Persistent stapedial artery and chronic otitis media DIEGO ZANETTI, MD, CESARE PIAZZA, MD, and ANTONINO R. ANTONELLI, MD, Brescia, Italy
A 55-year-old woman was referred for bilateral chronic otitis media with hearing loss and purulent otorrhea, associated with a persistent pulsatile tinnitus in the right ear that had been present from birth. The last symptom had been previously attributed to the middle ear disease. Her medical and family history were otherwise unremarkable. A pure-tone audiogram showed moderate bilateral conductive hearing loss in the lowfrequency range. Otoscopic examination showed a large pulsatile vessel through a right subtotal tympanic membrane perforation. Its course and relationships with adjacent anatomic structures were suggestive of a persistent stapedial artery (PSA). A high-resolution CT scan of the temporal bones was therefore performed to rule out middle or inner ear malformations, often associated with this finding.1 Radiologic examination was negative in this respect and indirectly confirmed the presence of a PSA by enlargement of the tympanic portion of the right facial canal close to the geniculate ganglion. Absence of the foramen spinosum on the right indicated a lack of normal middle meningeal artery branching from the internal maxillary, consistent with a diagnosis of PSA.2 No cholesteatoma was detected, and there was no clinical indication for an angiography. Micro-otoscopy allowed visualization of the complete course of the vessel toward the intracranial compartment. An underlay myringoplasty with autologous tragal perichondrium was performed with the patient under general anesthesia. During surgery the vessel was found to be 2 mm in diameter, coursing from the floor of the hypotympanum across the promontory and between the stapedial crura (Fig 1). The artery entered the facial canal just behind the cochleariform process. No stapedial ankylosis or ossicular malformations were seen. Any surgical maneuver on the aberrant artery was avoided to minimize the risks of profuse bleeding and neurologic sequelae.1 The postoperative course was uneventful, and at 1-year follow-up the right neotympanum was intact and no recurrence of the inflammatory process was detected. The patient reported no subjective change of the tinThis section is made possible through an educational grant from AstraZeneca, LP, makers of Rhinocort Aqua. From the Department of Otolaryngology, University of Brescia. Presented at the 86th National Congress of “Societ Italiana di Otorinolaringologia e Chirurgia Cervico-Cefalica,” Venice, Italy, May 26-29, 1999. Reprint requests: Diego Zanetti, Spedali Civili di Brescia, Piazzale Spedali Civili 1, 25123 Brescia, Italy. Otolaryngol Head Neck Surg 2000;123:663-4. Copyright © 2000 by the American Academy of Otolaryngology– Head and Neck Surgery Foundation, Inc. 0194-5998/2000/$12.00 + 0 23/11/109931 doi:10.1067/mhn.2000.109931
nitus. A myringoplasty was then performed in the opposite ear, where no anatomic abnormalities were observed. DISCUSSION The prevalence of PSA is low and reported to range between 0.14% and 0.48%.3 Embryologically, it arises from the hyoid artery, a branch of the internal carotid artery at about the fifth intrauterine week. Its intratympanic course, as observed in our patient, begins from the anterior part of the hypotympanum, then crosses the promontory laterally to the round window niche, and bridges over the footplate, between the crura. Entering into a dehiscence along the horizontal portion of the fallopian canal, the PSA can considerably enlarge the transverse dimension of the canal. The vessel leaves the facial nerve 2 mm behind the geniculate ganglion and courses superiorly. It branches intracranially through a special foramen in the anterior aspect of the petrous bone, replacing the middle meningeal artery. Diagnosis of PSA is usually accidental, and there are frequently no peculiar symptoms or signs that would suggest its presence before otoscopic examination or middle ear surgical procedures. A pulsatile tinnitus, synchronous with the heartbeat, is not always associated with a PSA, and even in its presence other causes must be ruled out. A true PSA tinnitus would be explained only by an artery large enough to transmit the mechanical energy of its bloodstream to the footplate of the stapes, thus resulting in auditory perception. In rare cases this problem is the most important symptom, however, and it does not justify, in our opinion, any attempt to intentionally interrupt the artery. Although several reports of accidental or intentional discontinuation of a PSA without postoperative complications
Fig 1. Intraoperative micro-otoscopic view of the right middle ear. Asterisk, Large PSA coursing through the stapes arch (open arrow); arrowhead, malleus handle; TMF, tympanomeatal flap. 663
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have been described,1 permanent hemiplegia, tabes dorsalis–like symptoms, and hearing loss are a significant risk for a congenital, usually well-tolerated, pulsatile tinnitus. The occasional discovery of a PSA does not represent an absolute contraindication to middle ear surgery.1 In our patient the PSA did not interfere with the correct performance of an underlay myringoplasty. High-resolution CT scan and angiography are useful tools to evaluate the role of this vessel and its possible relationships with intracranial vascularization. One case has been reported of a PSA supplying a glomus tympanicum tumor.4 Rare angiographic findings described in association to this abnormality always involve the internal carotid artery, which can be absent,4 bulging into the middle ear,2 dilated by an intratympanic aneurysm, and fenestrated or duplicated.5 Moreover, associated congenital middle or inner ear malformations fre-
quently occur with a PSA and can be radiologically detected and a proper single-step procedure planned. REFERENCES 1. Govaerts PJ, Cremers CWRJ, Marquet TF, et al. Persistent stapedial artery: does it prevent successful surgery? Ann Otol Rhinol Laryngol 1993;102:724-8. 2. Guinto FC Jr, Garrabrant EC, Radcliffe WB. Radiology of the persistent stapedial artery. Radiology 1972;105:365-9. 3. Mutlu C, da Costa SS, Paparella MM, et al. Clinical-histopathological correlations of pitfalls in middle ear surgery. Eur Arch Otorhinolaryngol 1998;225:189-94. 4. Boscia R, Knox RD, Adkins WY, et al. Persistent stapedial artery supplying a glomus tympanicum tumor. Arch Otolaryngol Head Neck Surg 1990;116:852-4. 5. Koenigsberg RA, Zito JL, Patel M, et al. Fenestration of the internal carotid artery: a rare mass of the hypotympanum associated with persistence of the stapedial artery. AJNR Am J Neuroradiol 1995;16(4 Suppl):908-10.