Patient Story
A 10-year-old girl has a 2-week history of daily headaches and rhinorrhea. She is admitted from the emergency department to the pediatric intensive care unit for a 2-day history of worsening left frontal headache, mental status changes including lethargy and slurred speech, nausea, and mild periorbital edema. Computed tomography (CT) demonstrates opacification of bilateral frontal, maxillary, and anterior ethmoid sinuses as well as pneumocephalus (Figure 27-1A). Magnetic resonance imaging demonstrated extensive left sided subdural empyema (worse frontal and temporal) and diffuse bilateral dural enhancement (Figure 27-1B). She is urgently treated via a combined surgical approach with pediatric otolaryngology for bilateral endoscopic sinus surgery and pediatric neurosurgery for left craniotomy. She subsequently had 10 weeks of intravenous antimicrobial therapy. Her immediate postoperative course was complicated by seizures; she has now made a full recovery and is doing well.
FIGURE 27-1
A. Coronal CT scan demonstrating bilateral ethmoid and left maxillary sinus opacification along pneumocephalus, in a 10-year-old with intracranial extension from frontal sinusitis leading to subdural empyema. B. Same patient, coronal T2 MRI demonstrating a hyperintense extra-axial collection (arrow) along the falx to the left of midline and uniform dural enhancement overlying both cerebral hemispheres. (Used with permission from Prashant Malhotra, MD.)

Introduction
Synonyms
Epidemiology
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Orbital complications account for 90 percent of acute complications from sinusitis and approximately 3 percent of all acute rhinosinusitis.1
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Children younger than age 7 years of age develop isolated orbital complications associated with acute ethmoiditis.2
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Children older than 7 years, mostly teenage males, are more likely to develop intracranial complications.2,3 This is likely related to the age related development of the frontal and sphenoid sinuses.
Etiology and Pathophysiology
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Children have a high rate of upper respiratory infections (URI) and viral rhinosinusitis.
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Congenital or traumatic dehiscences in the lamina papyracea and skull base provide potential routes for direct spread.
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The diploic veins of the skull and ethmoid bone as well as the ophthalmic veins are valveless and allow for communication between the nose, sinuses, face, orbit, cavernous sinus, and intracranial system.
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The combination of phlebitis and direct entry of bacteria into perivascular structures results in a continuum of inflammatory and infectious changes.
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The valveless intracranial venous system allows for further spread of thrombophlebitis and septic emboli.
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Complications can be orbital (Table 27-1),4 intracranial, or involving adjacent bone.
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Intracranial complications can include meningitis, epidural or subdural abscess or empyema, and intracerebral abscess or venous sinus thrombophlebitis.
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Culprit bacteria in children include the usual acute rhinosinusitis bacteria (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis); however, suppurative complications are also associated with other Streptococcus species, Staphylococcus aureus, anaerobes (such as Bacteroides and Fusobacterium species), and polymicrobial infections.9
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Local bony complications include mucocele, pyocele, or mucopyocele, as well as osteomyelitis.
I | Preseptal cellulitis |
II | Subperiosteal abscess |
III | Orbital cellulitis |
IV | Orbital abscess |
V | Cavernous sinus thrombosis |
Risk Factors
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Children with immune deficiencies, cystic fibrosis, and ciliary dyskinesias are more likely to develop acute bacterial rhinosinusitis.5,6
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Orbital complications are associated with ethmoiditis in 86 percent of cases.1
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Intracranial complications are more likely in children with frontal sinusitis, adolescent age, and male gender.3,7
Diagnosis
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Every patient with a possible complication of sinusitis should have an examination with anterior rhinoscopy or nasal endoscopy to evaluate for polyps or purulent drainage in the middle meatus.
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Endoscopy can also assist in identifying local complications and anatomic abnormalities such as mucopyocele.
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The eye must be assessed for visual acuity, extraocular movements, and proptosis. Upper and lower lid edema and erythema are common, and conjunctiva should be assessed for chemosis. Fluctuance of lids consistent with abscess is rare (Figure 27-2A, B).
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The orbital septum is a fascial continuation of the periosteum extending into the upper and lower eyelids, and is a physiologic barrier to the orbit. When post-septal involvement is suspected an ophthalmologic consultation should be obtained immediately to help with surgical planning.
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Generalized symptoms indicative of increased intracranial pressure include frontal or retro-orbital headache, nausea and vomiting, altered mental status, nuchal rigidity, abducent nerve palsy, and papilledema.
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Late intracranial findings include seizures, hemiparesis, and focal neurologic findings.8
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Specific complications of sinusitis and their common clinical findings are summarized in Table 27-2.
Complication | Clinical Findings |
Preseptal cellulitis | Eyelid edema, erythema, and tenderness (Figure 27-3). No deficits in extraocular movement or visual acuity. |
Subperiosteal abscess | Eyelid edema, erythema, and tenderness, and possibly proptosis and impaired extraocular muscle movement. Can have downward and laterally displaced globe (Figures 27-4 and Figure 27-5). |
Orbital cellulitis | Eyelid edema and erythema, proptosis, chemosis, limited or no impairment of extraocular movements or vision. Normal visual acuity. |
Orbital abscess | Significant exophthalmos, chemosis, ophthalmoplegia, and visual impairment (Figures 27-6). |
Cavernous sinus thrombosis | Bilateral orbital pain, chemosis, proptosis, ophthalmoplegia, cranial neuropathies (IV, V1, V2, and VI), picket-fence fevers, meningismus, lethargy. |
Meningitis | Headache, neck stiffness, and high fever, vomiting. |
Epidural abscess | Headache, fever, and local pain and tenderness. Unenhanced CT reveals a hypodense or isodense crescent-shaped area adjacent to the inner table of the skull. |
Subdural abscess | Headache, fever, meningismus, focal neurologic deficits, and lethargy with rapid deterioration. MRI demonstrates a low signal on T1 images and high signal on T2 images with peripheral contrast enhancement (Figures 27-1). |
Intracerebral abscess | Fever, headache, vomiting, lethargy, seizures and focal neurologic deficits. Frontal deficits can include changes in mood and behavior. Lumbar puncture can be life threatening. MRI demonstrates a cystic lesion with a distinct hypointense strongly enhancing capsule on T2 images. |
Venous sinus thrombosis | Extremely ill with meningeal signs or other serious neurologic symptoms. Picket fence fevers. MRI may reveal focal defects of enhancement. MR angiogram and venogram can further delineate. |
Pott’s puffy tumor or frontal bone osteomyelitis | “Puffy” fluctuant forehead swelling, frontal pain, fever (Figures 27-7). |
Mucocele, pyocele, mucopyocele | Proptosis and impaired extraocular muscle movement (Figure 27-8). |

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