Updated: Aug 19, 2009
Traditionally, sinusitis is defined as an inflammation of the mucosal lining of one or more of the paranasal sinuses. The term rhinosinusitis is now used interchangeably with sinusitis to emphasize the concurrent inflammation of the nasal passages that occurs with sinus mucosal inflammation. Sinusitis is subdivided into acute (symptoms lasting <4 wk), subacute (symptoms lasting 4-12 wk), and chronic (symptoms lasting >12 wk).1
The paranasal sinuses are in direct communication with the nasopharynx. The sinuses are normally sterile, but their proximity to nasopharyngeal flora allows bacterial and viral inoculation following rhinitis. Diseases that obstruct drainage can result in a reduced ability of the paranasal sinuses to function normally. The sinus ostia become occluded, leading to mucosal congestion. The mucociliary transport system becomes impaired, leading to stagnation of secretions and epithelial damage, followed by decreased oxygen tension and subsequent bacterial growth.
Acute rhinosinusitis is most commonly associated with viral infections such as the common cold. In about 0.5-2% of cases, viral sinusitis can progress to acute bacterial sinusitis.2,3 Other factors that predispose to the development of acute bacterial rhinosinusitis include allergic rhinitis, impaired mucociliary transport as seen in cystic fibrosis, mechanical obstruction as seen secondary to foreign bodies, intranasal cocaine use and immunodeficient states.3
Acute bacterial sinusitis that does not completely resolve can progress to chronic sinusitis. Other factors associated with chronic sinusitis include allergic rhinitis, fungal colonization of the sinuses, and nasal polyposis. Nasal polyposis, more commonly seen in patients with aspirin sensitivity and asthma, results from a localized allergic hyperresponsivity to bacterial endotoxins. Diseases such as cystic fibrosis, primary ciliary dyskinesia, Wegener granulomatosis, Churg-Strauss vasculitis, and sarcoidosis have also been known to be affiliated with chronic rhinosinusitis.4
In the United States, approximately 1 billion cases of acute rhinosinusitis and 20 million cases of acute bacterial rhinosinusitis are diagnosed every year.3 About 50% of people with clinically diagnosed acute sinusitis have a bacterial sinus infection.2 Medical treatment of rhinosinusitis is expensive, with an estimated $3 billion spent annually.3
Sinusitis is rarely life threatening, but the close proximity of the paranasal sinuses to the central nervous system, the multiple fascial plains of the neck, and the associated venous and lymphatic channels can lead to serious complications.
Sinusitis occurs equally in males and females.
Sinusitis is more commonly seen in young or middle-aged adults.4 Sinusitis is rare in children younger than 1 year because the sinuses are poorly developed prior to that age.
Headache, Cluster
Headache, Migraine
Headache, Tension
Otitis Media
Dental infections
Periapical abscess
Upper respiratory tract infection
The treatment of sinusitis is mostly symptomatic and does not shorten the duration of the infection. Acute viral sinusitis usually resolves without treatment in 7-10 days.3 Up to 75 percent of cases of acute bacterial rhinosinusitis resolve without any treatment in 1 month.3 While in the emergency department and upon discharge, patients may obtain significant immediate relief with the administration of first-generation antihistamines, decongestants, and nonsteroidal anti-inflammatory drugs (NSAIDs).
Antibiotics are indicated for sinusitis that is thought to be bacterial (see History), including sinusitis that is severe or involves the frontal, ethmoid, or sphenoid sinuses, since this type of sinusitis is more prone to complications.7
Penicillins, cephalosporins, and macrolides seem to be equally efficacious.2 A 10-14 day regimen of amoxicillin 500 mg 3 times a day is considered first-line therapy.8 The risk of adverse effects should be weighed against the severity of disease and patient comorbidities prior to initiating antibiotic treatment.
These agents are used to loosen secretions for clearance.
Applied directly to mucous membranes, where it stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in blood pressure, vascular redistribution, or cardiac stimulation.
2-3 sprays or 2-3 gtt of 0.05% solution in each nostril bid
Use for maximum of 3 d only; patients can become dependent
<6 years: 2-3 gtt of 0.025% solution in each nostril bid
>6 years: Administer as in adults
Hypotensive action of guanethidine may be reversed; concurrent administration with methyldopa may result in an 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 such as oxymetazoline; TCAs potentiate vasopressor response and may result in dysrhythmias
Documented hypersensitivity; MAOI therapy
C - Fetal risk revealed in studies in animals but not established or not studies 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 with hypertension may experience change in blood pressure; do not use topical decongestants for longer than 3-5 d
A strong postsynaptic alpha-receptor stimulant with little effect on the beta-receptors of the heart.
1-2 sprays per nostril q3-4h
Administer as in adults
Bretylium may potentiate action of vasopressors on adrenergic receptors, possibly resulting in arrhythmias; MAOIs may significantly enhance adrenergic effects of phenylephrine, and pressor response may be increased 2- to 3-fold; guanethidine may increase pressor response of direct-acting vasopressors, possibly resulting in severe hypertension
Documented hypersensitivity; severe hypertension; ventricular tachycardia
C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Caution in elderly patients, hyperthyroidism, myocardial disease, bradycardia, partial heart block, or severe arteriosclerosis; in hypovolemia, use is not a substitute for replacement of blood, fluids and electrolytes, and plasma (these should be restored promptly when loss has occurred)
Stimulates vasoconstriction by directly activating the alpha-adrenergic receptors of the respiratory mucosa. Induces bronchial relaxation and increases heart rate and contractility by stimulating beta-adrenergic receptors. Available in 30- and 60-mg tablets, 30-mg/5 mL elixir, and in a sustained-release form 120 mg.
60 mg PO q4-6h; 120 mg SR q12h; not to exceed 240 mg/d
3-12 months: 3 gtt/kg q4-6h; not to exceed 4 doses/d
1-2 years: 7 gtt (0.2 mL)/kg q4-6h; not to exceed 4 doses/d
2-5 years: 15 mg PO q4-6h; not to exceed 60 mg/d
>5 years: 30 mg PO q4-6h; not to exceed 120 mg/d
Propranolol, MAOIs, and sympathomimetic agents may increase toxicity of pseudoephedrine; methyldopa and reserpine may reduce effects of pseudoephedrine
Documented hypersensitivity; severe anemia; postural hypertension and hypotension; closed-angle glaucoma; head trauma; cerebral hemorrhage
C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Caution in cardiovascular disease, diabetes mellitus, prostatic hypertrophy, and increased intraocular pressure
Empiric coverage for H influenzae and S pneumoniae is recommended, with the addition of M catarrhalis coverage in children.
Inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid. By inhibiting the enzyme dihydrofolate reductase, the production of tetrahydrofolic acid decreases. These effects inhibit bacterial growth. Bacterial resistance appears to develop more slowly with this drug combination than with either drug alone. DOC along with AMP/CL. Available in elixir 40/200 per 5 mL, single strength (80/400) and double strength (160/800).
5 mg/kg (based on trimethoprim) IV q6h; 1 tab (double strength) PO bid
5 mL/10 kg/dose elixir PO bid
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; 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 studies in humans; may use if benefits outweigh risk to fetus
Discontinue at first appearance of rash or sign of adverse reaction; obtain CBCs 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, chronic alcoholism, elderly persons, those receiving anticonvulsant therapy, or 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
Drug combination that extends the antibiotic spectrum of penicillin to include bacteria normally resistant to beta-lactam antibiotics. Administer treatment for a minimum of 10 d. Available in 125-, 250-, and 500-mg tablets and in 125 and 250/5 mL elixir.
500 mg PO q12h; 250 mg PO q8h
30-40 mg/kg/d PO divided tid
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
Give for a minimum of 10 d to eliminate organism and prevent sequelae (endocarditis, and rheumatic fever); following treatment, perform cultures to confirm eradication of streptococci
These agents are indicated for the management of infections caused by susceptible mixed aerobic-anaerobic microorganisms. Proper dosage and route of administration should be determined by the condition of the patient, severity of the infection, and susceptibility of the causative organism.
250 mg PO tid
20-40 mg/kg/d PO divided tid
Alcoholic beverages consumed <72 h after taking cefaclor may produce disulfiramlike reactions; may increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics and aminoglycosides (eg, loop diuretics) may increase nephrotoxicity
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 one fourth if <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy
Treats infections caused by susceptible organisms and can be used as prophylaxis in minor procedures. An alternative therapy, but some resistant organisms are beginning to be seen in the US.
250-500 mg PO q8h; not to exceed 3 g/d
20-50 mg/kg/d PO divided tid
Reduces the 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
Reversibly binds to the P site of the 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating the dissociation of peptidyl tRNA from ribosomes.
250-500 mg PO q12h for 7-14 d
15 mg/kg PO divided bid
Toxicity increases with coadministration of fluconazole, astemizole, and pimozide; clarithromycin effects decrease, and GI adverse 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; cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
Documented hypersensitivity; coadministration of pimozide
C - Fetal risk revealed in studies in animals but not established or not studies 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
Advanced-generation macrolide works similarly to clarithromycin but with shorter dosage time.
Day 1: 500 mg PO
Days 2-5: 250 mg PO qd
<6 months: Not established
>6 months:
Day 1: 10 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg PO qd; not to exceed 250 mg/d
May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Documented hypersensitivity; hepatic impairment; do not administer with pimozide
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients
The S-enantiomer of ofloxacin, a fluoroquinolone antibiotic with improved activity against gram-positive organisms. Best used only in severe or refractory sinusitis.
500 mg PO qd for 7-21 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; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin 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 studies 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
Second-generation cephalosporin maintains gram-positive activity that first-generation cephalosporins have. Adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis. Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.
100-400 mg PO bid
10 mg/kg/d PO divided bid
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 dosage in renal impairment
Second-generation cephalosporin maintains gram-positive activity that first-generation cephalosporins have; adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis. Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.
250-500 mg PO bid
250 mg PO bid for 20 d
Disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patient receiving potent diuretics such as loop diuretics; coadministration with aminoglycosides increases nephrotoxic potential
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Administer half dose if creatinine clearance is 10-30 mL/min and one-fourth dose if <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy
American Academy of Pediatrics. Clinical practice guideline: management of sinusitis. Pediatrics. Sep 2001;108(3):798-808. [Medline].
Ah-See, K. Sinusitis (acute). BMJ Clin Evid. 2008;03:511.
Hwang PH, Getz A. Acute sinusitis and rhinosinusitis in adults. UpToDate. Available at www.uptodate.com. Accessed June 7th, 2009.
Hamilos DL. Clinical manifestations, pathophysiology, and diagnosis of chronic rhinosinusitis. UpToDate. Available at www.uptodate.com. Accessed June 7th, 2009.
Lusk RP, Stankiewicz JA. Pediatric rhinosinusitis. Otolaryngol Head Neck Surg. Sep 1997;117(3 Pt 2):S53-7. [Medline].
Brook I. Microbiology and management of sinusitis. J Otolaryngol. Aug 1996;25(4):249-56. [Medline].
Falagas ME, Giannopoulou KP, Vardakas KZ, Dimopoulos G, Karageorgopoulos DE. Comparison of antibiotics with placebo for treatment of acute sinusitis: a meta-analysis of randomised controlled trials. Lancet Infect Dis. Sep 2008;8(9):543-52. [Medline].
[Guideline] National Guidelines Clearinghouse: Adult Sinusitis. Accessed June 28, 2009. [Full Text].
Benninger MS, Sedory Holzer SE, Lau J. Diagnosis and treatment of uncomplicated acute bacterial rhinosinusitis: summary of the Agency for Health Care Policy and Research evidence-based report. Otolaryngol Head Neck Surg. Jan 2000;122(1):1-7. [Medline].
Chow JM. The diagnosis and management of sinusitis. Compr Ther. 1995;21(2):74-9. [Medline].
Duncavage JA. Management of sinusitis. Compr Ther. Apr 1996;22(4):211-6. [Medline].
Joe SA, Thambi R, Huang J. A systematic review of the use of intranasal steroids in the treatment of chronic rhinosinusitis. Otolaryngol Head Neck Surg. Sep 2008;139(3):340-7. [Medline].
Osguthorpe JD, Hadley JA. Rhinosinusitis. Current concepts in evaluation and management. Med Clin North Am. Jan 1999;83(1):27-41, vii-viii. [Medline].
Piccirillo JF. Clinical practice. Acute bacterial sinusitis. N Engl J Med. Aug 26 2004;351(9):902-10. [Medline].
Snow V, Mottur-Pilson C, Gonzales R. Principles of appropriate antibiotic use for treatment of acute bronchitis in adults. Ann Intern Med. Mar 20 2001;134(6):518-20. [Medline].
Williams JW, Simel DL. Does this patient have sinusitis? Diagnosing acute sinusitis by history and physical examination. JAMA. Sep 8 1993;270(10):1242-6. [Medline].
sinusitis, sinus inflammation, sinus infection, paranasal sinuses, inflammation of paranasal sinuses, infection of paranasal sinuses, nasopharyngeal flora, sinus disease, upper respiratory infections, URI, acute sinusitis, subacute sinusitis, chronic sinusitis, bacterial sinusitis, allergic rhinitis, severe allergic rhinitis, rhinoviral infection, maxillary sinusitis, Haemophilus influenzae, H influenzae, Streptococcus pneumoniae, S pneumoniae, Bacteroides, Peptostreptococcus, Fusobacterium, Moraxella catarrhalis, M catarrhalis, Staphylococcus aureus, S aureus, Candida, Aspergillus, Phycomycetes
Hina Z Ghory, MD, Chief Resident Physician, Department of Emergency Medicine, New York Presbyterian Hospital
Hina Z Ghory, MD is a member of the following medical societies: American Medical Women's Association and Phi Beta Kappa
Disclosure: Nothing to disclose.
Rahul Sharma, MD, MBA, FACEP, Assistant Professor, Weill Medical College of Cornell University; Attending Physician, Department of Emergency Medicine, New York Presbyterian Hospital-Weill Cornell Medical Center
Rahul Sharma, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Associate Professor, Department of Emergency Medicine, University of Texas-Houston
Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Mark W Fourre, MD, Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Elicia S Kennedy, MD, and previous editor, Charles V Pollack, Jr, MD, to the development and writing of this article.
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