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Aneurysms of the Temporal Bone

Martin Papazian, MD"

Michae l Paparella, MD"

Edward Hames, MD, PhDb Minneapolis, Minnesota J ames Frisk, MD

Fargo, North Dakota

Abstract

Aneurysms ofthe internal carotid artery in the temporal bone are rare lesions which can present clinically as a growth in the middle ear cleft . Hemorrhage, occurring spontaneously or iatro genically, is a primary concern. This study describes morphological and embryological charac- teristics of the internal carotid artery in relationship to the protympanum and temporal bone. Concepts ofpath ogenesis and pathology are discussed, with referen ce to the neurosurgical andotolaryn gologic literature. Clinical char- acteristics, including methods of surgical repair, are pre- sented using thre e illustrative case reports. Methods of surgical repairinclude: 1)reinforcement;2) ligation; and3) primary excision andreanastotnosis.

Introduction

Aneurysms ofthe intrapetrous carotid artery are rare; more common are ane urysmal dilatations of the intracra nial and cervical caro tid artery. It is, however, vitally important to the otolaryngologist to know the clinical manifestations of this lesion in the more unusual location in the temporal bone because inadvertent manipulation or biopsy can result in massive and sometimes fatal hemorrhage. These lesions commonly present as growths in the middle ear cleft and are most often confused with glomus tumors. The purpo se of this paper is to familiarize the otolaryngologist with the emb ry- ology, morphology, pathogenesis, clinical presentation,and treatment modalities ofaneurysms of the intrapetrous carotid artery . The pertinent literature is reviewed and three illustra-

' Minnesota Ear Clin ic, P.A., Minneapolis, MN . Department of Otolaryn- gology--Head and Neck Surgery, Otopathology Laboratory, Univer- sity of Minne sota, Minne apolis.

"Neurcsurgical Associates, Ltd., Minneapolis, MN.

Supported in part by NIH NIDCD grant #POI-DCOO I33 and the Interna- tional Hearing Found ation.

Presented at the meetin g of the Southern Section of The American Laryngolog ical, Rhino logical and Otological Society, Inc. January 16, 1993 at Boca Raton, Florida.

474

tive cases are presented. Forty -nine previous case reports were found, 35 of which invol ved congenital aneurysms and 37 of which had undergone some type of surgical interven- tion.':"

Embryology

In the fourth to fifth week of gestation, each developing branchial arch recei ves its own artery , embedded in the mesench yme and arising ventrally from the aortic sac (Figure 1). With each new arch com es a new artery, until a total of six pairs have been formed." Not all six are present simul - taneou sly. The artery of the first arch undergoes involution (and its remnant becomes maxillary artery) when the embryo is at 4 mm, about the time the fourth arch is developed. The arter y of the second (stapedial) arch will soon disappear, before the artery of the sixth (pulmonary) arch is fully developed (when the embryo is about 10 mm). Th is phase of

"branchial archarteries"ends when the embryo is developed to about 13mm."

The segment of the dorsal aorta between the third and fourth arch on each side then disappears, and so does the

3rd Arch IF ..t.,o ~W. _ Ct. _''' "V ''I)

6lh Ax'l -~--\---;,.L ff

c,...p""""""''''...,,4o''\',

Figu re 1. Schematic drawing demonstrating origin of branchial arch arteries.

ENT Journal " July 1993

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ANEURYSMS OFTHE TEMPORAL BONE

segment between the left dor sal aorta and the light fourth arch. The aortic sac and the artery of the left fourth arch become the definitive aOIta.47The ventral junctions between the third and fourth arches become the common carotid arteries. The distal portions of each third arch become the internal carotids." The external carotid arteries begin as midline ventral pharyngeal arteries from the aortic sac, then migrate laterally." This structure continues to develop into what is recognized as theexternal carotid artery with all ofits cervical branches. The developing internal carotid and stapedial arteries become the anlage of several otic and orbital vessels.

Comprehension of the formation of the stapedial artery is critical to the understanding of abnormalities in the petrous carotid artery . The vascul ature in this region evolves as a late stage in the development ofthe firsttwo aortic arches." In the embryo at 14 mm , the distalportionofthe ventral pharyngeal artery ends at the root of the mandibular nerve and is no longer attached to the proximal remnant (the external carotid artery). The hyoid artery , no longer in the hyoid bar, is now cranial to the first pharyngeal cleft. The stapedial artery develops from this hyoid root and is annexed with the distal pharyngeal artery ." A cranial stem of this complex forms the supraorbital division, while the junction with the ventral pharyngeal artery forms the maxillomandibular division.

The supraorbital division eventually becomes the supraor- bital, frontal, anterior ethmoid and lacrimal arteries. From the internal maxillary artery, the maxillo-mandibular divi- sion forms precursors of the inferior alveolar, infraorbital, and middle meningeal arteries." By the time the embryo is at 20 mm, the stapedial artery begins to degenerate at the level of the stapes. The caudal (hyoid) portion becomes the caroticotympanic artery . The caroticotympanic and stape- dial arteries do not usually persist into adult life.

Anatomy

In order to understand the development of aneurysms of the petrous carotid artery,one must also have a fundamental know ledge of its anatomy. The internal carotid artery passes through its cervical course without branching. At the skull base, the artery enters into a periosteally lined canal anteromedial to the jugular foramen . The canal can be divided up into vertical, genu, and horizontal portions. The vertical segment is approximately 9 mm long, and is located anterior to the jugular fossa, anteromedial to the tympanic cavity, and posterior to the Eustachian tube.? In this portion, the carotid artery is approximately 1.5 mm from the co- chlea."

As the genu is approached, the canal lies inferomedial to the tensor tympani and directly medial to the thin bone of the Eustachian tube. The horizontal portion, which begins at the genu, is approximately 20.5 mm long ." The carotid artery

traverses the temporal bone anteroinferior and medial to the cochleariform process, medial to the Eustachian tube , ante- rior to the cochlea, and inferolateral to the Gasserian gan- glion , to emerge near the petrous apex. At the level of the tensor tympani, it lies approximately 2.8 mm from the basal tum of the cochlea." The artery then begins another S- shaped series of bends within the cavemous sinus, while heading toward the anterior clinoid process, where it perfo- rates the dura mater." The petrous canal at some points becomes quite thin, often less than 0.5 mm , most notably in areas adjacent to the Eustachian tube , Gasserian ganglion, and tympanic cavity. " In fact , dehiscence at this latter site occurs in 1-2% of the general population.v -"

The horizontal intrapetrous carotid artery gives lise to one or two branches, the caroticotympanic and Vidian arteries, in about 38% of cases. " The caroticotympanic artery exits through its own foramen to anastomose with the anterior tympanicartery. The Vidian artery exits into the foramen lacerum to travel eventually in the Vidian canal. Other smaller periosteal branches have also been identified.

Also, the petrous carotid artely is surrounded by a sympa- thetic nerve plexus that branches near the genu: a posterior branch accompanying the cerebral arteries, and an anterior, deep petrosal branch joining the Vidian nerve. A venous plexus surrounds the distal artery in 76 % ofcases , sometimes extending into the vertical portion."

Radiographically, the carotid artery passes upward in the petrous canal, makes a 90° bend at the genu, and angles forward 35-40°. If dehiscence is present near the tympanic cavity, a buckling of the artery is noted, lateral to a vertical line extending down from the vestibule." Normal arteries lie a mean distance of 5.35 mm medial to this line.

Etiology/Pathogenesis Intracranial

Due to the infrequent occurrence of aneurysms of the petrous carotid artery, concepts ofetiology and pathogenesis are best extrapolated from our knowledge of intracranial aneurysms. Intracranial (saccular) aneurysms are often referred to as"berry' aneurysms and are frequently thought of as congenital lesions. This may be because over 99%

occur at forks in the vasculature, in presumed areas of thinning of the vessel walls.59 .In fact, intracranial aneurysms may have numerous causes.

Hemodynamics appear to play an important role in forma- tion of these aneurysms. Hypertension has often been considered a significant etiologic factor in the formation of cerebral aneurysmsr?" some studies, however, question whether the relationship is cause-and-effect.S'" Even in the normotensive individual, hemodynamic factors, over time, are thought to damage the intemal elastic lamina of cerebral

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PAPAZIAN , PAPARELLA, HAMES, FRISK

arteries, leading to formation of aneurysms." Aging plays a significant role due to progressive arterial stiffening and thinning related to the repeated transmission of systolic forces." Because of the increased stiffness, these affected areas are under greater stress at any given pressure and may eventually lead to yielding ofthe vessel wall. This process of progressive thinning and eventual dilatation is more com- mon in the intracranial vessels , possibly due to the presence ofonly one elastic lamina, with a thin media and little external structural support.66Areas of vascular branching may be at particularrisk,due to the presence of fenestrations in the elastic lamina at theselocations." Branching also increases turbulence in the flow of blood , which may raise local forces in vessel walls, making formation of aneurysms more likely at theselocations."

Once an aneurysm forms, further disturbances in flow occur which may perpetuategrowth." Also , the increased stiffness and size of an aneurysm compared to the native vessel increases the relative local forces, further fatiguing the wall of the aneurysm." Progressive dilatation and eventual rupture may occur over time if this process is allowed to continue. At the same time, however, as an aneurysm increases in size, so does the likelihood of partial and sometimes even total thrombosis. Thrombosis occurs in about 1-15% of cases and is enhanced by processes that reduce flow such asvasospasm."

Several other factors have been associated with formation of cerebral aneurysms.f '' " Although frequently implicated, a congenital predisposition to the formation of aneurysms probably only occurs in association with aortic coarctation and polycystic kidney disease. Other disease states such as fibromuscular dysplasia, Ehlers-Danlos syndrome, Marfan' s syndrome, pseudoxanthoma elasticum, and Moyamoya dis- ease carry an increased risk of formation of intracerebral aneurysms. Changes in connective tissue and/or abnormali- ties in blood pressure are thought to be the basis of dilatation of the cerebral artery in several of these processes.

Inflammatory intracranial aneurysms may also occur, often caused bystreptococcus orstaphylococcus species.

Septic emboli are thought to enter distal branches of the cerebral vasculature and invade the adventitia through nor- mally occluded penetratingvessels." The resultant weak- ened wall dilates, due to the applied hemodynamic forces.

Underlying disease such as bactetial endocarditis is the source of emboli.

Intratemporal

Aneurysms of the intrapetrous carotid artery can be either

"true," where all layers are involved, or "false" (pseudo- aneurysm), where the dilated region demonstrates no archi- tecture charactetistics of a vessel wall. A variety of causes have been implicated, including bactetial or fungal infection, 476

syphilis, atherosclerosis, neoplasia, cystic medial necrosis , fibromuscular hyperplasia and post-traumatic or idiopathic causes.v-" Of the 49 cases reviewed, four were considered pseudoaneurysms, five post-traumatic, five infectious, and 35 congenital and idiopathic. Pseudo-aneurysms are usually a result of trauma, either from closed-head injury or surgery.

Inadvertent laceration of the outer vessel wall of an aberrant artery can result in pseudo-aneurysmal dilatation if the diagnosis is not suspected. Infectious aneurysms are thought to arise from bacterial or fungal invasion of the arterial wall, with secondary thrombosis. The toxins from the inflamma- tory process thin the wall, leading todilatation." Chronic otitis is a common etiology (and caused three of the five infectious cases reviewed). Syphilis and Varicella-Zoster infection were also causative agents.

Idiopathic or congenital aneurysms are believed to arise at the point of obliteration of an embryonic artery. An area of weakness in the media layer of the petrous carotid artery is thought to occur where the hyoid and caroticotympanic arteriesinvoluted."This corresponds to the anterior-inferior location of aneurysms found in the middle ear.

The symptomatology associated with aneurysms of the petrous carotid artery are a result of its restricted location.

Hearing loss is often related to inhibited ossicular transmis- sion ofsound. Deficits of the cranial nerves, most commonly V and VII,are likely related to direct pressure on these nerves . When they are large, petrous aneurysms may erode adjacent structures, causing multiple deficits.16,34In one report, 84%

of bones studied had a dehiscence somewhere between the carotid artery and the trigeminal nerve." As stated previ- ously, dehiscence may also occur into the middle ear, weak- ening structure support.

Enlargement may occur related to weakness of the vessel wall caused by the same hemodynamic forces described for intracranial aneurysms. Hemorrhage may result not only from progressive enlargement and rupture, but also from exposure to the frequent movement of an ossicular chain, exposure to chronic otitis with granulation, or to inadvertent biopsy or laceration. In a sense, aneurysms of the petrous carotid may be at greater risk for rupture than are cerebral aneurysms because of the unique anatomic position and exposure to the environment in the former.

Pathology Intracranial

The normal intracranial artery is composed of a single endothelial layer, an internal elastic lamina, a musculatis layer, and an adventitia. In arterial tissue adjacent to an aneurysm,there is intimal thickening with reflection of the internal elasticlamina." The aneurysmal sac itself contains little to no media or elastic lamina, and is primarily made up ENT Journal" July1993

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ANEURYSMS OF THE TEMPORAL BONE

of an endothelial layer, fibromuscu lar and fibrohyaline tis- sue, with a surro unding adve ntitia/" The media and internal elastic lamina ofte n end abruptly at the aneurys mal neck.

Intimal calc ification associated with atherosclerotic changes may also occ ur in areas adjace nt to an aneurys m. Th e wall of the aneurys mal sac itself has a variable thickness. Inflam- matory cells may also be prese nt in the aneurys mal wall, especially in areas of rupture.59.66

The petrou s carotid artery, although intracranial, is an extradural structure that has different characteristics than its intracra nial counterpart . The average diamet er in the petrous portion is 5.6 mm, while the intradur al portion has 25-40% of that diameter.? " The artery has an intima, media , and adve ntitia, with assoc iated elastic, muscle, and collage n. The intim a is a thin endothelial layer, with a moderat e-sized med ia. The adventitia is thickerthan that found intradurally.

Calcium is co mmo nly found within all lamin a of the petrous caro tid artery, but in contrast to the intradural portion, it is not here necessarily associated with atherosclerosis. Due to the surrounding bony canal,this calcification may not be eviden t radiog raphically." Formation of aneurysms in this regio n is often associated with bony dehiscence into the middle ear. As the ane urysmal sac grows, other bony eros ion occurs. Although relatively few morphologic studies have been perform ed, petrous aneurys ms would be similar in this respect to their intracra nial counterpart. In one report asso - ciated with chronic mastoiditis, the aneurysm was assoc iated with an athero matous plaque and demonstrated almos t total destruction of the media and intima."

Diagnosis in the Temporal Bone Age, Sex

The age of patients at presentation ranged from seve n to67 yea rs (average 31.5 years). The female:male incidence was nearly I:1, For congenital aneurys ms, the average age was 33,7 years, with a slight female predominance (4:3). Trau- matic aneurys ms were reported excl usively in males, with an average age of 29.6 years.

Clinical Presentation

Aneurysms of the petro us carotid may present as a silent mass in the middle ear cleft. Such a mass may sometimes be misdiagnosed as a glomus j ugulare, glomus tympaniciu m, high j ug ular bulb, jugul ar di verticulum, otitis medi a, cholesteatoma, granulation tissue, or cholestero l granuloma, Biopsy under these assumptions could result in massive hemorrh age. Sympt om s co mmonly associated with a clini- cal presentation of petrous carotid aneurysm including head- ache, otalgia, tinnitus , and hearing loss, Without othe r, more

objective findings, however, many with aneurysms have bee n diagnosed only after bleeding occurs. Seven teen of the 49 cases we reviewed (35%), for example, had some type of cranial nerve deficit, usually related to V or VII. Ptosis was prese nt in a small numb er of cases , Otorrh agia and epistaxis were not uncomm on presenting signs, and often led to a more urge nt work- up.

Work-Up

Any red or blue mass in the middl e ear should be ap- proa ched with caution. Several of the patients whose cases are reviewed here reported hemorrhage following biop sy or diagnostic myringotomyY·23.26.29.39 Most who perform ed a biopsy felt that they were dealing with a glomus tumor. A needle aspiration done first might raise suspicions and abort an attempt at biopsy." Biopsy should be deferred unt il the surgeo n is certain that the lesion is neither an aneurys m nor anomalous caro tid artery ,

Ang iog raphy is an accurate meth od of diagno sing ane u- rysm s of the carotid. These provide a good estimation of size, loc ation, patency, collateral flo w, and the presence of oth er anom alies. Bone detail is poor in this case, and thus a co mputed tomogram (CT) migh t be helpful if surgical interven tion is contemplated, Magne tic resonance (MR) angiography (MRA) is a necessary preoperative examina- tion . Pre operatively , o culoplethysmography and electroencephalography can help determine the adequacy of contralateral flow with carotid occlusion." More re- ce ntly, xenon 133 (XeI 33) has been used to delineate flow patterns of blood within the cerebral circulation." An audiogram and tympanogram can help predict ossicular or cochlear involvement.

Treatment

Therapy of petro us carotid aneurysms should be individu- alized to the case at hand, account ing for the age, health , risk factors, and desires of each patient. Using experience from intracra nial aneurysms, the options include watchful obser- vation, intenuption of the vesse l with or without bypass, reinforcement of the wall, resection, or selective intenuption of flow into the aneurysm , Of the 49 cases reviewed, 27 utilized vasc ular intenuption, I I were observed, five were resected, five utilized reinforcement (three in combina tion with vascular intenuption), three resulted acutely in death, and one was selectively occl uded.

ObseNation - Intracranial Lesions

The long-term morbid ity from observa tion alone is best extrapolated from experience with intracranial aneurysms, Expec tant observation may be appropriate in certain settings, especially for an elderly individu al with a small aneurysm, or for someo ne in whom the lesion can be imaged on a regular

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PAPAZIA N, PAPARE LLA, HAMES, FRISK

basis. Aneurysms may expand very slowly , causing only mild symptoms, or they may even spontaneously thrombo se.

They might also expa nd rapidly, with hemorrhage, resulting in profound neurologic deficits.

Twenty-eight percent with an unruptured symptomatic intracranial aneurys m subsequently die of hemorrhage."

Unruptured asymptomatic aneurysms carry a betterprogno- sis. If they are small (less than 5 mm), then the rate of hemorrhage is about 3-4% per year. Larger lesions carry a greaterrisk,"Approxi mately 60% of untreated patients with a rupture of the intracranial carotid artery die within the first year." The yearly incidence of bleeding from a previously ruptured untreated aneurysm of the carot id artery is about 3%.76 Overall mortality can be as high as 70% with a "wait and see"approach."

Lesions in the Temporal Bone

The number of cases is too few, and the documented follow-up too short, to evaluate the relative risk of observa- tion of these lesions. Patients were observed in I I of the cases reviewed. Many presented with hearing loss, otalgia , or diploplia; none demonstrated any bleeding. A diagnosis was made at angiography. Many reported "good" outcome s; the length of follow-up, however, was rarely mentioned in reports.

Vascular Occlusion - Intracranial Lesions

Vascular interruption of the carotid artery can be traced back to Pare in 1585,78and later Hunter in 1785.89 Dandy, in 1942, stressed the importance of preoperative assessment of blood flow, and provided data on long-term morbidity after ligation." Immedi ately after carotid occlusion, cerebral profusion relies on collateral circulation. Incomplete anasto- moses may lead to rapid neurologic changes ifblood flow is not adequate. Cerebral infarction will then ensue unless imperforate collaterals begin to dilate, allowing reversal of symptoms." Even with adequate collaterals, cerebra l blood flow may not be adequate if shunts exist, distal to the site of occlusion. Once past the immediate post-ligation alterations in blood flow, forma tion of thrombosis may still occur and may cause life-threatening embolization or extension into the circle of Willis . Ligation of the carotid artery may even increase the risk for aneurysms within the circle ofWillis,"

Interruption of carotid blood flow is done in an attempt to decrease the pressure into an aneurysm, with the hope that thromb osis will be induced, and that the clot will organize, preventing rupture of the vessel. Currently these techniques are utilized for inacce ssible aneurysms or for life-threatening hemorrhage. The simplest method is ligation ofthe common or internal carotid artery in the neck. This can decrease the rebleed rate to I% peryear." Carotid ligation, however, has been associated with acute cerebral ischem ia in 20-59% of 478

cases,83.84 with an associated mortalityof about4 %.81Landolt"

reported on 65 carotid occlusions, of which 32% had acute cerebral ischemia beginning an average of 17 hours after ligation. Forty-three percent resolved, leaving an 18% long- term rate of ischemic complication.

Angiograp hic imaging of cross-circulation has been used for some time, in an effort to predict the safety of carotid occlusion. The mere presence of collaterals, however, does not predict the blood flow, which is the critical factor. Xenon 133 CT flow studies may better estimate cerebral blood flow." :" Electroencephalography at the time of occlusion may warn of impending stroke. Carotid stump pressures have also been used to estimate the degree of cross-circula- tion, where pressures of 25-50 mm Hg indicate adequate flow . However, even those with minimally decreased cere- bral blood flow on tested occlusion can have a 5% incidence of stroke and 2 1% incidence of temporaryischemia."

Occlusion using endovas cular balloons is a techniqu e alternate to ligation , for vascular interrupti on. With this method, small percutaneously placed detachable balloons are placed either proximal or proximal and distal to the aneurysm . In certain cases, the balloon may be placed in the aneurysm itself, without interruption of flow in thevessel."

Although occlusion is often a highly successful techniqu e, incomplete occlusion can occur in 23% ofcases." Some difficulties with this technique include localization of the balloon, inflation without aneurysmal rupture, and deflation and migratio n of theballoon."

Attempts to decrease the morbidity of vascular occlusion have centered on methods to preserve distal blood flow. The simplest method involves slow occlusion of the vessel to allow opening of collaterals; hence the development of the silverstone clamp. The Cooperative Study of 765 patients, however, offered "no meaningful statistical evidence that grad ual carotid occlusion carries a lower ischemic comp lica- tion rate than abruptocclusion.?" Extracranial-intracranial (EC-IC) bypass offers a way to reestablish flow distal to the site of occlusion. Usually the superficial temp oral or parietal artery is anastomosed to the middle cerebral artery, after which the carotid isoccluded." Long-term patency occurs in a high percentage of grafts ;79 retrograde flow, however, may lead to rupture unless the aneurysm istrapped."

Currently, clipping is the treatment of choice for electively treated intracranial saccular aneurysms." Th rough a craniotomy approach, the aneurysm isdirectly accessed. The size and configuration of the aneurysm determine the type of clip utilized. Surgical results are excellent with this tech- nique, and morbidity islow."

In a related technique, an aneurysm may be balloon- occluded, after which chemically induced thrombosis of the aneurysm is performed through an intracranial approach."

M ore recent inve sti gator s ha ve induced an eurys ma l ENT Journal · July1993

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ANEURYSMS OF THE TEMPORAL BONE

thrombosis endovascularly, utilizing positively charged plati- num coils placed within the aneurysmallumen.v?' Lesions in the Temporal Bone

Small numbers and short follow-up (less than 12 months) do not allow a conclusion on the efficacy of treatment using this modality. Of the 27 cases reviewed, ten utilized ligation of the common carotid and 11 of the internal carotid artery ; six trapped the aneurysm. Overall, 22 demonstrated good results with no new neurologic deficits, and five had transient weakness. No post-treatment aneurysmal bleeds were re- ported. Results from ligation of the common carotid and of the internal carotid arteries were similar (10 % had transient weakness), while one-halfofthe group with "trapping" ofthe aneurysm had transient deficits. The one case of selective occlusion of an aneurysmal neck reported good results.

Resection - Intracranial Lesions

Resection is rarely necessary, and often is not feasible for intracranial saccular aneurysms. Large broad-based aneu- rysms are occasionally excised at the neck and reconstructed with a series ofmalleable clips orsutures.'?Plastic adhesives have been utilized in the past to repair cerebralarterotomies;"

this has, however, largely been abandoned.

Lesions in the Temporal Bone

A skull-base approach was used to resect five aneurysms of the petrous carotid artery. All demonstrated profuse bleeding preoperatively, often requiring packing of the ear.

In two , the lesion was excised with transection of the carotid artery.v" One of these was thought preoperatively to be a glomus jugulare tumor. Another two involved aneurysmal resection, but the postoperative status of carotid arterial flow was not mentioned.F-"

In an unusual case from Glasscock,"an aneurysm of the petrous carotid artery was resected with carotidreanastomosis.

This patient had demonstrated repe ated profuse bleeding even after wrapping ofthe aneurysm. An infratemporal fossa approach was utilized, including ma stoidectomy, superficial parotidectomy, rerouting of the facial nerve, resection of the zygomatic arch, removal of ossicles, and condylectomy.

Rerouting and primary arterial anastomosis allowed the reestablishment of vessel flow. The patient demonstrated a facial palsy, Homer's syndrome, and ipsilateral anacousis, postoperatively.

Reinforcement - Intracranial Lesions

The reinforcement of carotid aneurysms with fascia or muscle offers another method to decrease the chances of bleeding. Dott" was the first to describe wrapping cerebral aneurysms with muscle. There have since been numerous adhesives and plastics used to reinforceaneurysms." These

polymers are sometimes supported by materials such as oxicellulose." A report of 58 cases utilizing muscle or muslin gauze demonstrated no rebleeding in 81% of pa- tients." Six percent had a fatal rebleed, often within the first few weeks ofthe surgery. Others have demonstrated that this method can decrease the rate oflate rebleeding to 1.5% per year." Currently, most reserve wrapping for situations not amenable to clipping.

Lesions in the Temporal Bone

Wrapping has been used successfully in the treatment of aneurysms of the petrous carotid artery.36.39 The aneurysm may be visualized through a standard otologic approach, to delineate its dimensions and to identify other pathologic conditions. The relationship of the aneurysm to the ossicles deserves special attention where, if they are in close proxim- ity, removal of one or more of these bones might lessen the chance of future rupture. The middle ear or mastoid cavities may also need to be enlarged by performing an atticotomy, curetting the posterior tympanic ring, or performing an open- cavity procedure. Muscle or fascia may then be placed to cover and reinforce the aneurysm. Foreign materials are not used to reconstruct the hearing, as good results may be obtained with a type III tympanoplasty. The objective is that ingrowth offibrous tissue will add enough support to prevent aneurysmal rupture.

Illustrative Case Reports Case #1

Rarely, a patient may coincidentally be found to have an aneurysm of the internal carotid artery in the temporal bone.

This discovery might occur, for example, in the process of treating the patient for chronic otitis media and mastoiditis with cholesteatoma. In a small subset of patients we have coincidentally seen dehiscences occur in the region of the internal carotid artery as it anatomically relates to the protympanum. At the medial aspect ofthe protympanum and especially its inferior dimension, a dehiscence of the carotid artery might coincidentally be found during surgery on the middle ear cleft, usually for chronic ea r disease.

A sizable aneurysm was coincidentally found in an 18- year-old woman with a typical history ofchronic otitis media, chronic mastoiditis, conductive hearing loss, and occasional discomfort, but no other otological or neurological symp- toms. She had evidence of a cholesteatoma, and X-rays indicated pathological findings of a hypoplastic mastoid air- cell system. There was a lesion of the pars flaccida in the posterior superior quadrant, suggestive of a cholesteatoma.

Having failed medical therapy, she underwent post-auricular tympanomastoidectomy. Cholesteatoma was identified in the mesotympanum, and adjacent antrum, along with granu-

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PAPAZIAN, PAPARELLA, HAMES , FRISK

lation tissue and pathological findings in the middle ear cleft.

While removing this cholesteatoma it become clear that there was a bilobed aneurysm protruding from the region of the protympanum, as described above. This was identified and carefully avoided. An open-cavity tyrnpano- mastoidectomy procedure wasaccomplished. The pathologic tissue around the lesion was thoroughly removed, and no attempt at ossicular reconstruction was made. A double fascial graft, previously pressed and dried in the fascial press, was used to protect and reinforce the aneurysm, and it was followed by a split-thickness skin graft for additional protec- tion. With four-year follow-up, this patient has done well, has a dry ear, and has not had any untoward sequelae such as neurological or otological complications or difficulty.

This patient demon strates how, in rare cases, it is possible for an aneurysm to be identified coincidentally during the process of the treatment of chronic otitis media and chronic mastoiditis. It is also interesting to speculate whether the aneurysm was part of the etiologic process and pathogenesis for chronic otiti s media and chronic mastoiditis with cholesteatoma, by virtue of causing Eustachian tubal de- struction or dysfunction. It is also possible that the chronic otitis media was followed by development of this aneurysm . Our beliefis that the former possibility occurred, namely that there was an aneurysm in this region which contributed to chronic otitis media.

Case #2

This patient was a 49-year-old white man who had a small conductive loss and symptoms of pressure, occasional light- headedness, and occasional pain of a mild nature, relating to symptoms of the right ear, for a duration of II to 12 months . Otoscopy suggested a possible mass or tumor involving the middle ear cleft. Mastoid X-rays indicated a normal pneumatization ofthe mastoid air-cell system and there was a small conductive deficit with a speech reception threshold (SRT) of 25 dB. CT scan indicated a mass identified as a possible glomus lesion; it seemed, however, to occupy a mesotympanic orientation rather than a hypotympanic orien- tation.

Angiography was done, which substantiated an aneurysm protruding into the mesotympanum and protympanum at least 0.5 em. Electronystagmographic (ENG) findings were negative, and no other pathologic condition was identified from examination of the ear, head, and neck, nor systemi - cally.

This patient underwent surgical exploration whereby an aneurysm was identified fairly close to the description above . The incus and malleus were removed while preserving the stapes and the tympanic membrane. The middle ear was enlarged by removal of attic bone and posterior inferior bony annulus, to the level of the vertical facial nerve. Thus, the 480

diamet er, as well as the depth , of the middle ear space was enlarged to treat and protect the aneurysm.

Removal of ossicle s helps to avoid irritation of the aneurysm as it expands and thus avoid hemorrhage from irritation from, for example the incus. A large tympanomeatal flap was developed, and an open-cavity- intact-bridge tympanomastoidectomy was accomplished.

A double layer offascia previously pressed and dried was used to reinforce the aneurysm, and the tympanomeatal flap was placed on top of this to prov ide additional protec- tion to the aneurysm. The patient has done well to date, has a conductive loss of approximately 30 dB and has had no problems or complicat ion s for six years .

Case #3

This Caucasian woman was born in 1939 (52 years of age) and was in good health. During the past year she had developed minor symptomatology consisting of a sensation of pressure and tinnitu s and a slight hearing loss in the left ear.

She was seen by an otolaryngologist who, following X-ray studies and CT scan, explored the middle ear, thinking that this represented a glomus tumor . During the procedure it was identified that this was not a jugular bulb dehiscence, but an aneurysm of the internal carotid involving the middle ear.

Angiography was ordered; the lesion was not biopsied; and the tympanomeatal flap was replaced to its usual position .

Angiography indicated an aneurysm ofthe internal carotid artery which occupied the protympanum, asdescribed above, and also indicated an aberrant course of the left internal carotid artery that extended abnormally laterally into the petrous tempora l bone, projecting into the hypoty mpanic region where there was evidence of foca l aneurysmal out- pouc hing which measured approximately 3.5 mm (Figure 2).

There was a small focal irregularity along the superior contour of this aneurysmal out-pouching and narrowing of the cervical left internal carotid artery. There were no findings to suggest the presence of a glomu s tumor nor other abnorm alities of the vascular system relating to the carotid arterial system on this side of the head.

The angiogram resulted in a small sub-intimal collection of contra st associated with a small intimal tear. The patient was placed on Coumadin® for a period of a few months, and subsequently underwent exploration of the tympanomastoid region in which the middle ear was enlarged by extending its diameter inferiorly and posteriorl y. The ossicles were re- moved, and the tympanic membrane was carefully dissected off from a lesion which expanded literally to enlarge and fill the middle ear to approximately half its volume. The stapes wa s preserved, and an open-cavity endaural tyrnpanomastoidectomy was accomp lished. The lesion was isolated, possible irritative structures were removed, and a triple layer of fascia, previous ly processed and dried, was ENT Journal " July1993

(8)

ANEURYSMS OFTHETEMPORAL BONE

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Figure 2. Left carotid angiogram, Case 3. Note laterally displaced course through temporal bone with an aneurysm at level of the middle ear. At the time of surgery, the aneurysm filled one-half of the middle ear.

Discussion

The discovery of an aneurysm of the petrous carotid artery is a rare finding. Of 2,300 operations for aneurysms, Beall found only seven in the extracranial carotid artery."? Our review found only 49 previous reports of aneurysms in the intrapetrous carotid artery. The present series adds three cases to the world's literature.

Concepts of etiology, pathogenesis, pathology, and treat- ment were reviewed in the neurosurgical and otolaryngologic literature. Although usually protected in a hard bony shell, a petrous carotid artery can be exposed to the outside world by pathophysiologic events leading to defects in the middle ear, or can be exposed by such events to vital neural structures intracranially or at the skull base. Knowledge of the patho- genesis and resultant pathologic conditions is important, to avoid iatrogenic injury, afford early diagnosis, and allow a rational treatment plan.

Aneurysms of the petrous carotid artery are most often idiopathic and may be related to a combination of congenital weakness of the vessel wall and degenerative changes that occur with aging." Th e site of degeneration of the caroticotympanic artery at the level of the carotid siphon may leave an area that is predisposed to aneurysmal dilatation when it is subjected to systolic pressures over many years."

Congenital or acquired dehiscence of the carotid canal in this region may further weaken the vessels' structural support.

Once it is exposed to the middle ear, chronic otitis, irritation from adjacent ossicles, or iatrogenic injury can further dam- age the arterial wall and lead to rupture. In an alternative sequence, an aneurysm might erode into the middle ear cleft and obstruct the Eustachian tube, resulting in the develop- ment of chronic otitis. Aneurysmal dilatation without exten- sion into the middle ear may cause bony erosion and exten- sion into the middle cranial fossa or the region of the cavernous sinus.

The clinical presentation of petrous carotid aneurysms relates to its surrounding anatomy and associated pathologic placed upon the aneurysm. The tympanomeatal flap was placed on top of this.

The patient subsequently received a Thiersch graft to enhance healing of the raw surfaces of the tympanomastoid cavity. The patient has done well to date (approximately seven month s). She is essentially asymptomatic, and at present she has a 25 dB conducti ve hearing loss in the speech frequencies (Figure 3), similar to the loss she had prior to the procedure. The patient has been provided a card to suggest that in the future she should not have myringotomy nor other treatment ofthe middle ear, so as to avoid the possibilities of iatrogenic rupture of this area. She is also advised to seek medical consultation if she has any other otological symp- toms or difficulties.

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PAPAZIA N, PAPARELLA, HAMES, FRISK

conditions. These lesions may be asymptomatic and may be discovered by otoscopy for hearing loss or tinnitus. On the other hand, profound otorrha gia or epistaxis may herald their presentation . In Case 1, exploration for chronic otitis and masto iditis led to the discovery of a petrou s carotid aneu- rysm. It is intriguing to wonder whether the chronic otitis led to aneurysma l forma tion or whether aneurysmal obstruction of the Eustachian tube resulted in chro nic otitis. The cholesteatoma found in this case was not adjacent to the carotid canal and is thus unlikely to have caused erosion of the canal.

Cases2and3initially had hearing loss and otalgia. Both had a space-occupying lesion in the middle ear cleft that acco unted for the conductive nature of the loss, and had a sense of fullness in the ear. Otoscopy demo nstrated a vascular mass, presumed to be a glomus tumor. In both cases an aneurysm was diagnosed, in Case 2 by angiog ram prior to any surgery, and in Case3,atthe time of exploration. Neither demonstrated typical findings of a glom us tumor, and thus biopsy was not performed.

Inadvertent biopsy for diagnostic purposes in any of the above three cases would have resulted in hemorrhage. Diag- nosis is made either by angiograp hy or by discovery at the time of exploration for other disease along with a high index of suspicion. Biopsy should never be performed, and has been associated with catastrophic hemorrhage. Needle aspi- ration has been reported, however, with little ill effect."

The treatmentofpetrouscarotid aneurysmsdependslargely on their clinical behavior. Observation alone may be associ- ated with a high incidence of growth and potential rupture of these lesions, as demonstrated by intracranial aneurysms.

Life-threatening hemo rrhage would dictate immediate pack- ing of the ear canal , with strong consideration towards occlusion of the vesse l. Several options exist including arterial ligation in the neck, along or in combination with ligation (trapping) of the intracranial carotid artery; ligation with EC-IC bypass; and percutaneous occlusion of the artery with a balloon. Selective occlusion of the aneurysmal neck is rarely feasible in the temporal bone. Occlusion of the vessel carries a risk of temporary (up to 59%83)or permanent (up to 18%81) cerebral ischemi a. If bleeding can be stopped by packing alone, then other options exist for long-term management.

Aneurysmal resection, through a skull base approac h, has been reported with or without reestablishing vascular flow due to recurrent bleeding orfailure of othertherapies.9.'2.'4.27.38 Although these techniques are feasible, especia lly with the recent advances in skull base surgery , these procedures are extensive and may result in multiple cranial nerve deficits.

We feel that such an approach should be reserved for truly unique situations not amenable to other types of treatment.

For unruptured aneurysms, reinforcement of the vessel 482

provides a safe treatment modality with little morbidity. As illustrated in the three case reports above, the aneurys m is supported with fascial grafts through an endaural or mastoid approac h. An important adj unct is enlargement of the middle ear space and removal of ossicles in proximity to the aneu- rysm. Insertion of foreign bodies that could lead to further irritation of the aneurysm, such as a PORP or TORP, is avoided. Rather, a type III reconstruction (tympanic mem- brane to stapedial capitulum) is performed, usually with acceptable hearing results. The lesion should then be fol- lowed radiographically and clinically to monitor for any growth. Future manipulation of the ear should be performed with great care, and myringotomy should never be per- formed. The patient is advised to carry a warning card to this effect.

Conclusion

Aneurysms of the petrous carotid artery are rare lesions that may appear as a mass in the middl e ear cleft. Such masses should be approached with great caution and if an aneurysm is suspected, biopsy should not be per form ed, but rather the lesion should be eva luated radiographica lly.

If the aneurysm is unru ptured , then reinforcemen t would be the treat ment of choice. Aneurysms that have bled, either spontaneously or iatrogenically, ofte n need more urge nt intervention, and are treated with some form of vessel occlusion. Unu sual cases, with poor cerebral cross circulation, or other co mplica ting factors, might warra nt aneurys mal resection.

The present report adds three cases of unruptured petrous carotid aneurysms to the world ' s literature, all treated suc- cessfully by reinforcement. A high index of suspicion avoided iatrogenic traum a. An increased awareness through additional case reports in the literature will help to encourage a better understanding of the etiology, pathogenesis, and pathology of these uncommon but importa nt lesions.

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ENT Journal" July 1993

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ENT Journal " July 1993

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If this can be done, the size of the packed code will be two times the original shellcode (each non-printable address is represented by two printable 4-byte operands) plus the size

Purpose: Propose a modeling and analysis methodology based on the combination of Bayesian networks and Petri networks of the reverse logistics integrated the direct supply

Involvement of the pelvis is unusual even in reDorts describing large numbers of cases of osteomyelitis.'89 The ilium is most commonly affected in both acute hematogenous pelvic

Our experiments, on three different pairs of corpora, con- firm that our probabilistic model for estimating word translation probabilities is helpful for cross-lingual