Updated: Feb 10, 2009
Sinusitis is characterized by inflammation of the lining of the paranasal sinuses. Because the nasal mucosa is simultaneously involved and because sinusitis rarely occurs without concurrent rhinitis, rhinosinusitis is now the preferred term for this condition.1 By definition, symptoms of acute rhinosinusitis last less than 3 weeks, symptoms of subacute rhinosinusitis last 21-60 days, and symptoms of chronic rhinosinusitis last more than 60 days. The Agency for Healthcare Research and Quality accepted this terminology in 1999.
Rhinosinusitis may be further classified according to the anatomic site (maxillary, ethmoidal, frontal, sphenoidal), pathogenic organism (viral, bacterial, fungal), presence of complication (orbital, intracranial), and associated factors (nasal polyposis, immunosuppression, anatomic variants).
The vast majority of rhinosinusitis episodes are caused by viral infection. Most viral upper respiratory tract infections are caused by rhinovirus, but coronavirus, influenza A and B, parainfluenza, respiratory syncytial virus, adenovirus, and enterovirus are also causative agents.
Almost 90% of patients with upper respiratory tract infections have radiographic evidence of paranasal sinus involvement. However, only 0.5-2% of viral rhinosinusitis cases are complicated by bacterial infection.2
The pathophysiology of rhinosinusitis is related to 3 factors: obstruction of sinus drainage pathways (sinus ostia), ciliary impairment, and mucus quantity and quality.
Rhinosinusitis affects 35 million people per year in the United States and accounts for close to 16 million office visits per year.3 According to the National Ambulatory Medical Care Survey (NAMCS), approximately 14% of adults report having an episode of rhinosinusitis each year, and it is the fifth most common diagnosis for which antibiotics are prescribed. In 1996, Americans spent approximately $3.39 billion treating rhinosinusitis.4
Approximately 0.5-2% of cases of viral rhinosinusitis are complicated by bacterial superinfection.
Sinusitis is more common from early fall to early spring.
Forty percent of acute rhinosinusitis cases resolve spontaneously. Untreated or inadequately treated rhinosinusitis may lead to complications such as meningitis, cavernous sinus thrombophlebitis, orbital cellulitis or abscess, and brain abscess.
Acute rhinosinusitis has no racial predilection.
Acute rhinosinusitis has no sexual predilection.
Sinusitis occurs in all age groups.
A history of occupational or allergic rhinitis, vasomotor rhinitis, nasal polyps, rhinitis medicamentosa, or immunodeficiency should be sought in an evaluation for rhinosinusitis. Rhinosinusitis is more common in individuals with congenital defects that affect humoral immunity and ciliary motility, in those with cystic fibrosis, and in persons with AIDS. Obtain a history of diabetes or organ transplant if invasive fungal sinusitis is being considered.
Acute bacterial rhinosinusitis is commonly overdiagnosed. In fact, acute bacterial rhinosinusitis is the correct diagnosis in only 40-50% of cases in which a primary care physician initially classifies a patient as likely having the condition.5
The natural history of rhinovirus infection, as described by Gwaltney et al, lasts from 1-33 days. One fourth of patients have symptoms that last longer than 14 days.6
The most common pathogens isolated from maxillary sinus cultures in patients with acute bacterial rhinosinusitis include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Streptococcus pyogenes, Staphylococcus aureus, and anaerobes are less commonly associated with acute bacterial rhinosinusitis.
| Adenoviruses | Mucormycosis |
| Allergic and Environmental Asthma | Parainfluenza Virus |
| Asthma | Rhinitis, Allergic |
| Bronchitis | Rhinocerebral Mucormycosis |
| Haemophilus Influenzae Infections | Rhinoviruses |
| Human T-Cell Lymphotrophic Viruses | Sarcoidosis |
| Immunosuppression | Sinusitis, Chronic |
| Influenza | Staphylococcal Infections |
| Kartagener Syndrome | Streptococcus Group A Infections |
| Lymphoma, B-Cell | Streptococcus Group B Infections |
| Moraxella Catarrhalis Infections |
Gastroesophageal reflux
Cystic fibrosis
Immotile cilia syndrome
Migraine headache
Sinonasal polyposis
Chemical rhinitis
Nasal foreign body
Chronic invasive fungal sinusitis
Sinonasal neoplasm
The goals of therapy in rhinosinusitis are to improve mucociliary function and to control infection.
Antral puncture and irrigation are used for diagnostic culture and sensitivity testing in immunosuppressed or critically ill patients if the organism must be identified. However, more recent data support the role of endoscopically guided middle meatus cultures instead.
Viral rhinosinusitis does not require antimicrobial treatment.
Standard nonantimicrobial treatment options include topical steroids, topical and/or oral decongestants, mucolytics, and intranasal saline spray.
A recent meta-analysis of 4 double-blind, placebo-controlled trials of intranasal corticosteroid treatment in acute rhinosinusitis supports its use as monotherapy or as an adjuvant therapy to antibiotics.11 However, a recent randomized controlled trial of antibiotics and intranasal steroid showed no treatment benefit of intranasal steroids, either alone or with antibiotics.12
Ahovuo-Saloranta et al, in a 2008 Cochrane Review meta-analysis of 57 studies, concluded that antibiotics yield a small treatment effect in a primary care setting in patients with uncomplicated sinusitis whose symptoms have lasted more than 7 days.13 However, another meta-analysis found no treatment effect of antibiotics, even in patients whose symptoms had persisted for more than 10 days.14
No available data suggest that antihistamines are beneficial in acute sinusitis. In fact, antihistamines may cause harm by drying mucous membranes and decreasing clearance of secretions.
Antibiotic efficacy rates are as follows:
Based on the 2000 Sinus and Allergy Health Partnership treatment guidelines for acute bacterial rhinosinusitis, patients are divided into 3 groups, as follows:
Patients who remain symptomatic despite appropriate antibiotic therapy may be evaluated with sinus endoscopy, CT scanning, or sinus aspiration/culture.
First-line antibiotic choice. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
250 mg PO q8h for 10-12 d
Not established
Reduces efficacy of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; use during mononucleosis produces a characteristic rash
First-line antibiotic choice. Inhibits biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached and most effective during stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.
250 mg PO q6h for 10-12 d
Not established
Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, causing a decrease in effectiveness when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal impairment; superinfections may occur with prolonged use; reduces efficacy of oral contraceptives
First-line treatment in patients allergic to penicillin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
250 mg PO q6h for 10-12 d
Not established
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, benzodiazepines, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; may prolong QT interval, resulting in cardiac arrest if combined with nonsedating antihistamines
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
First-line agent with more convenient dosing. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
160 mg TMP/800 mg SMZ PO q12h for 10-12 d
<2 months: Do not administer
>2 months: Not established
May increase PT when used with warfarin (perform coagulation tests, and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, people with long-term alcoholism, elderly people, those receiving anticonvulsant therapy, those with malabsorption syndrome); hemolysis may occur in G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation
Second-line agent. Binds to one or more of the penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.
250-500 mg PO q12h for 10 d
Not established
Probenecid increases effect; coadministration with furosemide and aminoglycosides increases nephrotoxic effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Second-line agent. Second-generation cephalosporin maintains gram-positive activity of first-generation cephalosporins. Adds activity against Proteus mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and M catarrhalis.
250 mg PO bid for 10 d
Not established
Disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patients receiving potent diuretics such as loop diuretics; coadministration with aminoglycosides increases nephrotoxic potential; concomitant use with agents that lower gastric pH decreases absorption
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Reduce dosage by half if CrCl is 10-30 mL/min and by three fourths if <10 mL/min (high doses may cause CNS toxicity); bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy
Second-line agent. Binds to one or more penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.
100 mg PO q12h for 10 d
Not established
Probenecid increases effect; coadministration with furosemide and aminoglycosides increases nephrotoxic effects; antacids and H2 blockers decrease absorption
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Reduce dosage by half if CrCl is 10-30 mL/min and by three fourths if <10 mL/min (high doses may cause CNS toxicity); bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy
Second-line agent. By binding to one or more penicillin-binding proteins, arrests bacterial cell wall synthesis and inhibits bacterial growth.
400 mg PO qd for 10 d
Not established
Increases carbamazepine levels; coadministration of aminoglycosides increases nephrotoxicity; probenecid may increase effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Second-line agent. Drug combination treats bacteria resistant to beta-lactam antibiotics.
875 mg PO q12h or 500 mg PO q8h for 10 d
Not established
Coadministration with warfarin or heparin increases risk of bleeding
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Presence of mononucleosis produces skin rash; interstitial nephritis and renal failure may occur in high doses
Second-line agent. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
500 mg PO bid for 10 d
Not established
Toxicity increases with coadministration of fluconazole, astemizole, and pimozide; effects decrease and adverse GI effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors; serious cardiac arrhythmia may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmia and increase in QT intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
Documented hypersensitivity; coadministration of pimozide or cisapride
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; give half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies
Used to treat acute maxillary sinusitis caused by S pneumoniae, H influenzae, or M catarrhalis. Fluoroquinolones should be used empirically in patients likely to develop exacerbation due to resistant organisms to other antibiotics. This is the L stereoisomer of the D/L parent compound ofloxacin, the D form being inactive. Good monotherapy with extended coverage against Pseudomonas species, as well as excellent activity against pneumococcus. Agent acts by inhibition of DNA gyrase activity. PO form has bioavailability that is reportedly 99%.
500 mg PO qd for 7-14 d
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Inhibits protein synthesis, and thus bacterial growth, by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
100-200 mg PO bid for 14 d
<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO in 1-2 divided doses; not to exceed 200 mg/d
Bioavailability decreases with antacids that contain aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
These agents cause vasoconstriction, which reduces nasal congestion.
Produces vasoconstriction. Possibly helpful, not harmful.
2 puffs q4h prn; not to exceed 3 d of use
Not established
May cause hypertensive crisis in the presence of MAOIs
Documented hypersensitivity; severe hypertension or ventricular tachycardia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use may produce rhinitis medicamentosa; caution in hypertension
Applied directly to mucous membranes. Stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in blood pressure, vascular redistribution, or cardiac stimulation.
2 puffs in each nostril bid; not to exceed 3 d of use
Not established
Hypotensive action of guanethidine may be reversed; concurrent administration with methyldopa may result in increased vasopressor response; concurrent use of MAOIs and ephedrine may result in hypertensive crisis; pressor sensitivity to mixed-acting agents, such as ephedrine, may be increased; guanethidine potentiates effects of epinephrine and inhibits effects of ephedrine; phenothiazines may reverse action of nasal decongestants; TCAs potentiate vasopressor response and may result in dysrhythmia
Documented hypersensitivity; MAOI therapy; angle-closure glaucoma
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hyperthyroidism, coronary artery and ischemic heart disease, diabetes mellitus, increased intraocular pressure, or prostatic hypertrophy; because of increase in vasoconstriction, patients who are hypertensive may experience change in blood pressure; may produce rhinitis medicamentosa
Increases respiratory tract fluid secretions and helps to loosen phlegm and bronchial secretions. Indicated for patients with bronchiectasis complicated by tenacious mucous and/or mucous plugs.
600-mg SR tab 1-2 tab PO q12h
<2 years: Not recommended
2-6 years: One-half tab PO q12h
6-12 years: 1 tab q12h
>12 years: Administer as in adults
May increase renal clearance of urate and lower serum uric acid levels
May interfere with urine laboratory tests for 5-hydroxyindoleacetic acid and urine testing for catecholamines
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
When prescribing medication that may suppress cough, important to identify cause of the cough and that suppression will not increase risk of clinical or physiologic complications
These agents are beneficial, especially if underlying rhinitis is present.
Has potent vasoconstrictive and anti-inflammatory activity. Has a weak hypothalamic-pituitary-adrenocortical (HPA) axis inhibitory potency when applied topically.
2 puffs in each nostril bid for 3 wk
Not established
None reported
Documented hypersensitivity; viral, fungal, and bacterial skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria; nasal septum perforation, angioedema, and bronchospasm may occur
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
2 puffs in each nostril qd
Not established
None reported
Documented hypersensitivity; fungal, viral, and bacterial skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use can result in systemic absorption, which may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria; nasal septum perforation, angioedema, or bronchospasm may occur
Inhibits bronchoconstriction mechanisms. Produces direct smooth muscle relaxation. May decrease number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness.
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Does not depress the hypothalamus.
2 sprays/nostril bid/tid (25 mcg/spray)
<6 years: Not established
>6 years: 1 spray/nostril tid or 2 sprays/nostril bid (25 mcg/spray)
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Educate patient that this agent is not to be used as a rescue treatment for acute bronchospasm
Lanza DC, Kennedy DW. Adult rhinosinusitis defined. Otolaryngol Head Neck Surg. Sep 1997;117(3 Pt 2):S1-7. [Medline].
Gwaltney JM Jr. Acute community-acquired sinusitis. Clin Infect Dis. Dec 1996;23(6):1209-23; quiz 1224-5. [Medline].
Lucas JW, Schiller JS, Benson V. Summary health statistics for U.S. adults: National Health Interview Survey, 2001. Vital Health Stat 10. Jan 2004;(218):1-134. [Medline].
Ray NF, Baraniuk JN, Thamer M. Healthcare expenditures for sinusitis in 1996: contributions of asthma, rhinitis, and other airway disorders. J Allergy Clin Immunol. Mar 1999;103(3 Pt 1):408-14. [Medline].
Hansen JG, Schmidt H, Rosborg J, Lund E. Predicting acute maxillary sinusitis in a general practice population. BMJ. Jul 22 1995;311(6999):233-6. [Medline].
Gwaltney JM, Hendley JO, Simon G. Rhinovirus infections in an industrial population. II. Characteristics of illness and antibody response. JAMA. Nov 6 1967;202(6):494-500. [Medline].
Hickner JM, Bartlett JG, Besser RE. Principles of appropriate antibiotic use for acute rhinosinusitis in adults: background. Ann Intern Med. Mar 20 2001;134(6):498-505. [Medline].
Jacobs MR, Bajaksouzian S, Windau A, Good CE, Lin G, Pankuch GA. Susceptibility of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis to 17 oral antimicrobial agents based on pharmacodynamic parameters: 1998-2001 U S Surveillance Study. Clin Lab Med. Jun 2004;24(2):503-30. [Medline].
Payne SC, Benninger MS. Staphylococcus aureus is a major pathogen in acute bacterial rhinosinusitis: a meta-analysis. Clin Infect Dis. Nov 15 2007;45(10):e121-7. [Medline].
Brook I, Foote PA, Hausfeld JN. Increase in the frequency of recovery of meticillin-resistant Staphylococcus aureus in acute and chronic maxillary sinusitis. J Med Microbiol. Aug 2008;57:1015-7. [Medline].
[Best Evidence] Zalmanovici A, Yaphe J. Steroids for acute sinusitis. Cochrane Database Syst Rev. Apr 18 2007;CD005149. [Medline].
[Best Evidence] Williamson IG, Rumsby K, Benge S, Moore M, Smith PW, Cross M, et al. Antibiotics and topical nasal steroid for treatment of acute maxillary sinusitis: a randomized controlled trial. JAMA. Dec 5 2007;298(21):2487-96. [Medline].
[Best Evidence] Ahovuo-Saloranta A, Borisenko OV, Kovanen N, Varonen H, Rautakorpi UM, Williams JW Jr, et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev. Apr 16 2008;CD000243. [Medline].
Young J, De Sutter A, Merenstein D, van Essen GA, Kaiser L, Varonen H, et al. Antibiotics for adults with clinically diagnosed acute rhinosinusitis: a meta-analysis of individual patient data. Lancet. Mar 15 2008;371(9616):908-14. [Medline].
Cunha BA. Antibiotic Essentials. 7th ed. Boston, MA: Jones and Bartlett Publishers; 2008.
Bachert C, Meltzer EO. Effect of mometasone furoate nasal spray on quality of life of patients with acute rhinosinusitis. Rhinology. Sep 2007;45(3):190-6. [Medline].
Bailey BJ, Calhoun KH, et al. Head & Neck Surgery - Otolaryngology, 3rd edition. 2001;vol 1.
Benninger MS, Payne SC, Ferguson BJ, Hadley JA, Ahmad N. Endoscopically directed middle meatal cultures versus maxillary sinus taps in acute bacterial maxillary rhinosinusitis: a meta-analysis. Otolaryngol Head Neck Surg. Jan 2006;134(1):3-9. [Medline].
Berkow R, Beers MH, eds. Sinusitis. In: The Merck Manual of Diagnosis and Therapy. 16th ed. Whitehouse Station, NJ: Merck & Company; 1992. [Full Text].
Fagnan LJ. Acute sinusitis: A Cost-Effective Approach to Diagnosis and Treatment. In: American Family Physician. Leawood, Kans: American Academy of Family Physicians; 1998. [Full Text].
[Best Evidence] Karageorgopoulos DE, Giannopoulou KP, Grammatikos AP, Dimopoulos G, Falagas ME. Fluoroquinolones compared with beta-lactam antibiotics for the treatment of acute bacterial sinusitis: a meta-analysis of randomized controlled trials. CMAJ. Mar 25 2008;178(7):845-54. [Medline].
Meltzer EO, Bachert C, Staudinger H. Treating acute rhinosinusitis: comparing efficacy and safety of mometasone furoate nasal spray, amoxicillin, and placebo. J Allergy Clin Immunol. Dec 2005;116(6):1289-95. [Medline].
Meltzer EO, Hamilos DL, Hadley JA, Lanza DC, Marple BF, Nicklas RA, et al. Rhinosinusitis: developing guidance for clinical trials. J Allergy Clin Immunol. Nov 2006;118(5 Suppl):S17-61. [Medline].
National Ambulatory Medical Care Survey. Ambulatory Health Care Data. [Full Text].
Sinus and Allergy Health Partnership. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Sinus and Allergy Health Partnership. Otolaryngol Head Neck Surg. Jul 2000;123(1 Pt 2):5-31. [Medline].
Skoner DP. Complications of allergic rhinitis. J Allergy Clin Immunol. June 2000;105:605-609. [Medline].
Varonen H, Rautakorpi UM, Nyberg S, Honkanen PO, Klaukka T, Palva E, et al. Implementing guidelines on acute maxillary sinusitis in general practice--a randomized controlled trial. Fam Pract. Apr 2007;24(2):201-6. [Medline].
acute sinusitis, rhinosinusitis, acute rhinosinusitis, common cold, seasonal allergy, bacterial infection, flu, Streptococcus pneumoniae, S pneumoniae, Haemophilus influenzae, H influenzae, acute ethmomaxillary sinusitis, rhinitis, subacute sinusitis, subacute rhinosinusitis, maxillary sinusitis, ethmoidal sinusitis, frontal sinusitis, sphenoidal viral sinusitis, bacterial sinusitis, fungal orbital sinusitis, intracranial sinusitis, maxillary rhinosinusitis, ethmoidal rhinosinusitis, frontal rhinosinusitis, sphenoidal viral rhinosinusitis, bacterial rhinosinusitis, fungal orbital rhinosinusitis, intracranial rhinosinusitis, acute viral rhinosinusitis, acute bacterial rhinosinusitis, acute viral sinusitis, acute bacterial sinusitis
Brian E Benson, MD,, Attending Physician, Department of Otolaryngology, St Luke's-Roosevelt Hospital Center; Clinical Assistant Professor, Department of Otolaryngology, Hackensack University Medical Center; Director, The Voice Center, Hackensack University Medical Center
Brian E Benson, MD, is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, and Sigma Xi
Disclosure: Nothing to disclose.
Linas Riauba, MD, Assistant Professor of Clinical Medicine, Department of Medicine, Section of Infectious Disease, University Hospital, University of Medicine and Dentistry of New Jersey
Linas Riauba, MD is a member of the following medical societies: American Medical Association and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Tracey Quail Davidoff, MD, Senior Clinical Instructor, Department of Emergency Medicine, Rochester General Hospital
Tracey Quail Davidoff, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Forensic Examiners, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.
Thomas Herchline, MD, Professor of Medicine, Wright State University Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio
Thomas Herchline, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Gordon L Woods, MD, Consulting Staff, Department of Internal Medicine, University Medical Center
Gordon L Woods, MD is a member of the following medical societies: Society of General Internal Medicine
Disclosure: Nothing to disclose.
Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthors Michael Cunningham, DO, and Erhun Serbetci, MD, to the development and writing of this article.
Further Reading© 1994-
by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)