Etiology and Pathogenesis

Paranasal sinus development begins in utero and continues until adolescence. The ethmoid and maxillary sinuses are present at birth, although the maxillary sinuses are not pneumatized until approximately 4 years of age. The sphenoid sinus is pneumatized by about 5 years of age. The frontal sinuses are present at 7 to 8 years of age, but they do not fully develop until adolescence (Figure 33-1).

Figure 33-1 Paranasal sinuses: changes with age.

The frontal, anterior ethmoid, and maxillary sinuses drain into the middle meatus of the nasal cavity through the osteomeatal complex. This structure forms a direct communication between the sinuses, which are normally sterile, and the nasopharynx, which is heavily colonized with bacteria. Under normal circumstances, sinus sterility is maintained by the mucociliary apparatus of the sinuses, which mobilizes secretions (and any bacteria that may have entered the sinus cavity) in the direction of the sinus ostia (Figure 33-2). This clearance mechanism may be compromised when the ostia are obstructed (because of mucosal inflammation and swelling, as in viral or allergic rhinitis or mechanical obstruction). The cilia do not function properly, resulting in stasis of secretions and hypoxia, which worsens edema and inflammation and creates an ideal environment for the overgrowth of bacteria (Figure 33-3).

Figure 33-2 Histology and physiology of nasal cavity and sinuses.

Figure 33-3 Pathogenesis of sinusitis.

The pathogens most commonly responsible for ABS are similar to those for acute otitis media (AOM): Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. The microbiology of ABS, as of AOM, is thought to be changing in the era of the pneumococcal conjugate vaccine and an increasing prevalence of penicillin-resistant S. pneumoniae.

Chronic sinusitis is a poorly understood phenomenon, defined by symptoms lasting for longer than 90 days without interval improvement. It is unclear how significant a role is played by bacterial infection in chronic sinusitis, with some theorizing that an inciting infection causes a prolonged inflammatory response. No clear data exist as to the most common causative agents; these infections are generally considered polymicrobial.

Rhinitis without sinus involvement is also an extremely common pediatric complaint and may be confused with sinusitis. The majority of these cases result from infection or allergy. Infectious rhinitis is caused by a number of common viruses, including rhinovirus, respiratory syncytial virus, and adenovirus, among others. Allergic rhinitis results from an immunoglobulin E–mediated response to allergens in the nasal airway, in which mast cell degranulation effects an inflammatory response resulting in edema of the nasal mucosa and the characteristic symptoms of rhinorrhea, congestion, and pruritus.

Clinical Presentation

ABS most commonly presents in a patient with a preceding upper respiratory infection (URI), and the signs and symptoms of the two conditions are similar. Although most uncomplicated URIs will at least have begun to resolve by the tenth day of illness, however, a URI complicated by an evolving bacterial sinusitis will not have lessened in severity by day 10.