Rhinosinusitis comprises a spectrum of medical conditions that are characterized by

inflammation in the nose and paranasal sinuses. These are divided into acute, subacute, and
chronic rhinosinusitis, depending on duration.
Pathophysiology
The etiologies of acute and chronic rhinosinusitis differ widely. In the case of acute
rhinosinusitis, the role of viral and bacterial pathogens has been well-established. Rhinovirus is
responsible for approximately half of the cases, with other viruses such as coronavirus, influenza,
parainfluenza, respiratory syncytial virus, adenovirus, and enterovirus accounting for the rest. Of
these, approximately 1% to 2% will become complicated by a secondary bacterial sinusitis.
During the acute viral infection, multiple inflammatory mediators including interleukins, tumor
necrosis factor alpha, and cytokines are up-regulated. Acute inflammation of the sinus mucosa,
manifested by mucosal hypersecretion and edema, may cause obstruction of the sinus outflow
tracts (particularly the ostiomeatal complex). The resulting mucus stasis may provide a rich
environment for bacterial proliferation. Viruses may also damage or disrupt the nasal epithelium
and impair mucociliary clearance, further predisposing the patient to a secondary bacterial
infection. Although acute viral infection is a primary etiology of acute sinusitis, host factors such
as atopy, immunodeficiency, or anatomic obstruction may be secondary predisposing factors.
With multiple potential inflammatory triggers acting through various and often overlapping
physiologic pathways, it appears that CRS may represent a syndrome with multiple etiologies.
Predisposing factors for CRS can be categorized into three broad and overlapping categories:
genetic or physiologic factors, environmental factors, and structural factors.
Genetic/Physiologic Factors
A substantial number of patients with CRS appear to be physiologically predisposed to chronic
paranasal sinus inflammation. The prevalence of rhinosinusitis in several well-studied, inherited
disorders also points to a probable genetic contribution. Airway hyperreactivity is a well-known
risk factor associated with the development of CRS. Multiple studies have shown a strong
association between asthma and CRS, and exacerbations of the latter can adversely affect
pulmonary function in these patients. The identification of the ADAM-33 gene in asthma has
raised the possibility of a relationship to CRS given the close association between the two
diseases (5). Aspirin sensitivity with concurrent asthma and nasal polyposis (Samter's triad) is
another example that presents with a typically more severe form of CRS.
Immune deficiencies, whether innate or acquired, can also contribute to sinusitis. Hyperimmune
states such as is seen in Churg-Strauss and Job syndromes can also predispose to rhinosinusitis.
Inherited disorders such as cystic fibrosis (CF) and Young's syndrome may be associated with
abnormal mucociliary clearance from the sinuses. The increased viscosity of nasal secretions in
patients with CF impedes adequate clearance and leads to ciliary injury, local mucosal edema,
and further inflammation.

Ciliary dysfunction is the hallmark of a group of disorders known as primary ciliary dyskinesia.
Morphologic ciliary defects, such as absent ATPase-containing dynein arms, result in ciliary
dysmotility that predisposes patients to both acute and chronic rhinosinusitis. Kartagener
syndrome, the most common form of primary ciliary dyskinesia, is associated with a triad of
chronic sinusitis, bronchiectasis, and situs inversus.
Environmental Factors
The association between allergic rhinitis and rhinosinusitis has been well studied and well
documented, although a causal relationship has not necessarily been established. In patients with
ABRS, the incidence of allergy has been found to be higher than in the general population. The
same is true for patients with CRS, where prevalence estimates of allergic rhinitis range from
25% to 50%. The severity of sinus disease has also been associated with the presence of allergic
rhinitis. Smoking and environmental pollution have both been identified as risk factors for
rhinosinusitis.
Although the role of viruses in acute rhinosinusitis has been well established, their role in CRS is
not clear. In a large epidemiologic study, Gable et al. (1994) found a higher incidence of CRS
during the winter upper respiratory tract infection season. In both human and animal models,
viruses have been shown to cause multiple morphologic and functional changes in nasal
epithelial cells, including increased shedding of cells, shorter cilia, decreased ciliary beat
frequency, and decreased mucociliary clearance. Whether this translates into increased
susceptibility to CRS requires further investigation.
In CRS, the bacteriology of the sinuses is distinct when compared to acute rhinosinusitis, with a
greater presence of gram-negative bacilli and trend toward increased antimicrobial resistance.
Research suggests that bacteria may directly activate the inflammatory cascade, apart from their
traditionally perceived role as infectious agents. In susceptible individuals, bacterial
superantigens such as staphylococcal enterotoxin may activate T-cells, bypassing the normal
antigen-presenting mechanism of T-cell activation. Bachert et al. have suggested that bacterial
superantigens may be responsible for the chronic inflammation present in nasal polyps. Bacterial
biofilms have also been suggested as possible instigators of persistent sinus disease. A biofilm is
a complex polysaccharide matrix synthesized by bacteria that serves as a protective
microenvironment for bacterial colonies. Biofilms have a tenacious quality that renders them
relatively resistant to antimicrobial therapy. Cryer et al. have identified bacterial biofilms on the
sinus mucosa of patients infected with Pseudomonas aeruginosa, a known biofilm former (16).
The presence of these biofilms may help explain the refractory nature of some forms of CRS
despite treatment with potent antimicrobials.
The potential pathogenic role of fungus in the nose has garnered much attention after Ponikau et
al. (1999) demonstrated positive fungal cultures in 96% of 210 patients with CRS and 100% of
normal controls. The presence of fungus in the nose does not imply a causal relationship with
CRS. Fungus may be a cause of CRS because it appears to stimulate an inflammatory reaction

that is not seen in controls. Although the current evidence does not implicate fungus as the sole
cause of CRS, further investigation is warranted.
Structural Factors
The ostiomeatal complex is a functional unit rather than an anatomic structure. It refers to the
physiologic arrangement of structures into which the frontal, maxillary, and anterior ethmoid
sinuses drain. Patency of the pathways through which the sinuses drain is crucial for adequate
mucociliary function and subsequent sinus drainage. The nasal and sinus mucosa produces
approximately 1 L of mucus per day, which is cleared by mucociliary transport. Ostial
obstruction may lead to fluid accumulation and stagnation, creating a moist, hypoxemic
environment ideal for growth of pathogens.
Sinus obstruction may be caused by multiple anatomic variants, including septal deviation,
concha bullosa, paradoxic middle turbinates, and infraorbital (Haller) cells. Scarring from
previous surgery or trauma can also impair sinus drainage. Dental disease may be the source of a
persistent maxillary sinusitis through seeding directly into the sinus cavity. Craniofacial
anomalies in which the anatomy of the sinuses is altered may predispose patients to rhinosinusitis. In children, the presence of foreign bodies should always be considered as another
possible cause of sinusitis.

Diagnosis
To foster effective communication among physicians and researchers and to standardize the
reporting of rhinosinusitis, the Task Force on Rhinosinusitis was created in 1996, sponsored by
the American Academy of Otolaryngology Head and Neck Surgery. The Task Force proposed a
symptom-based format for the diagnosis of rhinosinusitis, with major and minor symptom
categories (Table 29.2). According to the duration of the symptoms, rhinosinusitis was defined as
acute when symptoms lasted 4 weeks or less, subacute when symptoms were present for 4 to 12
weeks, or chronic for symptoms lasting longer than 12 weeks. The term recurrent acute
rhinosinusitis was reserved for patients with 4 or more episodes per year with disease-free
intervals in between. An acute exacerbation of CRS was defined as a sudden worsening of
symptoms in a patient already diagnosed with CRS, with return to baseline symptoms after
treatment. A strong history consistent with rhinosinusitis would require the presence of either 2
major factors or 1 major and 2 minor factors. When only 1 major factor or 2 or more minor
factors were present, this constituted a suggestive history in which rhinosinusitis should be
included in the differential diagnosis.

In 2003 a new task force, the Task Force for Defining Adult Chronic Rhinosinusitis, described
objective criteria that must be present in addition to symptoms for a diagnosis of CRS (2). These
objective criteria may take the form of physical examination findings or imaging studies (Table
29.3).

History and physical examination usually provide enough information to make the diagnosis of
rhinosinusitis. In some instances, particularly in CRS, radiologic imaging may be required. Plain
films have a very limited role in the contemporary workup of CRS (2). Currently, CT scans are
considered the standard for imaging the sinuses. CT scans provide excellent bony anatomic
detail, readily depict anatomic variants, and provide a roadmap for presurgical planning (Figure
29.5 and 29.6). Usually, coronal cuts are obtained with a slice thickness of 2 to 3 mm using a
bone algorithm. Axial cuts can be helpful in evaluating anatomic variations of the frontal recess
or sphenoethmoid complex.
Classification
Most of the early staging systems proposed, including the ones put forth by Friedman et al.
(1990), Kennedy et al. (1992), May et al. (1993), and Gliklich and Metson (1994), assign
patients into four stages depending on the areas of involvement of disease. Notably, all of these
systems are based purely on CT scan findings except for the Kennedy system, which uses a
combination of CT findings and endoscopic grading of mucosal disease (Table 29.4).

Treatment
Acute Rhinosinusitis
Although the pathophysiologies of acute and chronic rhinosinusitis are markedly different, the
therapies used to treat both of these conditions are fairly similar and overlapping. In acute
rhinosinusitis, the most important factor in deciding whether to treat is differentiating viral from
bacterial rhinosinusitis. This may present a clinical challenge because the symptoms and signs
may be similar. Studies have shown that individual signs or symptoms such as discolored nasal
discharge, fever, or facial pain lack the necessary sensitivity and specificity to differentiate viral
from bacterial infections. Because bacterial sinusitis occurs in only a small proportion of viral
upper respiratory tract infections, discerning bacterial from viral sinusitis is critical to avoid
unnecessary antibiotic use. As a general guideline, ABRS should be suspected in a patient with a
viral upper respiratory tract infection that has not resolved in 10 days or worsens after 5 to 7 days
and is accompanied by some or all of the signs and symptoms outlined in the 1997 Task Force
criteria.
Once the diagnosis of ABRS is made, antibiotics are the mainstay of treatment. Choosing the
right antibiotic depends on understanding the relevant microbiology of ABRS. The most
common pathogens in ABRS have been well-studied and include Streptococcus pneumoniae,
Haemophilus influenzae, and Moraxella catarrhalis (Table 29.6). The Sinus and Allergy Health
Partnership has published treatment guidelines for ABRS (1) (Table 29.7). More precise
antibiotic selection can be achieved if cultures can be obtained. The gold standard of sinus
cultures has traditionally been direct maxillary sinus puncture and lavage. More commonly,
endoscopically guided cultures are obtained transnasally (Figure 29.7). These may be performed
with sterile suction traps or small wire swabs because both have been shown to be equally
efficacious. Nonendoscopic cultures obtained from the vestibule or nasal cavity should be
avoided because these are not accurate and usually only demonstrate contaminant pathogens.

TABLE 29.7 ANTIMICROBIAL TREATMENT GUIDELINES FOR ACUTE

BACTERIAL RHINOSINUSITIS IN ADULTS (2004 SINUS AND ALLERGY HEALTH
PARTNERSHIP)
Calculate
d
Calculated
Clinical Bacteriolog Switch Therapy Options (No
Efficacy ic Efficacy Improvement or Worsening
Initial Therapy
(%)
(%)
After 72 hours)
Mild disease with no recent antimicrobial use in past 46 weeks
Amoxicillin/clavulanate (1.754.0 9091 9799

g/250 mg/d)
Amoxicillin (1.54.0 g/d)
8788 9192
Gatifloxacin/levofloxacin/moxiflox
acin
Cefpodoxime proxetil
87
91
Amoxicillin/clavulanate (4 g/250
mg)
Cefuroxime axetil
85
87
Ceftriaxone
Cefdinir
83
85
Combination therapy
-Lactam allergic
Trimethoprim-sulfamethoxazole
83
84

(TMP/SMX)
Doxycycline
81
80
Gatifloxacin/levofloxacin/moxiflox
acin
Azithromycin/erythromycin/clarithro 77
73
Rifampin plus clindamycin
mycin
Mild disease with recent antimicrobial use (past 46 weeks) or moderate disease
Gatifloxacin/levofloxacin/moxifloxaci 92
100

n
Amoxicillin/clavulanate (4 g/250 mg) 91
99
Reevaluate patient
Ceftriaxone
91
99

Combination therapy

-Lactam allergic
Gatifloxacin/levofloxacin/moxifloxaci 92
100
Reevaluate patient
n
Clindamycin and rifampin

Reevaluate patient
Adapted from Anon JB, Jacobs MR, Poole MD, et al. Antimicrobial treatment guidelines for
acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg 2004;130(1 Suppl):145, with
permission.

In ABRS, antibiotic therapy should be continued for a minimum of 10 to 14 days. Response to

therapy should be assessed at 72 hours, and if the patient is unimproved, a change in antibiotic
should be considered. Antibiotic use in the previous 4 to 6 weeks may be predictive of a more
resistant infection, an important consideration that has been incorporated into the guidelines for
antibiotic selection. Parenteral antibiotics should be reserved for complicated infections or
patients who are severely immunocompromised.
Other adjunctive treatments that may reduce sinus ostial edema and improve drainage include
both oral and topical decongestants. Topical decongestants in particular should be used with
caution and not for longer than 3 days to prevent a rebound effect and rhinitis medicamentosa.
Antihistamines in the setting of ABRS should generally be avoided because these may increase
the viscosity of secretions and diminish mucociliary clearance. Topical steroids may be
theoretically helpful as local antiinflammatory agents, but their role in this acute setting has not
been clearly established. Systemic steroids exert a potent antiinflammatory effect and are
sometimes beneficial in select cases of ABRS. Nasal saline irrigations have been shown to
improve patient symptoms related to the acute episode and are especially helpful in those
patients having a significant amount of secretions.
Chronic Rhinosinusitis
As in ABRS, antibiotics are the most commonly prescribed agents for CRS. Because of increased
prevalence of Staphylococcus species, gram-negative bacilli, and anaerobes in CRS, broader
spectrum antibiotics may be necessary if given empirically (26). Antibiotic selection should be
guided by appropriately obtained cultures whenever possible, especially in postoperative patients
and those who have failed an initial trial of first-line antimicrobials. Culture-directed therapy
may reduce the tendency to shift to multiply-resistant organisms over time (27). The most
effective duration of therapy for CRS has not been clearly established. Usually, most authors
recommend a prolonged course of 4 to 6 weeks of antibiotics. Topical delivery of antibiotics into
the nose and sinuses has also been reported and may be helpful in patients experiencing systemic
side effects of oral antibiotics. Topical antibiotics can theoretically treat resistant organisms as an

alternative to intravenous therapy. Parenteral antibiotics also have a selected role in the treatment
of CRS. They are usually indicated for severe or complicated infections, highly resistant
organisms, or patient intolerance of other therapies.
Adjunctive therapies for CRS are diverse and address different facets of the pathophysiologic
process. Topical nasal steroids are routinely used in CRS for their localized antiinflammatory
effect. As in ABRS, however, their actual clinical benefit has not been definitively shown in this
setting. Oral steroids are used frequently for exacerbations of CRS, and this is probably a
reflection of the increasingly recognized inflammatory nature of this disease. Other
antiinflammatory therapies that have been described include leukotriene inhibitors and longterm, low-dose macrolide therapy. Treatment of concomitant inhalant allergies with
antihistamines, topical steroids, or immunotherapy can reduce the background nasal
inflammation over both the short and long term. With the recent data published on the role of
fungus in CRS, antifungal therapy may also be beneficial in selected patients. These can be given
either orally or in a topical form. Other therapies that may be useful include decongestants,
mucolytics, and nasal saline irrigations.