Sinusitis affects an estimated 16% of the adult population in the United States, which translated into an astonishing 5.8 billion dollars of direct health care costs in 1996. The great majority of patients present to their primary care physician, resulting in approximately 18 million office visits a year.

From 1990 through 1992, total restricted activity days numbered 73 million. Degree of impairment from sinusitis is substantial, and is comparable to other chronic diseases, such as chronic obstructive lung disease, angina, and back pain.

The sinuses are air-filled cavities, which are lined with classical, pseudostradified and ciliated columnar epithelium. The host defense system works to keep this pathogen free in a number of ways. In an immunocompetent host, secretory IgA and proper mucocilliary clearance through a patent ostium prevent local mucosal damage.

Proper function of the sinuses involves several key points, including:

1. mucus that is of appropriate viscosity, composition, and volume
2. normal mucociliary flow, and
3. open ostia to allow adequate drainage and aeration.

The cilia help to clear secretions by sweeping them toward a patent ostial opening and into the nasal cavity.

In the maxillary sinuses, proper ciliary function is especially important because the direction of drainage is against the pull of gravity. The ostiomeatal complex (OMC) is a narrow drainage pathway located in the middle meatus, which allows ventilation of the anterior ethmoid, frontal, and maxillary sinus.

Sinusitis can be broadly defined as inflammation of one or more of the paranasal sinuses. Classically, sinusitis is characterized as the following:

• Acute-symptoms last less than 4 weeks
• Subacute-symptoms last 4 to 8 weeks
• Chronic-symptoms last longer than 8 weeks
• Recurrent three or more acute episodes a year

Acute sinusitis can be further defined as an infection of the paranasal sinuses, with accompanying symptoms present for more than 10 days and less than 4 weeks. To fully define chronic sinusitis has been difficult.

Because of the variation in clinical expression of the disease, and the discordance between patient symptoms and objective findings, no one set of diagnostic criteria has been agreed on by all clinicians.

Furthermore, before much of the microbiologic or pathologic data regarding this disease had been shown, chronic sinusitis was thought to be a chronologic extension of acute sinusitis. However, it is now thought that chronic sinusitis is a much different disease.

In contrast to acute sinusitis, most chronic sinusitis is not an infectious disease and is better thought of as an inflammatory disease, much akin to asthma. Several factors promote the development of acute sinusitis. In most cases, bacterial sinusitis is preceded by a viral upper respiratory infection, which in turn leads to sinus inflammation and obstruction of the OMC.

As a result, drainage and ventilation of the maxillary, anterior ethmoid, and frontal sinuses are compromised. Once this occurs, both the pH and oxygen content decrease, the cilia are less functional, mucosa are damaged, and the microenvironment becomes more susceptible to infection.

Approximately 0.5% to 2% of viral sinusitis progress into bacterial infections. To distinguish between bacterial and viral sinusitis can be difficult. Typically viral sinusitis resolves in 7 to 10 days, whereas bacterial sinusitis remains persistent.

Rhinovirus is the most common viral pathogen and is easily transmissible. In a study of healthy volunteers, 95% of individuals challenged with intranasal rhinovirus drops became infected, and three quarters of them became symptomatic.

Within 10 hours, newly replicating virus was found in the nasal secretions. As confirmed by sinus puncture, Streptococcus pneumoniae, Haemophilus influenza, and Moraxella catarrhalis make up the majority of the community acquired bacterial pathogens.

One possible mechanism for introduction of pathogens from the nasal passages into the sinuses may actually be through nose blowing. This processes creates a negative intranasal pressure with such force that nasal fluid is propelled from the middle meatus into the sinus cavity.

The pathogenesis of chronic sinusitis is poorly understood. The mechanisms that contribute to the chronicity of the disease include mucociliary dysfunction, mucostasis, hypoxia, and release of microbial products.

However, the initial stimulus and subsequent perpetuation of these processes is unclear. Some theories have implicated anatomic, infectious, allergic, and inflammatory disease, but none have been proven. Unlike acute sinusitis, the role of ostiomeatal complex blockage is uncertain.

In a comparison of CT scans between patients with chronic sinusitis and healthy controls, there was no difference in the patency of the ostiomeatal complex. Also in contrast to acute sinusitis, the role of infection as the driving force behind most chronic sinusitis has been brought into question.

While the most common pathogens in acute sinusitis include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, pathogens found in chronic sinusitis are usually a mixture of aerobic and anaerobic bacteria, including Staphylococcus aureus and coagulase-negative Staphylococci.

Whether these organisms are pathologic, or are merely colonizing agents, is difficult to determine. Reports of the prevalence of anaerobic species differ widely, and range from as high as 80% to 100% in children, or to as low as 0% to 25% in adults. Furthermore, treatment with antibiotics tends to provide only transient benefit.

Granted, a small subset of patients with chronic sinusitis may be infectious in nature, but it is usually in association with an underlying immunodeficiency, such as immunoglobulin deficiency, HIV, cystic fibrosis, or Kartagener syndrome. Several other mechanisms of disease have been previously proposed.

In these cases, the inflammatory response is against the microbe as an antigen, and not as an invasive pathogen per se. One theory proposes that immune hyperresponsiveness to colonizing bacteria, such as Staphylococcus aureus, may play a role in chronic sinusitis with polyps.

Yet another theory proposes that colonizing fungi serve as the antigen. Regardless of the initial stimulus, the inflammatory process ensues, with a predominance of eosinophils. Furthermore, chronic sinusitis with and without polyps differ in their specific histopathologic presentation.

In nasal samples of patients with polyps, there were significantly more eosinophils, plasma cells, and stromal edema compared with those without polyps. The investigators argued that because a substantial difference was found between these groups, they should be treated as separate entities, and not a continuum of one.

Perhaps an understanding of the pathophysiology of chronic sinusitis can be gleaned by its close association with other allergic diseases, such as allergic rhinitis, asthma, and aspirin sensitivity. Based on CT studies, anywhere from 74% to 90% of asthmatics have sinus mucosal abnormalities, albeit asymptomatic.

In addition, chronic sinusitis was associated with allergic rhinitis in 40% to 84% of adult patients. Even so, a direct causal role between these diseases has never been shown. Lastly, gastroesophageal reflux (GERD) has been implicated as a cause of sinusitis.

Gastric acid can reflux directly into the nasopharynx and, in theory, can cause inflammation of the sinus ostium, and pH probe studies have shown a much higher incidence of GERD in patients with chronic sinusitis.

In an uncontrolled study of 19 adults with chronic sinusitis, 68% had symptoms of GERD, and 78% had abnormal esophageal pH probe results. After a subset of these subjects was treated with proton pump inhibitors, 67% had an improvement in sinus symptoms.