Rhinosinusitis is defined as an inflammation of the mucosa of the nose and paranasal sinuses. It is classified as acute, subacute, and chronic according to whether the duration of symptoms persists as long as 4 weeks, between 4 and 12 weeks, and more than 12 weeks, respectively (Brook et al. 2000). More than $2 billion is spent annually in the United States for over-the-counter medications for rhinosinusitis (National Center for Health Statistics 1994).
Even though data regarding the incidence of rhi-nosinusitis in the world population are scarce in the literature, every year approximately 16% of adults in the United States receive a diagnosis of rhinosinusitis (National Center for Health Statistics 1994).
If the forms of rhinosinusitis exclusively arising in a single paranasal sinus, such as the maxillary sinus, in relation to tooth disease, facial trauma, or paranasal sinus neoplasms are excluded, the first step in the pathophysiology of most rhinosinusitis is almost invariably an inflammation with edema of the mucosa which involves one or both "pre-chambers" (ostiomeatal complex, sphenoethmoidal recess). This causes an obstruction of the dependent sinus outflow and creates an ideal environment for pathogen and saprophytic bacteria. In acute rhinosinusitis, the most frequently isolated bacteria are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catharralis in 41%, 35%, and 7% of cultures, respectively (Wald 1998).
Apart from the duration of symptoms, acute and subacute rhinosinusitis may be regarded as the same disease, since they share the same etiology (infectious), pathogenesis (obstruction of the sinus drainage), medical therapy, and complications. For this reason, they will be discussed together under the term acute rhinosinusitis.
Despite the widespread use of broad-spectrum antibiotics, complications of acute rhinosinusitis may still be a fatal event in a percentage ranging from 1% to 3.7% (PAtt and Manning 1991; Younis et al. 2002a). BrAdLEY et al. (1984) and Younis et al. (2002b) reported the occurrence of complications in 0.5% and 11% of patients admitted to their institutions for rhinosinusitis, respectively. Intraorbital and intracranial complications are more frequently reported, while osteomyelitis and toxic shock syndrome are rarely encountered (Lusk 1992; Younis et al. 2002a,b).
Orbital complications may be subdivided into five groups (ChANdLEr et al. 1970):
• Group 1. Preseptal cellulitis. Edema of the eyelids without tenderness and with no associated visual loss or limitation of extraocular motility
• Group 2. Orbital cellulitis without abscess. Diffuse edema of the adipose tissue in the orbit with no abscess formation
• Group 3. Orbital cellulitis with subperiosteal abscess. Abscess formation between the orbital periosteum and orbital bone; the abscess displaces the globe, usually down and laterally; if the pro-ptosis is severe, it will be associated with limitation of ocular motility and perhaps decreased visual acuity
• Group 4. Orbital cellulitis with abscess within the orbital fat. Proptosis may be purely frontally directed and not laterally or inferiorly displaced as in subperiosteal abscess; severe limitation of extraocular motility results and visual loss due to optic neuropathy may ensue
• Group 5. Cavernous sinus thrombosis. Orbital phlebitis extends into the cavernous sinus and across the basilar venous plexus to the opposite side, resulting in bilateral disease
In decreasing order of frequency, intracranial complications are: subdural empyema, intracerebral abscess, extradural abscess, meningitis, and, more rarely, cavernous and superior sagittal sinus thrombosis (Jones et al. 2002).
According to some authors (Lang et al. 2001; Noordzij et al. 2002; Younis et al. 2002a,b) complicated rhinosinusitis more frequently affects chil dren and adolescents, with a male/female ratio of 3:1 (KrAus and Tovi 1992).
Sinonasal infections reach the orbit and the intra-cranial cavity spreading through the neurovascular foramina, congenital or acquired bony dehiscences, or via a retrograde flow through the diploic valve-less veins secondary to a thrombophlebitis. Since in children the cranium has more diploic veins than in adults, infections spread more deeply and more rapidly. This accounts for a higher incidence of severe complications in children (Lusk 1992; Lang et al. 2001; Younis et al. 2002b).
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