The paranasal sinuses and their pathways are lined by mucosa composed of ciliated pseudostratified columnar epithelium. The cilia beat consistently in a fluid medium, moving sinus secretions out toward the natural ostia, along the drainage pathways, and eventually into the nasopharynx. It is this interplay of ostial patency, mucociliary functioning, and fluid secretions that allows for normal paranasal sinus physiology. When one or more of these elements is impaired, the potential for sinus dysfunction exists.
Patency of the paranasal sinus ostia with maintenance of drainage pathways is a key element in normal sinus physiology. The posterior ethmoid cells drain secretions through the superior meatus, and the sphenoid sinus drains into the sphenoeth-moidal recess. The frontal sinuses, anterior ethmoid sinuses (agger nasi cells and both supra- and infraorbital ethmoids), and maxillary sinuses drain into the osteomeatal complex (OMC). This area consists of the hiatus semilunaris, frontal recess, anterior ethmoid cells, ethmoid bulla, anterior wall of the middle turbinate, and the infundibulum. The infundibu-lum is a troughlike space just anterior to the anterior ethmoid cells, which acts as a common drainage pathway. Because of these anatomic and physiologic relationships, OMC or anterior ethmoid disease can induce mucosal edema and functional obstruction of the infundibulum and drainage of its related sinuses.7 Mechanical factors, as well as functional factors, may also precipitate obstruction, although viral URI with secondary mucosal swelling is by far the most frequent cause of ostial obstruction.3
Once the sinus ostia become obstructed, ventilation is impaired and there is a transient increase in intrasinal pressure, followed by a negative intrasinal pressure.8 The negative pressure within the sinus relative to the atmospheric pressure may allow nasal flora to flow against the mucosal ciliary beat patterns and enter the typically sterile sinus cavity. Sniffing, sneezing, and nose-blowing, associated with altered intranasal pressure, may also facilitate entry of bacteria into the sinus from a colonized nasal chamber.3 As nasal congestion increases, nasal breathing decreases; decreased gas exchange produces a decreased partial pressure of oxygen intrasinally, which favors multiplication of certain bacterial species. An acidic pH may also develop, promoting anaerobic conditions. As the immune system responds to the bacterial invasion, tissue congestion worsens secondary to the inflammatory response, further perpetuating the cycle of obstruction.
Normal mucociliary functioning usually protects respiratory epithelium from bacterial invasion, however, certain respiratory viruses appear to exert a direct cytotoxic effect on the cilia.3 Alteration of the number, morphology, and function of cilia in the respiratory epithelium may facilitate secondary bacterial infection of the paranasal sinuses. Ciliary activity may also be impaired with alterations in mucosal secretions, as cilia can only beat in a fluid medium. Thickened secretions typically seen in systemic disorders such as cystic fibrosis or asthma have the potential to impair ciliary movement. Purulent secretions from an infected sinus may also affect ciliary movement, however, reports on this are conflicting.9'10
Ostial obstruction thus initiates a vicious circle, with self-mediated mucosal edema and hyperplasia, obstruction of sinus drainage, retention of secretions, and ciliary dysfunction, cumulatively creating an environment ideal for long-standing infection. In children, OMC obstruction is recognized as a critical factor in chronic rhinosinusitis, however, it is unclear whether this is the primary cause of the disease.
Perhaps critical to our further understanding of this unique pathophysiologic model is the concept that there is rarely a single isolated cause. A number of conditions have been identified as predisposing to chronic rhinosinusitis in children, although an acute viral illness—the common cold—appears to be the most frequently recognized association.11,12 Data suggest children average 6 to 8 upper respiratory infections (URIs) per year, and acute sinusitis complicates 5 to 10% of cases.13,14 The precise mechanism whereby viruses predispose to rhinosinusitis is unknown, but it may involve local immune defense destruction and a subsequent increase in bacterial attachment to epithelial cells.15 An immature immune system and lack of previous exposures presumably make children more susceptible to common viral URIs, especially in settings where close contact with other children facilitates infectious transfers.16 Also, the smaller size of developing sinuses and a shorter distance between ostial mucosal surfaces may further facilitate OMC obstruction, and encourage the development of rhinosinusitis after a viral URI in children.16 Potentially modifiable predisposing factors involved in the pathogenesis of this disease have also been identified, and are addressed later in the chapter.
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