EDUCATIONAL OBJECTIVE

INTRODUCTION

University of Wisconsin-Madison Email: JBrucker@uwhealth.org www.radiology.wisc.edu

Radiology In the Nosebleed Section: How to Pick Out A Diagnosis Justin L. Brucker, M.D.1, Tabassum A. Kennedy, M.D.1, Shirley Chan, M.D.2

University of Wisconsin-Madison Department of Radiology1 University of Rochester Department of Radiology2

RELEVANT ANATOMY

DISCUSSION

SUMMARY

VARIOUS NEOPLASMS JUVENILE NASOPHARYNGEAL

ANGIOFIBROMA ESTHESIONEUROBLASTOMA NEUROFIBROMATOSIS TYPE 1 GLOMANGIOPERICYTOMA SINONASAL MELANOMA

ARTERIOVENOUS FISTULA ARTERIOVENOUS MALFORMATION POSTTRAUMATIC PSEUDOANEURYSM BACTERIAL SINUSITIS FUNGAL SINUSITIS

(acute invasive type) c-ANCA + GRANULOMATOSIS

WITH POLYANGIITIS

Figure 3 (A-C): Multiplanar contrast-enhanced CT images demonstrate a large uniformly enhancing soft tissue mass (✪), centered within the left pterygopalatine fossa. There is expansive remodeling of the adjacent osseous strucutres, as well as invasion into the adjacent maxillary sinus and masticator space. The tumor protrudes slightly into the sphenopalatine foramen ().

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Fig 1: Conventional Angiography of the Relevant Arterial Anatomy A) Lateral digital subtraction angiography (DSA) of the internal carotid artery (ICA). The ophthalmic artery (black arrows) rises off of the distal ICA siphon, and gives rise to the posterior ethmoidal artery, anterior ethmoidal artery, and terminal dorsal nasal artery. Please note the choroid blush of the retina (white arrow).

B-C) Selective angiography of the terminal external carotid artery (ECA) in the lateral and anteroposterior (AP) projections. The ECA terminates into the internal maxillary artery (black arrows), which gives rise to the sphenopalatine artery (white arrows). The sphenopalatine artery splits into the posterior septal branches, posterior lateral nasal branches, and gives rise to the greater palatine artery via the descending palatine artery. D-E) Selective angiography of the linguo-facial trunk ( * ) in the lateral and AP projections. The ascending pharyngeal artery (black arrows) and lingual artery (white arrows) are seen in addition to the facial artery. The terminal branches of the facial artery include the alar artery (a), the superior lingual artery (sl), and angular artery (at the level of the medial canthus – not shown).

Fig 2: Anatomical Landmarks & Vascular Territories On Multiplanar CT A-D: Serial axial CT images descending in the cranial to caudal direction, from left to right. E-I: Serial coronal CT images obtained in the anterior to posterior direction, from left to right. J-M: Serial sagittal CT images obtained in the medial to lateral direction, from left to right. The superimposed color-coded maps (see descriptions below) illustrate the approximate vascular territories of the arteries that comprise the majority of vascular supply to the nasal cavity. There is a high degree of variability in vascular anatomy between individuals, and well as robust collateralization between adjacent vascular territories. Anastomotic connections between ICA and ECA circulation can be a potential pitfall in sinonasal embolization cases. ICA SUPPLY: Dorsal Nasal Artery: Terminal branch of the ophthalmic artery (in addition to the superior trochlear artery), providing vascular supply to the anterior superior sinonasal cavity and nasal root, at the level of the superomedial orbital ridge. Anterior Ethmoidal Artery: Medial branch of the ophthalmic artery, which enters the ethmoid air cells via the anterior ethmoidal foramen ( on A and G) at the level of the olfactory fossa, posterior-adjacent to the second ethmoid lamellae ( image K). Posterior Ethmoidal Artery: Medial branch of the ophthalmic artery, which enters the posterior ethmoid air cells via the posterior ethmoidal foramen ( on A, H, and K) posterior-adjacent to the third ethmoid lamellae. ECA SUPPLY: Posterior Lateral Branches of the Sphenopalatine Artery: Supplies blood to the posterior lateral walls of the nasal cavity. It enters the nasal cavity via the sphenopalatine foramen, superior-adjacent to the posterior apex of the middle turbinate ( on B, I , and K). Posterior Septal Branches of the Sphenopalatine Artery: Blood supply to the posterior nasal septum. They also enter the nasal cavity via the sphenopalatine foramen. Greater Palatine Artery: Arises from the descending palatine artery of the sphenopalatine artery, which travels through the greater palatine canal ( on M), inferior to the pterygopalatine fossa (*). Distal Branches of the Facial Artery: The alar, superior lingual, and angular arteries provide vascular supply to the anterior nasal cavity and perinasal soft tissues.

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Figure 3 (D-F): Multiplanar contrast-enhanced T1 weighted images with fat saturation, redemonstrate the CT findings with improved soft tissue delineation. Better seen is vascular engorgement and tumor infiltration of the left posterior nasal mucosa in the posterior lateral sphenopalatine () and posterior ethmoidal arterial territories ().

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Figure 3 (G-H): AP and lateral images from ICA angiogram, demonstrate tumoral blush in the region of the posterior nasal cavity, fed by branches of the posterior ethmoidal artery (), and nasopharynx. Figure 3 (I-J): AP and lateral images from ECA angiogram, demonstrate large tumoral blush in the region of the pterygopalatine fossa, centered over the branching point of the sphenopalatine artery ().

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Figure 4 (A-C): Axial and coronal T2-weighted images with fat saturation, demonstrate a uniformly hyperintense lobulated mass centered within the anterior superior sinonasal cavity, eroding into the suprasellar cistern, cavernous sinus, and right ostiomeatal unit. As suggested by superimposed vascular maps (C), this tumor may possess both ethmoidal and posterior septal/lateral sphenopalatine arterial supply.

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Figure 4 (D-F): Mutiplanar T1-weighted images before the administration of intravenous contrast, demonstrate a uniformly T1-hypointense mass filling the ethmoidal and frontal air cells, with obstruction of the sphenoid and right maxillary sinuses. The mass has eroded through the cribriform plate and displaces the orbitofrontal cortex.

Figure 4 (G-I): Mutiplanar T1-weighted images following the administration of contrast. The mass is diffusely enhancing, but with preferential hyperenhancement of the tumor margins and relative hypoenhancement of the central mass. There is no abnormal enhancement within the maxillary or sphenoid sinuses, confirming the presence of debris.

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Figure 5 (A-C): Axial and coronal T1-weighted postcontrast images with fat saturation, demonstrate diffuse thickening and enhancement of the sinonasal mucosa. There are several small areas of discrete nodularity () superimposed on this background of mucosal prominence, with near complete obliteration of the posterior nasal apertures.

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Figure 5 (D-E): Axial and sagittal postcontrast T1-weighted images with a larger field of view demonstrate an additional area of confluent heterogeneously enhancing soft tissue, centered in the right suboccipital scalp and eroding through the adjacent osseous structures ().

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Figure 5 (F-H): Axial and sagittal T2-weighted images with fat saturation demonstrate the soft tissue mass to composed of a collection of multiple rounded T2-hyperintense nodules, which replace most of the right paraspinal cervical soft tissues and infiltrate along the fascial planes. These are compatible with plexiform neurofibromas, which the patient possessed all over his entire body.

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Figure 6 (A-E): Serial axial (A-D) and coronal (E-F) contrast enhanced CT images demonstrate a sessile uniformly enhancing solid mass, arising form the posterior superior nasal septum (), with apparent attachment to the adjacent middle turbinate.

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Figure 6 (G-N): Serial axial (G-I) and coronal (J-L) postcontrast enhanced T1-weighted images better delineate the margins of the mass; based on its location and extent, branches of the posterior septal sphenopalatine and posterior ethmoidal arteries are presumably involved (colored maps).

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Figure 6 (O-P): Gross pathology images obtained with intranasal endoscope (O) and after resection (P). These images reveal a vascular lobulated mass with areas of ulceration and active oozing. The intact tissue is smooth, pink, and firm.

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Figure 7 (A-D): Serial axial (A-B) and coronal (C-D) images from an unenhanced CT demonstrate a isodense solid mass filling the posterior left middle turbinate, at the level of the sphenopalatine foramen ().

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Figure 7 (E-F): Corresponding coronal and axial fused PET/CT images from the previous month demonstrated hypermetabolic level 2 lymphadenopathy on the left side, as well as a subcentimeter faintly hypermetabolic nodule in the perihilar location of the left upper lobe (), as identified on noncontrast chest CT (G). These findings were compatible with biopsy-proven melanoma.

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Figure 8 (A-C): Multiplanar CT images demonstrate an isodense periorbital mass within the right medial canthus ()

Figure 8 (D-F): MultiplanarT1-weighted postcontrast images demonstrate transcranial extension of an enhancing mass through the cribriform plate and along the right frontal dura. There is a small intranasal component that penetrates the frontoethmoidal air cells.

Figure 8 (J-K): Time-resolved MR angiography demonstrates a dural AVF arising from the anterior falx, with brisk drainage into the superior sagittal sinus, and peri-iorbital and intranasal varices.

Figure 8 (J-K): Sequential images from right ICA angiogram in the lateral projection, redemonstrates and high flow AVF fed by meningeal branches of the ICA and and superior trochlear branch of the ophthalmic artery (), with brisk intranasal and periorbital drainage ().

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Figure 8 (L-M): Late arterial phase images from selective right facial artery angiogram in the AP (L) and lateral (M), demonstrate a small canthal portion of the AVM fed by the angular arterial branch () of the facial artery.

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Figure 8 (N-O): Rotational 3-D reconstruction of the conventional angiogram, demonstrating the complexity of the AVF.

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Figure 9 (A-C): Patient initially presented after a high speed collision. Multiplanar CT images at the time of trauma demonstrate multiple minimally displaced fracture of the sphenoid sinus and midface, with involvement of the bilateral carotid canals ().

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Figure 9 (D-I): The patient presenting a short interval later, with epistaxis and a hyperdense mass expanding the sphenoid sinus. Angiographic images demonstrate a bilobed ICA pseudoaneurysm protruding in the sphenoid sinus, surrounded by hemorrhage.

Figure 9 (J): A 3-D reconstruction of the ICA pseudoaneurysm.

Figure 9 (K-L): Lateral angiographic images, showing the pseudoaneurysm before and after coil embolization.

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Figure 10 (A-C): Patient with history of Osler-Weber-Rendu. Multiplanar images from a CT angiogram, demonstrating multiple enlarged tortuous vessels with arterial enhancement, coursing throughout the scalp and nose, with deformity of the soft tissues and midface.

Figure 10 (D-G): Lateral angiographic images of the bilateral internal maxillary arteries, before (left) and after (right) particle embolization of numerous abnormal distal branching vessels, notable for their dysplastic appearance and prominent nasal mucosal blush, compatible with multiple telangiectasias.

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Figure 11 (A-B): Young patient with facial pain, epistaxis, fevers, and altered mental status several weeks after sinus surgery. Skull radiograph and corresponding coronal maxillofacial CT demonstrate opacification of the left maxillary and ethmoid sinuses ().

Figure 11 (C-E): Serial axial images demonstrate the extent of unilateral sinus disease, involving the left maxillary, ethmoid, and frontal sinuses. Also noted is a left subperiosteal abscess ().

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Figure 11 (F-H): Additional multiplanar CT images after administration of contrast reveal an epidural air-fluid collection along the frontal lobes (), and scalp swelling along the frontal bone.

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Figure 11 (I-J): Multisequence MR images demonstrating the extent of sinus disease, epidural collection, cortical signal changes, and leptomeningeal enhancement. The latter is compatible with cerebritis.

Figure 11 (K-L): The fluid collections in the sinuses and epidural space demonstrate restricted diffusion (e.g. the left maxillary sinus on L).

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Figure 12 (A-C): 45 year old female with history of liver transplant. Serial axial postcontrast CT images demonstrate unenhancing isodense material filling the majority of the sphenoid sinus ().

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Figure 12 (D-F): Serial axial T1-weighted postcontrast images demonstrate heterogeneous peripheral enhancement within the sphenoid sinus, with T1 hypointense debris.

Figure 12 (G-I): Serial axial T2-weighted images demonstrate that the debris is has heterogeneous T2 signal intensity, with central hypointensity. The surrounding mucosa is hyperintense and thickened.

Figure 12 (J-K): Multiplanar, multisequence images redemonstrate T1-hypointense, T2-hypointense debris with peripheral mucosal enhancement. There is associated restricted diffusion within the sphenoid sinus debris (L).

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M N Figure 12 (M-N): Intraoperative photos demonstrate dark, friable debris filling and eroding the sphenoid sinus.

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Figure 13 (A-I): Serial multiplanar images from a sinus CT, demonstrate asymmetric mucosal thickening and debris throughout the right ethmoid and sphenoid sinuses. Semisolid debris fills the posterior nasal cavity and nasopharynx.

Figure 13 (J-L): Multiplanar images from a thoracic CT performed the same day, demonstate innumerable cavitary thick-rimmed nodules and masses scattered throughout the bilateral lung fields.

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Figure 12 (M-N): AP chest radiographs obtained at the time of presentation (M) and one month after initiation of treatment (N). There has been interval decrease in the overall conspicuity and number of the pulmonary lesions. A few of the larger cavities are still apparent.

Epistaxis is a commonly encountered, albeit nonspecific, clinical presentation, which can on occasion indicate the presence of a serious underlying pathology. In particular, high volume and recurrent epistaxis are more likely to be caused by any number of worrisome medical conditions, including: benign and malignant neoplasms, accidental and iatrogenic trauma, granulomatous disease, vascular malformations (both acquired and hereditary), and various infections. These conditions can be associated with high morbidity or mortality, so effective and appropriate treatment relies upon timely diagnosis.

1) Familiarize the reader with the normal vascular anatomy of the nasal cavity, with attention to the areas of shared vascular supply and potential anastomotic connections. 2) Provide a framework for deciding which vascular territories are involved in epistaxis, which may facilitate diagnosis and management. 3) Introduce a broad range of diagnoses that can be associated with morbid epistaxis, with emphasis on their classic radiologic findings across various imaging modalities.

Epistaxis can be caused by any process that leads to injury or derangement of the normal vasculature. Therefore, the differential for intranasal bleeding is broad. In general, epistaxis can be categorized by location: anterior vs. posterior, lateral vs. septal, and internal vs. external carotid supply. The nasal cavity receives blood supply from both the internal carotid (via branches of the ophthalmic artery) and external carotid arteries (via branches of the sphenopalatine and facial arteries). The territories of these arterial branches demonstrate a high degree of overlap, which carries two important consequences: 1) it provides a robust network of collateral flow to preserve the viability of delicate soft tissues throughout the nasal cavity, and 2) it allows for anastomotic routes between the internal and external arterial circulation. Both scenarios can complicate the management of epistaxis, which can be refractory in some cases or associated with unintentional embolization of the retina or brain in others. In the region of the anterior nasal cavity, two important anastomotic sites should be considered. One is between the dorsal nasal artery (terminal branch of the ophthalmic artery) and angular artery (terminal branch of the facial artery), at the level of the medial canthus; sometimes called the “orbital point.” Another is between the superior labial artery (another terminal branch of the facial artery) and the anterior ethmoidal artery, at the level of the columella; sometimes referred to as the “nasal point.” In the posterior nasal cavity, anastomotic connections exist between the branches of the sphenopalatine artery and ethmoidal branches of the ophthalmic artery, as well as with the greater palatine artery. The branches of the anterior and posterior vascular supply intersect at a rich vascular plexus along the anterior nasal septum, also known as “Kiesselbach plexus” or “Little’s area”. This is a common site for epistaxis, particularly in children, and is often easily treated with tamponade. Treatment of posterior epistaxis can be attempted with tamponade, but often will require more invasive interventions, such as clipping or embolization.

The eruption of blood from the nasal cavity is usually a self limited condition bearing little to no significant clinical consequence. Most cases are associated with irritation or injury to a rich vascular plexus within the anterior nasal septum, and easily treated with tamponade. However, epistaxis originating from the posterior vascular territories or secondary to the presence of an underlying lesion may require more invasive treatment. It is wise to maintain a broad differential in such patients The vascular supply to these lesions is often multifold, and awareness of collateral pathways can help plan treatment and anticipate outcomes.

• Indolent tumor of the sinonasal cavity, occurs in older adults • Sinonasal type of hemangiopericytoma. • Composed of perivascular glomus-like myoid cells. • Behaves less aggressively than hemangiopericytomas in

other parts of the body. • Low malignant potential and surgical resection is usually

curative. • Ddx: solitary fibrous tumor, capillary hemangioma,

leiomyoma

• Seen in 6-8% of head and neck melanoma cases, but less than 1% of all melanoma cases.

• Most common location is along the nasal septum, followed by the middle nasal turbinate (41%), inferior nasal turbinate, lateral nasal wall, then nasal floor (1%).

• Associated with poor prognosis, due to high degree of invasion at the time of diagnosis.

• Ddx: squamous cell carcinoma, minor salivary gland neoplasm, lymphoma

• Formerly known as “Wegener’s granulomatosis.” • Multiorgan vasculitis, most commonly affecting

the sinuses, upper respiratory tract, and kidneys. • Highest incidence in the 5th decade of life, and

slightly more common in men than women. • Early sinonasal disease is nonspecific, but

advanced disease is associated with marked erosions, nasal septal destruction, and orbital involvement.

• Poor prognosis in untreated patients, but >75% respond well to steroids and cyclophosphamide.

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• Fungal sinusitis can be invasive (acute, chronic, or granulomatous subtypes) or chronic (allergic or mycetoma).

• The “acute invasive” subtype is most commonly seen in diabetic patients or immunocompromised patients; Aspergillus is the most common fungal agent encountered in the latter group.

• Associated with a high mortality rate if diagnosis and treatment are delayed, due to invasion.

• Classically T2-hypointense and destructive.

• Associated with obstruction of maxillary ostiomeatal complex and other sinonasal drainage pathways.

• Classically associated with Haemophilus or Streptococcus species.

• Polymicrobial infections more common in chronic sinusitis patients.

• Classically T2-hyperintense with restricted diffusion

• Ddx: Fungal sinusitis, allergic sinusitis, chronic inflammatory sinusitis, Wegener’s granulomatosis

• Epistaxis secondary to nasal cavity telangiectasias is reported in 96% of patients with Hereditary Hemorrhagic Telangiectasias (HHT; Osler-Weber-Rendu).

• 50% of patients with HHT have related epistaxis prior to the age of 20.

• May be associated with gastrointestinal bleeding secondary to intestinal telangiectasias (present in 80%).

• Pulmonary and cerebral AVM’s are common.

• Pseudoaneurysm formation of the cavernous portion of the internal carotid artery or carotid-cavernous fistula formation is associated with any destructive skull base process.

• Etiologies include: trauma, infection, neoplasm, atherosclerosis, and radiation therapy.

• Presenting symptoms include: epistaxis, proptosis, chemosis, 3rd-6th cranial nerve deficits, Horner’s syndrome

• Intranasal passage of medical implements (e.g. nasogastric tube) should be avoided in such cases.

• Autosomal dominant inheritance; chromosome 17 • Isolated sinonasal neurofibromas are rare. • Sinonasal involvement in neurofibromatosis Type 1 (NF1) is

usually a consequence of secondary dysplasia of the sphenoid bone and orbit, due to plexiform neurofibromas arising from branches of the trigeminal nerve.

• Plexiform neurofibromas tend to occur early in life and are associated with deformities of the skull, ribs, and spine.

• Also known as olfactory neuroblastoma • Bimodal age distribution, with largest incidence in young

men and secondary peak in 5th-6th decade. • Arises from the olfactory epithelium and often erodes

through the cribriform plate. • T1-hypointense and T2-iso/hyperintense relative to brain

parenchyma • Moderate enhancement and tumoral cysts along the

superior margin is classic. • Ddx: nasopharyngeal carcinoma, adenocarcinoma

• Rare, benign, but locally aggressive vascular tumor • Most commonly seen in adolescent males • The pterygopalatine fossa and posterior nasal cavity are the

most common sites of involvement. • Tumoral vessels lack normal wall musculature and

perivascular elastic fibers, and are therefore prone to epistaxis.

• Treatment usually involves surgical resection following preoperative embolization, but recurrence is common.

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VASCULAR ANOMALIES INFECTIOUS/INFLAMMATORY

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