Embolization Therapy: Principles and Clinical Applications, 1 Ed.


Long Chen • Ali Akber Hazari • Laura MacNeil • Kieran Murphy

Epistaxis, commonly known as a nosebleed, is the most common otolaryngologic emergency.1 It is estimated that 60% of people have experienced at least one episode of epistaxis, with 6% requiring medical attention.2 Although this medical condition is not always recognized as life-threatening, there have been incidences where epistaxis has led to serious complications, and if not treated effectively, it can be fatal. Therefore, it is crucial that the techniques and treatments used in prevention are well understood.

Many studies indicate that the severity of the epistaxis depends on where the bleed originates. Clinically, anterior bleeds are usually less severe than posterior bleeds, and in about 80% of cases, epistaxis originates from the anterior septal area.1,3 Kiesselbach plexus, an “anastomosis with branches from both the internal and external carotid artery systems,” is responsible for most anterior septal nosebleeds, for example, those which children experience in the winter time.3 Anterior septal nosebleeds would also include epistaxis resulting from trauma, digital irritation, and dryness.3 The posterior septal area is where epistaxis can be severe, more specifically the Woodruff area where the “anastomoses of the sphenopalatine and pharyngeal arteries is found.”3

In a case of epistaxis, the aim of treatment is to do at least one of the following: reduce bleeding through decreasing arterial inflow pressure, reduce mucosal irritation, or reduce blood flow by inducing clot formation. The initial treatment of epistaxis is based on nasal packing and chemical or electrocautery.4 This is usually successful for the anterior septal area and is also a first-line therapy for posterior epistaxis.4,5 However, the posterior nasal vault is located in an inaccessible region, causing this method to prove ineffective 25% to 50% of times.6,7 Nasal packing can also be painful for the patient.6 Patients with preexisting pulmonary or cardiac problems are at serious risk for hypoxia, cardiac arrhythmias, or sepsis when treated with nasal packing.8 This is a particular risk in patients with heart disease where the mucosal absorption of epinephrine can result in ischemia.

If the prior proves unsuccessful, patients are treated with nasal packing along with transantral maxillary artery and ethmoid artery ligation.8 The aim of this treatment is to surgically achieve homeostasis at the affected area by decreasing arterial blood flow so epithelial repair and clotting may occur.8 However, this procedure is not always successful in achieving the desired homeostatic result and also puts the patient at risk for anesthetic problems, septal perforation, infraorbital nerve dysfunction, ophthalmoplegia, blindness, or myocardial infarction.8 Rarely, postsurgical pseudoaneurysms develop.

Therefore, both these methods have been proven to carry a relatively high number of risks and possible complications, making alternative therapies more favorable for patients with severe cases of epistaxis.

One such alternative therapy, which has proven to be very effective, is endovascular embolization. Embolization is the process of inducing blood clots or embolus to occlude blood flow. In 1974, Sokoloff et al.9 reported the first successful percutaneous embolization of the internal maxillary artery causing nasal hemorrhage. A later study conducted in 1995 by Elahi et al.7 demonstrated a 96% success rate in treating patients with intractable epistaxis using embolization. Embolization is a relatively short procedure, which increases both safety and accuracy.7 Moreover, a patient who has undergone embolization is able to remove his or her posterior nasal pack earlier, which allows for a reduced hospital stay and increased patient comfort.7 The technique has since then been widely accepted and its efficacy confirmed.10Nevertheless, in some institutions and in case the of conservative treatment failure, angiographic embolization remains the procedure of first choice.11


Once a year, our group is asked to review strokes that occur during epistaxis embolizations. Usually, this happens in a procedure performed by a well-intentioned interventional radiologist who uses a 5-Fr glide catheter to close the internal maxillary. This is a recipe for disaster. Strict guiding catheter and microcatheter technique must be used. Embolization is a procedure that can be conducted using various techniques or materials, for example, microcoils, gelfoam, glue, and polyvinyl alcohol (PVA) foam. Microcoils are overused by inexperienced practitioners and are a major problem in patients with recurrent bleeding as they recanalize, allowing reperfusion but obstructing embolization access. In transarterial embolization, physicians will use 6-Fr guiding catheters, microcatheters, and microwires to access the sphenopalatine branch of the internal maxillary artery.12 As it is difficult to reach areas in the nasal cavity, microcatheters are often preshaped in a 30- to 45-degree angle.12 The materials mentioned earlier are sometimes used in combination with one another. Patients should be heparinized during procedures to decrease the risk of periprocedural stroke.

PVA particles with a diameter of 300 to 500 μm are used for embolization of epistaxis.13 Particles with a smaller diameter should be avoided as they can navigate through the skull base extracranial–intracranial dangerous anastomosis and cause stroke. On the other hand, a larger diameter can clump and block the microcatheter. To balance the benefit of embolization therapy and the risk of complications, it is recommended that the range in diameter is between 300 and 500 μm.4,14

N-butyl cyanoacrylate (NBCA), detachable balloons, and microcoil embolization should be reserved for massive bleeding, when it is necessary to sacrifice internal carotid artery for epistaxis caused by internal carotid artery lesion such as a gunshot wound.15 For arteriovenous malformation (AVM) or dural arteriovenous fistula (DAVF), NBCA or Onyx (Covidien, Irvine, California) can be employed for embolization.1618


Transarterial embolization therapy should be conducted under conscious sedation, but in an agitated patient, general anesthesia (GA) should be used.19,20 Embolization under GA is recommended for patients with major blood loss, especially for cases of epistaxis caused by trauma, which are usually accompanied with a major blood loss and of higher risk for aspiration. Confused patients move and you lose your road map guidance. In that situation, it is harder to detect excessive reflux of embolic material retrograde from the catheter tip and potentially into the carotid bifurcation and hence internal carotid artery and cause stroke.

Complete common carotid and bilateral internal and external carotid arterial angiography should be conducted before embolization19,21 (Fig. 15.1). Preembolization angiography should be performed to indentify lesions such as AVMs, DAVF, and pseudoaneurysms. Preembolization diagnostic angiography can identify if extracranial–intracranial dangerous anastomosis exist. The key dangerous anastomosis exists between the middle meningeal artery and the ophthalmic artery. Due to anatomical variation, dangerous anastomoses exist between external and internal carotid arteries and their ophthalmic artery branches. Even if there is no extracranial–intracranial dangerous anastomosis detected by conventional angiography, potentially dangerous anastomosis will still open with an increase in the injection pressure during the embolization process. Internal and external carotid artery anastomoses can occur with vidian artery, artery of the foramen rotundum, the ascending pharyngeal artery, branches of middle meningeal artery and accessory meningeal artery, sphenopalatine artery, and branches between sphenopalatine artery and ophthalmic artery (Fig. 15.2).4,19 If embolic materials traverse through these anastomosis from external carotid artery to internal carotid artery or ophthalmic artery, it may cause cranial nerve palsy, loss of vision from retinal artery embolization, or even stroke.19,22

The internal carotid artery angiography could directly reveal if the ophthalmic artery branches out from the internal carotid artery and if there is development of choroidal blush. The blood supply to the ophthalmic artery from the branches of the middle meningeal artery should be closely watched for. The recommended sequence for performing angiography is to start from the common carotid and internal carotid artery, followed by external carotid artery of the diseased side. Then the same procedure is repeated on the other side.19

The main blood supply to the nasal cavity is from the sphenopalatine artery, which is branched from the internal maxillary artery. The normal embolization method is through a superselective microcatheter to the distal end of internal maxillary artery for angiography before embolization. In some cases, it can be difficult to place a catheter into the distal end of the internal maxillary artery or the inside of sphenopalatine artery or if the parent artery is extremely tortuous.

The operator should always bear in mind that the purpose of treating epistaxis is not to devascularize the nose but rather to reduce the blood flow pressure in certain areas so as to facilitate the formation of local thrombus and self-healing of the hemorrhage area. Thus, it is recommended that the diameter of embolization particles should not be less than 150 μm to avoid the possibility that a smaller particle could go intracranial through dangerous anastomosis and cause catastrophic consequences. Before embolization, it is important that a wedged catheter position is avoided and there is still forward blood flow in the distal end of the microcatheter. If a wedged catheter position and complete cutoff of forward blood flow occurs, the injection pressure can increase during the embolization process, incurring the risk of opening potential extracranial–intracranial dangerous anastomosis. It would also increase the risk of reflux of embolic materials into nontargeted vessels. In addition, it is very important to keep the microcatheter stable during the embolization process. This is especially true in the later stages of the process to avoid displacement of the microcatheter, which can be caused by increased injection pressure. During the embolization, a suspension of embolic and contrast material is subsequently injected under fluoroscopic control until significant flow reduction is noted in the target vessel (Figs. 15.3 to 15.5).19


Idiopathic Epistaxis

At least 70% of epistaxis cases are idiopathic.10,23 In this situation, there is often no characteristic angiography manifestations, and even otolaryngologist are unsure which side is the cause of bleeding. There is an extensive branch anastomosis among blood vessels of the two sides of nasal cavity, and thus the bilateral sphenopalatine artery may sometimes need to be embolized. Normally, successful hemostasis is achieved with internal maxillary route embolization alone, although rarely, it is necessary to embolize both facial artery branches. This has an additional risk of minor complications such as skin or mucosal necrosis, particularly if very small embolic material is used (50 to 199 μm).4,20,24 PVA particles with sizes 300 to 500 μm are the material of choice. It is not recommended to use microcoils to occlude main vessels as these become road blocks if a reembolization is needed in the future. Compared with other cases of epistaxis, the success rate of embolization therapy for idiopathic epistaxis is higher, and the long-term success rates could reach as high as 93.5%.20

Trauma or Iatrogenic Injury

For epistaxis caused by trauma or iatrogenic injury, bleeding usually occur immediately after the injury or medical procedure but can be delayed.15 Most would happen within 3 weeks after injury.15 For epistaxis caused by trauma or iatrogenic injury, diagnostic angiography may reveal a pseudoaneurysm of internal or external carotid artery, and in an active situation, you may see contrast media extravasation. For epistaxis caused by external carotid artery injury, the treatment method is similar to that for spontaneous epistaxis. However, trauma patients in shock may have injured vessels that are constricted or in spasm. Although bleeding can be controlled temporarily with embolization, blood pressure will increase once bleeding has stopped, the peripheral vascular bed will reopen, and the chances of bleeding reoccurring can be high. Using particles for embolizing diseased vessels, gelfoam pledgets, or microcoil for embolizing main branches of diseased vessels could be considered to consolidate the embolization effect and reduce the rate of bleeding. In urgent cases, NBCA is an excellent tool to achieve instant closure of a rapidly bleeding vessel. NBCA is, however, a complex material to use and should not be used by the inexperienced.

Pseudoaneurysm induced by injury of the internal maxillary or proximal external carotid can be difficult to handle. This is usually either traumatic or a complication of an endoscopic approach.25 Permanent vessel occlusion is the best solution.

Infectious Aneurysm

The wall of infectious aneurysm is thin; direct embolization of an aneurysm could possibly cause rerupture due to the fragile nature of the aneurysmal wall. Principally, treating infectious aneurysm of branches of external carotid artery is done to embolize the parent artery. The operational procedure is the same as previously described. For treatments of infectious aneurysm of the internal carotid artery, the principle is similar to that for traumatic pseudoaneurysm. In cases where a balloon occlusion test is tolerated, sacrificing the internal carotid artery of the diseased side can be considered for treatment. Another alternative therapy is a stent graft.

Hereditary Hemorrhagic Telangiectasia

The treatment of epistaxis in patients with hereditary hemorrhagic telangiectasia (HHT) is initially conservative. The success rate of embolization for treating HHT-induced epistaxis is only 20% to 25%, whereas the rate is as high as 90% for idiopathic epistaxis.20,26 It is difficult for embolization therapy to achieve radical treatment of HHT, and the purpose of the treatment is mainly to reduce the frequency of epistaxis occurrence and lessen the severity of each episode.27 Due to the fact that abnormal angiogenesis constantly exists, it is very difficult to conduct permanent embolization therapy for diseased vessels caused by HHT.26 In considering the refractory nature and high rate of recurrence for epistaxis induced by HHT, it is not recommended to use such permanent embolic materials as microcoil to embolize the main branches of diseased vessels so as to preserve the interventional approach for future treatment.27


The complication of embolism therapy for epistaxis fall into two categories: minor transient adverse event and major complications. Major complications can be further categorized as major transient or persistent.19 Patients with minor transient adverse event such as headache, facial pain, jaw pain, trismus, facial edema, or facial numbness are able to recover quickly without any disturbing aftereffects. Major transient complications include skin slough, temporary hemiparesis, temporary monocular visual field loss, and mucosal necrosis.19 Persistent complications include facial scarring following ischemia, monocular blindness, peripheral facial nerve paralysis, cerebral infarction, and ischemic sialadenitis requiring surgery.19 Larger series report minor transient complications in 25% to 59%, major transient in 0% to 1%, and persistent in 2% of cases.19 Smith4 retrospectively analyzed 15 clinical studies on embolism therapy for epistaxis and found that the occurrence rate of serious complication was 0% to 8% and the average rate was 3%.


• Create a separate table for the embolization materials and keep the bowls with the PVA, the contrast used for control injections, and all other equipment that have contact with embolic material. Do not cross-contaminate your diagnostic equipment.

• Do not do a final control injection with the guiding catheter in a common carotid ever. Most strokes occur from clot in the guide around the microcatheter.

• Use a negative road map. Foot on road map. Inject nothing, then use that image as the guide for the embolization. It allows you see dangerous anastomosis easier.

• Some of our patients have been elderly women with left-sided nosebleeds and a horrible ecstatic aortic arch. Keep a few Simmons 2 (Cook Medical Inc., Bloomington, Indiana) Envoy guide catheters on your shelf for this situation. If that is not working for you, look at some of the cardiology internal mammary guide catheters.

• Control the patient’s blood pressure.

• Heparinize the patient for the embolization. You can always give blood. You cannot give gray cells if you have a procedural stroke. The last thing you want to do is to give recombinant tissue plasminogen activator to someone with epistaxis.

• With a diagnostic catheter, do a complete preembolization angiography, common carotid to look for atheroma, then internal and external carotid arteries to identify extracranial–intracranial dangerous anastomosis.

• Appropriate range for diameter of PVA particles is 300–500 μm. Smaller particles increase the risk of skin necrosis and stroke.

• Do not wedge the catheter in the vessel and always maintain the forward flow of blood during embolization process; pay attention to the change of injection pressure or increase in resistance.

• If you block the microcatheter with PVA delivered by a 3-mL syringe, carefully unblock it using a contrast-filled 1-mL syringe or consider pulling the microcatheter out and recanalize it on the procedure table.

• Have a system to identify the syringes used in the embolization. We use 3-mL Luer lock syringes. We use Steri-Strips (3M, St. Paul, Minnesota) to identify the three different syringes, and they draw up from three different bowls. The syringes used for saline are bare, that is, no Steri-Strip; the contrast syringes have one Steri-Strip; and the PVA syringes have two Steri-Strips. The bowls have Steri-Strips that match this. The embolization space is self-sufficient. You never ever draw up saline or contrast from your diagnostic system with any syringe that came from the embolization table as a PVA particle can contaminate the clean system and cause a stroke.


 1. Shukla PA, Chan N, Duffis EJ, et al. Current treatment strategies for epistaxis: a multidisciplinary approach. J Neurointerv Surg. 2013;5(2):151–156.

 2. Small M, Murray JA, Maran AG. A study of patients with epistaxis requiring admission to hospital. Health Bull (Edinb). 1982;40(1):20–29.

 3. Fatakia A, Winters R, Amedee RG. Epistaxis: a common problem. Ochsner J. 2010;10(3):176–178.

 4. Smith TP. Embolization in the external carotid artery. J Vasc Interv Radiol. 2006;17(12):1897–1912; quiz 1913.

 5. Schlosser RJ. Clinical practice: epistaxis. N Engl J Med. 2009;360(8):784–789.

 6. Breda SD, Choi IS, Persky MS, et al. Embolization in the treatment of epistaxis after failure of internal maxillary artery ligation. Laryngoscope. 1989;99(8, pt 1):809–813.

 7. Elahi MM, Parnes LS, Fox AJ, et al. Therapeutic embolization in the treatment of intractable epistaxis. Arch Otolaryngol Head Neck Surg. 1995;121(1):65–69.

 8. Schaitkin B, Strauss M, Houck JR. Epistaxis: medical versus surgical therapy: a comparison of efficacy, complications, and economic considerations. Laryngoscope. 1987;97(12):1392–1396.

 9. Sokoloff J, Wickbom I, McDonald D, et al. Therapeutic percutaneous embolization in intractable epistaxis. Radiology. 1974;111(2):285–287.

10. Tseng EY, Narducci CA, Willing SJ, et al. Angiographic embolization for epistaxis: a review of 114 cases. Laryngoscope. 1998;108(4, pt 1):615–619.

11. Asanau A, Timoshenko AP, Prades JM. Strategy of modern epistaxis management. Cardiovasc Intervent Radiol. 2012;35(3):709–710.

12. Mahadevia AA, Murphy KJ, Obray R, et al. Embolization for intractable epistaxis. Tech Vasc Interv Radiol. 2005;8(3):134–138.

13. Koh E, Frazzini VI, Kagetsu NJ. Epistaxis: vascular anatomy, origins, and endovascular treatment. AJR Am J Roentgenol. 2000;174(3):845–851.

14. Christensen NP, Smith DS, Barnwell SL, et al. Arterial embolization in the management of posterior epistaxis. Otolaryngol Head Neck Surg. 2005;133(5):748–753.

15. Chen D, Concus AP, Halbach VV, et al. Epistaxis originating from traumatic pseudoaneurysm of the internal carotid artery: diagnosis and endovascular therapy. Laryngoscope. 1998;108(3):326–331.

16. Friedlander RM. Clinical practice: arteriovenous malformations of the brain. N Engl J Med. 2007;356(26):2704–2712.

17. Agid R, Terbrugge K, Rodesch G, et al. Management strategies for anterior cranial fossa (ethmoidal) dural arteriovenous fistulas with an emphasis on endovascular treatment. J Neurosurg. 2009;110(1):79–84.

18. Thiex R, Wu I, Mulliken JB, et al. Safety and clinical efficacy of Onyx for embolization of extracranial head and neck vascular anomalies. AJNR Am J Neuroradiol. 2011;32(6):1082–1086.

19. Willems PW, Farb RI, Agid R. Endovascular treatment of epistaxis. AJNR Am J Neuroradiol. 2009;30(9):1637–1645.

20. Strach K, Schrock A, Wilhelm K, et al. Endovascular treatment of epistaxis: indications, management, and outcome. Cardiovasc Intervent Radiol. 2011;34(6):1190–1198.

21. Lasjaunias P. Nasopharyngeal angiofibromas: hazards of embolization. Radiology. 1980;136(1):119–123.

22. Geibprasert S, Pongpech S, Armstrong D, et al. Dangerous extracranial-intracranial anastomoses and supply to the cranial nerves: vessels the neurointerventionalist needs to know. AJNR Am J Neuroradiol. 2009;30(8):1459–1468.

23. Elden L, Montanera W, Terbrugge K, et al. Angiographic embolization for the treatment of epistaxis: a review of 108 cases. Otolaryngol Head Neck Surg. 1994;111(1):44–50.

24. Fukutsuji K, Nishiike S, Aihara T, et al. Superselective angiographic embolization for intractable epistaxis. Acta Otolaryngol. 2008;128(5):556–560.

25. Redekop G, Marotta T, Weill A. Treatment of traumatic aneurysms and arteriovenous fistulas of the skull base by using endovascular stents. J Neurosurg. 2001;95(3):412–419.

26. Risley J, Mann K, Jones NS. The role of embolisation in ENT: an update. J Laryngol Otol. 2012;126(3):228–235.

27. Layton KF, Kallmes DF, Gray LA, et al. Endovascular treatment of epistaxis in patients with hereditary hemorrhagic telangiectasia. AJNR Am J Neuroradiol. 2007;28(5):885–888.