(1)
Nuffield Department of Surgical Sciences, Oxford University, Oxford, UK
Preamble
This tutorial is an example of the use of embolisation in a particular (and relatively easily defined) medical condition. Particle embolisation for epistaxis was first performed in 1972 by Sokoloff et al. and has remained part of the repertoire of interventional neuroradiology procedures ever since [1]. Some of the principles involved can be extended to almost all endovascular treatments. The tutorial is relatively short and is held at a time during the Oxford University MSc Course after students have had to read and learn a great deal of anatomy. It is thus a chance to take things a little slower and to apply some of the theoretical knowledge the course provides.
16.1 Epistaxis
Epistaxis is common. At least 60% of us will have episodes of nose bleeding at some time [2]. These occur with peak incidences in children (<10 years) and older adults (>50 years). Only 6% of episodes require medical treatment, and these are usually in the older age group. Bleeding can arise from veins, arteries or arterialised veins (e.g. associated with a vascular malformation or an arteriovenous shunt). Most episodes are idiopathic, though epistaxis in adults is frequently associated with systemic hypertension and other medical comorbidities.
Two clinical scenarios can be differentiated for idiopathic epistaxis. These are commonly termed anterior or posterior nasal bleeding, and the latter is more likely to arise from arteries.
16.1.1 Anterior Epistaxis
The anterior portion of the nasal cavity contains an area where small anastomotic mucosal arteries are concentrated. This is the usual site of anterior epistaxis which accounts for 90–95% of epistaxis. It is on the inferior-anterior surfaces of the septum and known as Kiesselbach’s plexus or Little’s area1 [3]. Bleeding in adults commonly occurs from the vessels of these areas or in children from the retrocolumellar vein. Since these areas are relatively accessible, treatment is by local compression, nasal packing and cautery. It is usually effective at stopping episodes of epistaxis.
16.1.2 Posterior Epistaxis
Bleeding in the posterior nasal cavity is far less frequent (5–10% of epistaxis) than anterior epistaxis [4]. It usually originates from the lateral nasal cavity, posterior to the middle turbinate, below the posterior end of the interior turbinate (an area called Woodruff’s plexus) or the roof of the nasal cavity [5]. The last area is the least accessible to anterior endoscopy and is the most frequent site for intractable epistaxis since effective packing in this region is difficult. Packing is also difficult if bleeding occurs from the upper pharynx.
16.2 Causes of Epistaxis
- (a)
Idiopathic
This is the commonest form of epistaxis, affecting 70–90% of all patients. No underlying structural cause is found, but factors considered to trigger spontaneous epistaxis include allergies, infections, cold weather and high atmospheric humidity. It affects men and women equally. In adults, it is associated with systemic hypertension, atherosclerosis, hypercholesterolaemia, smoking, liver disease and excess alcohol intake.
- (b)
Trauma
Acute bleeding following trauma is caused by direct vessel injury and is usually associated with facial fractures. Delayed bleeding may occur from pseudoaneurysms and false aneurysms in the nose or paranasal sinuses. Haemorrhage from posttraumatic aneurysms of the cavernous carotid artery (which may also cause a fistula) should be considered in the differential of delayed posttraumatic epistaxis. Surgical trauma, e.g. biopsy of a neoplasm, may precipitate epistaxis and bleeding may occur after radiotherapy [6].
- (c)
Tumours
Nasal and paranasal sinus tumours may present with epistaxis. Primary tumours include carcinoma (squamous, adenocarcinoma, adenoid cystic carcinoma), olfactory neuroblastoma, lymphoma, papillary angioma, angiomatous polyps and juvenile nasopharyngeal angiofibroma [7]. It has been reported in patients with the Wyburn–Mason (Bonnet Dechaume Blanc) syndrome. In this condition, retinal, nasal and intracranial angiomas or AVMs occur in a disease of abnormal metameric development. Secondary tumours occurring in the nose and paranasal tissues include metastases of renal cell carcinoma and malignant melanoma. A small point, when dealing with aggressive secondary tumours, is the possibility of embolisation inducing collateral blood supply. Thus, if the ethmoid arteries are enlarged, it has been suggested that they should be ligated before embolisation is performed in the internal maxillary artery (IMA) in case they become the route of additional collateral blood supply to the tumour from the ophthalmic artery.
- (d)
Hereditary haemorrhagic telangiectasia (Rendu–Osler–Weber syndrome)
Epistaxis is the most common presentation of this autosomal dominant disease that causes telangiectasia and AVMs in the nose, skin, gastrointestinal tract, lungs, liver and brain. Epistaxis affects 95% of patients. It is frequently recurrent with serial episodes which may be severe in a minority of episodes [8].
- (e)
Coagulopathies, blood dyscrasias and anticoagulation medication
Abnormal clotting should always be considered as a possible cause. It may be due to congenital conditions such as haemophilia, Von Willebrand disease and systemic disease such as cirrhosis or iatrogenic in patients on anticoagulant or antiplatelet drugs.
16.2.1 Vascular Anatomy
The blood supply to the nasal cavity is derived from branches of the internal maxillary artery (IMA), facial artery (FA), internal carotid artery (ICA) and the ascending pharyngeal artery (APA) (Fig. 16.1).
Fig. 16.1
Arterial supply to the nose: (a) nasal septum (lateral view), (b) lateral wall of the nose (lateral view), (c) left nasal cavity (frontal view) (Published with kind permission of © Henry Byrne, 2017. All rights reserved)
- (a)
Internal maxillary artery
The majority of the blood supply to the nasal mucosa comes from two terminal branches of the IMA: the sphenopalatine artery (SPA) and the greater palatine artery (GPA).
The larger SPA supplies the mucosa of the superior and middle turbinates and septum. It divides soon after passing through the sphenopalatine foramen into lateral short branches, which supply the lateral wall and turbinates and a medial long branch which supplies the nasal septum.
The greater palatine artery (GPA) or descending palatine artery arises from the distal IMA just before this artery enters the sphenopalatine foramen and becomes the SPA. It runs inferiorly to the hard palate in the greater palatine canal. A smaller companion branch of the IMA, the lesser palatine artery, parallels its course in a separate bony canal. They give branches to supply the palate and mucosa of the inferior part of the lateral nasal margin. The GPA is the more anterior branch of the descending palatine arteries, and a terminal branch runs forwards on the hard palate and enters the nose through the incisive foramen where, on the antero-inferior part of the nasal septum, it anastomoses with the septal branch of the SPA (i.e. at Kiesselbach’s plexus). It also gives small posterior branches, which supply the superior pharynx and anastomose with terminal branches of the SPA on the posterior inferior septum and inferior turbinate.
- (b)
Facial artery
Terminal branches of the facial artery (FA) supply the nostril and external nose. The alar artery (or lateral nasal artery) supplies the lateral nostril, and the superior labial artery gives small branches to supply the medial wall of the nasal vestibule and anterior septum. These branches are rarely seen on normal angiograms.
- (c)
Internal carotid artery branches
The anterior and posterior ethmoidal arteries are branches of the ophthalmic artery (OphA) and pass through the cribriform plate to anastomose with branches of the SPA and supply the roof of the nasal cavity. These vessels are rarely seen on normal angiograms and seeing prominent ethmoidal arteries usually means embolisation in the distal IMA will fail to control the epistaxis. Small branches of the ICA may also contribute to the nasal blood supply. These are the capsular branch arteries (capsular arteries of McConnell), artery of foramen rotundum (from the ILT) and the mandibular artery (from the mandibulo-Vidian trunk).2
- (d)
Ascending pharyngeal artery
The superior and middle pharyngeal arteries supply the medial and paramedial nasopharynx. They therefore border the territory of SPA and GPA branches.
The main supply to the posterior nose is from the SPA and this is the first target for endovascular treatment. Next, choose the FA and rarely the APA. The anterior and posterior ethmoidal arteries are best occluded by surgical ligation.
16.2.2 Indications for Embolisation
Embolisation is indicated for intractable epistaxis.
Failure of preliminary treatment by nasal packing or cautery. These techniques are generally successful in anterior epistaxis but have a relatively high failure rate in posterior epistaxis (about 25–50%) [9]. This is not surprising because it is difficult to tamponade the posterior nasal cavity from an anterior approach. More aggressive posterior packing with inflatable balloons is more likely to tamponade bleeding from the posterior nose but risks causing necrosis of the septum or alar cartilage. Endoscopic cautery is generally more successful, and in only a minority of patients (5–10%), bleeding becomes intractable.
Excessive blood loss with falling haemoglobin level.
Prior to surgical ligations. Embolisation is obviously best performed before surgical ligation of the SPA or IMA. Communication and collaboration with the surgical team should be ongoing so that patients are referred for embolisation at the appropriate stage.
16.2.3 Pretreatment Assessment
In practice, most patients have been bleeding for several hours (or days) by the time they are referred. Often, packing initially appears to work and natural optimism delays referral for embolisation. An important initial assessment is whether treatment needs to be performed under general anaesthesia.
- 1.
A detailed history is taken about the epistaxis episode. The details required are: source of bleeding, how long the patient has been bleeding and if they have had previous episodes and if so how they were treated. A general history of the patient’s health should include enquiry about any bleeding tendency, previous trauma or nasal disease. Imaging is not usually required (unless the history and examination suggests an underlying lesion causing the epistaxis) since catheter angiography will be performed as part of the endovascular procedure.
- 2.
Laboratory tests should include recent routine biochemistry and blood counts. In particular, current plasma haemoglobin and platelet levels should be available and the clotting time estimated. Abnormalities causing hypocoagulation such as low platelet counts or vitamin K levels should be corrected prior to embolisation.
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