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A practical evidence-based approach to rhinosinusitis

The Journal of Respiratory DiseasesThe Journal of Respiratory Diseases Vol 6 No 9
Volume 6
Issue 9

Abstract: Rhinosinusitis affects millions of persons annually and has a marked impact on quality of life and work productivity. Chronic rhinosinusitis (CRS) is characterized by symptoms that last at least 12 weeks. The history and physical examination should include a search for underlying conditions, such as allergic or nonallergic rhinitis and nasal polyposis. An evaluation of underlying immunodeficiency is warranted in certain patients, particularly those with severe or difficult-to-treat disease or other recurrent infections. When radiologic evaluation is indicated, coronal sinus CT scanning is the procedure of choice. While antibiotics are indicated for bacte- rial rhinosinusitis, intranasal corticosteroids represent the mainstay of treatment for CRS and are particularly useful when polyp disease is present. Nasal irrigation with a saline solution can be a very beneficial adjunctive therapy. Depending on coexisting conditions, additional treatments may include antihistamines, leukotriene modifiers, and immunotherapy. (J Respir Dis. 2006;27(9):372-379)

Rhinosinusitis affects 31 million persons and accounts for 18 million medical office visits annually in the United States, with an average work productivity loss of 4 days a year per person.1 It has significant diagnostic and treatment costs because of its insidious nature and likelihood of progressing to a chronic condition affecting quality of life.

In this article, we present an overview of the approach to the diagnosis and management of chronic rhinosinusitis (CRS), with an emphasis on evidence-based recommendations.


Rhinosinusitis refers to inflammation of 1 or more of the paranasal sinuses, typically accompanied by inflammation of the nasal mucosa. Sinusitis is typically preceded by an inflammatory response of the nasal mucosa, which extends into contiguous sinus tissues. The term "rhinosinusitis" is preferred in the literature to illustrate this interrelationship. Evidence-based practice focuses on evaluation and treatment of underlying nasal conditions, which are fundamental in the management of sinus inflammation.

Rhinosinusitis has been classified on the basis of duration of symptoms, presence or absence of nasal polyps, identification of an infectious cause, or the finding of nasal eosinophilia. A seminal article established definitions of the following rhinosinusitis subtypes: acute rhinosinusitis (and recurrent acute rhinosinusitis), CRS either with or without nasal polyposis, and allergic fungal rhinosinusitis.2

Acute rhinosinusitis is most often seen in the primary care office and is diagnosed when symptoms occur for less than 4 weeks. Symptoms persisting for 4 to 8 weeks may be referred to as subacute disease. Recurrent disease refers to 3 or more episodes of acute rhinosinusitis per year. In CRS, symptoms typically persist for at least 12 weeks. The classification of CRS is subdivided based on the presence or absence of nasal polyps, reflecting a different pathophysiology with distinct clinical features.

Allergic fungal rhinosinusitis is a specific entity characterized by fungal colonization of the nasal mucosa in an immunocompetent person, with evidence of an IgE-mediated reaction to the fungus (identified by allergen skin testing or specific in vitro serum IgE). Asymmetric heterogeneous sinus opacification on a CT scan is characteristic. Pathologic findings associated with fungal hyphae mixed within eosinophilic mucin show a macroscopic mucous exudate with the consistency of peanut butter. A clue to the diagnosis is an elevated total serum IgE level, usually more than 1000 IU/mL.


Several factors contribute to the pathogenesis of rhinosinusitis. Although infection--usually viral infection--represents the most common cause of acute rhinosinusitis, the role of infection in CRS is not well established.

The focus of evidence-based practice is the recognition of predisposing factors and comorbidities fundamental in the pathogenesis of rhinosinusitis. Allergic or nonallergic rhinitis, nasal polyposis, immunodeficiency, and mechanical factors such as impaired ciliary function may play a role in the etiology of rhinosinusitis.


Viral infection is by far the most common cause of acute rhinosinusitis, complicated by secondary bacterial infection in an estimated 0.5% to 2% of cases.1 The most frequently encountered bacteria in this setting are Streptococcus pneumoniae, Haemophilus influenza, and Moraxella catarrhalis.

In CRS, other bacteria have been isolated from sinus cultures, including Pseudomonas aeruginosa, group A streptococci, Staphylococcus aureus, and anaerobes. Evidence that these isolates have a primary pathophysiologic role in CRS is lacking.3,4 Nosocomial rhino- sinusitis is commonly caused by Gram-negative rods (Pseudomonas, Klebsiella, Enterobacter, Proteus, Serratia) and Gram-positive cocci (Streptococcus, Staphylococcus).

Fungal involvement can range from benign colonization to invasive life-threatening disease, depending in part on the patient's immune status. Allergic fungal rhinosinusitis represents an intense allergic reaction to microscopic amounts of colonizing fungus in an immunocompetent person. In contrast, invasive fungal rhinosinusitis is an acute fulminant process that predominantly occurs in immunocompromised patients, such as those with diabetes, febrile neutropenia, or impaired cell-mediated immunity and those who are receiving high-dose corticosteroids.


In patients with rhinitis, sinonasal mucosal edema results in obstruction of sinus drainage, predisposing to sinus inflammation and infection.5 Allergic and nonallergic rhinitis are the most common factors in CRS.6 In adults with acute maxillary sinusitis, the incidence of allergic rhinitis was reported to be 25% to 31%, while the incidence of allergic rhinitis in patients with CRS was 40% to 84%.7 The latter statistic emphasizes the importance of allergy as a contributing factor in disease outcome and progression of upper and lower airway disease.

Patients with chronic or recurrent acute rhinosinusitis should be evaluated for the presence of allergy by allergen skin testing performed by a specialist. Control of rhinitis is pivotal for the management of rhinosinusitis, by achieving a reduction of the mucosal inflammation and edema.

Nasal polyposis

Nasal polyps are familial, are not usually associated with atopy, have an unclear pathogenesis, and are characterized by increased eosinophilic infiltration.8 Nasal polyposis is often associated with other comorbidities, such as cystic fibrosis, ciliary dyskinesia, and Churg-Strauss vasculitis.

Interestingly, up to 90% of patients with aspirin hypersensitivity that triggers bronchospasm have nasal polyps; this complex is referred to as Samter triad. It is worth noting that patients with this triad may tolerate nonacetylated aspirin or selective cyclooxygenase-2 antagonists.


An underlying immunodeficiency should be considered in patients who have CRS or recurrent acute rhinosinusitis, especially when the symptoms are severe, unresponsive to therapy, or associated with other recurrent infections or bronchiectasis. Patients who have underlying immunodeficiency and rhinosinusitis most frequently have a defect in antibody-mediated immunity--most commonly selective IgA deficiency, which has an estimated prevalence of 1:500 in the United States. As many as one third of patients who have IgA deficiency experience recurrent infections, which include rhinosinusitis, pneumonia, otitis, and GI infections.9

Other antibody defects include common variable immunodeficiency (CVID) and specific antibody deficiency with normal levels of immunoglobulins. Another predisposing risk factor for rhinosinusitis is AIDS, which is characterized by combined humoral and cellular immune defects. The incidence of rhinosinusitis in patients who have HIV infection increases as the CD4+ cell count decreases. The prevalence of rhinosinusitis in patients infected with HIV has been reported to be between 10% and 68%.10,11

Evaluation for immunodeficiency starts with measurement of serum immunoglobulin (IgA, IgG, IgM, and IgE) levels. Undetectable serum IgA in the setting of normal IgG and IgM levels denotes selective IgA deficiency. A low IgG level with depressed IgA or IgM levels suggests CVID. If immunoglobulin levels are normal and immunodeficiency is still suspected, further evaluation starts with measuring pneumococcal titers before and after immunization with pneumococcal vaccine. HIV testing should be offered whenever risk factors are present.



Compared with acute rhinosinusitis, CRS tends to have a more insidious presentation that may consist of primarily 1 symptom, such as postnasal drip or nasal obstruction. In one survey, 322 adults with disease duration of 12 weeks or longer classified their rhinosinusitis symptoms as major or minor.12 Major symptoms include nasal discharge, nasal obstruction, facial congestion, facial pain/pressure/ fullness, and loss of smell. Minor symptoms include headache, ear pain/pressure, halitosis, dental pain, cough, fever, and fatigue.12

These symptoms may provide clues to further differentiation of disease pathogenesis. For example, patients who have nasal polyps predominantly experience a decreased sense of smell, while patients who do not have nasal polyps complain mostly of facial pain, pressure, and fullness.

Physical examination

An accurate diagnosis should be made by integrating physical examination findings with key elements obtained from a comprehensive history. Allergic diseases are associated with key findings, such as dark semicircles underneath the eyes, a nasal crease, and periorbital puffiness.

Anterior rhinoscopy is the fundamental physical examination tool used in the primary care office for evaluation of rhinosinusitis. The nasal mucosa is characteristically red and swollen in infectious rhinosinusitis, while it appears pale and swollen, with copious watery secretions, in allergic rhinitis.

Purulent secretions from the middle meatus are characteristic of rhinosinusitis and have the highest positive predictive value of all physical findings.5 However, these secretions may be difficult to visualize without a vasoconstrictor agent, such as a topical decongestant. Nasal polyps are smooth, round, gelatinous structures that most commonly originate from the ethmoidal sinuses and are visualized in the middle meatus. Polyps are typically bilateral; unilateral polyps should prompt investigation by an otolaryngologist for an inverting papilloma or a nasal tumor.


Imaging has no proven value in routine cases of acute rhinosinusitis, and it does not help in distinguishing viral from bacterial disease.13 An exception is made in the presence of certain findings that would necessitate immediate imaging and referral (Table 1).5 Patients who have recurrent or chronic sinus disease or who have a poor response to treatment often require imaging for further evaluation of the sinonasal anatomy and associated comorbidities.

Plain radiographs have very limited value in CRS; they do not provide adequate diagnostic information, and their radiologic interpretation may be quite variable. Moreover, the practical benefit of plain radiographs may be unjustified because of the unnecessary radiation exposure and expense.

Coronal CT without contrast is cost-effective and easily done, and it represents the gold standard diagnostic test.14,15 It is important to correlate CT results with the history and physical examination findings, since up to 40% of asymptomatic patients have been found to have at least 1 abnormality detected on sinus CT, such as mucosal thickening or a retention cyst.14

MRI is better than CT for evaluation of soft tissue, but it is less suited for bony imaging. It is superior for evaluation of malignant tumors and orbital or intracranial extension of disease, but it may be too sensitive for nasal mucosal evaluation, since normal mucosa in the edematous phase may appear indistinguishable from inflammatory disease.



Antibiotics are the primary treatment for bacterial rhinosinusitis. Select antibiotic regimens are listed in Table 2.

Most patients with acute rhinosinusitis have a viral infection that will spontaneously improve. When symptoms persist beyond 10 to 14 days, antibiotic therapy is warranted because of suspected bacterial superinfection. A 14-day antibiotic course is adequate for most acute cases; CRS may require a 4- to 6-week course.

In patients who have protracted or severe rhinosinusitis, anaerobes are more frequently encountered and can be appropriately covered by a penicillin with a ß-lactamase inhibitor (such as amoxicillin/ clavulanate) or a combination of metronidazole and a macrolide or a fluoroquinolone.16

In patients who continue to have clinical disease despite appropriate antibiotic therapy, it is beneficial to determine the underlying causative microorganism(s), especially in the setting of rising antibiotic resistance. The gold standard is a Gram stain and cultures of a sinus aspirate performed by an otolaryngologist. Endoscopically obtained culture specimens from the middle meatus represent a less invasive alternative, although more studies are needed to confirm the correlation of this method with sinus aspirates.7

Intranasal corticosteroids

These agents are essential in the management of CRS and have significant benefit in the control of underlying rhinitis. Corticosteroids inhibit cellular trafficking, improve ciliary flow, decrease mucosal edema, and may restore patency of the sinus ostia. In patients with polyp disease, corticosteroids are particularly useful in reducing polyp size, although they alone may not improve anosmia. Daily use of intranasal corticosteroids for 6 to 12 months may be necessary to reach maximal benefit.

Leukotriene modifiers provide alternative therapy for patients with polyposis who are intolerant of intranasal corticosteroids, and these agents have been found to reduce polyp recurrence following surgery.17

Nasal saline irrigation

This is a safe, well-tolerated, and inexpensive modality that can be very effective in reducing sinus symptoms and improving quality of life. Lavage with saline performed 2 or 3 times each day clears the nasal passages, prevents crusting of secretions, augments mucociliary clearance, and may assist in reducing mucosal inflammation.18

The nasal saline recipe consists of mixing 1 teaspoon of noniodized table salt with 1 pint of distilled water, prepared fresh every 1 or 2 days, and irrigating the nose at least daily using about 150 mL in each nostril per application.


The topical and oral a-adrenergic agents decrease nasal airway resistance by producing vasoconstriction while improving symptoms of nasal congestion. There are no evidence-based data regarding the role of these agents in the treatment of rhinosinusitis.

A common side effect of a-adrenergic nasal sprays is rhinitis medicamentosa (rebound hyperemia). The use of oral agents may result in increased blood pressure, particularly in patients with underlying hypertension.

Sinus surgery

Referral to an otolaryngology specialist for functional endoscopic sinus surgery (FESS) may prove beneficial in patients who fail to respond to maximal medical therapy (Table 3). FESS has become a minimally invasive procedure frequently performed on an outpatient basis.19

Ongoing medical management is appropriate after FESS, given the high rate of relapse in patients with CRS and nasal polyposis. Patient reassessment by the primary care physician is paramount to ensure long-term treatment success and adherence to the medical management plan.



Consultation with an allergy/immunology specialist is warranted in patients with chronic symptoms of rhinitis or refractory sinopulmonary disease (Table 4). For example, in patients with concomitant allergic rhinitis, precautionary measures should be undertaken to minimize environmental exposure to the sensitizing allergens.

In addition to nasal saline irrigation and intranasal corticosteroids, antihistamines and/or allergen immunotherapy play a pivotal role by significantly diminishing atopic symptoms.

Gastroesophageal reflux disease

Although not proved by a well-designed controlled study, it has been suggested that gastroesophageal reflux disease (GERD) could cause CRS by direct reflux of gastric acid into the patient's upper airway. In select cases, referral to a gastroenterologist may be warranted to delineate GERD by endoscopy and to more effectively manage persistent symptoms.7,20


Clinical and research evidence supports the theory that a sinopulmonary reflex stimulates a neural arc, which involves cellular, humoral, and immunologic factors that play a pivotal role in perpetuating bronchial hyperresponsiveness.21 It is important for the primary care physician to recognize the clinical implications of the association of CRS with asthma, since inflammation of the upper airway may directly affect the pathophysiol- ogy and long-term outcomes of asthma.22,23

Aggressive management of rhinosinusitis with intranasal corticosteroids, antihistamines, nasal saline irrigation, and decongestants has been demonstrated to lead to improvement and stabilization of associated lower airway disease. This results in reductions in hospitalization rates related to asthma, in the number of acute care visits, and in the cost of long-term management of asthma and rhinosinusitis.

An important take-home message is that acute rhinosinusitis is usually viral in origin and rarely requires diagnostic imaging or antibiotic therapy. In contrast, CRS may have several interrelated comorbidities, such as allergic rhinitis, nasal polyps, asthma, GERD, and immunodeficiency, which need to be thoroughly evaluated and addressed.



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