Cleveland Clinic Foundation
Disease Management Project
TITLE: SINUSITIS
AUTHOR: Cristine Radojicic, MD --
Department of Allergy and Immunology
    
PUBLISHED: September 14, 2004
    

SINUSITIS

DEFINITION

Sinusitis is defined as inflammation of the sinuses, which are air-filled cavities in the skull. The inflammation can be caused by infectious (bacterial, viral, or fungal) or noninfectious (allergic) triggers. This inflammation leads to blockade of sinus ostia (the normal sinus drainage pathways), which in turn leads to mucus retention, hypoxia, decreased mucociliary clearance, and predisposition to bacterial growth.

Sinusitis can be divided into the following categories:1

  • Acute sinusitis is defined as symptoms of less than 4 weeks' duration;
  • Subacute sinusitis is defined as symptoms of 4 to 12 weeks' duration;
  • Chronic sinusitis is defined as symptoms lasting longer than 12 weeks' duration;
  • Recurrent acute sinusitis is often defined as four episodes per year, with each episode lasting less than 2 weeks' duration.

PREVALENCE

The prevalence of acute sinusitis is on the rise, based on data from the National Ambulatory Medical Care Survey (from 0.2% of diagnoses at office visits in 1990 to 0.4% of diagnoses at office visits in 1995).2 In 2001, sinusitis represented 13.6 million outpatient visits according to the US Centers for Disease Control and Prevention.3 Approximately 40 million Americans are affected by sinusitis every year, with 33 million cases of chronic sinusitis reported annually to the US Centers for Disease Control and Prevention.4

When sinusitis is considered together with commonly associated comorbid conditions such as allergic rhinitis, asthma, and chronic bronchitis, exacerbation of these diseases affects more than 90 million people—nearly one of three Americans.5 The socioeconomic impact of this translates to more than $5.8 billion dollars spent in the treatment of sinusitis.6

PATHOPHYSIOLOGY

The most common cause of acute sinusitis is an upper respiratory tract infection (URTI) of viral origin. The viral infection may lead to sinus inflammation that usually resolves without treatment in less than 2 weeks. If symptoms worsen after 3 to 5 days or persist for longer than 10 days and are more severe than normally experienced with a viral infection, a secondary bacterial infection is diagnosed. The inflammation may predispose to the development of acute sinusitis by causing sinus ostial blockage. Although inflammation in any of the sinuses can lead to blockade of the sinus ostia, the most commonly involved sinuses in both acute and chronic sinusitis are the maxillary and the anterior ethmoid sinus.7 The anterior ethmoid, frontal, and maxillary sinuses drain into the middle meatus, creating an anatomic area known as the "ostiomeatal complex." The nasal mucosa responds to the virus by producing mucus and recruiting mediators of inflammation, such as white blood cells, to the lining of the nose, which add to congestion and swelling of the nasal passages. The resultant sinus cavity hypoxia and mucus retention cause the cilia—the hairlike projections in the nasal/sinus cavity that move mucus and debris from the nose—to function less efficiently, thereby creating an environment for bacterial growth.

If the acute sinusitis does not resolve, chronic sinusitis develops from the persisting mucus retention, hypoxia, and anatomic blockade of the ostia. This promotes mucosal hyperplasia, continued recruitment of inflammatory infiltrates, and the potential development of nasal polyps.

However, other factors may predispose to sinusitis8 (Table 1).

Table 1:
Conditions Associated with Sinusitis
Infectious
Organisms
Noninfectious
Factors
Anatomic
Problems
Immune
Deficiencies
Genetic
Disease
  • Viral
  • Bacterial
  • Fungal
  • Allergic rhinitis
  • Nasal polyps
  • Irritants
    (eg, tobacco smoke)
  • Hormonal conditions (eg, progesterone-induced congestion of pregnancy, rhinitis of hypothyroidism)
  • Septal deviation
  • Concha bullosa
  • Paradoxic middle turbinate
  • Ethmoid bulla hypertrophy
  • Choanal atresia
  • Adenoid hypertrophy

Primary Deficiency

  • Selective IgA deficiency
  • Common variable immunodeficiency

Acquired Deficiency

  • Human immunodeficiency virus
  • Transplantation
  • Chemotherapy
  • Cystic fibrosis
  • Primary ciliary dyskinesia
  • Kartagener's syndrome
  

When bacterial growth occurs, the most common organisms in acute sinusitis include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.9 When chronic sinusitis is suspected, these organisms, plus Staphylococcus aureus, coagulase-negative Staphylococcus species, and anaerobic bacteria, are the most likely involved organisms. Organisms isolated from patients with chronic sinusitis increasingly are showing antibiotic resistance. In fact, the reported penicillin resistance rates for Streptococcus pneumoniae are 28% to 44% across the United States.10 These resistant organisms are more commonly found in patients who have received two or more recent courses of antibiotics, a common scenario in patients with chronic sinusitis.

A distinct entity, allergic fungal sinusitis (AFS), occurs in non-immunocompromised patients and results from an immunologic reaction to fungi that colonize the sinuses.11 Fungi are ubiquitous in the environment, and most people tolerate exposure to mold spores in the air. However, people with AFS develop a colonization of fungus in the mucus, which leads to a hypersensitivity reaction involving an intense eosinophilic inflammatory response. The common fungi causing this syndrome include Bipolaris specifera and Aspergillus, Curvularia, and Fusarium species.11 This allergic response to the fungus is not invasive and should be distinguished from invasive fungal sinusitis, which is more common in diabetic patients and in those with immunocompromised states. The diagnostic criteria for AFS include chronic sinusitis, with CT of the sinuses showing chronic mucosal thickening, opacification, polyps, and high-intensity signaling from the high protein content in the mucus. On sinus culture, fungi can be isolated with associated "allergic mucin," which is mucus loaded with degranulated eosinophils.

SIGNS AND SYMPTOMS

Acute bacterial sinusitis in adults most often presents with more than 7 days of nasal congestion, purulent rhinorrhea, postnasal drip, and facial pain and pressure, alone or with associated referred pain to ears and teeth. There may be a cough, frequently with a worsening at night.12 Children with acute sinusitis may not be able to relay a history of postnasal drainage or headaches, so cough and rhinorrhea are most commonly reported symptoms.13 Other symptoms may include fever, nausea, fatigue, impairment of smell and taste, and halitosis.

Chronic sinusitis may cause more indolent symptoms that persist for months. Nasal congestion and postnasal drainage are the most common symptoms of chronic sinusitis. Chronic cough that is described as worse at night or upon awakening in the morning is also a frequently described symptom of chronic sinusitis. Clinical evidence of chronic sinusitis may be subtle and less overt than in acute sinusitis unless the patient is having an acute sinusitis exacerbation. As this diagnosis may be more difficult to make in the primary care setting or in a setting without radiographic or rhinoscopic capabilities, Lanza and Kennedy have proposed14 a major and minor classification system to define chronic sinusitis by the presenting symptoms (Table 2).

Table 2:
Symptoms Associated with the Diagnosis of Chronic Sinusitis
Major Symptoms Minor Symptoms
  • Facial pain/pressure
  • Facial congestion/fullness
  • Nasal obstruction/blockage
  • Nasal discharge/purulence/postnasal drip
  • Hyposmia/anosmia
  • Headache
  • Fever
  • Halitosis
  • Fatigue
  • Dental pain
  • Cough
  • Ear pain/pressure/fullness
  

Physical Findings
Typical physical signs include bilateral nasal mucosal edema, purulent nasal secretions, and sinus tenderness (however, this is not a sensitive or specific finding). The location of sinus pain depends on which sinus is affected. Pain on palpation of the forehead over the frontal sinuses can indicate that the frontal sinuses are inflamed; however, this is also a very common area for tension headaches. Infection in the maxillary sinuses can cause upper jaw pain and tooth sensitivity, with the malar areas tender to the touch. Since the ethmoid sinuses are between the eyes and near the tear ducts, ethmoid sinusitis may be associated with swelling, tenderness, and pain in the eyelids and tissues around the eyes. The sphenoid sinuses are more deeply recessed and may present with more vague symptoms of earaches, neck pain, and deep aching at the top of the head.

However, in most patients with a suspected diagnosis of sinusitis, pain or tenderness is found in several locations, and their perceived area of pain usually does not clearly delineate which sinuses are inflamed.

Purulent drainage may be evident on examination as anterior rhinorrhea or visualized as posterior pharyngeal drainage with associated clinical symptoms of sore throat and cough.

The nose should be examined for a deviated nasal septum, nasal polyps, and epistaxis. Foreign bodies and tumors may mimic symptoms of sinusitis and should be in the differential diagnosis, especially if the symptoms are unilateral. The ears should be examined for signs of associated otitis media and the chest for the presence of asthma exacerbation, a common comorbid condition.

DIAGNOSIS

In a primary care setting, a good history and physical examination to detect the presence of most or all of the commonly presenting signs and symptoms can provide a reliable diagnosis of acute sinusitis. The presence of purulent secretions has the highest positive predictive value for clinically diagnosing sinusitis.

Differentiating it from a common viral URTI is most important, to avoid unnecessary antibiotics. Mucus in URTIs is typically thin, clear, and not described as persistently purulent. Nasal congestion is a predominant symptom without persistent or worsening head congestion, headache, or facial pain or fatigue. URTI symptoms would be expected to peak about day 3 to 5 and resolve within 7 to 10 days.

Most other diagnostic modalities, described below, aid in the differential diagnosis of persistent nasal symptoms.

Radiographic Evaluation
The two modalities most commonly used include the plain radiograph and computed tomography (CT).

Plain radiograph has does not adequately represent the individual ethmoid air cells, the extent of mucosal thickening in chronic sinusitis, or the anatomy of the ostiomeatal complex. Magnetic resonance imaging can be considered for evaluation of suspected tumors but is not recommended for acute sinusitis because it does not distinguish air from bone. For these reasons, CT of the sinuses is the imaging procedure of choice. In many centers, the cost is similar to that of plain radiographs due to the availability of limited axial views (usually comprising approximately 6 axial views that include views of the maxillary, ethmoid, sphenoid and frontal sinuses) that are optimally sufficient for ruling out sinusitis. More detailed coronal slices are useful for viewing the ostiomeatal complex and for surgical mapping.

Transillumination
A common practice before plain radiographs and CTs were widely available, it is of limited use, with a high rate of error.

Ultrasonography
This method has not been proven accurate enough to substitute for a radiographic evaluation. However, it may be considered to confirm sinusitis in pregnant women, for whom radiographic studies may pose a risk.

Nasal Smear
By examining the cellular contents of the nasal secretions, one may find polymorphonuclear cells and bacteria in sinusitis. In a viral infection, these would not be found, and in allergic disease, one would expect eosinophils.

Sinus Puncture
The most accurate way to determine the causative organism in sinusitis is a sinus puncture.7 After anesthetization of the puncture site, usually in the canine fossa or inferior meatus, the contents of the maxillary sinus are aspirated under sterile techniques, and bacterial cultures are performed to identify the organism. Culture specimens obtained from nasal swabs correlate poorly with sinus pathogens found by puncture due to contamination of the swab with normal nasal flora. However, since sinus puncture is an invasive procedure, it is not routinely performed. More recently, studies have shown close correlation between organisms found by sinus puncture and by endoscopically guided aspiration of the sinus cavities through the middle meatus.7 Although this needs to be done by an otolaryngologist trained in the procedure, it may be necessary for defining the pathogenic organism when standard therapy has failed or in an immunocompromised patient who is at high risk of sequelae of untreated sinusitis, such as orbital or central nervous system complications.

THERAPY

Treatment of Acute Sinusitis
Antibiotics, such as amoxicillin for 10 to 14 days, have been the recommended first-line treatment of uncomplicated acute sinusitis. The antibiotic of choice in acute sinusitis must cover S pneumoniae, H influenzae, and M catarrhalis. Since most intracranial and orbital complications of acute bacterial sinusitis are caused by S pneumoniae (most commonly in the immunocompromised host), adequate coverage for this organism is important. Amoxicillin-clavulanate (Augmentin) for 10 to 14 days is also an appropriate first-line treatment of uncomplicated acute sinusitis.15 The addition of clavulanate, a beta-lactamase inhibitor, provides the complete coverage for H influenzae and M catarrhalis that is lacking in amoxicillin. In areas of high S pneumoniae resistance, higher doses of amoxicillin (up to 80 to 90 mg/kg/d, with a maximum of 3 g/d) should be considered. These doses are effective against S pneumoniae because resistance is related to alteration in penicillin-binding proteins, a mechanism distinct from the beta-lactamase enzymatic inactivation of H influenzae and M catarrhalis.15

Other options include cephalosporins such as cefpodoxime proxetil (Vantin) and cefuroxime (Ceftin). Trimethoprim-sulfamethoxazole (Bactrim), clarithromycin (Biaxin), and azithromycin (Zithromax) may be prescribed for patients allergic to beta-lactams but may not be adequate coverage for H influenzae or resistant S pneumoniae.16 Penicillin, erythromycin, cephalexin ( Keflex, Keftab), tetracycline, and cefixime (Suprax) are not recommended for the treatment of acute sinusitis because of inadequate antimicrobial coverage of the major organisms.

If treatment with one of these first-line agents has failed—and lack of clinical response within 72 hours on initial therapy should be considered as treatment failure—more broad-spectrum antibiotics should be considered. These include the newer fluoroquinolones, gatifloxacin (Tequin), moxifloxacin (Avelox), and levofloxacin (Levaquin), especially if amoxicillin-clavulanate, cefpodoxime proxetil, and cefuroxime were already tried. In April 2004, a new antibiotic in the ketolide class called telithromycin was approved for the treatment of acute bacterial sinusitis due to S pneumoniae, H influenzae, M catarrhalis, or Staphylococcus aureus.

Treatment of Chronic Sinusitis
Medical therapy should include both a broad-spectrum antibiotic and a topical intranasal steroid to address the strong inflammatory component of this disease. Medical therapy should be continued for 4 to 6 weeks.12 The antibiotics of choice include agents that cover organisms causing acute sinusitis but also cover Staphylococcus species and anaerobes.12 These include amoxicillin-clavulanate, cefpodoxime proxetil, cefuroxime, gatifloxacin, moxifloxacin, and levofloxacin. Currently used topical intranasal steroids such as fluticasone (Flonase), mometasone (Nasonex), budesonide (Rhinocort AQ), triamcinolone (Nasacort AQ) have a favorable safety profile as well as indications for the pediatric age group. However, a short course of oral steroids may be used for extensive mucosal thickening and congestion or nasal polyps.

Adjunctive Therapy
To temporarily alleviate the drainage and congestion associated with sinusitis, decongestant nasal sprays (oxymetazoline (Afrin) and phenylephrine hydrochloride (Neo-Synephrine) may be used for 3 to 5 days. Long-term use of topical decongestants may cause "rhinitis medicamentosa," which is rebound congestion caused by vasodilatation and inflammation. Oral decongestants (pseudoephedrine) may be a reasonable alternative if the patient has no contraindication such as hypertension. Mucolytic agents (guaifenesin) can help to decrease the viscosity of the mucus for better clearance and are often found in combination with decongestants. Some mucolytics are now available over the counter. Saline spray or irrigation may help clear secretions. Topical corticosteroids are not indicated for acute sinusitis but may be helpful for chronic sinusitis, nasal polyps, and allergic and nonallergic rhinitis. Antihistamines are not indicated for sinusitis but may be helpful for underlying allergic rhinitis.

Surgery
If medical therapy fails to adequately control symptoms or if complications are suspected, an otolaryngology consultation is warranted. This may begin with a nasal endoscopy for better visualization of the nasal cavity and ostiomeatal complex. This may also allow for endoscopically guided sinus culture. If surgical therapy is being contemplated, newer techniques of functional endoscopic sinus surgery are performed to clear sinuses of chronic infection, inflammation, and polyps. This may be combined with somnoturboplasty, ie, shrinkage of the turbinates using radiofrequency waves. Endoscopic sinus surgery is commonly performed on an outpatient basis using local anesthesia and has less morbidity than traditional open surgery for chronic sinus disease.1 Special consideration should be given for patients who have chronic sinusitis and nasal polyps and who also have aspirin-induced asthma. This is commonly referred to as the "aspirin triad" of aspirin sensitivity, asthma, and polyposis. Although most of these patients undergo sinus surgery and polypectomy, additional therapy with nasal steroids, leukotriene modifiers. and aspirin desensitization followed by 650 mg aspirin daily should be considered.17

Additional Evaluations:

Laboratory Evaluation
This may be necessary to look for an underlying disorder that may predispose to sinusitis. The evaluation may include a sweat chloride test for cystic fibrosis, ciliary function tests for immotile cilia syndrome, blood tests for HIV, or other tests for immunodeficiency, such as immunoglobulin levels.

Allergy Consultation
This should be done in any patient with recurrent acute or chronic sinusitis to rule out allergy to dust mites, mold, animal dander, and pollen, which trigger allergic rhinitis. An allergy consultation will provide immediate hypersensitivity skin testing to delineate which environmental aeroallergens may exacerbate allergic rhinitis and predispose to sinusitis. Medical management and environmental control measures are discussed. Treatment options such as medications and/or immunotherapy ("allergy shots") are considered. Addition evaluation for comorbid conditions such as asthma and sinusitis are addressed and treated. Allergists are also trained in aspirin desensitization for treatment of patients with the aspirin triad.

Treatment of Complications of Sinusitis
Orbital extension of sinus disease is the most common complication of acute sinusitis. This complication is more common in children. Immediate management includes broad-spectrum intravenous antibiotics, a CT to determine the extent of disease, and possibly surgical drainage of the infection if there is no response to antibiotics. Extension to the central nervous system can also occur. The most common intracranial complications are meningitis (usually from the from sphenoid sinus, which is anatomically located closest to the brain) and epidural abscess (usually from the frontal sinuses).

Treatment of Allergic Fungal Sinusitis
Because of the extent of sinus blockage and strong association with polyps, surgery is usually indicated to remove the inspissated allergic mucin and polyps, followed by systemic corticosteroids to decrease the inflammatory response.7 Treatment guidelines are based on the use of systemic steroids in allergic bronchopulmonary aspergillosis, in which steroids are tapered to daily or every-other-day dosing to control the disease. Commonly, nasal steroids are also added for topical treatment. Studies are currently being conducted to establish the role of antifungal agents or inhalant allergen immunotherapy for the treatment of AFS.

OUTCOMES

URTIs of viral origin should run their course, with gradual improvement in symptoms daily until complete resolution of symptoms occurs by day 7 to 10, with supportive treatment only and no antibiotics.

When a secondary bacterial infection is suspected and antibiotics are given for acute sinusitis, the expected clinical outcome would be resolution of the infection and associated symptoms. This was shown in a study by Wald, in which symptoms resolved in 79% of patients who had clinically and radiographically diagnosed sinusitis and who had been treated with amoxicillin or amoxicillin plus clavulanic acid.18

The data on outcomes of medical management of chronic sinusitis are showing that we can control symptoms to a degree, although with a high rate of recurrence. Hamilos7 reported a retrospective series of patients treated medically for chronic sinusitis. Treatment included systemic steroids for 10 days, antibiotic coverage for aerobic and anaerobic organisms for 4 to 6 weeks, nasal saline irrigation, and topical steroid nasal spray. There was symptomatic and radiographic improvement in 17 of 19 patients, but 8 of 19 had persistent ostiomeatal complex abnormalities. In addition, relapse of sinusitis has been significantly associated with nasal polyposis and a history of prior sinus surgery.7

Overall, we have many treatment options for the sinusitis patient: antibiotics for the bacterial infection; steroids, systemic or topical, for the inflammatory component; and surgery for the anatomic and structural abnormalities that may predispose to sinusitis. Although these have proven to help with initial improvement, we still see a high rate of recurrence of sinus disease. This forces us to address the role of comorbid conditions such as allergic rhinitis, environmental irritants (eg, cigarette smoke ), or the need for newer and better treatment modalities for this disease.

REFERENCES

  1. Dykewicz MS. Rhinitis and sinusitis. J Allergy Clin Immunol. 2003;111(suppl):S520-S529.
  2. Evidence Report/Technology Assessment no. 9. Diagnosis and Treatment of Acute Bacterial Rhinosinusitis. Rockville, Md: US Dept of Health and Human Services, Agency for Health Care Policy and Research. AHCPR Publication no. 99-EO16.
  3. Spiegel Jeffrey H. Sinusitis Otolaryngologic Clinics of North America Volume 37 Number 2 April 2004.
  4. Vital and health statistics. Current estimates from the National Health Interview Survey, 1995. US Dept of Health and Human Services, Centers for Disease Control and Prevention/National Center for Health Statistics.
  5. Ivker R. Respiratory disease: sinusitis, upper respiratory infection, otitis media. Clin Fam Pract. 2002;4:929.
  6. Ray NF, Baraniuk JN, Thamer M, et al. Healthcare expenditures for sinusitis in 1996: contributions of asthma, rhinitis, and other airway disorders. J Allergy Clin Immunol. 1999;103:408-414.
  7. Hamilos DL. Chronic sinusitis. J Allergy Clin Immunol. 2000;106:213-227.
  8. Winstead W. Rhinosinusitis. Prim Care. 2003;30:137-154.
  9. Dykewicz MS. The microbiology and management of acute and chronic rhino-sinusitis. Curr Infect Dis Rep. 2001;3:209-16.
  10. Doern GV, Pfaller MA, Kugler K, Freeman J, Jones RN. Prevalence of antimicrobial resistance among respiratory tract isolates of Streptococcus pneumoniae in North America: 1997 results from the SENTRY antimicrobial surveillance program. Clin Infect Dis. 1998;27:764-770.
  11. deShazo RD, Swain RE. Diagnostic criteria for allergic fugal sinusitis. J Allergy Clin Immunol. 1995;96:24-35.
  12. Spector SL, Bernstein IL, Li JT, et al. Parameters for the diagnosis and management of sinusitis. J Allergy Clin Immunol. 1998;102:S107-S144.
  13. American Academy of Pediatrics. Subcommittee on Management of Sinusitis and Committee on Quality Improvement. Clinical practice guideline: management of sinusitis. Pediatrics. 2001;108:798-808.
  14. Lanza DC, Kennedy DW. Adult rhinosinusitis defined. Otolaryngol Head Neck Surg. 1997;117(3 pt 2):S1-S7.
  15. Sinus and Allergy Health Partnership. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Executive summary. Otolaryngol Head Neck Surg. 2000;123(1 Pt 2):5-31.
  16. Wald ER. Microbiology of acute and chronic sinusitis in children and adults. Am J Med Sci. 1998;316:13-20.
  17. Hoban DJ, Doern GV, Fluit AC, Roussel-Delvallez M, Jones RN. Worldwide prevalence of antimicrobial resistance in Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis in the SENTRY Antimicrobial Surveillance Program 1997-1999. Clin Infect Dis. 2001;32(suppl 2):S81-S93.
  18. Szczeklik A, Stevenson DD. Aspirin-induced asthma: advances inpathogenesis and management. J Allergy Clin Immunol. 1999;104:5-13.