Radiological Diagnosis and Management of Epistaxis
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The majority of episodes of spontaneous posterior epistaxis treated with embolisation are idiopathic in nature. The angiographic findings are typically normal. Specific angiographic signs are rare and may include the following: a tumour blush, telangiectasia, aneurysm, and/or extravasation. Selective internal carotid artery (ICA) angiography may show rare causes of epistaxis, such as traumatic or mycotic aneurysms, which require different treatment approaches. Complete bilateral selective external and internal carotid angiograms are essential to evaluation. The images should be analysed for detection of central retinal blush in the external carotid artery (ECA) and anastomoses between the branches of the ECA and ICA. Monocular blindness and stroke are two of the most severe complications. Embolisation aims to decrease flow to the bleeding nasal mucosa while avoiding necrosis of the nasal skin and palate mucosa. Embolisation is routinely performed with a microcatheter positioned in the internal maxillary artery distal to the origin of the meningeal arteries. A guiding catheter should be placed in the proximal portion of the ECA to avoid vasospasm. Embolisation with microparticles is halted when the peripheral branches of the sphenopalatine artery are occluded. The use of coils is not recommended because recurrent epistaxis may occur due to proximal embolization; moreover, the option of repeat distal embolisation is lost. The success rate of embolisation therapy (accounting for late recurrence of bleeding) varies between 71 and 94 %. Results from endoscopic surgery are quite comparable. When epistaxis is refractory to nasal packing or endoscopic surgery, embolisation is the treatment of choice in some centres.
KeywordsPosterior epistaxis Selective percutaneous embolisation Endovascular intervention
Haemorrhage from the nose is formally referred to as “epistaxis.” Haemostasis within the nose can be compromised by mucosal abnormalities, vessel pathology, or coagulation disorders. The aetiology of epistaxis is divided into groups: local and systemic factors. Local factors include the following: trauma, local inflammatory reactions, foreign bodies, postsurgical anatomical deformities, intranasal tumours, chemical inhalants, nasal-prong oxygen administration, and continuous positive airway pressure therapy for obstructive sleep apnoea. Systemic causes of epistaxis include the following: vascular disorders, especially hereditary haemorrhagic telangiectasia (HHT); blood dyscrasias; hematologic malignancies; and drugs affecting the normal clotting mechanism. Epistaxis arising from the anterior septal area (anterior epistaxis) is more common in children and young adults; it is the most common type of epistaxis and is more often venous in origin. This condition is usually responsive to treatment because it is readily accessible for nasal packing if bleeding does not resolve spontaneously [1, 2]. Therefore, endovascular therapy is usually not indicated for anterior epistaxis.
Approximately 5 % of epistaxis episodes arise from the posterior and superior portions of the nasal cavity, and the majority of posterior epistaxis episodes arise from the arteries of the septum. Posterior epistaxis is more common in older patients than in children  The most common factors associated with posterior epistaxis are hypertension [4, 5], acetylsalicylic acid or nonsteroidal anti-inflammatory drug use , previous episodes of epistaxis, alcohol use, and anticoagulant use. However, the majority of these cases are idiopathic . Refractory epistaxis is defined as recurrent or persistent bleeding after appropriate packing or multiple episodes of epistaxis during a short period of time, each requiring medical attention. Embolisation for intractable epistaxis was first reported as an alternative to surgery and other methods by Sokoloff .
Nonendovascular Therapy for Epistaxis
The management of epistaxis should begin with general measures, including calming the patient (with sedatives if necessary), application of a cold compress to the nape of the neck, decreasing the blood pressure if the patient is hypertensive, fluid resuscitation, and correction of any underlying coagulopathy. Local measures include the following: various methods of bleeding control, such as local application of haemostatic agents, infiltration of the bleeding area with vasoconstrictive agents, and cautery. Anterior nasal packing is performed by positioning strips of ointment-saturated gauze so as to produce satisfactory pressure on the bleeding mucosa. Posterior nasal packing is an option if anterior packing is insufficient to stop the haemorrhage or if the bleeding originates posteriorly. Posterior nasal packing requires general anaesthesia. A balloon catheter is inflated in the nasopharynx to stop the flow of blood posteriorly, and the anterior part of the nasal cavity is packed. The catheter coming out of the nose is fixed in place [3, 9].The patient should be monitored because posterior nasal packing can lead to nasal trauma, vasovagal reaction, and infection. Traditional gauze packing or balloon devices may be left in the nasal cavity for ≤48 h to prevent such complications. The success rate of posterior packing is reported to be between 48 and 83 %. Subsequent therapy can include either surgical endonasal coagulation or ligation . An endoscopic approach has been used for direct electrocauterisation of the active bleeding site and endoscopic ligation of the sphenopalatine and ethmoidal arteries . Surgical intervention is clearly indicated in anterior ethmoid bleeding because the ethmoidal arteries arise from the ophthalmic artery, the embolisation of which is generally considered to be dangerous.
Endovascular Therapy of Epistaxis
Detailed knowledge of the arterial anatomy of this region is important for safe and successful treatment. Stroke and blindness are two of the most severe complications. When retinal opacification from branches of the external carotid artery (ECA) is identified, embolisation must not be performed, and the patient should be referred for surgical treatment [12, 13, 14, 15].
Branches of the maxillary artery (modified according Allen et al. )
I. First (mandibular) portion
a. Anterior tympanic
b. Deep auricular
c. Middle meningeala
d. Accessory meningeala
e. Inferior alveolar
II. Second (pterygoid) portion
a. Deep temporal
III. Third (pterygopalatine) portion
a. Posterior superior alveolar
c. Greater (descending) palatineb
d. Artery to foramen rotunduma
e. Artery of pterygoid canal (vidian artery)a
Distribution of the third (pterygopalatine) portion of the maxillary artery (modified according Allen et al. )
Route of exit
Posterior superior alveolar
Inferior orbital fissure
Artery of foramen rotundum
Artery of pterygoid canal
The descending palatine artery, another branch of the pterygopalatine portion of the IMA, supplies the nasal fossa. This artery courses through the pterygopalatine canal and emerges from the palatine foramen. It outlines the posterior wall and floor of the maxillary antrum. The terminal branch enters the incisive foramen and supplies the inferior nasal septum. Here, the branch anastomoses with the medial nasal branches of the sphenopalatine artery. The infraorbital artery enters the orbit through the infraorbital fissure and runs through the infraorbital foramen. Its branches supply the cheek, lower eyelid, and upper lip, and nose. This artery does not supply the nasal mucosa.
The ophthalmic artery gives rise to a collateral network with the sphenopalatine artery by way of the anterior and posterior ethmoidal branches. These arteries pass through the cribriform plate of the ethmoid. The superior labial artery, a small branch of the facial artery, contributes to the arterial supply of the nasal septum. This branch is not regularly visible on angiographic studies.
Some investigators state that a venous plexus, called Woodruff’s plexus, is a common source of bleeding in cases of posterior epistaxis. This plexus is located in the posterior part of the inferior meatus and around the choanae .
Endovascular Therapy for Idiopathic Posterior Epistaxis
Computed tomography (CT) or magnetic resonance imaging is not typically indicated for the investigation of epistaxis unless tumour or other local diseases are suspected as an underlying cause. Idiopathic epistaxis is classified after exclusion of local or systemic causes. The interventional radiologist should be aware of the laterality of the nose bleed, the current severity of bleeding, and the patient’s history. These factors are crucial in deciding whether general anaesthesia is required for the procedure. General anaesthesia is routinely used only in children, noncompliant patients, and patients having uncontrolled epistaxis with possible compromise of the airway. The majority of embolisation procedures can be performed with intravenous sedation and analgesia with standard monitoring of blood pressure, electrocardiogram, and pulse oxymetry. Nasal packing, which is radiopaque, should be avoided in patients who might be candidates for embolotherapy.
The presence of any underlying coagulopathy should be evaluated because embolisation with polyvinylalcohol (PVA) microparticles is more effective in patients with normal platelet and plasma protein functions .
Obtain full blood count, platelet count, and international normalised ratio (INR)
Patients with metallic heart valves on warfarin should be kept only on a therapeutic level of INR. A cardiologist should be contacted if life-threatening bleeding occurs
Patients with coronary stents treated with acetylsalicylic acid or other antiplatelet therapy should be discussed with a cardiologist for possible platelet transfusion in cases of life-threatening epistaxis
Angiography and Embolisation
Complete selective external and internal carotid angiograms are essential to evaluation. Angiograms should be analysed for the detection for arterial variants and anastomoses between branches originating from the external carotid and internal carotid arteries [14, 15]. Standard catheterisation of the common carotid artery (CCA) is performed. Depending on the type of the aortic arch, various diagnostic and guiding catheters are selected. The most frequently used are vertebral, Berenstein, Davis, Simmons, or Vitek catheters. A 5F or 6F guide catheter permits angiography while a microcatheter is in the target artery. A standard continual pressure flush with heparinised normal saline must be used to prevent the backflow of blood into the guiding catheter.
Angiographic and embolisation protocol in epistaxis
A. The ICA angiogram
1. Start on the side of epistaxis (if identified)
2. Check the carotid bifurcation for stenosis or occlusion
3. Look for central retinae blush, ophthalmic retina feeders to the nasal mucosa
4. Exclude source of epistaxis from the ICA
B. The ECA angiogram
1. Position the guide catheter with its tip just within the ECA to avoid vasospasm
2. Exclude filling of the ophthalmic artery (retinae blush on lateral view)
3. Exclude collaterals to the ICA
4. Show any arterial pathology as a source of bleeding
C. Embolisation of the IMA
1. Place microcatheter into the pterygopalatine portion of the IMA sufficiently distal to the accessory or middle meningeal arteries, preferably distal to the infraorbital artery
2. Perform flow-directed embolisation with PVA particles (250–500 μm) in nondiluted contrast agent using a 1-ml syringe
3. Avoid reflux and coil embolisation
D. Perform contralateral ICA and ECA angiograms as well as IMA embolisation
E. Remove the nasal packing and check the nasal pathway for bleeding; if no bleeding appears for 15 min, remove the microcatheter and perform a completion ECA angiogram
F. Perform embolisation of the ipsilateral facial artery with the microcatheter placed as distally as possible (at least distal to the submandibular part of the facial artery) using 250- to 350-μm PVA particles if significant contribution to the nasal mucosa is angiographically visible
Arterial vasospasm is an undesired but common consequence of forceful manipulation, particularly manipulation with the tip of the guiding catheter in the proximal part of the ECA or microwire manipulation in the branches of the ECA. The presence of proximal vasospasm impairing the arterial flow in the access artery can alter the hemodynamic pattern of the arterial feeders in the target area, thus rendering embolisation impossible. Vasodilators may be administered intra-arterially to treat or prevent vasospasm [24, 25].
Microparticle embolisation is performed using a standard free-flow technique. A wedged position of the microcatheter should be avoided (Fig. 3B). Ideally, the capillary bed of the nasal cavity is slowly saturated with embolic microparticles. This goal is accomplished using fluoroscopic guidance in the lateral view to assess blood flow velocity in the artery, potential backflow, and reflux of the embolic agent (Fig. 3C). During embolisation, the operator should perform selective angiograms, the quality of which enables not only assessment of occlusion progress but also the potential filling of collaterals. The tip of a microcatheter is placed into the IMA distal to the origin of the middle meningeal and accessory meningeal artery due to the anastomoses with the ICA (Fig. 2A) In addition to the medial and lateral branches of the sphenopalatine artery, it is also desirable to embolise the descending palatine artery (Fig. 3A). This artery originates distal to the infraorbital artery (Fig. 3A). Reflux of embolic particles into the infraorbital artery is generally considered to be safe. The penetration of microparticles into the middle deep temporal artery may cause pain and trismus after embolisation. The embolic microparticles are mixed with nondiluted contrast medium to achieve the best visibility during injection using a 1-ml syringe. The mixture should not be too concentrated and must be continually mixed because the PVA microparticles have a tendency to sediment and occlude the microcatheter. Spherical microparticles make a more stable mixture. Spherical microparticles can penetrate deeper into arteries than PVA microparticles of the same size. Particles should lodge distal enough to control haemorrhage and yet proximal enough to preserve the distal supply of the terminal alar artery, which supplies the skin of the nose. The PVA microparticles 200–500 μm in size are usually selected. It is useful to talk to the patient if he or she is awake to show any ischaemic neurological deficit as soon as possible. In the sleeping patient, we must rely on anatomical angiographic studies and a thorough knowledge of the anatomy .
Embolisation is halted when the peripheral branches of the sphenopalatine segment are not opacified and the arterial tree seems to be debranched (Fig. 3C). The amount of microparticles required varies. Special care must be taken as soon as the flow begins to slow because even small additional amounts of microparticles may result in unexpected arterial stasis or even reflux.
The strategy for embolisation in patients with idiopathic epistaxis relies on the identification of the side of bleeding and the collateral pathways involving the contralateral IMA and the ipsilateral facial artery (Fig. 2C). The distribution of embolised arteries varies significantly in published series. The bilateral IMAs together with the ipsilateral facial artery were embolised in 27–48 %, the bilateral IMAs in 15–35 %, and the unilateral IMA in 13–70 % of cases. The bilateral IMAs are embolised if the side of haemorrhage is unknown or bilateral IMAs and ipsilateral facial artery if the side of haemorrhage is known. There also exist published case reports describing embolisation of the ascending pharyngeal and accessory meningeal supply to the nasal fossa for the management of epistaxis [27, 28, 29].
Nasal Packing Removal
Two different strategies regarding nasal packing removal have been reported in the literature. Some operators remove the packs while the catheters are still in the arteries, check the nasal pathway for bleeding, and finish the procedure if the nasal pathway remains dry for 15 min. Persistent bleeding influences the decision to embolise the contralateral IMA or the ipsilateral facial artery . Other practitioners leave the packs in place to facilitate the synergistic effects of external compression and devascularisation. Nasal packing removal is influenced by the duration of its placement, the severity and intractability of the epistaxis, and occasionally by the time of day the procedure is performed. Care must be taken to prevent the aspiration of pooled blood into the respiratory tract.
Review of studies on posterior epistaxis treated with embolisation
First author (reference)
No. of patients
Mean age (year)
No. of procedures
Embolic material for ECA branches
Immediate clinical success (%)b
Severe complications (%)c
2 stroke, skin slough
5 nose necrosis
PVA, GS, coils
7 nose necrosis, palate necrosis
4 nose necrosis, hemiparesis
Failures of embolisation therapy to control epistaxis are due to dominant ICA supply by way of the anterior and/or posterior ethmoid arteries. This arterial supply requires external surgical ligation. Late rebleeds are dependent on the underlying pathology and are more frequent with HHT. Often these patients are included in studies involving idiopathic epistaxis .
Surgical Versus Endovascular Therapy
The decision between surgery and embolisation should be based on the individual patient’s comorbidities, the anatomical setting, and the availability of adequate interventional radiology . There are retrospective studies available comparing IMA ligation (with or without ethmoid artery ligation)  with PVA embolisation of the bilateral IMAs and ipsilateral facial artery  for the treatment of refractory epistaxis. The embolised arteries were not specified in one of those studies . The success rates for IMA ligation and embolisation were 89 and 94 %, respectively . The other study reported success rates of 73 and 79 %, respectively . The investigators in both studies concluded that complication and failure rates of IMA ligation and embolisation were comparable. However, although the major complication rates were not significantly different between the two therapies, the complications associated with embolisation were more serious than those associated with IMA ligation.
The advantages of PVA embolisation include the use of local anaesthesia; pretreatment angiogram, which may show less common causes of epistaxis; distal embolisation; and shorter hospitalisation times. Embolisation is indicated in patients with cardiovascular instability. However, embolisation is available only in specialised centres. Furthermore, if bleeding originates from the ethmoid arteries, embolisation by way of the ophthalmic artery is considered to be hazardous. Ophthalmic artery embolisation should be avoided, even in cases of long-standing blindness in the ipsilateral eye, because retinal necrosis may lead to autoimmune retinal inflammation and loss of vision in the contralateral eye . In the presence of dangerous collaterals, the embolisation material must be exchanged for microcoils, which results in a more proximal and less effective embolisation or referral for surgical treatment. Surgical ligation of the IMA with or without anterior ethmoid artery ligation seems to be the more common technique and requires general anaesthesia in all cases.
Embolisation should decrease flow to the bleeding nasal mucosa while avoiding necrosis of the nasal skin or palate mucosa. Skin necrosis requires plastic surgical repair [32, 33, 34, 35]. Smaller particles (45–150 μm) carry a greater risk of collateral tissue ischemia, including ischemia of the vasa nervorum .
The most frequent causes of neurologic deficit and blindness  after embolisation in the ECA territory are reflux of emboli due to vasospasm, nonselective injection, injection of excessive particles at an excessive rate, and failure to recognise dangerous anastomoses due to incomplete angiograms and inadequate analysis [27, 38].
Minor complications include postembolisation ischemic syndrome, which typically lasts for a short time and requires only symptomatic therapy. Acute ischemic sialadenitis has been reported after reflux of microparticles into the proximal branches of the facial artery .
Management of Angiographically Proven Causes of Epistaxis
The clinical presentation of traumatic epistaxis is life-threatening haemorrhage at the time of trauma . CT imaging is indicated in all cases of suspected arterial epistaxis. Angiogram may show focal active extravasation, pseudoaneurysm , or arterial pseudo-occlusion. The embolisation technique for these cases differs from that for idiopathic epistaxis. The tip of the microcatheter must be as close as possible to the arterial pathology. In the case of possibly dangerous collaterals, microcoils are preferred. The most common sources of bleeding are the sphenopalatine and facial arteries. In a significant number of cases, bilateral extravasation is present .
When trauma or infection  of the ICA arterial wall results in pseudoaneurysm formation, the patient can present with delayed epistaxis. This pseudoaneurysm should be expected in the cervical, petrous, or cavernous portions of the ICA . Arterial injuries during craniofacial surgery are uncommon but have been well described [45, 46, 47, 48].
Juvenile Nasopharyngeal Angiofibroma and Other Tumours
Juvenile nasopharyngeal angiofibroma (JNA) is a benign hypervascular tumour that occurs in young males between 8 and 23 years of age. Symptoms are related to the size and direction of spread. These symptoms may include recurrent epistaxis (observed in 59 % of cases), which may be life-threatening. The lesion originates from the posterolateral wall of the nasal cavity in close proximity to the superior aspect of the middle sphenopalatine foramen, the attachment site of the posterior part of the middle turbinate.
The systematic angiographic protocol for JNA begins with injection in the contralateral CCA followed by injections in the ICA ipsilateral common and internal carotid arteries. Next, ipsilateral external carotid angiography for evaluation of the maxillary and ascending pharyngeal arteries is performed. The maxillary, accessory meningeal, ascending pharyngeal, and ascending palatine arteries are most commonly embolised vessels. If the tumour crosses the midline, additional embolisation of the appropriate contralateral feeders is performed.
In cases with extensive tumour spread, the supply from the ICA branches may be embolised if possible, especially if the ICA must be sacrificed before surgery. Neurologic deficit is the most feared complication of preoperative embolisation. Blindness, in particular, is of major concern as a result of involvement of the ethmoidal blood supply .
Since the introduction of embolisation of JNA by Roberson , several studies have been published proving the benefit of preoperative embolisation by decreasing blood loss and operative times. Other sinonasal neoplasms that can cause life-threatening epistaxis include nasopharyngeal carcinoma and hemangiopericytoma .
Epistaxis in HHT
HHT, a hereditary disease, is associated with skin and mucosal telangiectasias and arteriovenous shunts most commonly involving the lung, brain, and liver. It is easily recognised in individuals displaying the classic triad of epistaxis, telangiectasia, and a relevant family history .
Epistaxis is caused by spontaneous bleeding from telangiectasias of the nasal mucosa (Fig. 2B). Recurrent epistaxis begins by the age of 10–21 years and the severity of the episodes increases with age .
Among numerous local and surgical treatments, transcatheter embolotherapy has been used with the intent of decreasing the number and severity of epistaxis episodes. Microparticle embolisation should decrease flow to the nasal mucosa, but care must be taken to leave the proximal arteries patent. Embolisation with coils should be avoided because the artery cannot be made again accessible distal to the proximal occlusion in recurrent epistaxis. Preventive embolisation is considered to have a questionable long-term effect [32, 52].
Ninety five per cent of all epistaxis episodes have their origin in the anterior septum and are easily controlled with local endonasal therapy using anterior packing if bleeding does not resolve spontaneously. Posterior epistaxis represents 5 % of cases and is more difficult to treat. The placement of posterior nasal packs may predispose patients toward vasovagal reaction, infection, and significant discomfort [53, 54, 55, 56]. Endoscopic ligation or electrocauterisation of the sphenopalatine and anterior ethmoidal arteries is a routine technique for local control of active bleeding. Embolisation of the distal branches of the bilateral IMAs and ipsilateral distal branches of the facial artery is the preferred therapy in patients with poor cardiovascular status because this procedure can be performed with the patient under local anaesthesia in a majority of cases . Embolisation is also used in the treatment of epistaxis refractory to previous endonasal or surgical therapy, including IMA ligation. Rare but major complications of embolisation therapy are mainly due to the penetration of embolic material into the intracranial and ophthalmic arteries. Embolisation therapy is relatively contraindicated when the bleeding originates mainly from the ethmoid branches of the ophthalmic artery or in the presence of anastomoses between the ECA and the ICA. In our experience, close collaboration between the otorhinolaryngologist and the interventional radiologist provides the best chance of controlling posterior epistaxis.
Conflict of interest
Antonín Krajina and Viktor Chrobok have no conflicts of interest.
- 2.Shukla PA, Chan N, Duffis EJ, Eloy JA, Prestigiacomo CJ, Gandhi CD (2012) Current treatment strategies for epistaxis: a multidisciplinary approach. J Neurointerv Surg 5(2):1–6Google Scholar
- 20.Lasjaunias P, Berenstein A, TerBrugge KG (2001) Anatomy and variations of the extracranial carotid artery branches. In: Lasjaunias P, Berenstein A, TerBrugge KG (eds) Surgical neuroangiography, vol 1., Clinical vascular anatomy and variation (2nd ed)Springer, Berlin, pp 292–385Google Scholar
- 23.Walker FDL, Rutter C, McGarry GW (2008) The use of anticoagulants in epistaxis patients. Rhinology 46:346Google Scholar
- 26.Krajina A, Cesak T, Zelenak K, Rehak S (2011) Therapeutic embolisation of cranial tumours. In: Abujamra AL (ed) Diagnostic techniques and surgical management of brain tumours. Intech, Rijeka, pp 493–516Google Scholar
- 31.Strong EB, Bell A, Johnson LP, Jacobs JM (1995) Intractable epistaxis: transantral ligation versus embolisation: efficacy review and cost analysis. Surgery 113:674–678Google Scholar
- 44.Chen D, Concus AP, Halbach VV, Cheung SW (1998) Epistaxis originating from traumatic pseudoaneurysm of the internal carotid artery. Diagn Endovasc Ther 108:326–331Google Scholar
- 54.Godard JC, Reiter ER (2005) Inpatient management of epistaxis: outcomes and cost. Head Neck Surg 132:707–712Google Scholar
- 60.Oguni T, Korogi Y, Yasunaga T et al (2000) Superselective embolisation for intractable idiopathic epistaxis. British J Radiol 73:1148–1153Google Scholar
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