What are the possible complications of allergic fungal sinusitis (AFS) surgery?

Updated: Apr 13, 2020
  • Author: John E McClay, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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In most patients, surgery is performed without incident, but the pathologic behavior of allergic fungal sinusitis (AFS) theoretically increases surgical risk. Nasal polyposis, expansile accumulations of allergic mucin, and poor intraoperative hemostasis may increase spatial disorientation. Additionally, areas of bony dehiscence may confuse or distort anatomic boundaries while offering little protection to the orbit and intracranial cavities. Conversely, a less than complete surgical procedure (in an attempt to decrease iatrogenic injury) is likely to lead to incomplete retrieval of allergic fungal mucin and rapid recurrence of allergic fungal sinusitis (AFS).

On the basis of currently accepted pathophysiology of allergic fungal sinusitis (AFS), little risk of fungal invasion into adjacent tissues should exist in an immunocompetent host. However, rare exceptions may occur. Tsimikas et al report a single case of an Aspergillus frontal lobe abscess that occurred following surgical treatment of allergic fungal sinusitis (AFS) that had expanded into the anterior cranial fossa. [29, 30] This case may represent seeding of the intracranial cavity as a result of inadvertent dural penetration, and it emphasizes the importance of mucosal preservation.

In addition to fungal or bacterial seeding, penetration of the dura or periorbita iatrogenically during surgery may result in injury of structures within the orbit or intracranial cavities. Such transgressions can cause diplopia, blindness, hemorrhage, stroke, intracranial hemorrhage, encephalocele, and/or cerebrospinal fluid (CSF) rhinorrhea (see the Medscape article Pediatric Sinusitis Surgery).

Erosion by allergic fungal sinusitis (AFS) of the osseous boundaries separating the intracranial fossa from the sinonasal cavities may increase the risk of subsequent encephalocele formation. The otologic community commonly accepts that dural exposure in the absence of dural injury along the tegmen mastoideum rarely results in development of an encephalocele. Unfortunately, no analogous information within the rhinologic literature exists. However, it is logical to assume that eventual encephalocele formation may occur as a result of a combination of factors, including dural injury, location of bony dehiscence, and/or size of the bony dehiscence. In rare cases, accumulations of allergic fungal mucin actually may appear to support intracranial structures. Monitoring for development of encephaloceles is important, because their occurrence may require subsequent repair of bony dehiscence.

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