Coil embolization of a palatine artery pseudoaneurysm in a gelding

Coil Embolization of a Palatine Artery Pseudoaneurysmin a GeldingNathaniel R. McClellan1, DVM, Margaret C. Mudge1, VMD, Diplomate ACVS, ACVECC,Brian A. Scansen1, DVM, MS, Diplomate ACVIM, Stephen S. Jung2, MD, FACR,and Duncan Russell3, BVMS (Hons), Diplomate ACVP1 Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio ,2 Radiology Incorporated and Mount Carmel HealthCare, The Ohio State University, Columbus, Ohio and 3 Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio

Corresponding AuthorMargaret C. Mudge, VMD, Diplomate ACVS,ACVECC, Department of Veterinary ClinicalSciences, The Ohio State University, 601Vernon L. Tharp Street, Columbus, OH43210.E‐mail: [email protected]

Submitted November 2011Accepted June 2012

DOI:10.1111/j.1532-950X.2014.12174.x

Objective: To describe successful transarterial coil embolization of a palatine arterypseudoaneurysm that extended into the caudal maxillary sinus of a gelding.Study Design: Clinical report.Animal: A 24‐year‐old Morgan gelding with right‐sided epistaxis.Methods: The right maxillary sinus was imaged by radiography, computedtomography, and sinoscopy. Angiography was performed to locate the source ofbleeding, and transarterial coil embolization of a right palatine artery pseudoaneurysmwas performed.Results: There was some mucoid nasal discharge and an intermittent coughpostoperatively. No epistaxis was seen after embolization. There was moderateswelling of the surgical incision over themid‐cervical common carotid artery. The horsewas discharged from the hospital 4 days after surgery, and had been doing well, with nosigns of bleeding, for 2 months postoperatively. The horse had acute colic secondary toa strangulating lipoma at 2 months and was euthanatized after exploratory celiotomy.Placement of embolization coils in the right palatine artery was confirmed by CT andnecropsy.Conclusions: Severe epistaxis in the horse may be caused by a ruptured major palatineartery pseudoaneurysm. Occlusion of this vessel can be successfully accomplished bytransarterial coil embolization.

Severe epistaxis in the horse has been reported secondaryto guttural pouch mycosis, sinonasal trauma, and is occasion-ally associated with paranasal sinus neoplasia or ethmoidhematoma. Most commonly, rupture or erosion of the internalcarotid, external carotid, and/or maxillary arteries have beenreported to occur secondary to fungal infection of these vesselsas they course through the guttural pouch.1–5

Transarterial coil embolization has been described inhorses to control hemorrhage from the internal carotid, externalcarotid, and maxillary arteries individually or in combinationwith one another related to guttural pouch mycosis inducedaneurysm.1,2 We are unaware of any reports describingtransarterial coil embolization to control hemorrhage fromother sites of aneurysm or pseudoaneurysm in the horse. Ourobjective was to report an unusual cause of life‐threateninghemorrhage in the horse and to describe the technique oftransarterial coil embolization to successfully occlude theaffected vessel.

CLINICAL REPORT

A 24‐year‐old Morgan gelding (482 kg) was admitted forevaluation of moderate to severe right‐sided epistaxis.

Moderate to severe bleeding from the right nostril was noted3 weeks before, and again 6 days before admission. Right‐sided guttural pouch mycosis was suspected based on theseverity of hemorrhage and endoscopic observation of clottedblood at the right salpingopharyngeal opening. The horse hadbeen treated with sulfamethoxazole trimethoprim since the firstepisode of bleeding and was also being administeredisoxsuprine, cyproheptadine, and levothyroxine (Thyro‐L,Usp, Lloyd, Inc., Shenandoah, IA) for management of equinepituitary pars intermedia dysfunction and chronic laminitis.

On admission, the gelding was quiet, alert, responsive,and afebrile, with a heart rate of 52 beats/min and respiratoryrate of 20 breaths/min. Mucous membranes were pale pinkwith a capillary refill time of 1–2 seconds. A moderate amountof blood was observed on the muzzle, chest, and forelimbs. Noother abnormalities were identifies on physical examination.On hematologic examination, there was anemia (PCV, 16%),mild hypoproteinemia (5.4 g/dL) and a blood lactate of2.1mmol/L.

Endoscopic examination of the upper airway revealed aregion of swollen red tissue interpreted as hematoma in thepharynx, immediately rostral to the right salpingopharyngealopening (Fig 1A). A small amount of fresh blood was seen atthe right nasomaxillary opening. Both guttural pouches were

Veterinary Surgery 43 (2014) 487–494 © Copyright 2014 by The American College of Veterinary Surgeons 487

free of blood and exudate. Skull radiographs revealedhomogenous soft tissue opacity within the right rostral andcaudal maxillary sinuses as well as the dorsal and ventralconchal sinuses, consistent with sinusitis and/or hemorrhage.There was no evidence of distortion of bony structures or fluidline present in the paranasal sinuses. Widening of theperiodontal space along the left upper PM3, PM4, M1 (Triadan207, 208, 209) and mild remodeling of the tooth roots of theright upper PM3 and rostral root of PM4 (Triadan 107 and 108)were seen, indicating periodontal disease (Fig 1B–D). Oralexamination revealed good alignment of all premolar andmolar teeth with mild points on the lingual surfaces of bothmandibular cheek teeth arcades and the buccal surfaces of bothmaxillary cheek teeth arcades. There was no evidence of anyfractures, fistula, masses, or foreign bodies.

Considering the signalment and history top differentialdiagnoses were neoplasia or ethmoid hematoma with unusualhemorrhage. Because of a lack of a definitive radiographicdiagnosis, computed tomography (CT) was recommended todiagnose the problem and determine if surgical interventionwould be an option. The day after admission, cross‐matchingwas performed in preparation for blood transfusion before

general anesthesia and if indicated during/after any potentialsurgical intervention. Based on the gelding’s anemia andcontinued mild epistaxis, 4 L whole blood was administeredbefore anesthesia. Immediately after the horse was anesthetizedand positioned in dorsal recumbency for the CTscan, there wasprofuse hemorrhage from the right nostril. Additional wholeblood was transfused and the right nasal cavity was packed tohelp reduce hemorrhage during CT.

On the CT scan, there was diffuse soft tissue attenuatingmaterial that filled the entire right paranasal sinuses as well asthe nasopharynx (interpreted as hemorrhage). The areas ofattenuating material were later analyzed using Hounsfield units(HU) and were determined to have a CT density of �60HU.This value of Hounsfield unit falls within the range of freshblood, early hematoma, and some soft tissue structures.6

Unfortunately, because of the severity of hemorrhage thatstarted before CT evaluation, the entire right paranasal sinuseswere completely filled with blood which may have masked anaccurate diagnosis of any potential difference in CT density ofan abnormal soft tissue structures versus fresh hemorrhage. CTimages demonstrated the presence of both expansion and lysisof the right wing of the basisphenoid bone and right maxillary

Figure 1 (A) Endoscopic image showing hematoma (white arrows) on the right pharyngeal wall immediately rostral to the right salpingopharyngealopening (black arrow). (B) Dorsoventral radiograph of the skull demonstrating increased radiopacity in the right paranasal sinuses (outlined by blackarrows). (C) Right lateral oblique radiograph of the skull demonstrating increased radiopacity within the right paranasal sinuses compared to the left(Fig 1D).Mild widening of the periodontal space and remodeling of the tooth roots of the right upper PM3 and rostral root of PM4 (black arrows). (D) Leftlateral oblique radiograph of the skull demonstrating mild widening of the periodontal space along the left upper PM3, PM4,M1 (black arrows). The leftparanasal sinuses appear clear (radiolucent) in this image.

488 Veterinary Surgery 43 (2014) 487–494 © Copyright 2014 by The American College of Veterinary Surgeons

Coil Embolization of a Palatine Artery Pseudoaneurysm McClellan et al.

bone of the ventral aspect of the caudal maxillary sinus,including the bone surrounding the right maxillary third molarand right ventral aspect of the infraorbital canal (Fig 2A–C).These CT findings did not definitively diagnose the problem,but with the bony lysis and expansile nature of the lesion,neoplasia or large sinus ethmoid hematoma was consideredhighly likely.

During the CT scan, mean arterial blood pressuredecreased to 52mmHg. The previously placed nasal cavitypacking was producing an inadequate level of hemostasis, sothe decision was made to stop the CT scan and proceed toemergency temporary ligation of the right common carotidartery. The right neck was clipped and scrubbed withchlohexidine and alcohol. A 7 cm skin incision was madeimmediately dorsal to the jugular vein in the right mid‐cervicalregion. The incision was then extended through the brachio-cephalicus and omohyoid muscles using a combination ofblunt and sharp dissection. Once located, the right carotidsheath was carefully incised so that the right carotid arterycould be isolated from both the vagosympathetic trunk andrecurrent laryngeal nerve. Once isolated, the right commoncarotid was ligated using sterile umbilical tape. The hemor-rhage appeared to decrease after carotid artery ligation, but didnot stop completely. Therefore, the decision was made toproceed directly to surgery for an emergency right frontonasalsinusotomy in an attempt to achieve both a definitive diagnosisand stop the hemorrhage by application of direct pressure withgauze packing.

The right frontonasal sinus region was prepared for afrontonasal sinusotomy, which was performed using anoscillating bone saw.7 Hemorrhage from the sinus continuedonce the flap was elevated, and bleeding was reduced withmanual pressure and gauze packing. One soft friable red/blackmass �6 cm diameter was discovered in the right frontal sinus

and another firm fibrous tan mass �4 cm diameter wasobserved in the right caudal maxillary sinus. Portions of bothmasses were removed using sponge forceps which significantlyincreased the severity of hemorrhage. Gauze packing was usedto apply pressure within the sinuses, and this stopped thehemorrhage. The end of the packing was exited through theright nostril by attaching it to a Chamber’s catheter passedretrograde through the nostril with 3 polymerized caprolactumsuture (Braunamid; Jorgensen Laboratories, Loveland, CO)and then removing the catheter from the nostril. The packingwas then tacked to the external surface of the right nares using 0polypropylene suture in a simple interrupted pattern. Thefrontonasal bone flap was repositioned and secured. Afterbeing in place for �45minutes, the umbilical tape wasremoved from the right common carotid artery and theapproach incision was closed in 2 layers. Total anesthetic timewas 105minutes and total surgical time was 60minutes.Anesthetic recovery time was �30minutes and the quality ofrecovery was subjectively graded as smooth and uneventful.

Intraoperatively, the PCV and total solids were 11% and3.8 g/dL. Whole blood transfusion (12 L) was initiated duringsurgery and continued after recovery, for a total transfusionvolume of 16 L. Potassium penicillin (22,000U/kg intrave-nously [IV] every 6 hours), gentamicin (6.6mg/kg IV every24 hours), flunixin meglumine (1.1mg/kg IV every 12 hours),and aminocaproic acid (40mg/kg IVonce) were administeredpostoperatively.

Biopsies obtained during surgery were evaluated bycytology (impression smears made with fresh tissue) andhistopathology (formalin fixed tissue). Cytologic evaluationswere made the same day as surgery and revealed mild tomoderate neutrophilic inflammation with a large amount of redblood cells; however, no definitive causative agents orneoplastic cells were observed. By Day 5, the histopathology

Figure 2 (A) Transverse CT image of the skull at the level the third maxillary molars demonstrating bony lysis and remodeling surrounding the rightmaxillary thirdmolar (black arrow). The right paranasal sinuses and nasopharynx are diffusely filledwith a soft tissue attenuatingmaterial (60Hounsfieldunits [HU]). (B)Transverse CT image of the skull at the level of the caudal maxillary sinus demonstrating bony lysis/remodeling of the ventral aspect ofthe caudal maxillary sinus (black arrows) and the ventral aspect of the right infraorbital canal (white arrow). The right paranasal sinuses and nasopharynxare diffusely filled with a soft tissue attenuating material (60HU). (C) Transverse CT image of the skull at the level of the caudal aspect of the caudalmaxillary sinus, demonstrating bony lysis in the right caudal maxillary sinus (black arrows). The right paranasal sinuses and nasopharynx are diffuselyfilled with a soft tissue attenuating material (60HU).


McClellan et al. Coil Embolization of a Palatine Artery Pseudoaneurysm

results were available and were inconclusive for the cause ofhemorrhage. Histopathology was consistent with subacutehemorrhage and organizing hematoma. At this point the PCVhad stabilized at 25% and without a definitive diagnosis, thedecision was made to reopen the sinus flap for furtherevaluation of the soft tissue mass noted in the right maxillarysinus during the previous surgery.

The sinus flap was reopened with the horse standing andsedated (0.1mg/kg morphine IV; 18mg/kg detomidine IV) andlocal anesthesia to avoid the hemorrhage experienced duringgeneral anesthesia. The gauze packing material was removedfrom the sinuses, the sinuses were lavaged with sterile salinesolution, and several blood clots were removed. A 4 cmdiameter round firm, white to tan mass was present in the rightcaudal maxillary sinus. Sinoscopy was performed through theprevious right frontonasal sinus flap to aid viewing of the rightcaudal maxillary mass. After closer examination with sino-scopy, the mass was observed to be pulsating leading tosuspicion that the mass was an aberrant arterial structure(Fig 3A). Gauze packing material was placed in the rightfrontal and maxillary sinuses to prevent further bleeding.

Transarterial Surgical Technique

Angiography was performed 2 days later, with the geldinganesthetized and positioned in left lateral recumbency. The

right common carotid artery (CCA) was accessed through theprevious mid‐cervical incision, and elevated after ensuring thatit was separated from the vagosympathetic trunk and recurrentlaryngeal nerve. The CCAwas isolated with umbilical tape. An18 g, 7 cm arterial access needle (ArgonMedical Devices, Inc.;Athens, TX)was placed into the CCA, and a 0.889mm, 150 cmangled hydrophilic guidewire (Weasel Wire; Infiniti Medical,LLC; Menlo Park, CA) was advanced through the needle. Thearterial needle was exchanged over the wire for a 7 Fr 55 cmlong sheath (Flexor Check‐Flo Introducer, RAABE; Cook,Inc.; Bloomington, IN). Angiograms were performed throughthe sheath and with a 5 Fr 100 cm straight marker catheter(Royal Flush II Angiographic Catheter with Beacon‐Tip;Cook, Inc.) to delineate the anatomy. After entering the rightexternal carotid artery, the right maxillary artery was selected,and angiography revealed a focal dilation (interpreted as apseudoaneurysm) in the proximal to mid aspect of the greaterpalatine artery (Fig 3B). The frontonasal bone flap wasreopened to ensure that the abnormality seen on angiographycorrelated with the aberrant arterial structure in the maxillarysinus.Metallic hemostats were placed into the caudal maxillarysinus to the level of the mass through the previous frontonasalsinus flap site, and confirmed by fluoroscopy to preciselyoverlie the pseudoaneurysm diagnosed with angiography. Thepseudoaneurysm was not readily accessible through thesinusotomy, as the full extent could not be seen, even withan endoscope. A maxillary sinusotomy was considered to gainmore direct access to the area of the pseudoaneurysm; however,it was decided that a transarterial approach would be lessinvasive and would be more likely to ensure completeocclusion of the abnormal vasculature.

A 5 Fr 100 cm multipurpose end‐hole (MPA Beacon‐TipTorcon NB Advantage Catheter; Cook, Inc.) catheter was usedto place a 10mm to 5mm tapered platinum embolization coil(Tornado Embolization Coil; Cook, Inc.) in the greater palatineartery beginning distal to and extending into the pseudoaneur-ysm. Two more tapered platinum embolization coils weredeployed within the pseudoaneurysm and extended into theproximal greater palatine artery. A final 5mm� 3 cm coil(Embolization Coil; Cook, Inc.) was placed at the entrance tothe pseudoaneurysm. Digital subtraction angiography (DSA)performed immediately after coil embolization showed a smallamount of flow into the pseudoaneurysm, which rupturedunder pressure. Complete hemostasis was achieved withinseconds as the pseudoaneurysm thrombosed and there was nolonger flow through the right greater palatine artery (Fig 3C,D).The catheter was withdrawn to the maxillary artery and furtherDSA in both the maxillary artery and right ECA failed toidentify any other vascular abnormalities or tumor blush. Exitangiography in the right ECA and CCA showed normal flowwith profound vasospasm. All catheters were withdrawn andthe carotid access was closed with a single cruciate suture of3‐0 polydioxanone. The brachiocephalicus and omohyoidmuscles and skin were closed and a Penrose drain placed. Totalanesthesia time was 185minutes and total surgical/proceduretime was 140minutes. Recovery time from anesthesia was�35minutes and the quality of recovery was subjectivelyassessed as good.

Figure 3 (A) Sinoscopy image showing a portion of the palatine arterypseudoaneurysm in the caudal maxillary sinus (white arrow) via rightfrontonasal sinus flap approach. (B) Pseudoaneurysm pre coil emboliza-tion observed under digital subtraction angiography (�) in the proximal tomid aspect of the greater palatine artery, infraorbital artery (black arrow),and maxillary artery (white arrow). (C) Pseudoaneurysm post coilembolization observed under digital subtraction angiography (�). (D)Embolization coils observed within the palatine artery pseudoaneurysmon fluoroscopy (�).



Postoperative Care

The gelding was hospitalized for 4 days after the coilembolization procedure. Trimethoprim‐sulfa tablets (25mg/kgorally every 12 hours) and phenylbutazone (2.2mg/kg orallyevery 12 hours) were administered for another 5 daysafter discharge. Levothyroxine and cyproheptadine wereadministered throughout hospitalization. The skin staples andsutures were removed from the sinus flap and neck incision,respectively, at 14 days postoperatively. Exercise was restrictedto a small paddock for 30 days followed by a return to normalturnout and exercise.

Outcome

There was no active bleeding seen after the coil embolizationprocedure. The gelding developed mild mucoid nasaldischarge and had an intermittent cough while in the hospital.There was moderate swelling and drainage associated with thecarotid access incision, and some incisional discharge from thesinus flap site was noted �5 days after hospital discharge. Allcomplications were self‐limiting and resolved within 30 daysafter discharge.

Two months after surgery, the gelding had acuteabdominal pain. On exploratory celiotomy, ischemic necrosisof the jejunum secondary to a strangulating lipoma wasidentified and resection and jejunocecostomy performed. Thegelding was euthanatized 1 day after surgery because of hispoor prognosis following severe postoperative abdominal painand endotoxemia.

Necropsy Findings

CTwas performed on the head before and after infusion of a 1:4barium/latex mixture infused into the right external carotidartery. Bariumwas used to add contrast to the vasculature to aididentification of any vascular anomalies on CT. Figure 4A–Cdemonstrates the location of the coils in the right greaterpalatine artery along with the unaffected left side for anatomiccomparison. Gross dissection of the head revealed bonyproliferation in the caudal and rostral maxillary sinuses withdisruption of the septum dividing the maxillary sinuses. Therewas also severe thickening of the infraorbital canal as it coursedthrough the affected area. A small 7–8mm segmentallydistended vessel was noticeable in the right caudal maxillarysinus at the level of the nasomaxillary opening with the coilspresent within its lumen (Fig 5A,B).

Histopathology performed on the palatine artery at the siteof coil embolization showed a luminal obstruction byfibrovascular connective tissue interpreted as a recanalizedthrombus. The arterial wall had severe myointimal hyperplasia(remodeling), with chronic intramural hemorrhage, andmoderate lymphoplasmacytic arteritis (Fig 5C). Elastic fiberswithin the tunica media were disrupted, coiled, and fragmented(degeneration) and the wall contained multiple, small calibervascular profiles (neovascularization). Both the tunica intimaand tunica media contained amoderate amount of myxomatousmaterial and foci of mineralization. Special stains for fungal

elements (periodic acid‐Schiff [PAS] and Grocott’s methena-mine silver [GMS]) were unremarkable; however, previousfungal disease could not be excluded. In the associated sinusmucosa there were reactive, non‐specific changes consistentwith chronic hemorrhage and granulation tissue. Other findingsincluded moderate lymphoplasmacytic and neutrophilic sinus-itis, periosteal reaction, and mild Wallerian degeneration ofperipheral nerves.

DISCUSSION

We are unaware of reports of pseudoaneurysm of the palatineartery in horses. Arterial pseudoaneurysms are rare in people,but have been reported after orthognathic surgery, gunshotwounds, penetrating knife injuries, facial fractures, placementof circummandibular wires, visceral transplantation, obstetricand gynecological procedures, and vascular and endovascularinterventions.8–10

Pseudoaneurysms are believed to form after trauma to anarterial vessel wall that allows the flow of blood to bemaintained through the vessel. Arterial trauma may be causedby infection/inflammation, vasculitis, iatrogenic causes, andtumor invasion.10 As a result of arterial damage, a hematomacan be formed when hemorrhage occurs into the soft tissuessurrounding the vessel. The hematoma will continue toincrease in size until the periarterial pressure becomes greaterthan the mean arterial pressure. After pressure equilibration,the hematoma and perivascular connective tissue becomesmore organized to form a fibrous “sac” like structure around theinjured artery. The “sac” is contained by themedia or adventitiaor simply by soft‐tissue structures surrounding the injuredvessel.11 As the hematoma resolves, the mass or “sac” expandswith arterial pressure producing pulsations. Once formed, apseudoaneurysm can either progressively enlarge or rupture.9

This can be distinguished from a true aneurysm which has all 3layers of the arterial wall ‐ intima, media, and adventitia.10

Angiography in this gelding was supportive of pseudo-aneurysm, though the histopathology was not confirmatory,likely because of distortion of the vessel secondary to the coildeployment and associated thrombosis. Histopathology re-vealed sections that contained evidence of chronic arterialthrombosis and recanalization. Products of blood breakdownwere identified in the vessel wall and surrounding connectivetissue, indicating long‐standing hemorrhage. Because of thechronicity and extensive vascular remodeling from coilembolization it was difficult to make the distinction betweenaneurysm and pseudoaneurysm.

Although an inciting cause was not apparent, possibleexplanations for the vascular pathology might include primaryintramural degeneration, vascular trauma or previous inflam-matory disease (vasculitis), external or foreign body relatedtrauma, or severe dental disease. The level of dental diseaseaffecting the right upper PM3 and rostral root of PM4 wasdiagnosed on radiographs and CTas mild disease; therefore wedid not suspect that the inciting cause was secondary to dentaldisease. In fact the overall alignment and condition of all 4dental arcades were considered excellent given the gelding’s



Figure 4 (A) Postmortem CT 3D reconstructions with barium:latex (1:4) vascular contrast, right sagittal view; embolization coils in the palatine artery(�), external carotid artery (1), linguofacial trunk (2), maxillary artery (3), lingual artery (4), and facial artery (5) infraorbital artery (6). B) Postmortem CT 3Dreconstructions with barium:latex (1:4) vascular contrast, left sagittal view; external carotid artery (1), linguofacial trunk (2), maxillary artery (3),infraorbital artery (6), uncoiled palatine artery (7). (C) Postmortem CT 3D reconstructions with barium:latex (1:4) vascular contrast, dorsoventral view;embolization coils in the palatine artery (asterix), maxillary artery (3), uncoiled palatine artery (7).

Figure 5 (A) Dorsal view of the right nasomaxillary opening with the remnant of the palatine artery pseudoaneurysm (�) observed by sectioning of theskull in a dorsal to ventral direction. (B) Close up view of the right nasomaxillary opening with the remnant of the palatine artery pseudoaneurysm. (C)Equine, longitudinal section through palatine artery. There is severe thickening of the tunica intima, with occlusion of the arterial lumen (black arrow).The tunica intima contains loosely arranged mesenchymal cells with intramural hemorrhage and recanalization (�); multiple deposits of hematoidin arealso present, indicating chronic hemorrhage (white arrow). Hematoxylin and eosin. Bar¼ 500mm.



age. The owner was unable to recall any specific incidences,but did inform us that the gelding shared a pasture with anothergelding and they would sometime play roughly. There was noobvious sign of trauma on physical examination or skullradiographs that would indicate that the vascular anomalyoccurred secondary to external trauma. Although a foreignbody penetration sometime before admission could not beruled out we were unable to identify a foreign body presencewith any of our diagnostic modalities performed. Potentially astick or other organic foreign body may have caused trauma tothe palatine artery several months before admission. We feelthat the client would have noticed some bleeding associatedwith such trauma, but we cannot rule out the possibility.Another striking, yet puzzling aspect of this lesion was theamount of bony lysis and remodeling associated with the rightmaxillary sinus and infraorbital canal. One potential explana-tion is that the remodeling is simply a response to the chronicexpansile and inflammatory nature of the lesion as it relates tothe pressure placed on the surrounding bony and soft tissuestructures during the formation of the pseudoaneurysm. Orperhaps there was initial damage to the bony structures duringsome unidentified event that caused the formation of a palatineartery pseudoaneurysm. Unfortunately, we were unable to find aprimary cause for the bony lysis in this gelding, insteadwe believeit is all a result of the chronic inflammatory nature of the lesion.

Diagnosis of pseudoaneurysms may be extremely difficultbecause they are often clinically silent until weeks or monthsafter the initial trauma to the artery. In people, pseudoaneurysmis most commonly associated with a severe bleed �2 weeksafter orthognathic surgery, however as late as 11 weeks postsurgery has been reported.9 A pseudoaneurysm may bediagnosed with CT or DSA as a rounded structure arisingfrom the side of the artery.10 Advances in CT technologyincluding contrast‐enhanced multidetector CT angiography,have facilitated fast, non‐invasive, accurate diagnosis ofaneurysm/pseudoaneurysm in people. However, for rupturedpseudoaneurysm, DSA is the “gold standard” because of theability to diagnose and treat concurrently.10 In this gelding, wechose DSA because of the availability at our hospital,limitations of CT angiography in an adult horse, and thehigh potential for another life threatening bleed that wouldrequire immediate intervention.

In retrospect, standing CT angiography might haveavoided the bleeding complications encountered during theinitial anesthetic episode. However, standing CT is notavailable in our hospital and since we initially suspectedneoplasia or ethmoid hematoma we did not anticipate themarked hemorrhage that occurred.12 To address the severebleeding, the decision to ligate the ipsilateral common carotidartery wasmade when simple nasal packing failed to reduce theamount of hemorrhage. Clinically, we observed a decrease inthe amount of hemorrhage after ligation which is consistentwith previous reports of a reduction to 30% of normal bloodflow with ipsilateral common carotid artery ligation.13

However the reduction in hemorrhage could also have beenthe result of a decrease in blood pressure which prompted thedecision for an emergency right frontonasal sinusotomy withdirect pressure applied to the location of the hemorrhage.

Palatine artery occlusion was considered necessarybecause of previous life‐threatening hemorrhage; however,we had to consider the potential complications of transarterialembolization or ligation of the palatine artery such as localischemic tissue necrosis and inciting the “steal phenomenon.”In people, ligation of the descending palatine artery during LeFort I osteotomy produces no change in the maxillary gingivalblood flow between groups with and without arterial ligation.14

This is most likely a result of the large amount of collateralcirculation that exists in the head region of most species. The“steal phenomenon” is proposed to cause blindness afterarterial occlusion for the treatment of guttural pouchmycosis inthe horse. The phenomenon occurs when the major blood flowto the horse’s eye (external ophthalmic artery) is reducedindirectly through ligation of the external carotid artery inaddition to simultaneous ligation of the major palatine arterywhich is the largest terminal branch of the maxillary artery andanother potential path for blood to reach the externalophthalmic artery by retrograde flow.15,16 We felt that thiswas unlikely to occur if we could occlude only the palatineartery without the need to affect the external carotid arterywhich would preserve blood flow to the eye via the externalophthalmic artery.

Another decision we had to make was whether or not toattempt open surgical repair using ligatures, vascular clips,or other means of vascular hemostasis. In people, options fortreatment include open surgical repair, direct percutaneousthrombin injection, transarterial embolization with coils,glue, or Gelfoam, and deployment of covered stents ordetachable balloons.8–10 We choose transarterial emboliza-tion with coils because of anatomic inaccessibility of thepseudoaneurysm, availability of equipment, and expertise ofthe surgeons/interventional radiologists. We could notcompletely see or access the entire extent of the lesionthrough the frontonasal sinusotomy, and complete occlusionof the vessel could be easily performed and confirmed bytransarterial approach. It is possible that an additionalmaxillary sinusotomy would have provided better access tothe lesion, allowing occlusion by ligatures or vascular clips.Overall we found that the approach through the rightcommon carotid artery was uncomplicated and the pseu-doaneurysm was effectively treated with transarterial coilembolization.

ACKNOWLEDGMENT

The authors are indebted to ElizabethM. Santschi, Diplomate ACVSof The Ohio State University Veterinary Medical Center for hersurgical assistance/expertise, and Melissa A Milligan, DVM, MS,Diplomate ACVS of Equine Specialty Hospital, Burton, OH.

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Coil embolization of a palatine artery pseudoaneurysm in a gelding