Sinusitis may be classified as acute (completely resolved in < 30 days); subacute (completely resolved in 30 to 90 days); recurrent (≥ 4 discrete acute episodes per year, each completely resolved in < 30 days but recurring in cycles, with at least 10 days between complete resolution of symptoms and initiation of a new episode); and chronic (lasting > 90 days).
Acute sinusitis in immunocompetent patients in the community is almost always viral (eg, rhinovirus, influenza, parainfluenza). A small percentage develop secondary bacterial infection with streptococci, pneumococci, Haemophilus influenzae, Moraxella catarrhalis, or staphylococci. Occasionally, a periapical dental abscess of a maxillary tooth spreads to the overlying sinus. Hospital-acquired acute infections are more often bacterial, typically involving Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, Proteus mirabilis, and Enterobacter. Immunocompromised patients may have acute invasive fungal sinusitis (see Invasive Sinusitis in Immunocompromised Patients).
Chronic sinusitis involves many factors that combine to create chronic inflammation. Chronic allergies, structural abnormalities (eg, nasal polyps), environmental irritants (eg, airborne pollution, tobacco smoke), mucociliary dysfunction, and other factors interact with infectious organisms to cause chronic sinusitis. The organisms are commonly bacterial (possibly as part of a biofilm on the mucosal surface) but may be fungal. Many bacteria have been implicated, including gram-negative bacilli and oropharyngeal anaerobic microorganisms; polymicrobial infection is common. In a few cases, chronic maxillary sinusitis is secondary to dental infection. Fungal infections (Aspergillus, Sporothrix, Pseudallescheria) may be chronic and tend to strike older and immunocompromised patients.
Allergic fungal sinusitis is a form of chronic sinusitis characterized by diffuse nasal congestion, markedly viscid nasal secretions, and, often, nasal polyps. It is an allergic response to the presence of topical fungi, often Aspergillus, and is not caused by an invasive infection.
Invasive fungal sinusitis is an aggressive, sometimes fatal, infection in immunocompromised patients, usually caused by Aspergillus or Mucor species.
Common risk factors for sinusitis include factors that obstruct normal sinus drainage (eg, allergic rhinitis, nasal polyps, nasogastric or nasotracheal tubes) and immunocompromised states (eg, diabetes, HIV infection). Other factors include prolonged intensive care unit stays, severe burns, cystic fibrosis, and ciliary dyskinesia.
In an upper respiratory infection (URI), the swollen nasal mucous membrane obstructs the ostium of a paranasal sinus, and the oxygen in the sinus is absorbed into the blood vessels of the mucous membrane. The resulting relative negative pressure in the sinus (vacuum sinusitis) is painful. If the vacuum is maintained, a transudate from the mucous membrane develops and fills the sinus; the transudate serves as a medium for bacteria that enter the sinus through the ostium or through a spreading cellulitis or thrombophlebitis in the lamina propria of the mucous membrane. An outpouring of serum and leukocytes to combat the infection results, and painful positive pressure develops in the obstructed sinus. The mucous membrane becomes hyperemic and edematous.
Acute and chronic sinusitis cause similar symptoms and signs, including purulent rhinorrhea, pressure and pain in the face, nasal congestion and obstruction, hyposmia, halitosis, and productive cough (especially at night). Often the pain is more severe in acute sinusitis. The area over the affected sinus may be tender, swollen, and erythematous.
Maxillary sinusitis causes pain in the maxillary area, toothache, and frontal headache.
Frontal sinusitis causes pain in the frontal area and frontal headache.
Ethmoid sinusitis causes pain behind and between the eyes, a frontal headache often described as splitting, periorbital cellulitis, and tearing.
Sphenoid sinusitis causes less well localized pain referred to the frontal or occipital area.
Malaise may be present. Fever and chills suggest an extension of the infection beyond the sinuses.
The nasal mucous membrane is red and turgescent; yellow or green purulent rhinorrhea may be present. Seropurulent or mucopurulent exudate may be seen in the middle meatus with maxillary, anterior ethmoid, or frontal sinusitis and in the area medial to the middle turbinate with posterior ethmoid or sphenoid sinusitis.
Manifestations of complications include periorbital swelling and redness, proptosis, ophthalmoplegia, confusion or decreased level of consciousness, and severe headache.
Sinus infections are usually diagnosed clinically. Imaging is not indicated in acute sinusitis unless there are findings that suggest complications, in which case CT is done. In chronic sinusitis, CT is done more often, and x-rays of the apices of the teeth may be required in chronic maxillary sinusitis to exclude a periapical abscess.
Microbial cultures are rarely done because a valid culture requires a sample obtained by sinus endoscopy or sinus puncture; culturing a swab of nasal secretions is inadequate. Cultures are typically done only when empiric treatment fails and in immunocompromised patients and some hospital-acquired causes of sinusitis.
Sinusitis in children can initially be difficult to distinguish from an upper respiratory infection (URI). Bacterial sinusitis is suspected when purulent rhinorrhea persists for > 10 days along with fatigue and cough. Fever is uncommon. Local facial pain or discomfort may be present. Nasal examination discloses purulent drainage and should rule out foreign body.
Diagnosis of acute sinusitis in children is clinical. CT is avoided because of concerns about radiation exposure unless there are signs of orbital or intracranial complications (eg, periorbital swelling, vision loss, diplopia, or ophthalmoplegia), there is chronic sinusitis that has not responded to treatment, or there is concern about rare nasopharyngeal cancer (eg, based on unilateral nasal obstruction, pain, epistaxis, facial swelling, or, particularly concerning, diminished vision). Periorbital edema in a child requires prompt assessment for orbital cellulitis and possible surgical intervention to prevent visual impairment and intracranial infection.
In acute sinusitis, improved drainage and control of infection are the aims of therapy. Steam inhalation; hot, wet towels over the affected sinuses; and hot beverages help alleviate nasal vasoconstriction and promote drainage.
Topical vasoconstrictors, such as phenylephrine 0.25% spray every 3 hours or oxymetazoline every 8 to 12 hours, are effective but should be used for a maximum of 5 days or for a repeating cycle of 3 days on and 3 days off until the sinusitis is resolved. Systemic vasoconstrictors, such as pseudoephedrine 30 mg orally (for adults) every 4 to 6 hours, are less effective and should be avoided in young children.
Saline nasal irrigation may help symptoms slightly but is cumbersome and uncomfortable, and patients require teaching to execute it properly; it may thus be better for patients with recurrent sinusitis, who are more likely to master (and tolerate) the technique.
Corticosteroid nasal sprays can help relieve symptoms but typically take at least 10 days to be effective.
Although most cases of community-acquired acute sinusitis are viral and resolve spontaneously, previously many patients were given antibiotics because of the difficulty in clinically distinguishing viral from bacterial infection. However, current concerns about creation of antibiotic-resistant organisms have led to a more selective use of antibiotics. The Infectious Diseases Society of America suggests the following characteristics help identify patients who should be started on antibiotics:
Because many causative organisms are resistant to previously used drugs, amoxicillin/clavulanate 875 mg orally every 12 hours (25 mg/kg orally every 12 hours in children) is the current first-line drug. Patients at risk of antibiotic resistance are given a higher dose of 2 g orally every 12 hours (45 mg/kg orally every 12 hours in children). Patients at risk of resistance include those who are under 2 years of age or over 65 years, who have received antibiotics in the previous month, who have been hospitalized within the past 5 days, and those who are immunocompromised.
Adults with penicillin allergy may receive doxycycline or a respiratory fluoroquinolone (eg, levofloxacin, moxifloxacin). Children with penicillin allergy may receive levofloxacin, or clindamycin plus a 3rd-generation oral cephalosporin (cefixime or cefpodoxime).
If there is improvement within 3 to 5 days, the drug is continued. Adults without risk factors for resistance are treated for 5 to 7 days total; other adults are treated for 7 to 10 days. Children are treated for 10 to 14 days. If there is no improvement in 3 to 5 days, a different drug is used. Macrolides, trimethoprim/sulfamethoxazole, and monotherapy with a cephalosporin are no longer recommended because of bacterial resistance. Emergency surgery is needed if there is vision loss or an imminent possibility of vision loss.
In exacerbations of chronic sinusitis in children or adults, the same antibiotics are used, but treatment is given for 4 to 6 weeks. The sensitivities of pathogens isolated from the sinus exudate and the patient’s response to treatment guide subsequent therapy.
Sinusitis unresponsive to antibiotic therapy may require surgery (maxillary sinusotomy, ethmoidectomy, or sphenoid sinusotomy) to improve ventilation and drainage and to remove inspissated mucopurulent material, epithelial debris, and hypertrophic mucous membrane. These procedures usually are done intranasally with the aid of an endoscope. Chronic frontal sinusitis may be managed either with osteoplastic obliteration of the frontal sinuses or endoscopically in selected patients. The use of intraoperative computer-aided surgery to localize disease and prevent injury to surrounding contiguous structures (such as the eye and brain) has become common. Nasal obstruction that is contributing to poor drainage may also require surgery.
Most acute sinusitis in immunocompetent patients is viral.
Immunocompromised patients are at greater risk of aggressive fungal or bacterial infection.
Diagnosis is clinical; CT and cultures (obtained endoscopically or through sinus puncture) are done mainly for chronic, refractory, or atypical cases.
Antibiotics may be withheld pending a trial of symptomatic treatment, the duration of which depends on the severity and timing of symptoms.
The first-line antibiotic is amoxicillin/clavulanate, with doxycycline or respiratory fluoroquinolones as alternatives.
Aggressive and even fatal fungal or bacterial sinusitis can occur in patients who are immunocompromised because of poorly controlled diabetes, neutropenia, or HIV infection.
Mucormycosis (zygomycosis, also sometimes called phycomycosis) is a mycosis due to fungi of the order Mucorales, including species of Mucor, Absidia, and Rhizopus. This mycosis may develop in patients with poorly controlled diabetes. It is characterized by black, devitalized tissue in the nasal cavity and neurologic signs secondary to retrograde thromboarteritis in the carotid arterial system.
Diagnosis is based on histopathologic demonstration of mycelia in the avascularized tissue. Prompt biopsy of intranasal tissue for histology and culture is warranted.
Treatment requires control of the underlying condition (such as reversal of ketoacidosis in diabetes), surgical debridement of necrotic tissue, and IV amphotericin B therapy.
Aspergillus and Candida spp may infect the paranasal sinuses of patients who are immunocompromised secondary to therapy with cytotoxic drugs or to immunosuppressive diseases, such as leukemia, lymphoma, multiple myeloma, and AIDS. These infections can appear as polypoid tissue in the nose as well as thickened mucosa; tissue is required for diagnosis.
Aggressive paranasal sinus surgery and IV amphotericin B therapy are used to control these often-fatal infections. If mucormycosis is excluded, voriconazole, with or without an echinocandin (eg, caspofungin, micafungin, anidulafungin), can be used instead of amphotericin.