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Neuroradiology Case of the Week

Case 9

Matthew Cham, MD, and P-L Westesson, MD, PhD, DDS

Clinical Presentation: A 72-year-old diabetic male presented with left eye pain, headache, and chills. CT of the face and orbits was requested to evaluate for retro-orbital involvement.

Radiological Findings: Axial computed tomographic sections of the orbits demonstrate soft tissue thickening and inflammatory changes within the left periorbital region (Figs. 1-8). There is no evidence of retro-orbital extension.
   
There are small pockets of air (-1000 hounsfield units) in the venous structures (Figs. 1-8), including the right facial vein (green arrows), left superior ophthalmic vein (red arrows), and left cavernous sinus (blue arrows). There is asymmetric enlargement of the left superior ophthalmic vein.

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Figure 8

Diagnosis: Ophthalmic herpes zoster infection with periorbital cellulitis and orbital emphysema.

Discussion: Orbital infections account for about 60% of primary orbital disease processes [1].
   The infection may be acute, subacute, or chronic. The majority of acute inflammatory disorders are of paranasal sinus origin. However, the infection may develop from infectious processes of the face or pharynx, trauma, foreign bodies, or septicemia. The majority of orbital infections are estimated to occur secondary to sinusitis and occasionally due to orbital foreign bodies. The bacteria most commonly involved are staphylococcus, streptococcus, pneumococcus, pseudomonas, neisseriaceae, hemophilus, and mycobacterium [2,3].
   Our patient’s history places him at greater risk for several other infectious etiologies. Herpes simplex and herpes zoster are the major virus infections of the orbit. In the immune-suppressed patient and poorly-controlled diabetic patient, opportunistic infections such as fungal and parasitic pathogens may be responsible for severe sinonasal orbital infections.
   Acute inflammation is characterized by rapid onset associated with soft tissue swelling and infiltration, loss of the normal soft tissue, planes, local soft tissue destruction, and abscess formation. The location of the process is clinically important because a preseptal infection rarely affects orbital function. On the other hand, a restroseptal infection may have a profound and sudden effect on optic nerve and orbital motility function. Pathologically, in acute bacterial inflammation, polymorphonuclear leukocytes are usually the dominant cells, which along with their pharmacologic intermediates, lead to necrosis and rapid involvement and destruction of tissue planes.
   Sinusitis is the most common cause of orbital cellulitis. Even though antibiotics have reduced the incidence of complicated sinusitis with orbital involvement, it still occurs and may be the first sign of sinus infection in children [3,4].
   Pathophysiologically, infection originating within the sinuses can spread readily into the orbit via the thin and often dehiscent bony orbital walls and their many foramina or by means of the interconnecting valveless venous system of the face, sinuses, and orbit [1].
   The classification of orbital cellulitis includes five categories or stages of orbital involvement: 1) Inflammatory edema; 2) subperiosteal phlegmon; 3) orbital cellulitis; 4) orbital abscess; 5) ophthalmic vein and cavernous sinus thrombosis [1,3,4].
   Because ophthalmic venous gas and asymmetric ophthalmic vein dilatation were present in this patient, ophthalmic vein and cavernous sinus thromboses were of particular concern [5,6]. Follow-up CT and MRI of the orbits within 24 hours revealed interval resolution of the gas pockets in all venous structures. The dilatation of the left ophthalmic vein had also resolved. There was no evidence of ophthalmic vein or cavernous sinus thrombosis on MRI. Another differential consideration for orbital emphysema in this patient include air embolism from a peripheral venous injection, although this has not been previously reported in the literature.
   Our patient was treated with oxacillin eye drops, acyclovir, and clindamycin for 10 days, with subsequent symptomatic improvement.

References:

  1. Rootman J, ed. Diseases of the orbit. Philadelphia, Pa: JB Lippincott, 1988.
  2. Momose KJ, Infection of the orbit. In: Gonzalez CA, Becker MH, Flanagan JC, eds. Diagnostic imaging in ophthalmology. New York, NY: Springer-Verlag, 1985; 281-302.
  3. Hawkins DD, Clark RW. Orbital involvement in acute sinusitis. Clin Pediatr 1977; 16(5):464-471.
  4. Mafee MF, Dobben GD, Valvassori GE. Computed tomography assessment of paraorbital pathology. In: Gonzalez CA, Becker MH, Flanagan JC, eds. Diagnostic imaging in ophthalmology. New York, NY: Springer-Verlag, 1985; 281-302.
  5. Curnes JT, Creasy JL, Whaley RL, et al. Air in the cavernous sinus: A new sign of septic cavernous sinus thrombosis. AJNR: American Journal of Neuroradiology 1987; 8(1):176-7.
  6. Ahmadi J, Keane JR, Secal HD, et al. CT observations pertinent to septic cavernous thrombosis. AJNR: American Journal of Neuroradiology 1985; 6:755-758.