The surgical challenge of carotid artery and Fallopian canal dehiscence inchronic ear disease:

a pitfall for endoscopic approach

Pauna, H.F., Monsanto, R.C., Schachern, P.A., Costa, S.S.,§ Kwon, G., Paparella, M.M. & Cureoglu, S.

Objective: Endoscopic procedures are becoming common in middle ear surgery. Inflammation due to chronic ear disease can cause bony erosion of the carotid artery and Fallopian canals, making them more vulnerable during surgery. The objective of this study was to determine whether or not chronic ear disease increases dehiscence of the carotid artery and Fallopian canals.

Design: Comparative human temporal bone study.

Setting: Otopathology laboratory.

Participants: We selected 78 temporal bones from 55 deceased donors with chronic otitis media or cholesteatoma and then compared those two groups with a control group of 27 temporal bones from 19 deceased donors with no middle ear disease.

Main outcome measures: We analysed the middle ear, carotid artery canal and Fallopian canal, looking for signs of dehiscence of its bony coverage, using light microscopy.

Results: We found an increased incidence in dehiscence of the carotid artery and Fallopian canals in temporal bones with chronic middle ear disease. The size of the carotid artery canal dehiscence was larger in the middle ear-diseased groups, and its bony coverage, when present, was also thinner compared to the control group. Dehiscence of the carotid artery canal was more frequently located closer to the promontory. The incidence of Fallopian canal dehiscence was significantly higher in temporal bones from donors older than 18 years with chronic middle ear disease.

Conclusion: The increased incidence of the carotid artery and Fallopian canal dehiscence in temporal bones with chronic middle ear disease elevates the risk of adverse events during middle ear surgery.

Introduction

The internal carotid artery (ICA) is one of the largest blood vessels neighbouring the middle ear cavity. As it climbs through the petrous bone, it passes the middle ear cavity and cochlea anteriorly and then bends to run medially to the Eustachian tube1,2 (Fig. 1). Previous studies have reported dehiscence of the carotid artery canal in 4.9%–35.2% of human temporal bones with no middle ear disease. In patients with dehiscence of the carotid artery canal, middle ear procedures such as tympanostomies can cause devastating complications, including massive haemorrhage.

The facial nerve (FN) is important for both communication and expression, and impairment of its function may affect the quality of life. After entering the internal acoustic canal, the FN goes into the Fallopian canal, passing through the labyrinthine, tympanic and mastoid segments towards the stylomastoid foramen. The prevalence of dehiscence in the Fallopian canal is reported to range from 25% to 57%. Baxter et al., during operative observations, found that 91% of the tympanic segment of the FN was dehiscent. Thus, procedures performed in the middle ear cleft could potentially traumatise the FN at this site of dehiscence.

Endoscopic approaches to the middle ear have become popular. But serious complications can occur, given the close proximity of the ICA to the tympanic membrane. In mastoid surgery, variations in vascular structures related to the temporal bone can lead to severe complications during middle ear or skull base surgery, including trauma to the ICA, the jugular bulb or the sigmoid sinus. Therefore, to avoid damage to those structures, preoperative measurements of surgical landmarks are important. Dehiscence of the carotid artery and Fallopian canals increases the risk of complications during otologic surgery via the transcanal, posterior or endoscopic approach.

Chronic ear disease is usually associated with persistent inflammatory response. Many patients have viral or bacterial infections that lead to the production of several cytokines, such as tumour necrosis factor-alpha (TNF-a), interleukin (IL)-1b, IL-6 and IL-8, all known to have nonspecific and proinflammatory activity as well as the potential to damage the bony structures of the middle ear.

No studies, to the best of our knowledge, have described the incidence and location of ICA and Fallopian canal dehiscence in patients with chronic middle ear disease. In this study, we investigated the dehiscence of the carotid artery and Fallopian canals in temporal bones with chronic middle ear disease compared to non-diseased control group.

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