto mild hyposmia occurred at 3 months postoperatively
with olfactory declineto preoperative states between 3 to 6 months postoperatively. Rowe-Jones and
Mackay
64
followed 115 patients with CRS prospectively, evaluating the effects of surgery and
postoperative oral prednisone tapered over 3 weeks with amoxicillin/clavulinic acid. They found
improvementin87%subjectively,and82%byvisualanalogscale.DelankandStoll
43
measuredodorant
detectionthresholdsforCRSpatientsundergoingESSandfoundthatdespitea70%rateofpostoperative
olfactoryimprovement,only25%ofhyposmicsand5%ofanosmicsreachednormalolfactorythresholds.
PadeandHummel
65
examined387patientspreoperativelyand206patientspostsinussurgeryusingthe
“Sniffin’ Sticks” test battery, and were only able to measure an increase in olfactory function in 48
patientswhile140didnotshowanychangeintheirolfactoryfunction.Ithastobepointedoutthatitisof
great importance to measure olfactory function rather than evaluate olfactory function using a visual
analogscaleashascommonlybeendone,especiallyinearlierstudies.Thesedataconcerningolfactory
self-assessment are rather unreliable. The flowchart (Fig. 7.4) summarizes the work-up and possible
therapeuticoptionsinCRS.
Conclusion
CRS,typically the polypoidform, is associated with smell loss as a major complaint. Thepathology
probablyinvolvesdiminishedaccessofodorantstotheolfactorycleftaswellasdirectinflammationof
the neuroepithelium. Medical therapy including oral corticosteroids is standard, with surgery (ESS)
offeredtothosewhofailtoimproveorrequireexcessivecorticosteroidstocontrolsymptoms.Physicians
andpatientsshouldunderstandthatsmelllossmaybethemostdifficultofallCRSsymptomstotreatlong
term, often necessitating combined ESS and medical therapy. Studies indicate that long-term oral
corticosteroidsmaybenecessaryaswell,tomaintainolfactorysensationinthenormosmicrange.
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Fig.7.4 Treatmentalgorithm forsinonasalolfactory disorders. AR,allergicrhinitis;CRS,chronicrhinosinusitis;CT,computedtomography;
ENT, ear, nose, and throat; FESS, functional endoscopic sinus surgery; HDF, head-down-forward position; IR, idiopathic rhinitis; MRT,
magneticresonancetomography;PRN,asneeded;UPSIT,UniversityofPennsylvaniaSmellIdentificationTest.Olfactorycleftapplicator:see
Fig.7.2a.
Fig.7.5a–cCTofapatientwithnasalpolypsinvolvingandnearlyobstructingallsinusesoncoronal(a),sagittal(b),andaxial(c)images.
CaseStudy
A 37-year-oldmanwasreferredforevaluationofthegradualonsetofnasal symptomsover thepast5
months. He was severely hyposmic but his other CRS symptoms were described as relatively mild,
includingnasalobstruction,facialpressure,andincreasedsneezing.Hiswifenoticedthathehadstarted
snoring more often. He denied any symptoms of purulent discharge, Eustachian tube dysfunction, or
historyofasthma.Hehadbeentreatedwithintranasalcorticosteroidswithoutmuchimprovement.
Hewasotherwisegenerallyhealthywithnoknownallergies.Skinpricktestingwaspositivetotrees,
dustmites,cats,dogs,andcockroaches.Hedid notsmokeor drink alcohol.He workedasa financial
director.
A completeheadandneckexaminationwas performed,yielding onlyedematousinferiorturbinates.
Flexiblenasalendoscopydemonstratednasalpolypsoriginatingfromhismiddlemeatus,andoccupying
50%ofhisnasalairwaybilaterally.
CTdemonstratedthepresenceofpolypsinallofhissinuses(Fig.7.5)andacourseoforalandnasal
steroidswasinitiated.Hissymptomsimprovedonlyminimally,andheagreedtoESSwithpolypectomy.
Hispathologyrevealednasalpolypswithmarkedeosinophilia.
Postoperatively, he was able to obtain significant improvement on maintenance therapy with
fluticasone propionate only. His UPSIT scores increased from 23/40 (severe microsomia) to 36/40
(normal)at6monthspostsurgery.
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8PostinfectiousandPost-traumaticOlfactoryDisorders
CarlPhilpott,RonDeVere
Etiology,Prevalence,andPathophysiology
PostinfectiousOlfactoryDisorders
The commoncold, whilea minorinconvenienceformost, remainsascourgeofmodernmedicine,with
treatmentslimitedtoover-the-counterremedies.Allofuscanprobablyrecallhavinghadacoldwhere
our sense of smell and the pleasure of eating was lost for a few days. However, for an unfortunate
minority,thisdisturbanceinolfactoryfunctionpersistslongafterthenasalcongestionandrhinorrheahave
abated.Estimatesoftheprevalenceofolfactorydisordersofanycausesuggestthat~5%ofthepopulation
isaffected.
1–4
Postinfectiousolfactorydisordersarebelievedtoaccountfor11to40%ofcases
5,6
with
the higher figures likely to represent the prevalence in specialist centers. Extrapolation of the lower
figures suggests that an estimated 1.7 million people in the USA and 330,000 people in the UK are
sufferingfrompostinfectiousolfactorydisorderatanyonetime.Virusesthatgiverisetothecommoncold
are thought to be the pathological agents responsible for postinfectious olfactory loss. These include
rhinoviruses(30to50%),parainfluenzavirus(5%),coronavirus(10to15%),influenzavirus(5to15%),
coxsackievirus(<5%),adenoviruses(<5%),andrespiratorysyncytialviruses(10%).However,thereare
over200virusesintotalthatcancauseupperrespiratorytractinfections(URTIs).
7
WhenWangetalset
outtostudythemost likely culpritofthisdisparatebandofviruses,theyfoundthatparainfluenzavirus
waspresentin88%ofpatientswithpostviralolfactorylosscomparedwith9%ofcontrols
8
;Sugiuraetal
hadsimilarfindings.
9,10
However,anotherstudypublishedthesameyearbySuzukietalshowedthatat
least four viruses were identified in biopsies from patients with post-viral olfactory loss and
parainfluenza virus only accounted for 1 of the 24 cases examined. Other identified viruses included
Epstein–Barrvirus,rhinovirus,andcoronavirus.
11
Themechanismbywhichthe viruswreaksitshavoc
usuallyinvolveshijackingofthecellularapparatus,buttheexactdetailsmaydependontheactualvirus
implicated.Rhinovirus,forinstance,causesaselectiveneutrophilandmonocyterecruitmenttooccur.The
ensuing inflammatory cascade includes an increase in bradykinin, cytokine, chemokine, and soluble
intercellular adhesion molecule-1 concentrations.
12
The response in an immunocompetent individual
involvesT-lymphocyteactivation,allowingtheviralpathogentobeeliminated.
Withspecificrespecttotheolfactoryapparatus,thesevirusesappeartocausepartiallossofreceptors
inthe olfactory epithelium.Ultrastructurally, previous studies of olfactoryepithelial biopsyspecimens
have revealed a decrease inthe number ofolfactory receptor cellsandnerve bundles, withsquamous
metaplasiaoccurringinafewcases.
13
Thisreductioninciliatedolfactoryreceptorsmeansthereisalack
ofdendritesandvesiclesattheepithelialsurfaceand,therefore,adecreaseintheareaavailableforodor
moleculedetection.
14
Studiesofpatientswithcongenitalanosmiahaveshownthatthenumberofolfactory
receptors in the neuroepithelium is likely to reflect the severity of the loss.
15
It is unclear why an
individualmaybe susceptible to theviralagents,but, asthe agerange ofaffectedpatients istypically
afterthefourthdecadeoflife,thereisweightbehindtheargumentofacumulativeeffectofthevirus(es)
onthe olfactoryepithelium.Thismayexplainwhysomepatients donotrecovertheir olfactoryability,
especiallyastheregenerativeabilityoftheolfactoryepitheliumdenudeswithadvancingage.
16
Itisbyvirtueofthispartiallossofreceptorsthatpatientstypicallycomplainofhyposmiaratherthan
anosmia, but, more importantly, they frequently describe various forms of dysosmia.
17
Decreased
olfactory inputtothe OBs(1–3)down-regulatesdopaminergicinterneurons(arrows),which mayaffect
transmissionfromtheolfactorynervetothebulbandsubsequentprocessingofthosesignalsfromthebulb
(solid/dottedlines)(Fig.8.1).Asall inflammatoryedemaassociatedwiththe initialviral URTIshould
have dissipated after the initial event, postinfectious disorders are considered to be sensorineural
olfactorydisorders(SNODs)andarenotcausedbypathologyinthenasalcavity,olfactorycleft,orthe
paranasal sinuses; that is to say, airflow into the olfactory cleft is normal both orthonasally and
retronasally. Thatdoes not, ofcourse, mean that postinfectious olfactorydisorders are exclusive from
those secondary tochronicrhinosinusitis;indeedtheviralURTI may havebeentheprecursor toacute
bacterial rhinosinusitis that then fails to resolve; there may also be septal deviation. The physician
assessingpatientswithpostinfectiousolfactorylossshouldbear in mind thatthesepatientsmayhavea
multifactorialetiologyimplicatedintheirdisorder.
Fig.8.1a–cEffectsofviralinsult.ORNs,olfactoryreceptorneurons.
aOlfactoryreceptors.
bViralinjurytoolfactoryepithelium.
cCentralmodulationofdamagedneuroepithelium.
Beyond the peripheral theory described above, central theories have also been mooted for the
qualitativedisordersthatencompassparosmias.However,inthepresenceofthepostinfectiousdisorder,
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viralreceptordamageisstronglybelievedtobethekeyculprit.Infact,itislargelyduetothefactthat
postinfectiousandpost-traumaticdisordersaccountformostparosmia,andthatsomedegreeofolfactory
functionispreserved,thattheperipheraltheoryisthemostpopular.CertainlyOBvolumehasbeenshown
tobe decreased inparosmicversus nonparosmicpatients, indicating possible decreased andincorrect
rewiring between theneuroepithelium and theOB.
18,19
Functional magnetic resonance imaging studies
have shown the impact that the addition of parosmia to hyposmia can have upon central olfactory
processing.
20
Theanteriorcingulategyrus,thalamus,andorbitofrontalcortexshowedmoreactivationin
patientswithonlyhyposmia,addingfurtherweighttothetheory ofdecreasedsignaltrafficbetweenthe
neuroepitheliumandtheOB.Itshouldberemembered,whendiscussingthemechanismofviralimpacton
the olfactory epithelium, thatthe olfactory systemis aportal ofentry forviruses to invadethecentral
nervoussystemandsocentraleffectsofvirusescannotbediscounted.
21,22
•Atleast10%ofolfactorydisordersareduetoviralURTIs.
•Rhinovirusesarethemostcommoninfectiveagent.
•Postinfectiousolfactorylosstypicallyoccursafterthefourthdecadeoflife.
Post-traumaticOlfactoryDisorders
The clinical term post-traumatic anosmia (PTA) is commonly used to describe olfactory impairment
followingaheadinjury.Theinjurycanincludedirectinjurytothefaceandnasalstructuresoranypartof
theskull.Thereportedincidencevariesfrom5%
23
to66%,
24
butthisextremedifferenceisbecauseofthe
inclusionofspecializedsmellcentersthathaveahighincidenceofreferrals.Theimportantpointisthat
PTAisnotanuncommoncauseofolfactoryimpairmentanditshouldbeclinicallypursuedasacausein
anypatientpresentingwitholfactorylossortasteimpairment.Ofcasesofolfactorylosspresentingtoa
physician,17to24%
3
are duetoheadorfacial trauma.
25,26
Olfactory lossduetohead trauma canbe
dividedintofourmechanismsasdiscussedbelow,andcanbetheresultofanycombinationsofthese.
Head or facial trauma is responsible for 17 to 24% of all cases of smell loss presenting to a
physician.
DirectInjurytotheNoseandFacewithorwithoutNasalandFacialFractures
Headtraumaassociatedwithdirectfacialandnasalinjuries,with or withoutfractures, often resultsin
edema and mucosal hematoma of the nasal passages, which can lead to olfactory impairment by
preventing odors from reaching the olfactorycleft and olfactory receptors (conductive disorder) (Fig.
8.2).Thissametraumacancauseinjurytotheolfactoryreceptorsdirectly,orlateronbyscarringofthe
olfactoryepitheliumandpossibledevelopmentofrhinosinusitis.
24
Withtime,astheedemaandpossible
hematoma subside, the conductive block improves, with possible recovery of olfactory function.
However, injury to the olfactory receptors at the onset or secondary to scar tissue, or presence of
rhinosinusitis,canleadtolongertermolfactoryloss.Theincidenceofolfactorylossinfacialandnasal
fracturesvariesfrom 11to60%.
27,28
Itishardattimestoisolatethe pathophysiology ofolfactory loss
specifically,becauseinjuriestothefaceandnose(e.g.,fractureofthenasalskeleton)maynotonlycause
ablockageofthenose,butalsoproducedirectimpairmentoftheolfactory organandindirectinjury to
olfactorynervesowingtotheaccelerationanddecelerationoftheheadwhenthenasaltraumaoccurs.
Fig.8.2Septaldeviationcontributingtoconductiveolfactorydeficit.
DirectInjurytoAnyPartoftheSkullwithoutContusionorHemorrhageintothe
Brain
In directskull injury, acceleration and deceleration forces shift the brain forward and backward very
rapidly,andtheolfactorynerves,passingthroughthecribriformplateoftheanteriorcranialfossaenroute
totheOB,getshearedorstretched(Fig.8.3).Somestudieshavesuggestedthatoccipitalheadtraumais
more likely to cause olfactory injury than trauma to other areas.
29
In a series of 168 post-traumatic
anosmiacases,itwasfoundthatinjurytotheocciputandthesidesoftheheadwasmorelikelytocause
greater olfactorynervedamagethanfrontalheadinjuries.
24
Itisbelieved that the frontal sinus may be
somewhatprotectiveinhelpingtodecreasetheforceoftheblow.Fracturesofthecribriformplatewere
relativelyrare.Inthismechanismofolfactoryloss,biopsyoftheneuroepitheliumintheolfactoryclefthas
found degeneration of the olfactory vesicles and cilia.
30
Other studies of the histopathology of post-
traumaticanosmiahaveconfirmedsimilarfindingstopostinfectiouschanges,withdisorganizationofthe
olfactoryepitheliumaswellasdamagetoolfactorynervefibersandchangesintheOB.
14,31
Injuriestotheoccipitalandtemporalregionsoftheheadaremorelikelytocausesmellimpairment
thanfrontalinjuries.
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