Sinus Infections

Anatomic Considerations

The paranasal sinuses (maxillary, ethmoid, frontal, and sphenoid) are air-filled cavities lined by pseudostratified, ciliated columnar epithelium. They are interconnected through small tubular openings, the sinus ostia, which drain into different regions of the nasal cavity ( Fig. 31.1 ). The frontal, anterior ethmoid, and maxillary sinuses open into the middle meatus, whereas the posterior ethmoid and sphenoid sinuses open into the superior meatus. The osteomeatal complex, an area between the middle and inferior nasal turbinates representing the confluence of drainage from the paranasal sinuses, is a particularly important anatomic site because of its potential for mucosal thickening and impaired drainage leading to sinus infection even without mechanical obstruction of the ostia.

The maxillary sinuses, either alone or in combination with the ethmoid or frontal sinuses, are the most frequent site of infection. The ostium of the maxillary sinus lies at an obtuse angle toward the roof (see Fig. 31.1 ), so the maxillary sinus does not empty well in the erect posture but drains best when the patient is lying on the side opposite the affected sinus. The floor of the maxillary sinus directly adjoins the maxillary bone in which the apices of the first, second, and third molar teeth reside; hence, extraction or root infection of these teeth is a frequent cause of maxillary (odontogenic) sinusitis. Furthermore, because the superior alveolar nerves (branches of the maxillary nerve) supply both the molar teeth and the mucous membranes of the sinus, maxillary sinusitis may frequently manifest as a toothache.

The frontal sinus is not a frequent site of infection but may be a focus for spread of infection into the orbit or the brain ( Fig. 31.2 ). The frontal sinus is supplied by the supraorbital branch of the ophthalmic division of the trigeminal nerve. Thus headache is a prominent symptom of frontal sinusitis.

The ethmoid sinuses are composed of multiple air cells that are separated by thin bony partitions, and each air cell drains by an independent ostium. The ethmoid sinuses are separated from the orbit by a paper-thin orbital plate. Perforation of the plate allows direct spread of infection into the retro-orbital space. Ethmoid sinusitis can also spread to the superior sagittal vein or the cavernous venous sinus (see Fig. 31.2 ).

The sphenoid sinus occupies the body of the sphenoid bone in proximity to the pituitary gland above; the optic nerve and optic chiasm in front; and the internal carotids, the cavernous sinuses, and the temporal lobes of the brain on each side (see Fig. 31.2 ). Therefore sphenoid sinusitis can spread locally to cause cavernous sinus thrombosis, meningitis, temporal lobe abscess, and orbital fissure syndromes. The superior orbital fissure syndrome, characterized by orbital pain, exophthalmos, and ophthalmoplegia, is caused by involvement of the abducens, oculomotor, and trochlear nerves and the ophthalmic division of the trigeminal nerve as they pass through the orbital fissure.

A patent osteomeatal complex and normal mucociliary clearance function are the key defense mechanisms of the paranasal sinuses.

Epidemiology and Risk Factors

According to the 2017 National Health Interview Survey, approximately 30 million cases of sinusitis are diagnosed each year, representing 12% of all adults 18 years of age or older. Children younger than age 15 and adults 25 to 64 years old are the most frequently affected. It is the fifth leading cause for antimicrobial prescriptions in office practice. Total direct costs for treating sinusitis are estimated at $6 billion per year, not to mention significant indirect costs such as days lost from work, decreased productivity, and impaired quality of life.

Several risk factors predispose to acute or chronic sinusitis ( Box 31.1 ). The most common cause of acute sinusitis is a viral upper respiratory infection or the common cold. Adults typically develop two to three colds per year, and children have six to eight episodes per year. However, only up to 2% of adults and 6% to 13% of children with viral upper respiratory infections develop a secondary bacterial infection of the sinuses. Nose blowing that generates excessive positive intranasal pressures and propels contaminated fluid from the nasal cavity into the paranasal sinuses may be an important predisposing mechanism.

A strong association exists among allergic rhinitis, asthma, and recurrent sinusitis in both children and adults. It has been suggested that allergic rhinitis may be a predisposing factor for acute maxillary sinusitis in 25% to 30% of patients, and as many as 60% to 80% of patients with chronic sinusitis. The observation that asthma, allergic rhinitis, and rhinosinusitis frequently coexist raises the possibility that these conditions are manifestations of an inflammatory process within an integrated and contiguous upper and lower airway (the integrated airway hypothesis).

Mild and selective immune deficiencies have been frequently demonstrated in children and adults with recurrent or persistent symptoms of sinus disease. One study found that 52% of patients had selective immunoglobulin (Ig) deficiencies (IgG2, IgG4 subclass, or IgA) or poor responsiveness to some polysaccharide antigens. In addition, chronic or recurrent sinusitis is an important source of morbidity in patients with cystic fibrosis and patients infected with human immunodeficiency virus (HIV).

Certain actions, such as sustaining head trauma, swimming, diving, cocaine sniffing, and nasotracheal or nasogastric intubation, may repeatedly traumatize the nasal mucosa and facilitate microbial invasion of the paranasal sinuses. Dental extraction and periapical infections of the maxillary molar teeth are particularly important causes of odontogenic sinusitis.

Microbiology

Sinus puncture and aspiration is the gold standard for establishing the microbial cause of sinusitis. Although acute sinusitis is primarily caused by respiratory viruses such as rhinoviruses, influenza A, parainfluenza, respiratory syncytial virus, and adenoviruses, direct isolation of these viruses from antral aspirates has been relatively uncommon. In acute bacterial sinusitis, Streptococcus pneumoniae and nonencapsulated Haemophilus influenzae are the causative agents in 70% of adults, whereas the addition of Moraxella catarrhalis accounts for 80% of cases in children ( Table 31.1 ). Staphylococcus aureus together with viridans streptococci and S. pneumoniae are the predominant isolates in acute sphenoid sinusitis. Anaerobes are uncommonly isolated in acute sinusitis but are the predominant flora in chronic sinusitis. The isolation of anaerobes during acute sinusitis suggests an odontogenic source. Nosocomial sinusitis secondary to prolonged nasotracheal intubation is commonly a polymicrobial infection caused by gram-negative bacteria, S. aureus, and anaerobes.

Up to 40% of H. influenzae , 80% of M. catarrhalis , and 30% of respiratory tract anaerobes produce β-lactamase. Over 25% of S. pneumoniae is now resistant to trimethoprim-sulfamethoxazole (TMP-SMX). Macrolide-resistant H. influenzae and S. pneumoniae are also isolated with increasing frequency.

The microbiology of chronic sinusitis is more closely linked to underlying comorbid diseases and differs considerably from that of acute sinusitis. In patients with cystic fibrosis, Pseudomonas aeruginosa and nontypable H. influenzae are the most frequent pathogens. Sinusitis in patients with HIV infection is often caused by gram-negative bacilli and unusual pathogens such as Aspergillus species and cytomegalovirus. In debilitated and severely immunocompromised hosts, such as those with uncontrolled diabetes mellitus, advanced HIV infection, or chemotherapy-induced neutropenia, invasive fungal infection with Aspergillus, Mucor, Pseudallescheria boydii, Fusarium, and other saprophytic fungi may occur. In chronic sinusitis associated with nasal polyposis or allergic fungal rhinosinusitis, hypersensitivity to and colonization by Aspergillus and other saprophytic fungi in the paranasal sinuses can often be demonstrated. In addition, there is an increased prevalence of nasal colonization by enterotoxin-producing S. aureus in patients with chronic sinusitis associated with nasal polyposis. Such patients typically demonstrate local production of enterotoxin-specific IgE antibodies and coexisting aspirin sensitivity or asthma.

Clinical Features