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Review
. 2009 Oct;30(9):1637-45.
doi: 10.3174/ajnr.A1607. Epub 2009 Apr 16.

Endovascular treatment of epistaxis

Affiliations
Review

Endovascular treatment of epistaxis

P W A Willems et al. AJNR Am J Neuroradiol. 2009 Oct.

Abstract

Epistaxis is a common condition that can be managed conservatively in most cases. When these measures, including anterior and posterior packing of the nasal cavity, are unsuccessful at controlling the bleeding, interruption of the blood supply to the sinonasal area can be performed, either by surgical ligation or by transarterial embolization. Embolization should be preceded by thorough diagnostic angiography. Aside from aiding with subsequent selective catheterization and embolization, such angiography may reveal significant anatomic anomalies, anastomoses, or an unsuspected cause of epistaxis. Taking these findings into account, the interventionalist may decide to refrain from embolization or adjust the technique to minimize the risk of adverse events, which are mostly related to inadvertent embolization of the internal carotid artery or ophthalmic artery. We present a review of the various causes of epistaxis and the treatment options, with emphasis on endovascular embolization. We also describe the protocol of our institution for endovascular management of this condition.

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Figures

Fig 1.
Fig 1.
Schematic representation of normal arterial anatomy of the sinonasal region. ACA indicates anterior cerebral artery; AEA, anterior ethmoidal artery; APA, ascending palatine artery; APhA, ascending pharyngeal artery; DPA, descending palatine artery; ECA, external carotid artery; FA, facial artery; ICA, internal carotid artery; ILT, inferior lateral trunk; IMA, internal maxillary artery; OFA, orbitofrontal artery; OphA, ophthalmic artery; PEA, posterior ethmoidal artery; SLA, superior labial artery; SPA, sphenopalatine artery.
Fig 2.
Fig 2.
Oblique view of a right internal carotid arteriogram in a 19-year-old man, presenting with uncontrollable epistaxis 2 weeks after being struck in the face by a baseball bat, demonstrating a 5-mm pseudoaneurysm (arrow) arising from an AEA.
Fig 3.
Fig 3.
A 35-year-old woman, who presented with severe recurrent epistaxis. A, Nonenhanced axial CT scan shows a soft-tissue attenuation projecting from the carotid canal into the eustachian tube (arrow). B, AP view of a left internal carotid arteriogram, revealing a 6-mm aneurysm (arrow) projecting off the region of the petrous genu.
Fig 4.
Fig 4.
Oblique right internal carotid arteriogram of a 52-year-old woman with a 6-month history of severe recurrent epistaxis following a motor vehicle crash, revealing 2 large intracavernous traumatic pseudoaneurysms (curved arrows).
Fig 5.
Fig 5.
Left external carotid arteriography in a 26-year-old woman presenting with unrelenting epistaxis several hours after septorhinoplasty. Mid (A) and late (B) arterial phases demonstrate contrast extravasation (arrow), indicating the site of hemorrhage.
Fig 6.
Fig 6.
Angiographic imaging of a 35-year-old man with a history of recurrent epistaxis due to an AVM of the nose and upper lip. He had undergone previous surgical ligation of the proximal right ECA. A, Lateral view of a right internal carotid arteriogram demonstrates a large AVM (open arrows) with primary supply from the OphA (arrowheads). Collaterals to the SPA via the artery of the foramen rotundum (arrow) and the vidian artery (curved arrow) are seen. B, Lateral view of a right vertebral arteriogram demonstrating retrograde filling of the proximally occluded right ECA (curved arrow) via the occipital artery (arrows). The IMA is reconstituted to supply the AVM (open arrows).
Fig 7.
Fig 7.
Left internal carotid arteriogram of a 53-year-old woman, who presented with a 4-week history of recurrent epistaxis uncontrolled by AP packs and requiring multiple transfusions. The image reveals a small cerebral AVM with a nidus measuring <1 cm (curved arrow). The AVM is fed by an orbitofrontal branch (straight arrow) of the right anterior cerebral artery. Two early draining cortical veins are seen (arrowheads) as well as a small venous aneurysm distal to the nidus (open arrow). A small venous network is opacified in the nasal fossa (double arrow).
Fig 8.
Fig 8.
Imaging of a patient with HHT, for whom embolization was requested to treat recurrent epistaxis. A, Right external carotid arteriogram shows typical vascular changes in HHT along the hard palate (arrow) and the premaxilla (double arrow). B, Right internal carotid arteriogram of the same patient shows a small incidental AVM fed by small branches of the pericallosal artery (arrow).
Fig 9.
Fig 9.
Right external carotid arteriogram in a 12-year-old boy with a juvenile nasopharyngeal angiofibroma, who presented with nasal obstruction and recurrent epistaxis. A hypervascular mass arises from the pterygopalatine portion of the IMA (arrows).
Fig 10.
Fig 10.
Imaging of a 65-year-old man who presented with intractable epistaxis and whose history included right nephrectomy for renal cell carcinoma 5 years earlier. A, Axial CT scan at the level of the ethmoid sinuses shows a soft-tissue mass in the posterior ethmoidal air cells (arrows). B, Left external carotid arteriogram demonstrates the neovascularity (arrow) supplied by the terminal IMA.
Fig 11.
Fig 11.
Angiography in a 62-year-old man with right-sided epistaxis, demonstrating a meningo-ophthalmic artery (ie, the OphA arises from the MMA). Selective catheterization of the IMA distal to the origin of the MMA was necessary to perform embolization safely. A, Right internal carotid arteriogram demonstrates the absence of the OphA arising from the internal carotid system. B, Right external carotid arteriogram, early arterial phase, reveals the meningo-ophthalmic artery (arrows). C, The same image as in B, late arterial phase, confirms the choroidal blush (arrows) arising from the external carotid system.
Fig 12.
Fig 12.
Angiography in a 72-year-old woman with intractable idiopathic epistaxis, who was referred to surgery because an ECA origin of the OphA rendered embolization unsafe. A, Left common carotid arteriogram demonstrates ICA occlusion (arrow). B, The same image as A shows no antegrade or retrograde opacification of the OphA. C, Selective left IMA injection, early arterial phase, demonstrates collaterals from the SPA to the OphA (arrow) via an ethmoidal branch (double arrows). D, The same image as in C but in the late arterial phase shows the OphA (arrow) and choroidal blush (arrowheads).

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