The economic impact of rhinosinusitis is staggering. Although references on this topic are few, thorough investigations were published in 1999 and in 2004, based on the 1996 and 1998 National Health Interview Surveys, respectively (6,7). The direct annual health care cost was estimated at $5.8 billion in 1996, of which about 30% was incurred to treat pediatric patients 12 years of age or younger (5,7). Nearly 90% of the expenditures were associated with ambulatory or emergency department visits (5,7). In 1996, there were 16.7 million outpatient physician, hospital office, and emergency department encounters attributed to the primary treatment of sinusitis (7). The majority of outpatient office-based physician care for sinusitis was delivered by primary care physicians (64.9% by family medicine and internal medicine doctors, and 15.4% by pediatricians) (7). Overall, outpatient visits with sinusitis as the primary diagnosis accounted for 36% of total medical expenditures in 1996, and medications to treat this condition added another 17% (7). In 1992, Americans spent $200 million on prescription medications and more than $2 billion on over-the-counter medications to treat sinusitis (8). The Integrated Health Interview Series for 1997 to 2006 shows that 55.8% of patients with sinusitis spend more than $500 annually on health care, higher than the amount spent by those suffering with chronic diseases such as chronic bronchitis, hay fever, ulcer disease, and asthma (9).

The indirect costs of rhinosinusitis are, as one would expect, not insignificant and are also increasing. The number of total restricted activity days due to rhinosinusitis rose from approximately 50 million per year in the period between 1986 to 1988 to 61.2 million per year between 1997 and 2006 (5,9,10). According to the 2007 estimates of workday productivity, this translates into $18.3 billion in lost opportunity cost (9). Based on the 2006 survey data, patients with sinusitis miss an average of 5.67 workdays due to illness annually, as opposed to 3.74 missed workdays for those without sinusitis (9). More difficult to quantitate, but certainly relevant within the realm of indirect costs, are the detrimental effects of rhinosinusitis on quality of life and the impairment of daily functioning due to the significant physical symptoms present when someone is suffering from rhinosinusitis (4).

The majority of acute rhinosinusitis is infectious in etiology (4) (Table 33.3). The leading pathogen is viral. A sinus puncture study in patients with acute community-acquired rhinosinusitis demonstrated the most common identifiable viral organisms in descending prevalence to be rhinovirus 15%, influenza virus 5%, parainfluenza virus 3%, and adenovirus 2% (4,13). The pathogenesis of infection by the most common of these, the rhinovirus, was very well delineated in the end of the twentieth century by Gwaltney’s group at the University of Virginia. The rhinovirus enters the body through the nose, either by direct inoculation or by large airborne particles (4,14). Viral particles travel in the mucus stream to the adenoid region where they attach to a specialized receptor (rhinovirus receptor intercellular adhesion molecule 1) on lymphoepithelial cells overlying lymphoid follicles (4,15,16,17). An inflammatory reaction is thus incited, and common acute viral rhinosinusitis (AVRS) symptoms, including sore throat, nasal obstruction, and rhinorrhea develop within hours of exposure (4,18).

Although historically viruses were thought to cause predominantly rhinitis, involvement of the paranasal sinuses in the clinical setting of AVRS is well documented radiologically in both adults and children (19,20). These studies were performed predominantly in the late 1980s and early 1990s at a time when people were comparing the relatively new modalities of computed tomography (CT) and magnetic resonance imaging (MRI) against the standard imaging modality for rhinosinusitis, plain film radiography. Abnormalities, including air-fluid levels, aerosolized secretions, and thickened mucosa are seen most often in the maxillary sinuses 87%, but also in the ethmoid sinuses 65%, the frontal sinuses 32%, and the sphenoid sinuses in 39% (4,21). These findings are associated with exocytosis of large amounts of mucin by goblet cells in the paranasal sinus epithelium after they have been stimulated
by inflammatory mediators in the setting of acute viral infection (4).

ABRS classically occurs when a patient with AVRS develops a superimposed or secondary bacterial infection (2). Only about 0.5% to 2.0% of AVRS are complicated by a bacterial infection (2,13). Yet, there are still about 20 million cases of ABRS annually in the United States (2,22). AVRS can promote development of ABRS by several mechanisms. The inflamed, edematous mucosa can obstruct sinus ostia and impair mucus drainage (2,23,24). Mucociliary function and clearance is also directly affected by inflammation; this deficit is magnified in a setting of increased mucus production (24). Infection by bacterial pathogens that colonize the nose and nasopharynx is promoted by mucus stasis and enabled as the bacteria are deposited into the paranasal sinuses by nose-blowing (2,13,25).

This concept of the transition from AVRS to ABRS is critical as we discuss patient presentation and accurate evaluation of progression of symptoms for diagnostic purposes. An episode of AVRS can be complicated by a bacterial infection at any point, but early in the presentation the clinical distinction between the two is essentially impossible. The more specific diagnostic criteria pertaining to the timeline of the infection will be discussed later in this chapter, and are directly related to recommended management of acute rhinosinusitis.

Knowledge regarding the microbiology of acute community-acquired bacterial rhinosinusitis in adults has been predominantly delineated from cultures of maxillary sinus mucus, as these are the most accessible of the paranasal sinuses (4). The majority of ABRS infections are due to a single bacterial isolate, but about one-fourth of cases have polymicrobial infection, more commonly seen in pediatric cases (4,26). The most common bacterial species isolated from the maxillary sinuses of patients with uncomplicated ABRS are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis (2,27) (Table 33.3). The relative frequency of bacterial isolates in ABRS has proven to be a reproducible relationship; S. pneumoniae is identified in 20% to 43% of cases, H. influenzae in 22% to 35%, and M. catarrhalis in 2% to 10% (2,26,27,28,29,30,31). The H. influenzae identified are predominantly the nontypeable organisms (4). In the last several decades of the twentieth century there was a very large increase in the prevalence of β-lactamaseproducing H. influenzae to greater than 50%; however, in the 21st century this appears to have stabilized at about 40% of the isolates (4,13,32,33). Macrolide-resistant S. pneumonia is an increasing concern, and has been associated with increased risk of treatment failure (34,35,36). Anaerobic bacteria account for only 2% to 6% of ABRS, some of which arise from primary dental pathology (4). Staphylococcus aureus and S. pyogenes play an interesting role in ABRS. Overall, they account for less than 5% of cases, although S. aureus is often overestimated based on culture from nasal swabs, as opposed to endoscopically-directed sinus cultures or direct sinus aspirates (4). Of note, S. aureus and S. pyogenes have a higher propensity to cause complications of acute rhinosinusitis, such as intracranial or orbital extension of the disease (4).

Nosocomial rhinosinusitis has a much higher prevalence of gram-negative organisms than community-acquired ABRS. Examples of organisms found in nosocomial infections include Pseudomonas aeruginosa, Klebsiella pneumoniae, Enterobacter species, Proteus mirabilis, Serratia marcescens, and gram-positive cocci, such as streptococci and staphylococci (4). For many years we have known that patients at high risk for nosocomial rhinosinusitis are those who require extended periods of intensive care with prolonged endotracheal intubation or nasogastric tubing (4,37). Nasotracheal intubation has a higher risk for nosocomial sinusitis than orotracheal intubation (4,38). Nosocomial sinusitis develops in 25% of patients requiring nasotracheal intubation for longer than 5 days (4,39).

Acute fulminant invasive fungal sinusitis is an aggressive disease characterized by the rapid spread of fungi from the sinonasal mucosa into the orbit, soft tissues, and brain parenchyma via direct and vascular invasion (40). Affected patients typically have a clinical condition associated with impaired neutrophil function, such as hematologic malignancies, aplastic anemia, diabetes, acquired immunodeficiency syndrome, organ transplant, or iatrogenic immunosuppression due to chemotherapy (40). The most common etiologic organisms are Aspergillus and Mucormycosis species. In this special patient population with decreased ability to mount an immune response to infectious organisms, the signs and symptoms of disease may be subtle. The most common physical finding on sinonasal endoscopy is an alteration in the mucosa of the nose and sinuses that suggest angioinvasion by the fungal organisms, with ultimate hypoperfusion of tissues. White discoloration may suggest tissue ischemia, whereas black discoloration is a late finding of tissue necrosis (40). Decreased mucosal bleeding and sensation of anesthetic regions of the face or oral cavity may be signs of this invasive process (40). The most common locations of mucosal abnormalities are middle or inferior turbinate, nasal septum, and palate (41). The gold standard for diagnosis of this disease is permanent section with Gomori methamine
silver stain showing “hyphal forms within the submucosa with or without angiocentric invasion and tissue necrosis with minimal host inflammatory infiltrate” (40) (Fig. 33.1A-C). Because prompt diagnosis is imperative with this condition, frozen section with histopathologic evaluation of any suspicious lesions is necessary to facilitate surgical resection and initiation of antifungal therapy without delay. The potassium hydroxide-calcofluor white method is an alternative rapid diagnostic technique in which potassium hydroxide is used to dissolve human material, and the calcofluor white is used as an optic brightener that binds to the cell wall of the hyphae and fluoresces when viewed with a fluorescent microscope (40).

When a patient presents with a constellation of symptoms consistent with acute rhinosinusitis, the care provider should document all relevant symptoms. Clarification of the severity of symptoms and their time course is critical in establishing an accurate diagnosis and forming an appropriate treatment plan. Assessment of the patient’s pain within this evaluation is strongly encouraged. Pain is one of the three cardinal symptoms described as the diagnostic criteria for ABRS, and pain is a major reason why patients seek medical care (4,42).

The early consensus report outlined by the Task Force on Rhinosinusitis in 1996 outlined a stratification of major and minor symptoms in order to facilitate appropriate diagnosis of ABRS and help emphasize its distinction from AVRS (1). Subsequent reports have replaced this model with a new concept, highlighting three cardinal
symptoms: purulent nasal discharge, nasal obstruction, and/or facial pain, pressure, or fullness (2,42) (Table 33.4). The logic behind this new slant in symptom interpretation for the diagnosis of ABRS is based upon the high sensitivity and relatively high specificity of these indicators for ABRS, especially when they are present for 10 days or longer (2,42,43,44). Presence of purulent nasal drainage, whether reported by the patient or seen on physical exam in the posterior pharynx or intranasally near the sinus ostia, correlates to the presence of bacteria on antral aspiration (2,45,46). Findings of purulence also correlate with radiographic evidence of ABRS (2,47). Nasal obstruction is associated with objective measures, such as rhinomanometry or nasal peak flow rate (2,48). Facial pain and dental pain are also predictive of ABRS according to culture results and to radiographic findings, but the location does not correlate with the specific sinuses involved (2,44,45,49).

After a thorough history of symptomatology is obtained, a physician can often distinguish ABRS from AVRS or from acute rhinosinusitis due to noninfectious etiologies (2). According to the 2007 guidelines, “ABRS is diagnosed when the three cardinal symptoms are present for 10 days or longer beyond the onset of upper respiratory symptoms, or when the symptoms or signs of acute rhinosinusitis worsen within 10 days after a period of initial improvement (double-worsening)” (2). In the first 3 to 4 days of illness, AVRS cannot be distinguished from an early transition to ABRS (2). Purulent discharge does not indicate the presence of bacteria within the mucus, but rather it demonstrates the presence of neutrophils, which is characteristic of acute inflammation regardless of the etiology. Clear rhinorrhea may be indicative of AVRS, allergic rhinosinusitis, or other causes of nonallergic rhinosinusitis, such as vasomotor rhinitis. At 10 days or more, inflammation and edema from AVRS may still be present; however, the condition should be improving. If the symptoms are progressing at the 10 day timeframe, a diagnosis of ABRS is suggested (2,42).

Fever is not included as a cardinal sign of ABRS because it only has a sensitivity and specificity of about 50% for this diagnosis (2,42,43,44). Patients with AVRS may have fever during the initial several days of illness, which does not necessarily implicate an evolving secondary bacterial infection. However, if a patient presents with the three cardinal symptoms, which seem to be particularly severe or with a high fever within the first 3 to 4 days of onset of illness, a diagnosis of ABRS may be considered early (2,4

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