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The diagnosis and management of sinusitis:

A practice parameter update

Chief Editors:Raymond G. Slavin, MD, Sheldon L. Spector, MD, and

I. Leonard Bernstein, MD

Sinusitis Update Workgroup: ChairmanRaymond G. Slavin, MD; MembersMichael

A. Kaliner, MD, David W. Kennedy, MD, Frank S. Virant, MD, and Ellen R. Wald, MD

Joint Task Force Reviewers:David A. Khan, MD, Joann Blessing-Moore, MD,

David M. Lang, MD, Richard A. Nicklas, MD,* John J. Oppenheimer, MD,

Jay M. Portnoy, MD, Diane E. Schuller, MD, and Stephen A. Tilles, MD

Reviewers:Larry Borish, MD, Robert A. Nathan, MD, Brian A. Smart, MD,

and Mark L. Vandewalker, MD

Theseparameterswere developed by theJointTaskForce on Practice

Parameters, representing the American Academy of Allergy, Asthma

and Immunology; the American College of Allergy, Asthma and

Immunology; and the Joint Council of Allergy, Asthma andImmunology.

TheAmerican Academy of Allergy, Asthmaand Immunology (AAAAI)

and the American College of Allergy, Asthma and Immunology

(ACAAI) have jointly accepted responsibility for establishing The

diagnosis and management of sinusitis: a practice parameter

update. This is a complete and comprehensive document at the

current time. The medical environment is a changing environment,

and not all recommendations will be appropriate for all patients.

Because this document incorporated the efforts of many

participants, no single individual, including those who served on

the Joint Task force, is authorized to provide an official AAAAI or

ACAAI interpretation of these practice parameters. Any request for

information about or an interpretation of these practice parametersby the AAAAI or the ACAAI should be directed to the Executive

Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy,

Asthma and Immunology. These parameters are not designed for

use by pharmaceutical companies in drug promotion.

Published practice parameters of the Joint Task Force

on Practice Parameters for Allergy and Immunology

include the following:

1. Practice parameters for the diagnosis and treatmentof asthma. J Allergy Clin Immunol 1995;96(suppl):S707-S870.

2. Practice parameters for allergy diagnostic testing.

Ann Allergy 1995;75:543-625.3. Practice parameters for thediagnosis and management

of immunodeficiency. Ann Allergy 1996;76:282-94.4. Practice parameters for allergen immunotherapy.

J Allergy Clin Immunol 1996;98:1001-11.5. Disease management of atopic dermatitis: a practice

parameter. Ann Allergy 1997;79:197-211.6. The diagnosis and management of anaphylaxis. J Al-

lergy Clin Immunol 1998;101(suppl):S465-S528.7. Algorithm for the diagnosis and management of

asthma: a practice parameter update. Ann Allergy1998;81:415-20.

8. Diagnosis and management of rhinitis: parameter

documents of the Joint Task Force on Practice param-eters in Allergy, Asthma and Immunology. AnnAllergy 1998;81(suppl):S463-S518.

9. Parameters for the diagnosis and management ofsinusitis. J Allergy Clin Immunol 1998;102(suppl):S107-S144.

10. Stinging insect hypersensitivity: a practice param-eter. J Allergy Clin Immunol 1999;103:963-80.

11. Disease management of drug hypersensitivity: apractice parameter. Ann Allergy 1999;83(suppl):S665-S700.

12. Diagnosis and management of urticaria: a practiceparameter. Ann Allergy 2000;85(suppl):S521-S544.

*This parameter was edited by Dr Nicklas in his private capacity and not in

his capacity as a medical officer with the Food and Drug Administration.

No official support or endorsement by the Food and Drug Administration

is intended or should be inferred.

Disclosure of potential conflict of interest: E. Wald has received grants from

GlaxoSmithKline, MedImmune, and Sanofi Pasteur. F. Virant has received

grants from Abbott, AstraZeneca, Boehringer Ingelheim, Bristol-Myers

Squibb, Dey Labs, Genentech, GlaxoSmithKline,Hoffman LaRoche, Immu-

nex, Key, Lederle, Lilly Research, Merck, Novartis, Pfizer, Purdue Fredrick,

Sandofi, Schering, Sepracor, TAP Pharmaceuticals, 3M Pharmaceuticals,

UCN Pharma, Upjohn Laboratories, and Med Point Pharmaceuticals; has

consultant arrangements with NeoRex; and is on the speakers bureau for

GlaxoSmithKline,Aventis, Merck, Pfizer, Schering,AstraZeneca,and IDEC.

S. Tilles has received grants from GlaxoSmithKline, Aventis, and Novartis

and is on the speakers bureau for GlaxoSmithKline, Aventis, and Pfizer.

J. Oppenheim has consultant arrangementswith Sepracor, GlaxoSmithKline,

AstraZeneca, and Roche; has received grants from Boehringer Ingelheim,

Schering, GlaxoSmithKline, Merck, Sepracor, AstraZeneca, Novartis and

Altana;and is on the speakers bureau for Sepracor, GlaxoSmithKline, Astra-

Zeneca, Novartis, and Merck. D. Khan has consultant arrangements withPfizer; has received grants from AstraZeneca; and is on the speakers bureau

for Merck, Pfizer, GlaxoSmithKline,and Aventis. D. Kennedy hasconsultant

arrangements with Medtronic-Xomed and Schering-Plough; has received

grants from Novartis; and is on the speakers bureau for Merck. M. Kaliner

hasconsultantarrangementswith Aventis,Medpoint, Glaxo, Gasser, Adams,

and King; has received grants from numerous pharmaceutical companies

that are researching allergies; and is on the speakers bureau for Aventis,

Medpoint, GlaxoSmithKline, Gasser, and Abbot.

Reprint requests: Joint Council of Allergy, Asthma and Immunology, 50 N

Brockway St, #3-3, Palatine, IL 60067.

J Allergy Clin Immunol 2005;116:S13-47.

0091-6749/$30.00

2005 American Academy of Allergy, Asthma and Immunology

doi:10.1016/j.jaci.2005.09.048

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13. Allergen immunotherapy: a practice parameter. AnnAllergy 2003;90(suppl):SI-S540.

14. Symptom severity assessment of allergic rhinitis:part I. Ann Allergy 2003;91:105-14.

15. Disease management of atopic dermatitis: an updatedpracticeparameter. Ann Allergy2004;93(suppl):S1-S21.

16. Stinging insect hypersensitivity: a practice parameterupdate. J Allergy Clin Immunol 2004;114:869-86.

17. The diagnosis and management of anaphylaxis: anupdated practice parameter. J Allergy Clin Immunol2005;115(suppl):S483-S523.

18. Practice parameter for the diagnosis and managementof primary immunodeficiency. Ann Allergy 2005;94(suppl):S1-63.

These parameters are also available on the internet at:http://www.jcaai.org.

CONTRIBUTORS

The Joint Task Force has made a concerted effort toacknowledge all contributors to this parameter. If anycontributors have been excluded inadvertently, the TaskForce will ensure that appropriate recognition of suchcontributions is made subsequently.

CHIEF EDITORS

Raymond G. Slavin, MD

Departments of Internal Medicine, MolecularMicrobiology and Immunology

Saint Louis University, Health Science Center

St Louis, MissouriSheldon L. Spector, MD

Department of MedicineUCLA School of MedicineDirector, California Allergy & Asthma Medical GroupLos Angeles, CaliforniaI. Leonard Bernstein, MD

Department of Medicine and Environmental HealthUniversity of Cincinnati College of MedicineCincinnati, Ohio

WORKGROUP MEMBERS

Michael A. Kaliner, MD

Department of MedicineGeorge Washington University School of MedicineWashington, DCDavid W. Kennedy, MD

Rhinology Professor and Vice DeanUniversity of Pennsylvania Medical CenterPhiladelphia, PennsylvaniaFrank S. Virant, MD

Department of PediatricsUniversity of WashingtonSeattle, Washington

Ellen R. Wald, MD

Department of PediatricsUniversity of Pittsburgh School of MedicineChief, Division of Allergy, Immunology and

Infectious DiseasesPittsburgh, Pennsylvania

JOINT TASK FORCE REVIEWERS

David A. Khan, MD

Department of Internal MedicineUniversity of Texas Southwestern Medical CenterDallas, TexasJoann Blessing-Moore, MD

Departments of Medicine and PediatricsStanford University Medical CenterDepartment of ImmunologyStanford, CaliforniaDavid M. Lang, MD

Allergy/Immunology SectionDivision of MedicineDirector, Allergy and Immunology Fellowship

Training ProgramCleveland Clinic FoundationCleveland, OhioRichard A. Nicklas, MD

Department of MedicineGeorge Washington Medical CenterWashington, DCJohn Oppenheimer, MD

Department of Internal MedicineNew Jersey Medical School

Pulmonary and Allergy AssociatesMorristown, New JerseyJay M. Portnoy, MD

Section of Allergy, Asthma & ImmunologyThe Childrens Mercy HospitalProfessor of PediatricsUniversity of Missouri-Kansas City School of

MedicineKansas City, MissouriDiane E. Schuller, MD

Department of PediatricsPennsylvania State University Milton S. Hershey

Medical College

Hershey, PennsylvaniaStephen A. Tilles, MDDepartment of MedicineUniversity of Washington School of MedicineRedmond, Washington

REVIEWERS

Larry Borish, MD, Charlottesville, VirginiaRobert A. Nathan, MD, Colorado Springs, ColoradoBrian A. Smart, MD, Chicago, IllinoisMark L. Vandewalker, MD, Columbia, Missouri

J ALLERGY CLIN IMMUNOL

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CLASSIFICATION OF RECOMMENDATIONS

AND EVIDENCE

Category of evidence

Ia Evidence from meta-analysis of randomized con-trolled trials

Ib Evidence from at least one randomized controlled trialIIa Evidence from at least one controlled study without

randomizationIIb Evidence from at least one other type of quasiexper-

imental studyIII Evidence from nonexperimental descriptive studies,

such as comparative studiesIV Evidence from expert committee reports or opinions,

clinical experience of respected authorities, or both

Strength of recommendation

A Directly based on category I evidenceB Directly based on category II evidence or extrapolated

recommendation from category I evidenceC Directly based on category III evidence or extrapo-lated recommendation from category I or II evidence

D Directly based on category IV evidence or extrapolatedrecommendation from category I, II, or III evidence

NR Not rated

PREFACE

Sinusitis is one of the most commonly diagnoseddiseases in the United States, affecting an estimated 16%of the adult population annually. It extracts an overall di-rect annual health care cost of $5.8 billion. Total restricted

activity days increased from 50 million per year during1986 through 1988 to 73 million per year during 1990through 1992.1 Sinusitis also significantly affects qualityof life in some symptom domains even more than otherchronic diseases, such as chronic obstructive pulmonarydisease, angina, and back pain.2

Because of the importance of sinusitis, the Joint TaskForce on Practice Parameters, representing the AmericanAcademy of Allergy, Asthma, and Immunology, theAmerican College of Allergy, Asthma, and Immunology,and the Joint Council of Allergy, Asthma and Immunol-ogy, developed the first set of Parameters for the diag-

nosis andmanagement of sinusitis, which was publishedin 1998.3 Much has happened since then with respect tonew concepts in diagnosis and management and new in-sights into pathogenesis. For these reasons, it was decidedthat a revision-update was indicated.

Four documents comprise this present practice param-eter on sinusitis: (1) an executive summary that reviews, innarrative format, the key clinical issues considered in theparameter documents; (2) a management algorithm withnarrative annotations designed to assist clinical decisionmaking; (3) a document listing only numbered summarystatements that is intended to promote rapid review andidentification of material comprehensively discussed in thefinal document; and (4) the complete guidelines docu-ment, which is organized so that the numbered key sum-mary statements precede relevant supporting text andcitations of evidence-based publications. This format pro-vides a ready reference for any physician who evaluatesand treats a patient with suspected sinusitis. In particular,the algorithm and its accompanying annotations aredesigned to present a global and useful approach to bothdiagnosis and management. Clinical decision points areclearly shown, and each of these proceeds stepwise tological implementation strategies. If further justification isrequired at any step in the algorithm, the evidentiary-basedguidelines text can and should be consulted. In addition,

The diagnosis and management of

sinusitis: A practice parameter update

Preface S15Executive summary S16Algorithm of sinusitis practice parameters (Fig 1)S17Annotations to the algorithm S17Complete guidelines and references S21

Definitions, anatomic considerations, sinusphysiology, and microbiology S21

Definitions S21Anatomic considerations S21

Sinus physiology S22Microbiology S22

Clinical diagnosis S24History S24Physical examination S25Imaging studies S26Laboratory tests S28

Predisposing factors S29Viral infections S29Allergic rhinitis S30Nonallergic rhinitis S30GERD S31

Immunodeficiency S32Cystic fibrosis S33Ciliary dysfunction S34

Associated conditions S34Otitis media S34Asthma S35

Treatment S35Medical S35

Antibiotics S35Antihistamines S37a-Adrenergic decongestants S38Glucocorticosteroids S38Adjunctive therapies: Saline, S39

mucolytics, and expectorantsIVIG S39Aspirin desensitization S40

Surgical S40Indications for referral S41


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guidance about appropriate referral of refractory cases,either because of treatment failure or for further investi-gation of possible associated conditions, is provided.

The great majority of patients with sinusitis seek carefrom their primary care physician. Various subspecialists(allergists and otolaryngologists) also see patients withsinusitis, especially patients who are more difficult to treat.It is incumbent on all physicians treating sinusitis to beknowledgeable concerning the latest information on path-ophysiology, diagnosis, and management, especially inlight of the rapidity with which infective organisms areable to change their character.

This practice parameter includes anatomic, allergic,immunologic, and physiologic considerations, as well asclinical diagnosis, differential diagnosis, diagnostic test-ing, and treatment. Predisposing factors, such as allergy,upper respiratory tract infections, anatomic abnormalities,immotile cilia syndrome, cysticfibrosis (CF), immunedefi-ciencies, and environmental factors, will be addressed.Medical and surgical therapies will be discussed.

An initial draft of parameters was prepared by a workgroup of experts in the field who carefully reviewed thecurrent medical literature. This material then underwentextensive peer review, revision, and annotation by exter-nal reviewers and by the Joint Task Force on PracticeParameters for Allergy and Immunology, a national panelof allergist-immunologists appointed by its cosponsoringorganizations: the American Academy of Allergy, Asthmaand Immunology; the American College of Allergy,Asthma and Immunology; and the Joint Council of Al-lergy, Asthma and Immunology. The parameters were re-viewed and approved by the cosponsoring organizationsand thereby represent an evidence-based, broadly ac-

cepted consensus opinion.The Joint Task Force is grateful for the cosponsoring

organizations financial support and encouragement. TheJoint Task Force would especially like to thank the manyindividuals who have donated substantial time and effortin producing this document that is intended to improve thequality of care of many millions of patients with sinusitis.

EXECUTIVE SUMMARY

Sinusitis, defined as inflammation of one or more of theparanasal sinuses, is characterized as acute when lasting

less than 4 weeks, subacute when lasting 4 to 8 weeks, andchronic when lasting longer than 8 weeks. Recurrentsinusitis consists of 3 or more episodes of acute sinusitisper year. A noninfectious form of chronic sinusitis istermed chronic hyperplastic eosinophilic sinusitis. Viralupper respiratory tract infections frequently precede sub-sequent bacterial invasion of the sinuses by Streptococcuspneumoniae, Haemophilus influenzae, and Moraxellacatarrhalis. These organisms can also be found in chronicsinusitis, as well asStaphylococcus aureus,Pseudomonasaeruginosa, and certain anaerobes. Fungi are being recog-nized increasingly as a factor in chronic sinusitis, particu-larly in the southeast and southwest parts of the country.

Prominent symptoms of acute sinusitis include nasalcongestion, purulent rhinorrhea, facial-dental pain, post-nasal drainage, headache, and cough. Chronic sinusitissymptoms are similar but might be even more subtle. Painis much less a feature of chronic sinusitis. Clinical signs ofboth acute and chronic sinusitis include sinus tendernesson palpation, mucosal erythema, purulent nasal secretions,increased pharyngeal secretions, and periorbital edema.There is an overlap in these symptomswith thoseof peren-nial rhinitis, and there is a frequent need to perform imagingprocedures to confirm the diagnosis. Because of this over-lap, some have suggested the use of the termrhinosinusitis.

Imaging techniques can provide confirmatory evidenceof sinusitis when symptoms are vague, physical findingsare equivocal, or clinical disease persists despite optimalmedical therapy. The imaging technique of choice is com-puted tomography (CT) because it can demonstrate abnor-malities both in the ostiomeatal complex and the sinuscavities.

Laboratory evaluation of acute, chronic, or recurrent

sinusitis might include nasal cytology, nasal-sinus biopsy,or tests for immunodeficiency, CF, or ciliary dysfunction.Nasal cytology is useful in the clinical evaluation ofconditions associated with sinusitis, including allergicrhinitis (AR), eosinophilic nonallergic rhinitis (NAR),neutrophilic rhinitis, and vasomotor rhinitis (VMR). Sinussecretionscan be obtainedfor culturein adults by meansofeither an aspiration of the maxillary sinus or an endoscop-ically directed catheter placed at the middle meatus. Forchildren, sinus secretions should be obtained by means ofaspiration only.

A number of factors associated with sinusitis shouldbe considered. Probably the most common is viral upper

respiratory tract infections. There is both clinical and ex-perimental evidence that ongoing AR might ultimatelylead to or augment acute bacterial sinusitis. NAR wasfound in 26% of patients with chronic sinusitis. Recently,gastroesophageal reflux disease (GERD) has been sug-gested as a cause of sinusitis, and there are several studiesin children and adults indicating that medical treatmentof GERD results in significant improvement in sinusitissymptoms. Tests for immunodeficiency, including quan-titative immunoglobulin measurement, functional anti-body tests, and HIV testing, might be useful if eithercongenital or acquired immunodeficiency is suspected incases of recurrent sinusitis. Quantitative sweat chloride

tests and genetic testing for diagnosis of CF should beconsidered in children with nasal polyps, colonization ofthe nose and sinuses with Pseudomonasspecies, or bothand in those who had chronic sinusitis at an early age.

Diseases associated with sinusitis are otitis media andbronchial asthma. Although no direct causal factor be-tween sinusitis and asthma has been found, a number ofstudies in both children and adults suggest that medicalmanagement, surgical management, or both of sinusitis re-sults in objective and subjective improvement of asthma.

The primary therapy for acute bacterial sinusitis isantibiotics. The choice is based on predicted efficacy,cost, and side effects. A 10- to 14-day course is generally


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adequate for acute disease, although shorter courses areindicated for newer antibiotics. If there is no improvementin 3 to 5 days, then an alternative antibiotic should beconsidered. The role of antibiotics in chronic sinusitis iscontroversial. For chronic infectious sinusitis, a longerduration of therapy might be required, with possible atten-tion to anaerobic pathogens. In the case of chronic non-infectious sinusitis, sometimes referred to as chronichyperplastic sinusitis, consideration should be given tosystemic corticosteroids.

Concern has been raised about the overdiagnosis ofsinusitis and unnecessary treatment with antibiotics. Ap-propriate criteria for the use of antibiotics are symptomsof sinusitis for 10 to 14 days or severe symptoms of acutesinus infection, including fever with purulent nasal dis-charge, facial pain or tenderness, and periorbital swelling.

Intranasal corticosteroids as an adjunct to antibiotictherapy might be helpful in treating recurrent acute andchronic sinusitis. Other adjunctive therapy, such as anti-histamines, decongestants, saline irrigation, mucolytics,

and expectorants, might provide symptomatic benefit inselected cases. The use of intravenous immunoglobulin(IVIG) is indicated only in patients with proved functionalimpairment of humoral immunity. The beneficial effectsof aspirin desensitization on aspirin-sensitive patients withsinusitis and asthma have been reported.

Medically resistant sinusitis might respond to appro-priate nasal-sinus surgery. In instances of localized per-sistent disease within the ostiomeatal complex, functionalendoscopic sinus surgery might result in significantimprovement.

Consultation with a specialist should be sought when(1) there is a need to clarify the allergic or immunologic

basis for sinusitis, (2) sinusitis is refractory to the usualantibiotic treatment, (3) sinusitis is recurrent, (4) sinusitisis associated with unusual opportunistic infections, and (5)sinusitis significantly affects performance and quality oflife. Consultation is also appropriate when concomitantconditions are present that complicate assessment or treat-ment, including chronic otitis media, bronchial asthma,nasal polyps, recurrent pneumonia, immunodeficiencies,aspirin sensitivity, allergic fungal disease, granulomas,and multiple antibiotic sensitivities.

ALGORITHM OF SINUSITIS PRACTICE

PARAMETERS (Fig 1)

Annotations to the algorithm

1. Symptoms suggestive of acute sinusitisd Acute sinusitis typically presents as a persistent

upper respiratory tract infection (10-14 days with-out improvement).

d In adults prominent symptoms include nasal conges-tion, purulent rhinorrhea, postnasal drainage, facialor dental pain, headache, and cough, frequently witha more severe nocturnal component.

d Any patient with orbital swelling or pain, swellingof the forehead, and/or diplopia should be urgentlyscheduled for evaluation.

d Children with acute sinusitis might also exhibit in-creased irritability and vomiting occurring in asso-ciation with gagging on mucus, prolonged cough,or both.

d In all age groups less frequent symptoms associatedwith acute sinusitis include fever, nausea, malaise,irritability, fatigue, halitosis, hyposmia, and sorethroat.

2. Office visitd Review medical history for diagnosis of sinusitis

and underlying risk factors.d General examination includes an evaluation for

signs of upper airway and sinus inflammation asso-ciated with nasal mucosal edema, purulent secre-tions, and increased localized blood flow. Typicalclinical signs include tenderness overlying thesinuses, dark circles beneath the eyes, and/or peri-orbital edema. Pharyngeal erythema, lymphoid hy-perplasia, and purulent material in the posteriorpharynx are also frequently observed.

d Nasal examination in patients with acute sinusitismight reveal mucosal erythema and purulent secre-tions. Nasal endoscopy, whether performed with arigid or fiberoptic instrument, offers a significantlybetter view than a nasal speculum. Nasal polypsmight contribute to nasal congestion and can be asource of recurrent sinusitis by obstructing the sinusostia. In adults nasal polyps might be associated withnonsteroidal anti-inflammatory drug sensitivity andasthma. Nasal polyps are relatively uncommon inchildren, and their presence should prompt evalua-tion for possible CF. Ear examination in patientswith suspected acute sinusitis frequently will reveal

middle ear effusions and associated eustachian tubedysfunction.

d Acute or chronic sinusitis might initiate or worsenasthma and bronchial hyperresponsiveness. Accord-ingly, chest auscultation and other objective mea-surements of airflow obstruction, such as officespirometry, should be considered in any patientwith possible sinusitis and cough.

d Patients with obvious acute sinusitis should be care-fully reviewed for any possible evidence of com-plicating factors, including the presence of facialswellingerythema over an involved sinus, visualchanges, abnormal extraocular movements, propto-sis, periorbital inflammationedemaerythema, anysuggestion of intracranial involvement, or centralnervous system involvement manifested as abnor-mal neurologic signs.

d In general, radiographs are not necessary in makingthe diagnosis of acute sinusitis, and plain radio-graphs have significant false-positive and false-negative results. Occasionally, imaging studiesmight be useful to support the diagnosis or provideevidence of the degree of mucosal involvement,thereby guiding more aggressive therapy. Plainradiographic signs compatible with sinusitis includegreater than 6 mm of mucosal thickening in the



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FIG 1. Algorithm of sinusitis practice parameters.


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maxillary sinuses in adults (>4 mm in children),greater than 33% loss of air space volume withinthe maxillary sinuses, or opacificationair-fluidlevels in any of the paranasal sinuses. Occipitomen-tal view radiographs might be helpful in screeningadults and children older than 1 year of age buthave inadequate sensitivity. A limited coronal sinusCT scan, with a focus on the ostiomeatal complex,might be helpful and should be considered if imag-ing is deemed necessary. Axial and coronal sinusCT is indicated in suspected orbital involvement,and sinus magnetic resonance imaging (MRI) canprovide useful information with related soft tissueinvolvement.

d Nasal cultures are not reliable for establishing thediagnosis of sinusitis or for determining a specificcausative microorganism. Maxillary antrum aspira-tion for culture is definitive but is indicated onlywhen precise microbial identification is essential.Obtaining cultures of the middle meatus through

endoscopically directed culture has shown promisein adults but not in children.

3. Acute sinusitisd Acute sinusitis is defined as symptoms and signs

for less than 4 weeks. The diagnosis of acute sinus-itis is based primarily on the clinical history, thephysical examination, and possibly other ancillaryevaluations, including nasal cytology or radio-graphic imaging. In most instances the diagnosisis made presumptively, and treatment is initiated.Clinical improvement usually occurs promptly;complete resolution of symptoms might require10 to 14 days.

4. Other diagnosesDifferential diagnoses include the following:

d AR and NAR;d viral upper respiratory tract infection;d nasal polyps;d sinonasal tumors;d nasopharyngeal tumor, granulomata, dental infections;d enlarged or infected adenoids in children.

5. Treatment

Antibiotics:

d Amoxicillin often is the drug of choice for childrenand adults. It is generally effective, inexpensive,

and well tolerated. Trimethoprim-sulfamethoxazolecan be used as an alternative drug in adults. Resis-tance is more commonly seen in children, and it isrecommended that the clinician refer to their localbiogram profile of antibiotic resistance. For patientswho do not respond to amoxicillin, high-doseamoxicillin-clavulanate (90 mg/kg amoxicillin and6.4 mg/kg clavulanate, not to exceed 2 g every12 hours) is recommended. For patients allergicto or intolerant of amoxicillin, alternatives includecephalosporins, macrolides, or quinolones.

d Acute sinusitis generally responds to treatment for10 to 14 days. Some physicians continue treatment

for 7 days after the patient is well to ensure com-plete eradication of the organism and prevent re-lapse. It is important to instruct the patient tocomplete the course of antibiotics.

d A reasonable approach would be to start the patienton amoxicillin for 3 to 5 days and determinewhether the signs and symptoms are improving.If the patients symptoms are improving, continuethis treatment until the patient is well for 7 days(generally a 10- to 14-day course). If after 3 to 5days the patient has not shown improvement,switch to a different antibiotic, such as high-doseamoxicillin-clavulanate or cefuroxime axetil.

Corticosteroids:

d The use of nasal corticosteroids might be helpful inpatients with acute and chronic sinusitis.

d Although efficacy has not yet been proved, theshort-term use of oral corticosteroids as an adjunctin treating patients with acute sinusitis is reasonable

when the patient fails to respond to initial treat-ment, demonstrates nasal polyposis, or has demon-strated marked mucosal edema.

Saline-mucolytics:

d Saline nasal sprays or lavage might be a useful ad-junct by liquefying secretions and decreasing therisk of crusting near the sinus ostia.

d There is no conclusive evidence that mucolytics,such as guaifenesin, are useful adjuncts in treatingacute sinusitis.

a-Adrenergic decongestants:

d Topicaldecongestants(eg,oxymetazolineandphenyl-

ephrine) and oral decongestants (eg, pseudoephe-drine) reduce mucosal blood flow, decrease tissueedema and nasal resistance, and might enhancedrainage of secretions from the sinus ostia.

d The use of topical decongestants beyond 3 to 5days might induce rhinitis medicamentosa, withassociated increased congestion and refractorinessto subsequent decongestant therapy.

Education:

d The following comfort measures might be helpful:adequate rest, adequate hydration, analgesics asneeded, warm facial packs, steamy showers, and

sleeping with the head of the bed elevated.d Prevention measures might include appropriate

treatment of allergies and viral upper respiratorytract infections and avoidance of adverse environ-mental factors, such as relevant allergens, cigarettesmoke, pollution, and barotrauma.

d Patients should be instructed to phone if symptomsworsen (eg, especially with headache or high fever)or if symptoms have not improved within 3 to 5days of treatment (see annotation 10).

6. Treatment successful?Complete response:

d Patient is improved symptomatically to near normal.



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Partial response:

d Patient is symptomatically improved but not backto normal at the end of the first course of antibiotics.

Poor response:

d Patient has little or no symptomatic improvementafter the first course of antibiotic therapy.

7. Follow-upd No further evaluation for resolved uncomplicated

sinusitis.d Consider further evaluation of underlying risk

factors, such as allergic rhinitis (AR) and NARand structural abnormalities.

8. Additional treatment and evaluationd For partial response, continue antibiotic treatment

for another 10 to 14 days or consider antibioticchoices listed under poor responses.

d For poor response to treatment with amoxicillin ortrimethoprim-sulfamethoxazole or in regions with ahigh incidence of antibiotic resistance, an antibioticshould be prescribed that covers resistant bacteria.

Appropriate choices include high-dose amoxicillin-potassium clavulanate, cefuroxime, cefpodoxime,cefprozil, and cefdinir. Quinolones, macrolides,and ketolides might also be a consideration.

d Sinusitis that fails to improve after 21 to 28 daysof initial antibiotic treatment might be caused bypathogens not adequately covered by prior antibio-tics, the presence of nasal polyps, or noncompli-ance. The use of broader-spectrum single agents,such as high-dose amoxicillin-potassium clavula-nate, cefuroxime, or cefpodoxime should be con-sidered with or without the addition of anaerobiccoverage with clindamycin or metronidazole.

d Reinforce the comfort and prevention measuresoutlined in Annotation 5.

d Consider sinus CT scan if not already done.d Underlying risk factors should be evaluated in a

more detailed manner.d Consider consultation with an allergist-immunolo-

gist for treatment of underlying allergic factorsand evaluation of unusual pathogens and immuno-deficiency. For structural abnormalities, consulta-tion should be sought with an otolaryngologist.

Recurrent sinusitis:

d Repeated episodes of acute sinusitis typically 3 ormore times per year.

d

Patients with chronic or recurrent sinusitis shouldbe evaluated for underlying inflammation, allergy,immunodeficiency, and anatomic abnormalities.

Rhinitis:

d Patients with suspected AR in conjunction withsinusitis should be evaluated for the presence ofIgE sensitization to inhalant allergens.

d Emphasis of therapy for AR includes environ-mental control, pharmacotherapy, and, in selectedpatients, allergen immunotherapy.

d Other rhinitic conditions (vasomotor, nonallergicrhinitiseosinophilia syndrome [NARES], and rhi-nitis medicamentosa) might also lead to sinusitis,

and the consultant must be capable of differentiat-ing these conditions and initiating an appropriatecourse of therapy.

Immunodeficiency:

d Referral to an allergist-immunologist is particularlyindicated in patients with chronic or recurrentsinusitis associated with such conditions as otitismedia, bronchitis, bronchiectasis, or pneumonia andin patients who have undergone prior surgical pro-cedures and continue to experience sinusitis. Thisevaluation might include measurement of quantita-tive serum IgG, IgA, and IgM level and assessmentof specific antibody responses to protein andpolysaccharide antigens, such as tetanus toxoid orpneumococcal polysaccharide vaccine.

9. Treatment successful?d See Annotation 6.

Follow-up

d See Annotation 7.10. Chronic sinusitis

d Signs and symptoms compatible with sinusitispersisting 8 weeks or longer.

d Consider a noninfectious form of sinusitis. Chronichyperplastic eosinophilic rhinosinusitis does notrespond to antibiotics and is marked by a prepon-derance of eosinophils and mixed mononuclearcells, with a relative paucity of neutrophils. A courseof systemic corticosteroids might have to beconsidered.

d If the patient has a significant nasal septal deviationthat compresses the middle turbinate into the ostio-meatal complex or obstruction of the sinus outflowtracts caused by middle turbinate deformity or the

presence of accessory structures that block sinusdrainage, consider consultation with an otolaryn-gologist. The presence of obstructing nasal polyps,after an appropriate course of treatment that mightinclude a trial of oral corticosteroids, is also anindication for referral. Finally, a patient with recur-rent or chronic symptoms and radiographic evidenceof ostiomeatal obstruction despite aggressive medi-cal management might also benefit from surgicalintervention.

d Evaluation should include coronal sinus CT withextra cuts through the ostiomeatal complex toclarify the extent of disease and specific location

or locations.d Evaluation might also include nasal-sinus biopsy in

suspected cases of neoplasia, fungal disease, gran-ulomatous disease, or tracheal biopsy for evaluat-ing ciliary structures, function, or both.

d In general, every effort should be made to maxi-mize medical treatment for underlying rhinitis be-fore proceeding with surgical intervention.

d Contemporary surgical therapy involves chieflyfunctional endoscopic sinus surgery.

d Most patients benefit from continued individualizedmedical therapy, including, when indicated, allergymanagement, after surgery.


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COMPLETE GUIDELINES AND REFERENCES

Definitions, anatomic considerations, sinus

physiology, and microbiology

Definitions

Summary StatementsSummary Statement 1: It has been suggested that theterm sinusitis be replaced by rhinosinusitis. NRSummary Statement 2: Sinusitis is defined as inflamma-tion of one or more of the paranasal sinuses. The mostcommon cause of sinusitis is infection. Classification ofsinusitis is frequently based on duration of symptoms,the specific sinus involved, or both. NRSummary Statement 3: The most commonly used classi-fication is as follows (NR):

a. Acute sinusitis: symptoms for less than 4 weeksconsisting of some or all of the following: persis-tent symptoms of an upper respiratory tract in-

fection, purulent rhinorrhea, postnasal drainage,anosmia, nasal congestion, facial pain, headache,fever, cough, and purulent discharge.

b. Subacute sinusitis: (unresolved acute) symptomsfrom 4 to 8 weeks.

c. Chronic sinusitis: symptoms for 8 weeks or longerof varying severity consisting of the same symp-toms as seen in acute sinusitis. In chronic sinusitisthere should be abnormal findings on CT or MRI.Some patients with chronic sinusitis might presentwith vague or insidious symptoms.

d. Recurrent sinusitis: 3 or more episodes of acute si-nusitis per year. Patients with recurrent sinusitismight be infected by different organisms at different

times.Summary Statement 4: A noninfectious form of chronicsinusitis is termed chronic hyperplastic eosinophilicsinusitis. NR

Although it is not universally accepted, the suggestionhas been made that the termrhinosinusitismight bemoreapplicable thansinusitisfor the following reasons4-6: rhi-nitis typically precedes sinusitis; sinusitis without rhinitisis rare; the mucosa of the nose and sinuses are contiguous;and symptoms of nasal obstruction and nasal discharge areprominent in sinusitis. Rhinitis associated with sinusitiscan be allergic, bacterial, viral, or perennial nonallergic.

Sinusitis is classified as acute, subacute, chronic, and recur-rent. It should be emphasized that this classification isentirely arbitrary, and the medical literature is unclear onthis point. Most treatment modalities are directed to acuteand chronic sinusitis. In acute sinusitis symptoms arepresent for less than 4 weeks. Symptoms consist ofsome or all of the following:persistent symptomsof an up-per respiratory tract infection, purulent rhinorrhea, postna-sal drainage, anosmia, nasal congestion, facial pain,headache, fever, and cough. Subacute sinusitis, also re-ferred to asunresolved acute sinusitisis the developmentof manifestations of minimal-to-moderate signs of sinusinflammation without an overt upper respiratory tract

infection or abrupt onset of symptoms. It might speak toinadequate or partial therapy of acute sinusitis or simpleinattention to acute problems. Chronic sinusitis is definedas persistent sinus inflammation for greater than 8 weeks.An operational definition of chronic sinusitis is persistentinflammation documented with imaging techniques atleast 4 weeks after initiation of appropriate medical ther-apy in the absence of an intervening acute episode.7 Incontrast to acute sinusitis, the roleof bacterial infectionin chronic sinusitis is less certain.8 Recurrent sinusitis in-cludes 3 or more episodes of acute sinusitis per year.

The symptom-based definition of chronic sinusitis hasbeen recently brought into question. In one study morethan 50% of patients with a strong history of chronicsinusitis had a normal CT scan. However, it is still debatedwhether CT also provides the definitive diagnosis of thisdisorder. A reevaluation of the way chronic sinusitisis defined and diagnosed appears necessary.9 Chronicsinusitis can be divided into infectious and hyperplasticcategories. Chronic infectious sinusitis might be due to

anaerobic bacteria, such as gram-positive streptococcus,bacteroides, andFusobacteriumspecies orS aureus. It isgenerally associated with a significant influx of neutro-phils. A noninfectious form of chronic sinusitis, some-times termed chronic hyperplastic eosinophilic sinusitis,is marked by a preponderance of eosinophils and mixedmononuclear cells, with a relative paucity of neutrophils.It is often associated with nasal polyps, asthma, and aspi-rin sensitivity.10

Anatomic considerations

Summary Statements

Summary Statement 5: The sinuses develop at differentages during childhood. BSummary Statement 6: The optic nerve, cavernous sinus,and carotid artery are adjacent to the sphenoid sinus.Tumors and infection in the sphenoid sinus might presentwith involvement of these structures. BSummary Statement7: Becauseof the location of the fron-tal and sphenoid sinuses, infection of these sinuses has agreater propensity to cause intracranial complications. ASummary Statement 8: The maxillary, anterior ethmoid,and frontal sinuses drain through the ostiomeatal com-plex and are dependent on this region for normal ventila-tion and mucociliary clearance. B

Summary Statement 9: The anterior ethmoid sinuses andmiddle meatus (ostiomeatal complex), as a result of theirlocation, are most frequently involved in sinusitis. DSummary Statement 10: Anatomic abnormalities of thenasal septum or within the ostiomeatal complex mightpredispose toward the development of sinusitis. B

Development. The maxillary sinus is the first to beginsignificant pneumatization between birth and 12 months.The floor of the maxillary sinus reaches the level of thefloor of the nose by approximately 12 years of age.Rudimentary ethmoid sinuses are present at birth andreach adult size at 12 to 14 years of age.11 Development of



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the frontal and sphenoid sinuses begins later than that ofthe ethmoid sinuses, and complete pneumatization is notachieved until mid to late adolescence.12 Although the de-gree of pneumatization of all sinuses is highly variable, thevariability in pneumatization of the frontal and sphenoidsinusesis greater than that of the ethmoid and maxillarysinuses.13 The frontal sinus is hypoplastic or completelyabsent in about 15% of the population, and the sphenoidsinus is rudimentary (conchal or presellar pneumatization)in 26% of patients. There is evidence to suggest thatsinusitis in childhood might inhibit sinus development.14

Because of their later development, frontal or sphenoiddisease is uncommon in childhood.Anatomy. The anterior ethmoid, frontal, and maxillary si-nuses all drain into the middle meatus through a relativelyconvoluted and narrow drainage pathway (ostiomeatalcomplex) rather than by simple ostia. The ethmoid sinusesthemselves consist of a honeycomb of cells lying medial tothe orbitalstructuresand varying between4 and 17 air cellsin number. Theymight also pneumatizeto a variable extent

above (supraorbital) or below (infraorbital) the orbit. Theethmoid sinus is divided into an anterior group of cells(draining into the middle meatus) and a posterior group ofcells (draining into the superior meatus).15 The maxillarysinus lies between the teeth and the orbit on both sidesand drains into the middle meatus through a channel inits supramedial aspect. The paired frontal sinuses arisefrom the region of the anterior ethmoid and extend superi-orly into the forehead. Valveless veins that pass throughthe posterior wall of the frontal sinus might allow thespread of frontal sinus infection intracranially, particularlyin acute infection.The sphenoid sinuses are also paired andlie posterior and slightly inferior to the posterior ethmoid

cells. They drain by separate ostia into the sphenoethmoi-dal recess on either side of the nasal septum posteriorly.The optic nerve courses over the sinus laterally and supe-riorly. The carotid artery indents the sinus laterally, and thesinus has an intimate relationship with thecavernous sinus,as well as the dura of both the anterior and middle cranialfossa.

The anatomic arrangement of the sinuses makes thefrontal anterior ethmoid and maxillary sinuses dependenton the ostiomeatal complex for their ventilation and mu-ciliary clearance. Significant obstruction of this complexcan predispose to the development of sinusitis. Becauseethmoid anatomy is extremely variable and dependent, to

some extent, on the position of the nasal septum, there isa potential for anatomic variations to cause ostiomeatalobstruction, although the importance of anatomic varia-tions in predisposing to chronic sinusitis either by meansof redirection of airflowor by means of direct compres-sion is still debated.16,17 In some situations the ethmoidcells might pneumatize into the head of the middle tur-binate (concha bullosa), and extreme middle turbinateaeration might narrow the ostiomeatal complex. The loca-tion of the anterior ethmoid sinuses and middle meatusmakes the ostiomeatal complex particularly at risk fromenvironmental exposures, and this region is typically thefirst and the most frequently involved region in chronic

sinusitis. Indeed, low-grade edema and inflammation canpersist within this region, resulting in intermittent episodesof inflammation in the dependent sinuses. When suchedema does not respond to medical therapy, endoscopicsurgical intervention might be required.

Sinus physiologyd The sinuses are air-filled cavities with classical, pseu-

dostratified, ciliated columnar epithelium interspersedwith goblet cells. The cilia sweep mucus toward theostial opening. Obstruction of sinus ostia might leadto mucous impaction and decreased oxygenation inthe sinus cavities.

d During obstruction of the ostia, the pressure in thesinus cavity can decrease, which in turn causes thesymptom of pain, particularly in the frontal region.

The sinus cavities are air filled, with classical, pseudos-tratified, ciliated columnar epithelium interspersed withgobletcells. Thecilia sweep mucus towardthe ostialopening.

Blood flow in the maxillary sinus is roughly estimated tobe 100 mL/100 g tissue per minute, which is similar to thatfound in the nose but higher than that found in the brain.Obstruction of the ostia can lead to mucous impaction anddecrease oxygenation in the sinus cavities. This in turnmight lead to further complications (discussed in furthersections). There is limited gas exchange in the sinuseswhen there is ostial obstruction, and then the oxygenconcentrations can decrease to close to 0% with purulentsecretionsbut not with nonpurulent secretions. The growthof bacteria is facilitated in this anaerobic environment.

During obstruction of the ostia, the pressure in the sinuscavity can decrease, which in turn causesthe symptoms of

pain, particularly in the frontal region.18

This pressure de-crease can range from 20 to 30 mm H2O, with the lowestpressure being 266 mm H2O. Transudation might startwhen the pressure is less than 20 to 30 mm H2O below0. This decrease in pressureis precededby a transient pres-sure increase caused by the increase in CO2, whereas thedecrease in pressure is principally caused by O2 absorp-tion.19 However, in acute purulent sinusitis the pressurecan sometimes be as high as 100 mm H2O.

20 Purulentsecretions have a low oxygen content, and the pain mightbe due to a combination of inflammation originating fromthe mucosa and pressure from the secretions on the insidewalls of the sinus.

During deep sea diving, the change in sinus pressurecanbe very high, causing transudation, bleeding, and edema,especially when pressures exceed 350 to 500 mm H2O.During flying, there is usually less change in pressurethan diving.When there is obstruction of the ostia, changesin sinus pressure similar to those of diving can occur.

Microbiology

Summary Statements

BacterialSummary Statement 11: In acute sinus disease viralupper respiratory tract infections frequently precede


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bacterial superinfection by S pneumoniae, H influenzae,and M catarrhalis. Both M catarrhalis and H influenzaecan produceb-lactamase and thereby be resistant to pen-icillin and its derivatives. ASummary Statement 12: The prevalence of penicillin-resistant S pneumoniae is increasing. Twenty-five per-cent to 50% of respiratory isolates ofS pneumoniae areresistant to penicillin. (A) There is wide geographicvariation.Summary Statement 13: In addition to the organismsmentioned above, the most common bacterial speciesin chronic sinusitis are S aureus, gram-negative entericorganisms (including P aeruginosa), and anaerobes,such as Prevotella species and fusobacteria. (A) Therole of infection in most patients with this disorder iscontroversial, and these culture results are similarly con-troversial and might reflect colonization only.Summary Statement 14: In contrast to community-acquired sinusitis, the usual pathogens in nosocomialsinusitis are gram-negative enterics (eg, P aeruginosa,

Klebsiella pneumoniae, Enterobacter species, Proteusmirabilis, Serratia marcescens, and bacteroides) andgram-positive cocci (occasionally streptococci and staph-ylococci). A

Fungal

Summary Statement 15: Fungal sinusitis can take one of3 forms: allergic fungal sinusitis, mycetoma, or fulminantinvasive disease. ASummary Statement 16: Common causes of allergic fun-gal sinusitis are Bipolaris species, Curvularia species,Aspergillusspecies, and Dreschlera species. A

To determine the microbiology of sinus infection

involving the maxillary sinus, the best measure, or goldstandard, is to perform an aspirate of the maxillarysinus.8,21 The nasal mucosa should be sterilized in thearea beneath the inferior turbinate through which thetrocar will be passed to insure that contamination is elim-inated or reduced. Quantitative cultures should be per-formed or at least a Gram stain should be prepared toestimate the density of infection. Infection is documentedwhen a bacterial species is recovered in a density of at least103 to 104 cfu/mL.

Recently, there has been interest in and enthusiasm forobtaining cultures of the middle meatus endoscopically asa surrogate for cultures of a sinus aspirate. Although some

studies have suggested good correlation between thepathogenic organisms isolated in the middle meatus andthose in the maxillary sinus, further verification of thisapproach is warranted. In healthy children the middlemeatus is colonized with the same bacterial species thatare commonly recovered from children with sinus infec-tions.22 Accordingly, the recovery of such organisms in asymptomatic child cannot confirm the presence of infec-tion. In adults the correlation between cultures of the mid-dle meatus and the sinus aspirate has been reasonable.23

The bacterial species recovered from the middle meatalsamples of normal adults were coagulase-negative staph-ylococci in 35%, Corynebacterium species from 23%

and S aureus from 8%.24 The presence ofS aureus as apresumed pathogen, as well as a common colonizer, canbe confusing.Bacterial. The microbiology of paranasal sinus infectionscan be anticipated according to the age of the patient,clinical presentation, and immunocompetency of thehost.25-37 In acute sinus disease viral upper respiratorytract infections frequently precede bacterial superinfectionby S pneumoniae, H influenzae, and M catarrhalis.25-27

BothM catarrhalisandH influenzaecan produce b-lacta-mase and thereby be resistant to amoxicillin. Increasingly,S pneumoniae is resistant to penicillin; 25% to 50% ofrespiratory isolates ofS pneumoniaewill be intermediateor highly resistant to penicillin.38,39 In adults with acutesinusitis, S aureus is another isolate from the paranasalsinuses.

Assessing the microbiology of chronic sinusitis hasbeen particularly difficult. Aspirates are frequentlyperformed immediately after or during a course ofantimicrobials that has failed to eliminate the patients

symptoms. Furthermore, sterilization of the mucosa andquantitation of isolates are infrequently performed. Thefrequent recovery of coagulase-negative staphylococci,viridans streptococci, and diphtheroids are good exam-ples of the dilemma. Often, patients are evaluated duringacute exacerbations of chronic sinusitis, which explainsthe frequent recovery of S pneumoniae, H influenzae,and M catarrhalis. A large multicenter study to assessbacteriologic findings in adults with chronic bacterialmaxillary sinusitis was recently reported.37 The mostcommonly isolated anaerobes were Prevotella species(31%), anaerobic streptococci (22%), andFusobacteriumspecies (16%). The aerobes most frequently recovered

included Streptococcus species (21%), H influenzae(16%), P aeruginosa (16%), S aureus (10%), and Mcatarrhalis(10%). In 2 small but recent series of patientswith chronic sinusitis, the commonly recovered bacterialspecies included S aureus, b-hemolytic streptococci,H influenzae, and various gram-negative enterics, in-cluding P aeruginosa, S marcescens, and Klebsiellaoxytoca.23,33

Three recent series of chronic sinusitis in pediatricpatients have been reported.34-36 Methods of obtainingmaterial for culturewere either an aspirate ofthe maxillarysinus34-36 or an irrigation of the sinus cavity.35 The micro-biology of this disorder was described to include primarily

H influenzae, S pneumoniae, M catarrhalis, coagulase-negative staphylococci, and a-hemolytic streptococci.Anaerobes were recovered from 40% and 13% of the spec-imens in 2 of these studies.34,36

In contrast to community-acquired sinusitis, the usualpathogens in nosocomial sinusitis are gram-negativeenterics (eg,P aeruginosa, K pneumoniae, Enterobacterspecies,P mirabilis, and S marcescens) and gram-positivecocci (occasionally streptococci and staphylococci).40-42

It has been suggested that staphylococcal enterotoxinacting as a superantigen might trigger an enhancedimmune response, resulting in polypoid formation andchronic sinusitis.43



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Fungal. Fungal sinusitis can take one of 3 forms: allergicfungal sinusitis, fungus ball, or fulminant invasive fungalsinusitis. Both allergic fungal sinusitis and fungus ball areconsidered to be noninvasive forms of sinus infection.Classical allergic fungal sinusitis invariably occurs inimmunocompetent patients with atopic disease, usuallywith nasal polyps and chronic nasal congestion andobstruction. The symptoms can be longstanding. In chil-dren there is frequently unilateraldisease, and there mighteven be some facial deformity.44 The material in the si-nuses has a peanut butterlike consistency, and histologicexamination shows fungal elements and abundant muci-nous material. The pathogenesis is an immunologicallymediated reaction to the presence of the fungal spores,which are acquired through inhalation of these commonsaprophytes.45 A positive skin test response to the relevantorganism is seen with an increase in total serum IgElevels.46 There might be dramatic encroachment on adja-cent structures (including the orbit and central nervoussystem) on the basis of expansion of the intrasinal con-

tents.46,47 True invasion of surrounding structures veryrarely occurs. This clinical syndromeis observed in certaingeographic areas more commonly than in others. In theUnited States it is most common in the south, southwest,and western regions of the country. Treatment involvesa very complete surgical exenteration, with mucosal pres-ervation and steroid therapy. The role of postsurgical anti-fungal therapy in this disorder has not yet been proved,but anecdotal reports suggest that it might be adjunctive.The most common fungi to cause this clinical syndromeare Bipolaris, Curvularia, Aspergillus, and Dreschleraspecies, although a wide variety of other fungi havebeen observed in a myriad of case reports.

Fungus ball typically occurs in themaxillary or sphe-noid sinuses and is usually unilateral.48 The symptoms ofsinus infection are again chronic and might lead to nasalobstruction and headache. Although pressure necrosiscan occur as the mass impinges on surrounding structures,invasion is rare. The principal way in which this entity isdistinguished from allergic fungal sinusitis is by meansof histologic examination, which shows dense accumula-tions of hyphae in concentric layers forming a fungusball.48 Eosinophilic mucin is not present. Surgical removalis indicated.

Invasive fungal sinusitis, a fulminant disseminateddisease, is usually observed in immunocompromised

patients, including diabetic patients, patients with leuke-mia or solid malignancies who are febrile and neutropenic(most of whom will have received broad-spectrum anti-microbial therapy), patients receiving high-dose steroidtherapy (eg, patients with connective tissue disease ortransplant recipients), and patients with severe impairmentof cell-mediated immunity (transplant recipients or per-sons with congenital or acquired T-cell immunodeficien-cies). Common clinical signs include fever, headache,epistaxis, and mental status changes. The patient mighthave insensate nasal ulcers. Thissymptom complex wasformerly calledmucormycosis.48 Aggressive debridementand systemic antifungal therapy is warranted.49,50

There is an evolving literature of the potential fornon-IgE immunologically mediated reactions tofungi toresult in an inflammatory process in the sinuses.51

Clinical diagnosis

History

Summary Statements

Summary Statement 17: Acute bacterial sinusitis is sus-pected in patients in whomupper respiratory tract infectionpersists beyond 10 to 14 days. A history of persistentpurulent rhinorrhea, postnasal drainage, and facial paincorrelates with increased likelihood of bacterial disease. ASummary Statement 18: Prominent symptoms of acutebacterial sinusitis include nasal congestion, purulent rhi-norrhea, facial-dental pain, postnasal drainage, headache,and cough. CSummary Statement 19: Predisposing factors for sinusitisinclude environmental exposures, genetic predisposition,

AR, eosinophilic NAR, VMR, rhinitis medicamentosa,nasal polyps and other causes of ostiomeatal obstruction,CF, ciliary dyskinesia, cocaine abuse, and immunodefi-ciency. DSummary Statement 20: The diagnosis of sinusitis isbased on a combination of clinical history, physical ex-amination, imaging studies, and/or laboratory tests. DSummary Statement 21: The differential diagnosis ofsinusitis includes AR, eosinophilic NAR, VMR, andvascular headaches-migraines. D

The diagnosis of sinusitis is based on a combination ofclinical history, physical examination, imaging studies,and/or laboratory tests. Acute bacterial sinusitis is sus-

pected in patients whose upper respiratory tract infectionhas persisted beyond 10 to 14 days.52,53 Prominent symp-toms in adults include nasal congestion, purulent rhinor-rhea, facial-dental pain, postnasal drainage, headache,and cough.54 Although all of these symptoms are nonspe-cific,55-58 a history of persistent purulent rhinorrhea andfacial pain appear to have somecorrelation with increasedlikelihood of bacterial disease.54,55 Symptoms of acutebacterial sinusitis are similar in children but often also in-clude increased irritability, even more prolonged cough,and vomiting that occurs in association with gagging onmucus.59-62

Less frequent symptoms include fever, nausea, malaise,

fatigue, halitosis, or sore throat.Chronic sinusitis symptoms are similartothoseof acutesinusitis but might be even more subtle.63,64 In fact, pa-tients with rhinitis might not even perceive that theyhave chronic sinusitis; instead, they might only sense amild increase in a subset of symptoms (eg, congestionand fatigue). Rather than expressing concern about anew problem, such a patient might simply complain thattheir usual medications for rhinitis are not effective. It isprobable that headache attributed to chronic sinusitiscould be a migraine equivalent.65,66

In reviewing a patients history, the differential diag-nosis of sinusitis (Table I) and predisposing conditions


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(Table II) should be considered. An accurate history has

implications for appropriate initial therapy and long-termmanagement.

Physical examination

Summary Statements

Summary Statement 22: Clinical signs of acute sinusitisinclude sinus tenderness on palpation, mucosal erythema,purulent nasal secretions, increased pharyngeal secre-tions, and periorbital edema. CSummary Statement 23: Rhinolaryngoscopy might be auseful adjunct to physical examination, providing directvisualization of abnormalities of the septum, turbinates,

mucosa, nasopharynx, adenoids, eustachian tube orifice,tonsils, posterior tongue, epiglottis, glottis, and vocalcords. The origin and extent of nasal polyps might bebetter identified after the use of topical decongestants,as well as the presence of purulent ostial secretions. D

When the clinical history suggests sinusitis, a directedphysical examination can help differentiate sinusitis froma simple upper respiratory tract infection or AR.54-58,61,67

The examination begins with careful inspection of theface. Acute sinusitis can be associated with swelling andtenderness overlying an affected area; rarely, with orbitalinvolvement, diplopia or proptosis can be observed. In

contrast, allergic facies demonstrate dark infraorbitalswollen semicircles. Allergic children frequently exhibita transverse nasal crease (caused by constant nose itching)or Morgan-Dennies lines (accentuated horizontal skinfolds on the lower eyelid running parallel to the lowerlid margin).

The nasal mucosa and quality of secretions should beassessed. Red, swollen nasal tissue is seen in infectiousrhinitis and sinusitis; pale boggy turbinates suggest AR.Secretions are clear and watery at the onset of upperrespiratory tract infections but become thicker, colored

(yellow-green), and opaque after a few days. Usually, thedischarge will remain purulent for several days and thenbecome clearer shortly before resolution. Typical coldslast5 to7 days and rarelyas long as10 days. Persistence ofpurulent secretions beyond 10 days in the middle meatusarea are characteristic of sinusitis, and secretions can beyellow-green, green, or gray.54,55 Allergic nasal secretionsare generally clear and watery; with extreme inflamma-tion, a pale yellow color might be observed.

Purulent exudates in the middle meatus are believedto be highly predictive of bacterial sinusitis54,55 but mightbe difficult to visualize unless the nasal mucosa is decon-gested with a vasoconstrictor. Accordingly, the absence of

purulent secretions does not exclude the possibility of ac-tive sinus infection. Protracted nasal-sinus inflammatorychanges in the mucosa might lead to polyps. Again, thesecould be difficult to see if the turbinates are swollen. Inchildren the presence of polyps should raise concernsabout CF. In all ages polyps are frequently seen withaggressive eosinophilic nonallergic sinusitis. Severe per-sistent asthma and nonsteroidal anti-inflammatory drugintolerance are frequently associated.68

The oropharynx should be examined for signs ofposterior pharyngeal mucopurulent secretions. On occa-sion, sinusitis might present with dental pain because theroots of the teeth project into the floor of the maxillary

TABLE I. Differential diagnosis of bacterial sinusitis*

Infectious rhinitis:

Viral upper respiratory tract infections

Allergic rhinitis:

Seasonal

Perennial

Nonallergic rhinitis:Vasomotor rhinitis

Aspirin intolerance

Eosinophilic nonallergic rhinitis

Rhinitis medicamentosa:

Decongestants

b-blockers

Birth control pills

Antihypertensives

Rhinitis secondary to:

Pregnancy

Hypothyroidism

Horner syndrome

Wegener granulomatosismidline granuloma

Anatomic abnormalities causing rhinitis:

Foreign bodyNasal polyps

Nasal septal deviation

Enlarged tonsils and adenoids

Concha bullosa and other middle turbinate abnormalities

Tumors

Cerebral spinal fluid rhinorrhea

Vascular headache (migraine)

Adapted from Kaliner MA. Medical management of sinusitis. Am J Med Sci

1998;16:21-8.

*Many of these conditions also predispose to sinusitis.

TABLE II. Conditions that predispose to sinusitis

Allergic and nonallergic rhinitis

Anatomic abnormality of the ostiomeatal complex

Nasal anatomic variants:

Septal deviation

Concha bullosa

Paradoxical curvature of the middle turbinateHaller cells

Cystic fibrosis

Common variable immunoglobulin deficiency

Specific antibody deficiency

IgG subclass deficiency

IgA deficiency

Ciliary dyskinesia, Kartagener syndrome, Young syndrome

Aspirin sensitivity

Acquired immunodeficiency syndrome

Churg Strauss syndrome

Rhinitis medicamentosa

Cocaine abuse

Adapted from Kaliner MA. Medical management of sinusitis. Am J Med Sci

1998;316:21-8.



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sinus. In fact, some cases of maxillary sinusitis are secon-dary to a dental root infection that erodes through the boneinto the adjacent sinus. Examination of the ears mightreveal otitis media, particularly in children with sinusitis;in fact, unresolved persistent bacterial sinusitis might leadto recurrent otitis media.61,67 Auscultation of the chestfor wheezing might disclose an asthmatic component ofa patients cough. The absence of audible wheezing doesnot exclude the possibility of asthma; subtle abnormalitiesmight only be apparent on spirometry (see the Labora-tory tests section).

Transillumination of the maxillary sinuses might bereported as opaque (no transmission), dull (reduced trans-mission), or normal, but thesensitivity and specificity ofthis technique alone is poor.69 Unless the clinician has ad-ditional knowledge of a patients sinus anatomy (eg, froma CT scan), it is impossible to differentiate active diseasefrom a congenitally small sinus or bilateral mild involve-ment of larger sinuses from normal size sinuses.70-73 Inone prospective study, however, abnormal transillumina-

tion combined with purulent nasal secretions and a historyof maxillary pain, poor response to decongestants, andcolored rhinorrhea was the best predictor of acute bacterialsinusitis.71

In reassessing patients with recurrent sinusitis, thephysical examination should be modified to evaluate forsigns of immunodeficiency (associated recurrent otitismedia, bronchiectasis, or pneumonia), complications ofprimary infections (eg, mastoiditis or orbital cellulitis),poor growth in children, unexplained dermatitis, absenceof lymphoid tissue, CF (poor growth, nasal polyps, barrelchest, digital clubbing, and diffuse chest abnormalities onauscultation), ciliary dysfunction (nasal polyps, digital

clubbing, dextrocardia, and situs inversus), and anatomicabnormalities (eg, septal deviation, nasal polyps, foreignbodies, and tumors).

In selected patients with chronic or recurrent sinusitis,nasal endoscopy should be considered. This procedureprovides ideal direct visualization of abnormalities of theseptum, turbinates, mucosa, nasopharynx, adenoids, eu-stachian tube orifice, tonsils, posterior tongue, epiglottis,glottis, and vocal cords. The origin and extent of nasalpolyps can be identified, as well as the presence ofpurulent ostial secretions.73,74

Imaging studiesSummary Statements

Summary Statement 24: Imaging techniques can provideconfirmatory evidence when symptoms are vague, phys-ical findings are equivocal, or clinical disease persists de-spite optimal medical therapy. BSummary Statement 25: Ultrasonography has limitedutility but might be useful in pregnant women or for de-termining amounts of retained sinus secretions. CSummary Statement 26: Standard radiographs might beused to detect acute sinusitis, but they are not sensitive,particularly for ethmoid disease. C

Summary Statement 27: CT is the optimal technique forevaluating the ethmoid sinuses and for preoperative eval-uation of the nose and paranasal sinuses, including as-sessment of the ostiomeatal complex areas. CSummary Statement 28: MRI is a sensitive techniquefor evaluating suspected fungal sinusitis and for differenti-ating between inflammatory disease and malignant tumors.MRI is limited in its ability to define bony anatomy.C

The diagnosis of acute sinusitis is generallymade on thebasis of history and physical examination.54,55 Occasion-ally, it might be difficult clinically to distinguish betweensinusitis and rhinitis, and it can be a challenge to documentthe extent of disease. As previously stated, the term rhino-sinusitishas been suggested in part to reflect this confu-sion. In this context imaging procedures, particularly CTand MRI, are the generally used imaging techniques forconfirmatory evidence in patients with both acute andchronic sinusitis.75 The clinical utility, relative safety,ease of performance, availability, and cost of these imag-ing techniques vary considerably, and all have inherent

limitations.58,76-79

Imaging procedures are often useful when symptomsare vague, physical findings are equivocal, or the responseto initial management is poor. The possibility of sinusitiscan also be confirmed by imaging patients with atypicalpresentations (eg, a child with refractory conjunctivitis ora patient with acute severe eye or occipital pain).

Some unusual causes of persistent disease, such as al-lergic fungal sinusitis and Wegener granulomatosis mightbe suggested by newer and more sophisticated imagingtechniques, such as MRI.80

Ultrasonography. A-mode ultrasonography is a safe,rapid, and noninvasive technique for evaluating the max-

illary and frontal sinuses. Unfortunately, several studiescomparing ultrasonography with radiographic techniques(as the gold standard) suggest that the sensitivity andspecificity of ultrasonography is poor, ranging from 39%to 61%and 42%to 53%, respectively.81-84 Another limita-tion is that ultrasonography can only be used to evaluatethe frontal and maxillary sinuses.85 Despite these issues,ultrasonography might have some utility as a sinus diag-nostic screen in pregnant women to avoid risks of ionizingradiation.Standard radiography. Caldwell (anterior-posterior) andWaters (occipito-mental) standard radiographs demon-strate the frontal and maxillary sinuses, respectively.86

Lateral views visualize the sphenoid sinus and adenoidsin children. The fine bony anatomy of the ethmoid sinusesis not well seen on any standard radiographs becauseof problems of normal structural superimposition.Although other sinuses might also be involved, acute si-nusitis commonly involves the maxillary sinuses. Accord-ingly, a single Waters view is a viable diagnostic substitutefor a 4-view sinus series in many patients.87 However,ethmoid involvement without maxillary sinus infectionoccurs in approximately 20% of patients.

The interpretation of standard radiographs remains con-troversial. It is generally believed that mild-to-moderatemucosal thickening is a nonspecific finding. In contrast,


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sinus opacification, air-fluid level, or severe mucosalthickeningin adults is more likely to reflect meaningfulpathology.88 Extrapolating from more recent CT studies,however, the correlation between radiographic extentof disease and likelihood of resolution without medicaltherapy is poor.76-78 The decision to treat with antibioticsshould therefore be made on clinical grounds alone.

Standard radiographs are of limited value in the eval-uation of chronic sinusitis; they are also inadequate forclarifying the need for endoscopicsurgery and the preciseareas that need surgical attention.89

Computed tomography. High-resolution CT scans dem-onstrate the extent of disease andthe degree of ostiomeatalcomplex obstruction; they might also delineate pathologicvariations and anatomic structures that are not apparent onphysical examination or rhinoscopy.89,90 Sinus CT is theimaging technique of choice in preparation for endoscopicsurgery.

Coronal scans provide a road map for surgery, bestdemonstrating the ostiomeatal drainage areas and intricate

relationships between the brain, fovea ethmoidalis, andethmoid sinuses. However, increasingly, surgeons areusing computer-assisted surgical navigation, particularlyin revision or other cases of complicated anatomy.Computer-assisted surgical navigation requires axialscans with scanning parameters specific for the computerdevice used, as well as standard coronal views.

The amount of radiation in standard sinus CTs is notnegligible. An alternative approach is a low-dose CT witha standard dose in 1 or 2 sections in which more intricatedetail is required (eg, in the ostiomeatal complex).91

In the past, a series of standard radiographs has beenfavored in preference to CT because of cost and time

considerations. More recently, however, some medicalcenters offer a limited 4- to 5-cut coronal sinus CT scan ata similar cost to a set of standard radiographs. Thistypically takes only 15 to 20 minutes and provides muchbetter high-resolution bone and soft tissue detail, includ-ing the ethmoids (which are poorly visualized on anystandard radiograph).92 This field is progressing rapidly,and current scanners take only 17 seconds for a completesinus set.

High-resolution sinus CT is considered a mandatorypreoperative study and is important for the planning andsafe performance of functional endoscopic sinus surgery.This is particularly crucialwhen the ostiomeatal complex

and ethmoids are involved.

93

Sinus CT is particularly helpful in the diagnosis offungal sinusitis. Classic findings for fungal disease are acombination of unilateral lesions of one or more sinuses,nodular mucoperiosteal thickening, focal areas of bonedestruction, and/or dense intrasinus concretions.94

Magnetic resonance imaging. MRI provides ideal imag-ing of soft tissues; it is less suited to imaging bonyanatomy because bone and air yield similar signal inten-sities on MRI. The value of MRI is further limited becausethe signal intensity from normal edematous mucosa isindistinguishable from extensively inflamed and diseasedtissue.

The differential diagnosis between inflammatory dis-

eases and malignant tumor is aided by MRI.

95

MRI assistsin clarifying the degree of orbital or intracranial extensionin complicated sinusitis. T2-weighted image intensity isuseful: high signal with bacterial and viral inflammation,intermediate bright signal with neoplastic processes (eg,squamous cell carcinoma), and verylow signal with fun-gal concretions, similar to that of air.86

MRI or CT is more sensitive than standard radiographyin defining the extent ofdisease, particularly with poste-rior sinus involvement.96 Table IIIcompares the indica-tions and limitations of CT and MRI.

All imaging should be performed more than 2 weeksafter an upper respiratory tract infection and more than

TABLE III. Indications and limitations of CT and MRI

Modality Indications

CT without contrast

(coronal views with

bone windows)

Images bone, sinus anatomy, ostio-

meatal complex, and shows soft

tissueairbone contrast

Indications:

Recurrent acute sinusitisChronic sinusitis

Preoperative for sinus surgery

Nasal polyposis

Persistent nasal congestion-

obstruction

Immunocompromised patient with

fever

Dentomaxillary pain

Facial pressureheadache unre-

sponsive to medical therapy

Anosmia after appropriate workup

CT with contrast (coronal

and axial views)

Allows some degree of differentia-

tion of soft tissue opacification

Indications:

Complications of sinusitis (periorbi-tal edema, subperiosteal abscess)

Sinonasal tumor

MRI with contrast (need to

specifically request coro-

nal views)

Provides excellent soft tissue differ-

entiation (eg, tumor vs retained

fluid) but does not image bone or

the bony anatomy required for

surgery. Images the nasal cycle

and thus might be oversensitive

for sinusitis.

Indications:

Skull base dehiscence with

opacification

Unilateral sinonasal opacification

(on CT)Sinonasal process with cranial

extension

Expansile sinonasal mass with bony

erosion (?remodeling)

Sinonasal mass with orbital

extension

Biopsy -proved tumor

Fungal sinusitis



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4 weeks after acute bacterial sinusitis and after medicalmanagement if the aim is to identify the underlying extentof chronic sinusitis or potential causes of recurrent acutesinusitis.

Laboratory tests

Summary Statements

Summary Statement 29: Laboratory evaluation of acute,chronic, or recurrent sinusitis might include the follow-ing: nasal cytology, nasal-sinus biopsy, or tests for im-munodeficiency, CF, or ciliary dysfunction. NRSummary Statement 30: Nasal cytology is useful in theevaluation of conditions associated with sinusitis, in-cluding AR, eosinophilic NAR, neutrophilic rhinitis,and VMR. CSummary Statement 31: Nasal-sinus biopsy is useful inseveral clinical situations: determining whether a lesionis neoplastic and, if so, its nature; confirming the presenceof fungal disease; confirming the presence of granuloma-tous disease; and determining the ultrastructure of cilia.C

Laboratory tests might provide additional diagnosticinformation in patients with acute or chronic sinusitis.Nasal cytology can provide data that support or refute theclinical diagnosis of acute infectious sinusitis; resultsmight suggest the presence of underlying disease (eg,eosinophilic rhinitis). Antral puncture and endoscopicallyobtained culture were discussed in the Microbiologysection. Nasal-sinus biopsy is useful in suspected cases ofneoplasia, fungal disease, or granulomatous disease; thistechnique is also used in patients with ciliary dysmotilityto define the ultrastructural nature of the defect. Other tests

are used to assess disorders that might be causallyassociated with recurrent or chronic sinusitis (eg, immu-nodeficiency, CF, or ciliary dysfunction); these tests arediscussed in separate sections (see below).Nasal cytology. Nasal cytology demonstrates the type ofcellular inflammation in patients with acute or chronicsinusitis. This can provide useful adjunctive informationto the clinical history and examination with regard tolikely infection or associated eosinophilic disease. Sam-ples can be obtained by having the patient blow secretionsinto transparent plastic wrap or by the use of a cytologybrush or Rhinoprobe (Synbiotics Corp, San Diego, Calif).Samples collected by means of the blowing technique

often contain less cellular material butare still useful fordetecting eosinophils and neutrophils.1

Nasal secretions are transferred to a glass slide, fixed,and then treated with Hansel stain, a stain that highlightseosinophil granular contents. Additional stains (eg,Papanicolaou, hematoxylin and eosin, acidified toluidineblue, or May-Grunwald-Giemsa) might be used to identifyother elements, including mast cells, basophils, neutro-phils, nonciliated epithelial cells, squamous cells, or evenpollens or mold spores.

Nasal cytology results can be consistent with a varietyof syndromes, including AR, eosinophilic NAR, VMR,bacterial sinusitis, neutrophilic nonbacterial sinusitis, and

metaplasia caused by environmental exposures.97,98 Thepresence of eosinophils correlates with AR or eosinophilicNAR, a condition often associated with chronic sinusitis,nasal polyposis, asthma, and nonsteroidal anti-inflamma-tory drug sensitivity.99

Unfortunately, the clinical value of nasal cytology inthe assessment of sinusitis is limited, with specificityranging from 40% to 90% and sensitivity from 67% to80%.100,101 This occurs because acute viral infections caninducenasal neutrophilia and transient abnormal imagingstudies.101 In addition, patients with AR and acute bacte-rial sinusitis will demonstrate a mixture of nasal eosino-philia and neutrophilia, potentially creating diagnosticconfusion. At the same time, nasal cytology can providesome useful information: the absence of neutrophils (as-suming an adequate sample) argues against an infectiouscomponent, and the presence of more than 10% eosino-phils in a patient with chronic or recurrent disease suggeststhe potential for underlying AR or NARES.Nasal-sinus biopsy. Nasal-sinus biopsy should be con-

sidered to aid in the diagnosis of nasal or paranasal lesionsthat obstruct sinus cavities and give rise to chronic orrecurrent sinus disease. Clinical reasons to obtain a biopsyare (1) to determine whether a lesion is neoplastic and, ifso, to clarify the nature of the neoplasm; (2) to confirmthe presence of suspected invasive fungal disease; (3) toconfirm the presence of granulomatous disease when thediagnosis is unclear on the basis of clinical or radiographicgrounds; and (4) to provide an initial evaluation of theultrastructure of cilia in patients with known or suspectedciliary dysfunction. In the presence of chronic inflamma-tion, a tracheal biopsy is typically required for confirmation.Nasal and paranasal sinus neoplasms. Early signs of

sinus neoplasia are nonspecific and include nasal obstruc-tion, anosmia, rhinorrhea, and pain. Accordingly, clinicalsuspicion of tumor is often delayed until epistaxis, prop-tosis, trismus, facial swelling, or cranial nerve (I/VI)dysfunction develop. Early diagnosis is enhanced by theuse of CT or MRI. The most common tumor is an invertedpapilloma, which is characterized by a polypoid appear-ance and unilateral location seen on both physical exam-ination and imaging.

Tumors within the nose or sinuses are histologicallydiverse and both benign and malignant. Generally, aspecific diagnosis is not reliable on the basis of clinicalor radiographic findings, making a tissue biopsy invalu-

able.

102

Juvenile angiofibroma is a notable exception.Diagnosis is made on the basis of finding a vascular pos-terior nasal or nasopharyngeal mass in an adolescent orpreadolescent male. Biopsy should not be performedbecause of the risk of significant hemorrhage.103

Invasive fungal infections. Fungal infection produced byphycomycetes (Absidia, Mucor, and Rhizopus species)can progress from the sinuses to the central nervous sys-tem and is potentially fatal. Similar rapidly fulminant in-fections can be caused by Aspergillus species. Thesefulminant diseases occur essentially only in the immuno-compromised (eg, patients with diabetes mellitus, hemato-logic malignancies, adrenal suppression, chronic renal


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failure, hematologic dyscrasia or overt immunodeficiency[eg, patients undergoing chemotherapy, intravenous drugusers, and patients with HIV]) However, less fulminantand more indolent invasive disease might occasionallyoccur in the immunocompetent patient.

Patients with fulminant invasive fungal sinusitis oftenpresent with fever, which rapidly progresses to facial pain,proptosis, ophthalmoplegia, and/or facial necrosis. Lateradiographic findings can include sinus opacification,mucoperiosteal thickening, bone erosion, and cavernoussinus thrombosis. Endoscopically, early lesions mightappear brick red or as black necrotic areas. Suspiciouslesions should be biopsied immediately, with the samplesent for fungal staining and culture. Early diagnosis can becritical in determining patient prognosis.104

Granulomatous inflammatory disease. Sinusitis can beassociated with several granulomatous diseases, bothinfectious and noninfectious. Sarcoidosis is by far themost common of these disorders identified within theUnited States. Another noninfectious cause is midline

granulomaWegener granulomatosis. Infectious causesinclude Klebsiellaspeciesinduced rhinoscleroma, tuber-culosis, leprosy, syphilis, and fungal infections. Lesionscan cause ulceration, necrosis, or hyperplastic mucosa.When such lesions are apparent, biopsy should beobtained to exclude neoplasia, and special staining andcultures should be done for mycobacteria and fungi.105,106

Cilia ultrastructure. When ciliary dysfunction is sus-pected in patients (eg, with recurrent or persistent infec-tious disease in the absence of underlying rhinitis,anatomic defects, or immunodeficiency), biopsy shouldbe considered for ultrastructural analysis. Reported resultsinclude the type of defect (dynein defects are most

specific), the percentage of cilia having the defect, thedistribution of the defect (bronchial versus nasal if bothareas are assessed), and the number of cilia present.107,108

Because acquired ciliary defects can sometimes mimicprimary ciliary dyskinesia in the presence of chronic in-flammation, tracheal biopsy is frequently required forconfirmation of this diagnosis.Immunodeficiency tests. See the Immunodeficiencysection.Cystic fibrosis tests.See the Cystic fibrosis section.Ciliary tests. See the Ciliary dysfunction section.Miscellaneous tests. The role of nasopharyngeal culturein the diagnosis of acute sinusitis remains controversial.

In the past, studies have suggested a poor correlationbetween the presence of nasal bacteria and the likelihoodof active bacterial sinusitis; even in patients with culture-proved sinusitis, the bacteria present in the sinus wasdifferent from bacteria in the nasophayrnx. More recently,it has been suggested that the presence of pathogenicorganisms (S pneumoniae,H influenzae, orM catarrhalis)in the nasopharynx of patients presenting with upperrespiratory tract infection symptomsmight define patientsmore likely to have bacterial disease.109

The value of routine hematologic tests (eg, erythrocytesedimentation rate, white blood cell count, and C-reactiveprotein) was recently evaluated in 176 patients with acute

maxillary sinusitis. In general, these tests were not sensi-tive indicators of disease or specific cause (82% of testresults were normal). Increased C-reactive protein (>40mg/L) was associated with likely infection with Strepto-coccus pyogenesorS pneumoniae, afact that could influ-ence choice and duration of therapy.110

In suspected Wegener granulomatosis, an antineutro-phil cytoplasmicantibody test might be a useful adjunctto tissue biopsy.111 Similarly, increases of angiotensin-converting enzyme and soluble IL-2 receptor levels mightbe of help in clarifying a suspected tissue diagnosis ofsarcoidosis.112

Predisposing factors

Viral infections

Summary Statements

Summary Statement 32: Acute viral upper respiratorytract infections often precede acute bacterial sinusitis. B

Summary Statement 33: Viral upper respiratory tract in-fections are often (40% to 90% of the time) associatedwith CT evidence of sinusitis. Viral sinusitis appears toresolve w

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