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Patient Education
Headache Center

Sinus Infection Overview

Sinus Infection Causes

Sinus Infection Symptoms

Sinus Infection Treatment




Author: Steven E Sobol, MD, FRCSC, MSc, FAAP, Assistant Professor, Director of Pediatric Otolaryngology, Department of Otolaryngology Head and Neck Surgery, Emory University School of Medicine; Otolaryngologist-In-Chief, Children's Healthcare of Atlanta at Egleston

Steven E Sobol is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery

Coauthor(s): Melvin D Schloss, MD, FRCSC, Director of Pediatric Otolaryngology, Professor, Department of Otolaryngology, McGill University, Canada; Ted L Tewfik, MD, FRCSC, Professor, Department of Otolaryngology, McGill University Medical School, Canada; Director, Department of Otolaryngology, Montreal Children's Hospital, Canada

Editors: Jack A Coleman, MD, Assistant Clinical Professor, Department of Otolaryngology, Middle Tennessee Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Stephen G Batuello, MD, Consulting Staff, Colorado ENT Specialists; Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders; Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine

Author and Editor Disclosure

Synonyms and related keywords: medical treatment for acute sinusitis, sinus infection, cold, runny nose, sinus headache, acute sinusitis, infection of the sinuses, recurrent acute sinusitis, subacute sinusitis, paranasal sinuses, chronic sinusitis

Background

Many classifications, both clinical and radiological, have been proposed in the literature to define acute sinusitis. Although no consensus on the precise definition currently exists, acute sinusitis may be defined as a bacterial or viral infection of the sinuses of fewer than 4 weeks duration that resolves completely with appropriate treatment. Subacute sinusitis represents a temporal progression of symptoms for 4-12 weeks. Recurrent acute sinusitis is diagnosed when 2-4 episodes of infection occur per year with at least 8 weeks between episodes, and, as in acute sinusitis, the sinus mucosa completely normalizes between attacks. Chronic sinusitis is the persistence of insidious symptomatology beyond 12 weeks, with or without acute exacerbations, and is discussed in Sinusitis, Chronic, Medical Treatment.

Embryology

To properly diagnose and treat infectious disorders of the paranasal sinuses, the clinician should have knowledge of the developmental milestones. The development of the paranasal sinuses begins in the third week of gestation and continues until early adulthood.

During the third week of embryonic development, proliferation and medial migration of ectodermal cells form the notochord. After the heart tube and pericardium have rotated from the cranial position to lie anteriorly, the notochord, which is initially in the caudal region of the embryonic disc, rotates to lie posterior to the primitive foregut. The paraxial layer of mesenchyme, which lies adjacent to the notochord, differentiates into the somite ridges, intermediate cell mass, and lateral plate mesoderm. From these mesodermal structures the branchial arches develop, the first of which gives rise to internal nasal structures.

The paranasal sinuses develop in conjunction with the palate from changes in the lateral wall of the nasal cavity. At 40 weeks' gestation, 2 horizontal grooves develop in the mesenchyme of the lateral wall of the nasal cavity. Proliferation of maxilloturbinate mesenchyme between these grooves results in an outpouching of tissue medially into the nasal lumen. This outpouching is the precursor of the middle and inferior meatus as well as the inferior turbinate. Ethmoidoturbinate folds develop superiorly to give rise to the middle and superior turbinates. Once the turbinate structures are established, sinus development begins and continues until early adult life.

Anatomy

The paranasal sinuses are air-filled bony cavities that extend from the skull base to the alveolar process and laterally from the nasal cavity to the inferomedial aspect of the orbit and the zygoma. They are lined with pseudostratified columnar epithelium that is contiguous, via ostia, with the lining of the nasal cavity. This epithelium contains a number of mucous-producing goblet cells. The arterial supply of the paranasal sinuses is from branches of the internal and external carotid arteries, while the venous and lymphatic drainage path is through the sinus ostia into the nasal cavity plexus. In addition, venous drainage occurs through valveless vessels corresponding to the arterial supply. The focal point of sinus drainage is the ostiomeatal complex, which is located in the middle meatus and is composed of the maxillary, frontal, and anterior ethmoid ostia. The posterior ethmoids empty into the superior meatus, and the sphenoids empty into the sphenoethmoidal recess.

The exact function of the paranasal sinuses is not well understood. The possible roles of the sinuses may include reducing the weight of the skull; dampening pressure; humidifying and warming inspired air; absorbing heat and insulating the brain; aiding in sound resonance; providing mechanical rigidity; and increasing the olfactory surface area.

The sinus mucosa has less secretory and vasomotor function than the nasal cavity does. Cilia are concentrated near and beat toward the natural sinus ostia. Blockage of the ostium results in stasis of mucous flow, which can lead to development of disease.

Pathophysiology

The sinuses are normally sterile under physiologic conditions. Purulent sinusitis can occur when ciliary clearance of sinus secretions decreases or when the sinus ostium becomes obstructed, which leads to retention of secretions, negative sinus pressure, and reduction of oxygen partial pressure. This environment is then suitable for growth of pathogenic organisms. Factors that predispose the sinuses to obstruction and decreased ciliary function are allergic, nonallergic, or viral insults, which produce inflammation of the nasal and sinus mucosa and result in ciliary dysmotility and sinus obstruction. Approximately 90% of patients who have viral upper respiratory tract infections (URTIs) have sinus involvement, but only 5-10% of these patients have bacterial superinfection requiring antimicrobial treatment.

Anatomical variations that narrow the ostiomeatal complex, including septal deviation, paradoxical middle turbinates, and Haller cells, make this area more sensitive to obstruction from mucosal inflammation. Mechanical obstruction of the ostiomeatal complex from foreign bodies, polyps, or tumors can also result in acute sinus disease. Systemic diseases that result in decreased mucociliary clearance, including cystic fibrosis and Kartagener syndrome, can be predisposing factors for acute sinusitis in rare cases. Patients with immunodeficiencies (eg, agammaglobulinemia, combined variable immunodeficiency, and immunodeficiency with reduced immunoglobulin G [IgG]– and immunoglobulin A [IgA]–bearing cells) are also at increased risk of developing acute sinusitis.

Acute sinusitis in the intensive care population is a distinct entity, occurring in 18-32% of patients with prolonged periods of intubation, and is usually diagnosed during the evaluation of unexplained fever. Cases in which the cause is obstruction are usually evident and can include the presence of prolonged nasogastric or nasotracheal intubation. Moreover, patients in an intensive care setting are generally debilitated, predisposing them to septic complications, including sinusitis.

Ciliary function is also reduced in the presence of low pH, anoxia, bacterial toxins, smoking, dehydration, foreign bodies, and drugs (eg, atropine, antihistamines, phenylephedrine). Approximately 10% of cases of acute sinusitis result from direct inoculation of the sinus with a large amount of bacteria. Dental abscesses or procedures that result in communication between the oral cavity and sinus can produce sinusitis by this mechanism. Facial trauma or large inoculations from swimming can produce sinusitis as well.

Frequency

United States

Sinusitis affects 1 out of every 7 adults in the United States, with over 30 million individuals diagnosed each year. Acute bacterial sinusitis is the fifth most common diagnosis prompting antibiotic administration and accounts for 0.4% of ambulatory diagnoses.1 The economic burden of acute sinusitis in children is $1.77 billion per year.2



History

Acute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is of paramount importance in differentiating this entity from allergic or vasomotor rhinitis and common URTIs. No specific clinical symptom or sign is sensitive or specific for acute sinusitis, so the overall clinical impression should be used to guide management.

A recent consensus statement published in Otolaryngology-Head and Neck Surgery made strong recommendations that clinicians should distinguish between acute rhinosinusitis caused by bacterial causes and those episodes caused viral upper respiratory infections and noninfectious conditions.3 The panel suggests that the diagnosis of acute bacterial sinusitis be entertained when (a) symptoms or signs of acute rhinosinusitis are present 10 days or more beyond the onset of upper respiratory symptoms, or (b) symptoms or signs of acute rhinosinusitis worsen within 10 days after an initial improvement. A history of purulent secretions and facial or dental pain are specific symptoms that may point to a bacterial etiology. In a patient in intensive care, acute sinusitis should be suspected in the presence of sepsis of unknown origin.

Physical

Anterior rhinoscopic examination, with or without a topical decongestant, is important to assess the status of the nasal mucosa and the presence and color of nasal discharge. Predisposing anatomical variations can also be noted during anterior rhinoscopy. Sinus transillumination and palpation are of little predictive value. A basic evaluation of ocular and neurological function is also necessary in order to rule out potential complications.

Endoscopic examination may reveal the origin of the purulent discharge from the middle meatus and may provide information about the nature of ostiomeatal obstruction. The use of endoscopy may also aid in the etiologic diagnosis of acute sinusitis by allowing the careful attainment of purulent secretions from the sinus ostia for culture.

Causes

The bacteria most commonly involved in acute sinusitis are part of the normal nasal flora. These bacteria can become sinus pathogens when they are deposited into the sinuses by sneezing, coughing, or direct invasion under conditions that optimize their growth. The most common bacterial pathogens in acute sinusitis are Streptococcus pneumoniae (30-40%), Haemophilus influenzae (20-30%), and Moraxella catarrhalis (12-20%). Staphylococcus aureus and Streptococcus pyogenes are isolated in rare cases. Sixty-six percent of patients with acute sinusitis grow at least 1 pathogenic bacterial species on sinus aspirates, while 26-30% percent of patients have multiple predominant bacterial species.

Anaerobic organisms have been found in fewer than 10% of patients with acute bacterial sinusitis, despite the ample environment available for their growth. The exceptions are in sinusitis resulting from a dental source and in patients with chronic sinus disease, in whom anaerobic organisms are usually isolated.

Gram-negative organisms, including Pseudomonas aeruginosa (15.9%), Escherichia coli (7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae, and Enterobacter species, predominate in nosocomial sinusitis, accounting for 60% of cases. Polymicrobial invasion is seen in 25-100% of cultures. The other pathogenic organisms found in nosocomial patients are gram-positive organisms (31%) and fungi (8.5%). Viruses are the most common trigger of acute sinusitis. Rhinovirus, influenza, and parainfluenza viruses are the primary pathogens in 3-15% of patients with acute sinusitis.

Fungal causes of sinusitis are discussed in Allergic Fungal Sinusitis and Sinusitis, Fungal.



Allergic Fungal Sinusitis
Sinusitis, Chronic, Medical Treatment
Sinusitis, Ethmoid, Acute, Surgical Treatment
Sinusitis, Frontal, Acute, Surgical Treatment
Sinusitis, Fungal
Sinusitis, Maxillary, Acute, Surgical Treatment
Sinusitis, Maxillary, Chronic, Surgical Treatment
Sinusitis, Sphenoid, Acute, Surgical Treatment


Lab Studies

  • Some authors have reported on the use of laboratory tests including sedimentation rate, white blood cell counts, and C-reactive protein levels to help diagnose acute sinusitis.4 These tests appear to add little to the predictive value of clinical findings in the diagnosis.
  • Cultures are not routinely obtained in the evaluation of acute sinusitis but should be obtained in a patient in intensive care or with immunocompromise, in children not responding to appropriate medical management, and in patients with complications of sinusitis. Because the nose is colonized with multiple nonpathogenic species of bacteria, care must be taken when evaluating culture results. A specific organism is considered pathogenic when more than 104 colony-forming units of the species are grown on culture or when polymorph counts are greater than 5000 cells/mL.

Imaging Studies

  • Imaging studies are not necessary when the probability of sinusitis is either high or low but may be useful when the diagnosis is in doubt, based upon a thorough history and physical examination. Plain sinus radiographs may demonstrate mucosal thickening, air-fluid levels, and sinus opacification. Limitations of plain films include interobserver variability, inability to distinguish infection from a polyp or tumor disease, and poor depiction of the ethmoid and sphenoid sinuses.
  • CT scanning has poor specificity for the diagnosis of acute sinusitis, demonstrating sinus air-fluid levels in 87% of individuals with simple URTIs and 40% of asymptomatic individuals. CT scanning is the modality of choice, however, in specific circumstances such as in the evaluation of a patient in intensive care, when complications are suspected, or in the preoperative evaluation of surgical candidates. CT scanning can give valuable information regarding the anatomical and mechanical contributions in the development of acute sinusitis. Coronal views with bone windows are the preferred sinus study for evaluating each of the sinuses as well as the ostiomeatal complex.
  • Magnetic resonance imaging (MRI) is excellent for evaluating soft tissue disease within the sinuses, but it is of little value in the diagnostic workup for acute sinusitis.



Medical Care

The primary goals of management of acute sinusitis are to eradicate the infection, decrease the severity and duration of symptoms, and prevent complications. Most patients with acute sinusitis are treated in the primary care setting. Further evaluation by an otolaryngologist is recommended when (1) continued deterioration occurs with appropriate antibiotic therapy, (2) episodes of sinusitis recur, (3) symptoms persist after 2 courses of antibiotic therapy, or (4) comorbid immunodeficiency, nosocomial infection, or complications of sinusitis are present. The goals of management of acute sinusitis are the provision of adequate drainage and appropriate systemic treatment of the likely bacterial pathogens.

Drainage of the involved sinus can be achieved both medically and surgically (see the Medication and Surgical Care sections). Aggressively treat patients in intensive care who develop acute sinusitis in order to avoid septic complications. Consider removal of nasotracheal and nasogastric tubes and promote drainage either medically or surgically.

Surgical Care

Sinus puncture and irrigation techniques allow for a surgical means of removal of thick purulent sinus secretions. The purpose of surgical drainage is to enhance mucociliary flow and provide material for culture and sensitivity. A surgical means of sinus drainage should be used when appropriate medical therapy has failed to control the infection and prolonged or slowly resolving symptoms result or when complications of sinusitis occur. Another indication for sinus puncture is to obtain culture material to guide antibiotic selection if empiric therapy has failed or antibiotic choice is limited. This is particularly important in patients who are immunocompromised or in intensive care. Sinusitis can be a prominent source of sepsis in these patients. In adults, sinus puncture can usually be achieved using local anesthesia; however, in children, a general anesthetic is usually necessary.

In today's era of minimally invasive surgical techniques, sinus endoscopy is commonly used to achieve sinus drainage. It offers the advantages of (1) being able to open multiple sinuses or to decompress the orbit in cases of complications and (2) allowing the surgeon to open the natural ostia of the involved sinuses.

The techniques and complications of open and endoscopic sinus surgical approaches are discussed in articles dealing with their individual surgical management.

Consultations

Ophthalmological or neurosurgical consultation should be obtained when either orbital or intracranial complications develop.



Medical drainage is achieved with topical and systemic vasoconstrictors. Oral alpha-adrenergic vasoconstrictors, including pseudoephedrine and phenylephrine, can be used for 10-14 days to allow for restoration of normal mucociliary function and drainage. Because oral alpha-adrenergic vasoconstrictors may cause hypertension and tachycardia, they may be contraindicated in patients with cardiovascular disease. Oral alpha-adrenergic vasoconstrictors may also be contraindicated in competitive athletes because of rules of competition. Topical vasoconstrictors (eg, oxymetazoline hydrochloride) provide good drainage, but they should be used only for a maximum of 3-5 days, given the increased risk of rebound congestion, vasodilatation, and rhinitis medicamentosa when used for longer periods.

Mucolytic agents (eg, guaifenesin, saline lavage) have the theoretical benefit of thinning mucous secretions and improving drainage. They are not, however, commonly used in clinical practice in the treatment of acute sinusitis. Intranasal steroids have not been conclusively shown to be of benefit in cases of acute sinusitis.

Antihistamines are beneficial for reducing ostiomeatal obstruction in patients with allergies and acute sinusitis; however, they are not recommended for routine use for patients with acute sinusitis. Antihistamines may complicate drainage by thickening and pooling sinonasal secretions.

In cases of suspected or documented bacterial sinusitis, the second principle of treatment is to provide adequate systemic treatment of the likely bacterial pathogens (ie, S pneumoniae, H influenzae, M catarrhalis). The physician should be aware of the probability of bacterial resistance within their community. Approximately 44 % of H influenzae and almost all of M catarrhalis strains have beta-lactamase–mediated resistance to penicillin-based antimicrobials in children. As many as 64% of S pneumoniae strains are penicillin resistant because of altered penicillin-binding proteins. Multiple drug–resistant S pneumoniae strains are also found in substantial numbers of children in daycare settings.5

Initial selection of the appropriate antibiotic therapy should be based on the likely causative organisms given the clinical scenario and the probability of resistant strains within a community. The course of treatment is usually 14 days. First-line therapy at most centers is usually amoxicillin or a macrolide antibiotic in patients allergic to penicillin because of the low cost, ease of administration, and low toxicity of these agents. Amoxicillin should be given at double the usual dose (80-90 mg/kg/d), especially in areas with known S pneumoniae resistance.

Table 1. Dosage, Route, and Spectrum of Activity of Commonly Used First-Line Antibiotics*

AntibioticDosage Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalisAnaerobic bacteria
SensitiveIntermediateResistant
Amoxicillin500 mg PO tid++++++++++
Clarithromycin250-500 mg PO bid+++++++++++
Azithromycin500 mg PO first day, then
250 mg/d PO for 4 days
+++++++++++

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism

Patients who live in communities with a high incidence of resistant organisms, those who fail to respond within 48-72 hours of commencement of therapy, and those with persistence of symptoms beyond 10-14 days should be considered for second-line antibiotic therapy. The most commonly used second-line therapies include amoxicillin clavulanate, second- or third-generation cephalosporins (eg, cefuroxime, cefpodoxime, cefdinir), macrolides (ie, clarithromycin), fluoroquinolones (eg, ciprofloxacin, levofloxacin, moxifloxacin), and clindamycin.

In patients with dental causes of sinusitis or those with foul-smelling discharge, anaerobic coverage using clindamycin or amoxicillin with metronidazole is necessary.

Table 2. Dosage, Route, and Spectrum of Activity of Commonly Used Second-Line Antibiotics*

AntibioticDosage Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalisAnaerobic bacteria
SensitiveIntermediateResistant
Amoxicillin/clavulanate500 mg PO tid+++++++++++++++
Cefuroxime250-500 mg PO bid+++++++++++++
Cefpodoxime
+
cefixime
200 mg PO bid

400 mg/d PO

-

++

+++

-

++

-

+

+++

+++

+++

+++

-

Ciprofloxacin500-750 mg PO bid++++++++++
Levofloxacin500 mg/d PO++++++++++++++++++
Trovafloxacin200 mg/d PO++++++++++++++++++
Clindamycin300 mg PO tid+++++++++--+++
Metronidazole500 mg PO tid-----+++

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism

Patients with nosocomial acute sinusitis require adequate intravenous coverage of gram-negative organisms. Aminoglycoside antibiotics are usually the drugs of choice for the treatment of such patients because of their excellent gram-negative coverage and sinus penetration. Selection of an antibiotic is usually based on the culture results of attained maxillary secretion.

In addition to surgical management, complications of acute sinusitis should be managed with a course of intravenous antibiotics. Third-generation cephalosporins (eg, cefotaxime, ceftriaxone) in combination with vancomycin provide adequate intracranial penetration, making them a good first-line choice.

Table 3. Dosage, Route, and Spectrum of Activity of Commonly Used Intravenous Antibiotics*

AntibioticDosageStreptococcus pneumoniaeHaemophilus influenzaeMoraxella catarrhalisGram-negativeAnaerobic bacteria
Piperacillin3-4 g IV q4-6h++++-++++++
Piperacillin/tazobactam3.375 g IV q6h++++++++++++++
Ticarcillin3 g IV q4h+++--+++++
Ticarcillin/clavulanate3.1 g IV q4h++++++-+++++
Imipenem500 mg IV q6h+++++++++++++++
Meropenem1 g IV q8h++++++++++++++
Cefuroxime1 g IV q8h+++++++++++++
Ceftriaxone2 g IV bid++++++++++++++
Cefotaxime2 g IV q4-6h++++++++++++++
Ceftazidime2 g IV q8h++++++++++++++
Gentamicin1.7 mg/kg IV q8h-++++++++-
Tobramycin1.7 mg/kg IV q8h-++++++++-
Vancomycin1 g IV q6-12h+++---++

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism

Described below are recommended antibiotic regimens.

Drug Category: Antibiotics

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Drug NameAmoxicillin (Trimox, Amoxil, Biomox)
DescriptionFirst-line antibiotic. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
Adult Dose250-500 mg PO tid
Pediatric Dose25-45 mg/kg/d PO divided bid
ContraindicationsDocumented hypersensitivity
InteractionsReduces efficacy of oral contraceptives
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsGastrointestinal irritation; black hairy tongue, glossitis, stomatitis; hypersensitivity may occur
Rare: pseudomembranous colitis, acute interstitial nephritis, hematologic disorders

Drug NameCefdinir (Omnicef)
DescriptionClassified as a third-generation cephalosporin and inhibits mucopeptide synthesis in the bacterial cell wall. Typically bactericidal, depending on organism susceptibility, dose, and serum or tissue concentrations.
Adult Dose600 mg/d PO for 10 d
Pediatric Dose14 mg/kg qd or divided bid for 10 d
ContraindicationsDocumented hypersensitivity
InteractionsMay increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics and aminoglycosides (eg, loop diuretics) may increase nephrotoxicity
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsReduce dosage by 1/2 if creatinine clearance is 10-30 mL/min, and by 3/4 if <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy

Drug NameClarithromycin (Biaxin)
DescriptionFirst-line antibiotic. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Adult Dose250-500 mg PO bid
Pediatric Dose15 mg/kg/d PO divided bid
ContraindicationsDocumented hypersensitivity; coadministration of pimozide
InteractionsToxicity increases with coadministration of fluconazole and pimozide; effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, carbamazepine, ergot alkaloids, triazolam, HMG-CoA reductase inhibitors
Plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increases in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCoadministration 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

Drug NameCefuroxime (Ceftin, Kefurox, Zinacef)
DescriptionSecond-line PO and first-line IV antibiotic. 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.
Adult Dose250-500 mg PO bid
Alternatively, 1 g IV q8h
Pediatric DoseAdminister as in adults
ContraindicationsDocumented hypersensitivity
InteractionsDisulfiramlike 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
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsReduce dosage by one 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; gastrointestinal irritation

Drug NameCeftriaxone (Rocephin)
DescriptionThird-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin binding proteins. Has good penetration.
Adult Dose2 g IV q12h
Pediatric Dose50-75 mg/kg IM/IV qd or bid
ContraindicationsDocumented hypersensitivity
InteractionsProbenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsAdjust 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; caution in breastfeeding women

Drug NameVancomycin (Vancocin, Lyphocin, Vancoled)
DescriptionPotent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci. For abdominal penetrating injuries, it is combined with an agent active against enteric flora and/or anaerobes.
To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients diagnosed with renal impairment.
Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing gastrointestinal or genitourinary procedures. Effective for resistant S pneumoniae.
Adult Dose500-1000 mg IV q6-12h
Pediatric Dose10 mg/kg/dose IV q6h
ContraindicationsDocumented hypersensitivity
InteractionsErythema, histaminelike flushing and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in renal failure, neutropenia; red man syndrome caused by too rapid IV infusion (dose given over a few min) but rarely happens when dose given IV over 2 h or PO/IP; red man syndrome is not an allergic reaction

Drug NameAmoxicillin/Clavulanate (Augmentin)
DescriptionDrug combination treats bacteria resistant to beta-lactam antibiotics.
Adult Dose250-500 mg PO bid/tid
Pediatric Dose<3 months: Not established
>3 months: Base dosing protocol on amoxicillin content; because of different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs more than 40 kg; 40 mg/kg/d PO divided q8h
ContraindicationsDocumented hypersensitivity
InteractionsCoadministration with warfarin or heparin increases risk of bleeding
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsGive 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



Complications

  • Local complications
    • Mucoceles are chronic epithelial cysts that develop in sinuses in the presence of either an obstructed sinus ostium or minor salivary gland duct. They have the potential for progressive concentric expansion that can lead to bony erosion and extension beyond the sinus.
    • Maxillary sinus mucoceles are usually found incidentally on sinus radiographs and are of little significance in the absence of symptomatology or infection. Surgical treatment is not usually necessary, and these lesions often regress spontaneously over time.
    • Frontoethmoidal and sphenoethmoidal mucoceles, on the other hand, tend to be symptomatic and have a high potential for bony erosion. Frontoethmoidal mucoceles should be completely removed and the sinus obliterated. Sphenoethmoid mucoceles should be widely opened into the nasal cavity.
    • Osteomyelitis is a potential local complication most commonly occurring with frontal sinusitis. Osteomyelitis of the frontal bone is called a Pott puffy tumor and represents a subperiosteal abscess with local edema anterior to the frontal sinus. This can advance to form a fistula to the upper lid with sequestration of necrotic bone. This rare complication should be managed with a combination of systemic antibiotics, surgical drainage of affected sinuses, and debridement of necrotic bone.
  • Orbital complications
    • Orbital complications are the most common complications encountered with acute bacterial sinusitis. Infection can spread directly through the thin bone separating the ethmoid or frontal sinuses from the orbit or by thrombophlebitis of the ethmoid veins. Diagnosis should be based on an accurate physical examination including ophthalmological evaluation and appropriate radiological studies. CT scanning is the most sensitive means of diagnosing an orbital abscess, although ultrasound has been found to be 90% effective for diagnosing anterior abscesses.6 The classification by Chandler, which is based on physical examination findings, provides a reasonable framework to guide management. This classification consists of 5 groups of orbital inflammation:7
      • Group 1 - Inflammatory edema (preseptal cellulitis) with normal visual acuity and extraocular movement
      • Group 2 - Orbital cellulitis with diffuse orbital edema but no discrete abscess
      • Group 3 - Subperiosteal abscess beneath the periosteum of the lamina papyracea resulting in downward and lateral globe displacement
      • Group 4 - Orbital abscess with chemosis, ophthalmoplegia, and decreased visual acuity
      • Group 5 - Cavernous sinus thrombosis with rapidly progressive bilateral chemosis, ophthalmoplegia, retinal engorgement, and loss of visual acuity; possible meningeal signs and high fever
    • Medical management, including sinus drainage and intravenous antibiotics, is advocated for any degree of orbital complication. The use of decongestant and antibiotic therapy is discussed in the Medical Care and Medication sections.
    • Among the classifications by Chandler, surgical drainage of both the infected sinuses and the orbit are advocated for groups 3-5 if inadequate improvement or progression of orbital cellulitis occurs despite medical therapy or if the patient has loss of visual acuity. Surgical procedures are discussed in Surgical Care.
  • Intracranial complications: Intracranial complications may occur as a result of direct extension through the posterior frontal sinus wall or through retrograde thrombophlebitis of the ophthalmic veins. Subdural abscess is the most common intracranial complication, although cerebral abscesses and infarction that result in seizures, focal neurological deficits, and coma may occur. Intracranial complications of sinusitis should be managed surgically with drainage of both the affected sinus and the cranial abscess.
  • Systemic complications: Sinusitis can result in sepsis and multisystem organ failure caused by seeding of the blood and various organ systems. Reports of bacteremia, thoracic empyema, and nosocomial pneumonia have been documented in the intensive-care population with acute sinusitis, and the mortality rate in this group can be as high as 11%.

Patient Education



  1. Bishai WR. Issues in the management of bacterial sinusitis. Otolaryngol Head Neck Surg. Dec 2002;127(6 Suppl):S3-9. [Medline].
  2. Ray NF, Baraniuk JN, Thamer M, Rinehart CS, Gergen PJ, Kaliner 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].
  3. Rosenfeld RM, Andes D, Bhattacharyya N, Cheung D, Eisenberg S, Ganiats TG, et al. Clinical practice guideline: adult sinusitis. Otolaryngol Head Neck Surg. Sep 2007;137(3 Suppl):S1-31. [Medline].
  4. Savolainen S, Jousimies-Somer H, Karjalainen J. Do simple laboratory tests help in etiologic diagnosis in acute maxillary sinusitis?. Acta Otolaryngol Suppl. 1997;529:144-7. [Medline].
  5. Slack CL, Dahn KA, Abzug MJ, Chan KH. Antibiotic-resistant bacteria in pediatric chronic sinusitis. Pediatr Infect Dis J. Mar 2001;20(3):247-50. [Medline].
  6. Sobol SE, Marchand J, Tewfik TL, Manoukian JJ, Schloss MD. Orbital complications of sinusitis in children. J Otolaryngol. Jun 2002;31(3):131-6. [Medline].
  7. Chandler JR, Langenbrunner DJ, Stevens ER. The pathogenesis of orbital complications in acute sinusitis. Laryngoscope. Sep 1970;80(9):1414-28. [Medline].
  8. AHCPR Evidence Report. Agency for Health Care Policy and Research. In: Diagnosis and treatment of acute bacterial rhinosinusitis. Rockville, MD. 1999.
  9. Brook I, Gooch WM III, Jenkins SG. Medical Management of acute bacterial sinusitis. Recommendations of a clinical advisory committee on pediatric and adult sinusitis. Ann Otol Rhinol Laryngol. 2000;109(Suppl):2-20.
  10. Conrad DA, Jenson HB. Management of acute bacterial rhinosinusitis. Curr Opin Pediatr. 2002;14(1):86-90.
  11. Eibling DE. Maxillary Sinus: Irrigation Techniques. In: Myers EN, ed. Operative Otolaryngology-Head and Neck Surgery. Philadelphia, Pa: WB Saunders; 1997:81-85.
  12. Frenkiel S. Embryology of the Nose and Sinuses. In: Tewfik TL, Der Kaloustian VM, eds. Congenital Anomalies of the Ear, Nose, and Throat. New York: Oxford University Press; 1997:183-187.
  13. Graney DO, Rice DH. Anatomy. In: Cummings CW, Frederickson JM, Harker LA, Krause CJ, Richardson MA, Schuller DE, eds. Otolaryngology-Head & Neck Surgery. 3rd ed. St. Louis: Mosby; 1998:1059-1064.
  14. International Rhinosinusitis Advisory Board. Infectious rhinosinusitis in adults: classification, etiology and management. International Rhinosinusitis Advisory Board. Ear Nose Throat J. Dec 1997;76(12 Suppl):1-22. [Medline].
  15. Johnson JT, Ferguson BJ. Infection. In: Cummings CW, Frederickson JM, Harker LA, Krause CJ, Richardson MA, Schuller DE, eds. Otolaryngology-Head & Neck Surgery. 3rd ed. St. Louis: Mosby; 1998:1107-1118.
  16. Josephson GD, Gross CW. Diagnosis & management of acute & chronic sinusitis. Compr Ther. Nov 1997;23(11):708-14. [Medline].
  17. Kaliner MA, Osguthorpe JD, Fireman P. Sinusitis: bench to bedside. Current findings, future directions. Otolaryngol Head Neck Surg. Jun 1997;116(6 Pt 2):S1-20. [Medline].
  18. Laine K, Maatta T, Varonen H. Diagnosing acute maxillary sinusitis in primary care: a comparison of ultrasound, clinical examination and radiography. Rhinology. Mar 1998;36(1):2-6. [Medline].
  19. Low DE, Desrosiers M, McSherry J. A practical guide for the diagnosis and treatment of acute sinusitis. CMAJ. Mar 15 1997;156 Suppl 6:S1-14. [Medline].
  20. Manning SC. Medical Management of Infectious and Inflammatory Disease. In: Cummings CW, Frederickson JM, Harker LA, Krause CJ, Richardson MA, Schuller DE, eds. Otolaryngology-Head & Neck Surgery. 3rd ed. St. Louis: Mosby; 1998:1135-1144.
  21. McCaig LF, Hughes JM. Trends in antimicrobial drug prescribing among office-based physicians in the United States. JAMA. Jan 18 1995;273(3):214-9. [Medline].
  22. Poole MD. A focus on acute sinusitis in adults: changes in disease management. Am J Med. May 3 1999;106(5A):38S-47S; discussion 48S-52S. [Medline].
  23. Rhys-Evans PH. Anatomy of the Nose and Paranasal Sinuses. In: Kerr AG, Groves J, eds. Scott-Brown's Otolaryngology. 5th ed. London: Butterworths; 1987:138-161.
  24. Talmor M, Li P, Barie PS. Acute paranasal sinusitis in critically ill patients: guidelines for prevention, diagnosis, and treatment. Clin Infect Dis. Dec 1997;25(6):1441-6. [Medline].
  25. Taylor JA, Weber W, Standish L, et al. Efficacy and safety of echinacea in treating upper respiratory tract infections in children: a randomized controlled trial. JAMA. Dec 3 2003;290(21):2824-30. [Medline].
  26. Wald ER. Expanded role of group A streptococci in children with upper respiratory infections. Pediatr Infect Dis J. Aug 1999;18(8):663-5. [Medline].
  27. Wald ER. Microbiology of acute and chronic sinusitis in children and adults. Am J Med Sci. Jul 1998;316(1):13-20. [Medline].
  28. Wald ER. Sinusitis. Pediatr Ann. Dec 1998;27(12):811-8. [Medline].
  29. Westergren V. Artificial ventilation-acquired sinopathy in the critically ill - the maxillary sinuses revisited. Clin Exp Allergy. Mar 1999;29(3):298-305. [Medline].

Sinusitis, Acute, Medical Treatment excerpt

Article Last Updated: Jan 23, 2008