Endovascular Treatment of Epistaxis

Abstract

Epistaxis is not uncommon, with up to 60% of the population suffering from at least one episode in their lifetime and as many as 6% presenting for medical attention. An analysis of emergency room (ER) visits in the United States between 2009 and 2011 identified 1.2 million encounters for epistaxis, accounting for 0.32% of ER visits. Approximately 6% of patients will require more aggressive, invasive management in the form of transnasal ligation of the sphenopalatine artery or endovascular embolization. This article reviews the epidemiology, rationale for endovascular treatment, strategy for treatment, endovascular technique, postprocedural follow-up, and complications and their management.

Epidemiology

Epistaxis is not uncommon, with up to 60% of the population suffering from at least one episode in their lifetime and as many as 6% presenting for medical attention. ¹ An analysis of emergency room (ER) visits in the United States between 2009 and 2011 identified 1.2 million encounters for epistaxis, accounting for 0.32% of ER visits. ² There is a bimodal distribution, with peak incidence in children younger than 10 years and adults 70 to 79 years old. ³

Anterior epistaxis accounts for 90 to 95% of all cases. ⁴ It is very common in children and usually responds to direct compression. Vasoconstricting agents, limited cautery, and/or packing are occasionally required. ⁵ Posterior epistaxis is generally seen in adults. While anterior epistaxis is largely spontaneous or related to trauma, underlying systemic conditions such as hypertension, coagulopathy, or use of anticoagulant/antiplatelet agents have been shown to be associated with more than one-third of cases of posterior epistaxis. ^{6 7} Posterior epistaxis is more likely to be severe or intractable, can be more challenging to manage, and can be life-threatening as a result of blood loss and airway compromise. More aggressive treatments such as vessel ligation and endovascular therapy may be required. ⁸ In one study, 73% of patients hospitalized for epistaxis had comorbidities. Antithrombotic use was noted in 61% of patients, often with a history of recent change in drug or dosage. Intervention was required in 47% of patients. ⁹

A subset of severe, intractable, or recurrent epistaxis (usually posterior) is related to underlying anatomic causes. Recurrent severe is common in patients with hereditary hemorrhagic telangiectasias (HHT). ^{10 11} Epistaxis in the setting of tumor can be the result of hypervascularity, tumor necrosis, or direct invasion and blowout of the internal or external carotid artery. ^{12 13 14} Rarely, a cavernous internal carotid artery can erode and rupture into a paranasal sinus (usually the sphenoid sinus). ^{15 16} Traumatic or infectious pseudoaneurysm of the internal carotid artery, internal maxillary artery, or (rarely) another major artery can also rupture. ^{17 18 19} Severe epistaxis can also be seen following surgical procedures, particularly transsphenoidal surgery. ²⁰ Epistaxis in the setting of any of these conditions can be rapidly life-threatening, requiring emergent intervention to gain control of the hemorrhage and treat the underlying cause. ⁸

Rationale for Endovascular Treatment

Conservative management of epistaxis unrelated to one of the underlying anatomic causes described earlier is generally successful. However, approximately 6% of patients will require more aggressive, invasive management in the form of transnasal ligation of the sphenopalatine artery or endovascular embolization. ^{6 21 22 23 24} Although a few studies have demonstrated that arterial ligation is more cost-effective and associated with fewer complications, relative expertise and local availability of specialists often dictate the choice of procedure. ^{23 25 26} Endovascular embolization is successful in greater than 75% of cases. ^{7 9 26} Transient, minor complications such as local pain or numbness, headache, and transient nasal ischemia have been reported in up to 20% of cases. Major complications such as stroke, blindness, tissue necrosis, and facial nerve paralysis have been reported in 2 to 4% of cases. ^{22 27 28 29 30 31} Cutaneous foreign body granulomas following particulate embolization have been reported. ³² While the majority of embolization procedures utilize particulates, the use of other embolic agents has been explored in an attempt to decrease the complication rate and improve outcome. ^{33 34} Embolization with microcoils has been reported in 12 patients, with a success rate of 75%. There was no reported stroke, visual disturbance, tissue necrosis, or other major adverse event. ³³ Embolization with nBCA (n-butyl cyanoacrylate) (TruFill, Codman), Onyx (Medtronic, Irvine, CA), or both has also been reported in a total of 46 patients. Five patients required retreatment. No other complications were reported. ³⁴ The choice of procedure in the setting of catastrophic hemorrhage due to underlying anatomic pathology is driven by what is most likely to be rapidly successful. ^{15 16 17 18 19}

Systemic (intravenous) treatment with the anti–vascular endothelial growth factor monoclonal antibody bevacizumab has been shown to be effective in decreasing the frequency of hemorrhagic complications of HHT. ^{35 36} However, it has been challenging to demonstrate any significant decrease in frequency and severity of epistaxis. ^{37 38} Intranasal submucosal injection of bevacizumab has also been utilized, but has not been shown to be universally successful. ^{39 40 41} Endovascular embolization can be utilized in the setting of severe epistaxis to gain immediate control and allow time for bevacizumab to be effective, or when there is inadequate response.

Strategy

The strategy for treatment of typical intractable epistaxis is to simply reduce the arterial pressure head to the region without causing any ischemic damage. This allows the inflamed/damaged mucosa to heal. Usually, the side of bleeding is known, but the angiography does not demonstrate ongoing extravasation because the patient has nasal packing in place and some control over the active bleeding has been attained. In addition, epistaxis is frequently episodic in nature. However, abnormal vessels can be seen, appearing dilated, beaded, and tortuous ( Fig. 1a ). Embolization is aimed at producing occlusion of proximal arterioles without true capillary devascularization ( Fig. 1a, b ). This is accomplished by superselective (not regional) embolization with particles in the 300- to 700-μm range. This will effectively decrease perfusion pressure to the area embolized while maintaining low-pressure collateral supply, preventing ischemic injury.

Fig. 1.

Typical posterior epistaxis. This is a 59-year-old man with allergic rhinitis and hypertension who is on warfarin for atrial fibrillation. He presents with recurrent epistaxis from the right nasal cavity. ( a ) Anteroposterior projection of angiography obtained following placement of the microcatheter in the internal maxillary artery. There is no filling of unexpected vascular structures. Note the irregular appearance of many of the arteriolar branches. ( b ). Following embolization with 300–500 μm spherical polyvinyl alcohol particles, there is stasis of flow in the arterial branches. The patient made an uneventful recovery with no further episodes of epistaxis.

If the underlying problem is bleeding from a tumor, the capillary bed itself must be eliminated to achieve a satisfactory result. The tumor is usually not bleeding secondary to necrosis, but due to the fact that the vessels themselves are intrinsically abnormal. These vessels must be devascularized by superselective, distal microembolization utilizing dilute particles (to prevent clumping) in the 100- to 300-μm range.

Intrinsic vascular pathology such as HHT requires a similar approach ( Fig. 2a–d ). Angiographic evaluation usually reveals innumerable abnormal blood vessels, not only in the nasal mucosa but involving the palate and tongue as well ( Fig. 2c ). In this setting, there is often recurrent epistaxis because of development of new abnormal vessels. Arteriovenous shunting may also be present ( Fig. 2d ). Embolization with particles in the 100- to 300-μm range is generally efficacious. ⁴² If there is significant arteriovenous shunting, larger particles (300- to 500-μm) may be required. Proximal occlusion of the maxillary artery not only prevents repeat treatment but also encourages development of collateral supply from the facial arteries, the ascending pharyngeal arteries, and ethmoidal branches of the ophthalmic arteries, increasing the difficulty of treatment ( Fig. 2c, d ). Collateral supply may develop after repeated successful distal embolization as well. Focused beam radiation therapy has occasionally been used successfully in this setting and may provide prolonged relief. ⁴³

Fig. 2.

Hereditary hemorrhagic telangiectasias (Osler–Weber–Rendu syndrome). This is a 59-year-old woman with HHT who has a history of recurrent severe epistaxis unresponsive to conservative measures up to and including cautery. She has previously required embolization of a pulmonary malformation and has required multiple transfusions. ( a ). Lateral projection of angiography obtained following microcatheter placement in the right internal maxillary artery. Note the hyperemic mucosa (arrow) with multiple abnormal vessels and telangiectasias. ( b ) Following embolization with 250–350 μm polyvinyl alcohol particles, there is significant devascularization. The left internal maxillary artery was similar in appearance and bilateral embolization was performed with control of the epistaxis. ( c ) Lateral projection of left common carotid arteriography. The patient required several additional embolizations for recurrent epistaxis. A subsequent angiography revealed that the dominant supply to the nasal mucosa was now from ethmoidal branches of hypertrophied ophthalmic arteries (arrow). It was felt that these could not be safely embolized. Note the telangiectasias in the tongue and soft palate (stars). Additional supply from the right facial artery was also identified. ( d ) Anteroposterior projection of angiography performed after selective catheterization of the right facial artery. Again, there is hyperemic mucosa with multiple telangiectasias. Note the early opacification of the draining venous structures (arrows). This facial artery supply was successfully embolized. The patient then underwent focused beam radiation therapy and has been free of epistaxis for 3 years.

Rupture of an aneurysm or pseudoaneurysm results in true arterial epistaxis and can be a life-threatening emergency. In this setting, the goal of treatment is to gain control of the bleeding source rapidly and, ideally, provide definitive treatment of the lesion. The standard endovascular techniques of aneurysm treatment, such as coil embolization without or with stent assist or flow diversion, can be employed if they are available and there is sufficient expertise with their use. The use of a balloon occlusion guide catheter to control the rate of bleeding may be advantageous. Although covered stents are not normally utilized in the treatment of aneurysms, the use of one in this setting as a life-saving measure can be considered if other options are not immediately available. Care must be taken when positioning the stent to avoid occluding major arterial branches. In the setting of a pseudoaneurysm, the use of a flow diverter or covered stent may be the most appropriate choice. If the bleeding source is a pseudoaneurysm or laceration of an external carotid artery branch such as the internal maxillary artery, occlusion of the artery with coils is usually sufficient. If the aneurysm/pseudoaneurysm cannot be treated endovascularly, inflation of a balloon across the bleeding site may allow for temporary control while definitive therapy (usually carotid sacrifice) is coordinated.

Internal carotid artery “blowout” caused by tumor invasion is best managed by deployment of a covered stent. It is important to choose a stent long enough to completely span the diseased segment of the artery. If it is not possible to cross the involved segment and gain distal access, carotid sacrifice may be necessary.

Technique

The management of the patient in the angiography suite depends on the patient's condition. If the epistaxis is not well controlled, general endotracheal anesthesia will allow protection of the patient's airway. If the patient is unstable, the assistance of the anesthesiologist in patient management is also welcome.

Treatment of epistaxis, like all endovascular procedures, should be started with a control angiography of the intracranial vasculature. This provides a baseline for comparison if there is any question of inadvertent intracranial embolization or other mishap during the procedure, and helps visualize any aberrant vascularity that may result in dangerous connections between the internal and external carotid artery or may lead to therapeutic failure. ^{44 45 46}

Guide Catheter Placement

Upon completion of the diagnostic angiography, the common carotid artery on the involved side is selectively catheterized with a standard diagnostic catheter. Utilizing a safe exchange wire with a coiled or “ J ”-shaped tip, the diagnostic catheter is exchanged for a guide catheter. Since there is usually no need for robust support, and spasm is to be avoided, a 6-Fr guide catheter with a soft atraumatic tip should be used. A balloon occlusion guide catheter can be used if the need for proximal flow control is anticipated. A true guide catheter is not absolutely necessary for particle embolization of “typical” epistaxis (no underlying anatomic pathology) owing to the clear goal (internal maxillary artery) and relatively constant anatomy. A microcatheter can be advanced through the diagnostic catheter. However, guide catheters are optimized for this purpose, as they are designed to sit safely in a brachiocephalic vessel, support advancement of a microcatheter, and allow injection of contrast around the microcatheter for road mapping and assessment of progress during treatment. The minimal inconvenience and time associated with exchanging for a guide catheter is more than offset by the degree of improvement in the efficiency of the procedure.

Depending on the target of the procedure, the external or internal carotid artery is then carefully catheterized with this guide catheter. A rotating hemostatic valve is attached to the end of the catheter. The side port is connected to a heparinized, pressurized flush through a three-way stopcock, allowing for contrast injection. As in any procedure, care should be taken not to introduce air bubbles into the system at any time.

Vasospasm

In the setting of epistaxis, it is better to avoid vasospasm caused by catheter and wire manipulation than to treat it with vasodilators, which may worsen the bleeding (and result in the need to secure the patient's airway). It is prudent, however, to have a premixed solution of nitroglycerin ready (50 μg/mL normal saline) to be used in the event of vasospasm secondary to catheter or wire manipulation.

The external carotid artery and its branches are particularly prone to vasospasm. Therefore, careful catheterization is necessary to prevent vasospasm. Not only will proximal vasospasm result in increased difficulty visualizing the abnormal vessels, the decreased pressure can cause shifts in hemodynamics. Distal anastomoses from other territories can reverse flow in the internal maxillary artery, resulting in misdirected embolization. In addition, potentially dangerous anastomoses with the intracranial circulation may not be visualized. It is imperative to treat vasospasm before continuing the procedure.

Initial Angiographic Evaluation

The control angiography is performed after the guide catheter is positioned in the internal or external carotid artery (and vasospasm, if any, has resolved). In the setting of planned embolization for typical epistaxis, this is carefully evaluated to identify any potentially dangerous collateral supply to the intracranial structures. It is also important to evaluate for anomalous vessels or aberrant supply to the nasal mucosa ( Fig. 2c, d ).

Microcatheter Placement

Most endovascular treatment strategies for epistaxis require the use of a microcatheter. The choice of microcatheter and microguidewire depends on the procedure to be performed and personal preference. The endovascular treatment of ruptured cerebral aneurysms with detachable coils, stent assist, and flow diverters is beyond the scope of this article. If the use of detachable coils or deployment of a covered stent is planned, the catheter chosen must be compatible with the delivery system. The remainder of the “Technique” section will focus on particulate embolization for typical epistaxis, intrinsic vascular pathology such as HHT, and tumor-related epistaxis not caused by carotid blowout.

When choosing a microcatheter and microguidewire for particulate embolization in the external carotid artery circulation, the guidewire must be capable of navigating the tortuous anatomy of the external carotid artery and its branches. The microcatheter must be able to track over the wire in its anatomy. Most microcatheters designed for neurointerventional procedures are capable of delivering the embolic particles without clogging in the hub or clogging the catheter (usually caused by the catheter lumen assuming an oval shape around a tight bend). It is important to verify that the catheter is capable of delivering the particle size that is to be used.

The microcatheter of choice is advanced through the guide catheter over the microguidewire into the target artery (the internal maxillary artery except in special circumstances). The internal maxillary artery provides variable supply to the intraorbital (or retro-orbital) region, cavernous sinus, nasal turbinates and septum, sphenoid and maxillary sinuses, hard palate, and other facial areas. Most importantly, it can provide supply to the retina. The middle meningeal artery arises just beyond the point where the internal maxillary artery transitions from an ascending to a horizontal, anteromedial course. The middle meningeal artery continues an ascending course. The pterygopalatine division of the internal maxillary artery supplies the branches typically involved in posterior epistaxis (the sphenopalatine artery, greater palatine artery, posterior superior alveolar artery, and pharyngeal and vidian arteries). These branches arise beyond the origins of the superficial temporal and anterior deep temporal arteries and the middle meningeal artery. They are medial to the mandibular ramus on frontal projections and continue anteromedially toward the nose. It is important to look for anastomoses between the vidian artery and the petrous internal carotid artery. The catheter tip should be placed distal to the origin of the middle meningeal artery, accessory meningeal artery, and deep temporal artery(ies) (the major superiorly directed branches of the internal maxillary artery; Fig. 1a , 2a ).

Once the microcatheter is in position, a baseline angiography is performed through the microcatheter ( Fig. 1a , 2a ). It is important to include the orbit during this examination. The images should be inspected for evidence of direct supply to the globe (presence of choroidal blush) or anastomoses with the intracranial circulation. It is wise to inject with enough force to produce reflux around the microcatheter; this may identify potentially dangerous branches that might be inadvertently embolized if there is reflux during particle embolization (which is not infrequent). Even if potentially dangerous communications are present, embolization can be undertaken if it is possible to protectively embolize the dangerous branches with coils prior to particle embolization, which will prevent any possible entry of particles into these vessels and allow more thorough particulate embolization of the target territory.

Embolization

The goal of therapy in a typical case of epistaxis, as noted earlier, is to reduce the pressure long enough for the mucosa to heal. Occlusion with a nonpermanent agent that occludes small arterial branches and large arterioles and allows low-pressure distal collateral perfusion would be ideal. The optimal particle size would be in the 200- to 700-μm range. Unfortunately, there is no true short-term temporary agent that is readily available in this size range. Gelfoam would be the ideal agent, but it is not available in specific size ranges. Gelfoam torpedoes are difficult to use with microcatheters and have to be prepared individually. Avitene or Gelfoam powder is not available in controlled particle size; particles less than 100 μm in size may result in tissue necrosis or nerve damage as well as possibly pass through small dangerous collaterals.

The commonly available particulate embolic agents (polyvinyl alcohol particles and gelatin microspheres) are not truly permanent agents. Recanalization of a variable percentage of the occluded vessels occurs, and there is rich collateral supply to the nose and face. Depending on factors such as catheter location, speed of flow, and degree of hemorrhage, particulate embolic agents 300 to 500 μm or 500 to 750 μm are typically used. If the source of bleeding is an abnormal capillary bed, such as a tumor or HHT, 100- to 300-μm particles are typically used unless the presence of arteriovenous shunting necessitates the use of larger particles. The particles are suspended per the manufacturer's instructions and diluted enough to prevent clogging the microcatheter hub during injection.

Embolization should be performed under fluoroscopic observation to avoid inadvertent reflux of particles. Serial angiograms are performed through the microcatheter as the embolization proceeds to carefully monitor flow. This procedure should not require a large amount of particles. Generally, one to three (3 mL) syringes of dilute particles are adequate to occlude the target vessels ( Fig. 1b , 2b ). Once the territory distal to the anterior deep temporal and meningeal vessels is occluded (there is near stasis in the arterial branches), a repeat bilateral external carotid angiography is performed.

Occasionally, the ascending pharyngeal and facial artery provide significant collateral supply to the nose or posterior nasal turbinates. The ascending pharyngeal artery supply can be difficult to demonstrate as the source of collateral supply if the artery is not selectively catheterized and injected. Not infrequently, collateral supply may be seen to arise from the opposite internal maxillary artery across the midline. These sources of collateral supply may need to be superselectively embolized, particularly the contralateral internal maxillary artery. Bilateral embolization is generally needed in the setting of true vascular pathology such as HHT.

If it is necessary to embolize the internal maxillary artery territory bilaterally, small (100–300 μm) particles should not be used on both sides. If it is necessary to use particles this small on the affected side, 500- to 700-μm particles should be used on the contralateral side to avoid excessive devascularization and the risk of ischemic complications. It is generally safe to use 300- to 500-μm particles in small territories on both sides. Devascularization of smaller territories decreases the likelihood of ischemic injury. This requires superselective catheterization. ⁴²

Completion of the Procedure

It is always prudent to perform a final injection of the common carotid artery bilaterally at the end of the procedure and to compare this with the initial examination to exclude intracranial embolization or other mishap.

The patient should be examined for evidence of ischemia in the embolized territory. It is important to perform a neurological examination as soon as possible, preferably before the patient leaves the angiography suite. The patient should be assessed for any evidence of cranial nerve deficit or stroke.

If there is any question regarding the efficacy of the embolization, the nasal packing can be removed on the angiography table. If the patient was intubated for the procedure, removal of the packing prior to extubation serves two purposes. First, it causes less discomfort for the patient. Second, the airway remains protected while the packing is removed. The timing of removal of the packing should be discussed with the otorhinolaryngologist.

Postprocedure Follow-up

It is important to check the patient postprocedure for signs of ischemic complications. Also, as with any devascularization procedure, patients may experience postprocedure pain even if there is no ischemic injury. This pain responds well to ketorolac tromethamine (Toradol; Roche, Indianapolis, IN; 10 mg PO qid). This aching pain is usually self-limiting and will resolve in 1 to 3 days.

Patients with typical epistaxis rarely require repeat embolization. While patients with bleeding from tumors may require more than one treatment, patients with HHT typically require multiple treatments. It is prudent to follow up these patients with the otorhinolaryngologist.

Complications and Management

No discussion of any procedure is complete without a discussion of potential pitfalls, how to avoid them, and how to manage them. Potential complications of embolization for epistaxis include tissue ischemia, stroke, and cranial nerve damage. ^{22 27 28 29 30 31}

Intraprocedural Ischemia

It is important to examine the patient for signs of nasal or facial ischemia prior to terminating the procedure. If there appears to be true ischemia after embolization (typically bilateral), nitroglycerin (50 μg/mL) can be infused superselectively at the end of the procedure. This will result in dilatation of collateral arterial channels and increased perfusion. This is the theory behind the use of nitroglycerin to treat the “no-reflow” phenomenon following coronary interventions. These channels would eventually dilate; this hastens the process.

Postprocedure Ischemia

If ischemia appears to be present in the embolized territory after the procedure, efforts should be made to increase the perfusion to the ischemic tissue. Local application of heat by means of warm compresses, warm towels, or a warm water bag is often successful. If this is not sufficient, further vasodilatation may be achieved by direct application of nitroglycerin paste.

Cranial Nerve Damage

Cranial nerve deficits following embolization for epistaxis are usually caused by perineural soft-tissue edema rather than ischemia of the nerve itself. If a cranial nerve deficit is noted after the procedure, administration of methylprednisolone (250 mg IV every 6 hours) may be helpful. The deficit will typically improve over a period of days to weeks. If embolization was performed with small particles for atypical pathology, true ischemia may be present. This may respond to efforts to treat the ischemia and administration of steroids.

Stroke

Careful evaluation of the preembolization angiographic images to exclude dangerous collaterals and anastomosis, along with careful embolization technique, should make embolization of routine epistaxis a safe procedure. However, it is important to review the final images carefully for any evidence of intracranial embolization and to perform a neurological examination as soon as possible after completing embolization.

In most instances, the stroke will be caused by occlusion of a small arterial branch to an eloquent territory (e.g., internal capsule). Since the occlusion is usually caused by the embolic material, it is not generally amenable to intra-arterial thrombolytic therapy and/or mechanical thrombectomy. Rarely, there may be a large embolus arising from the guide catheter, particularly if the continuous heparinized flush has been interrupted. In this instance, treatment should be attempted by mechanical thrombectomy.

If a small-vessel occlusion is suspected, oxygen should immediately be administered. Immediate heparinization may prevent further propagation of thrombus associated with the offending particles, but is of uncertain value. The mean arterial pressure should be raised (by ∼20–40 mm), generally by administration of intravenous fluids.

Conclusion

Epistaxis is a fairly common occurrence, with up to 60% of the population experiencing at least one episode. Anterior epistaxis accounts for the vast majority of cases, and usually responds to conservative management. Posterior epistaxis is more challenging to treat conservatively due to anatomic considerations and the fact that there is a higher percentage of underlying pathology. While there are often several treatment options, embolization can be utilized to treat both refractory spontaneous epistaxis and epistaxis associated with underlying pathology. In the setting of massive hemorrhage related to carotid blowout or rupture of an aneurysm, endovascular treatment may provide life-saving control of the hemorrhage as well as definitive treatment.