Radiology_Oct04 Abstract A total of 57 endovascular emboli- sation procedures were performed for intractable epistaxis in 51 patients over a 4-year period at the Unitas Interventional Unit near Pretoria. Long-term follow-up was possible in 36 patients. Three cases were due to trauma and 2 directly related to previ- ous facial surgery, 1 patient had here- ditary haemorrhagic telangiectasia (HHT), and the remaining 45 cases (88.2%) were classed as idiopathic. Eight patients (15.7%) had a rebleed between 1 and 33 days after the initial embolisation. Four were re-embolised once, 1 was re-embolised twice (the HHT patient), and 2 underwent addi- tional ethmoid artery ligation (with no further bleeding). This gives a pri- mary short-term success rate (in all 51 cases) of 86.3% and a secondary assisted success rate of 94.1% for embolisation alone. Long-term fol- low-up was obtained in 36 patients, with 35 (97.2%) reporting no further bleeding after the initial procedure(s). Only the patient with HHT developed multiple recurrent bleeds. The mor- tality rate was 0%, the major morbid- ity rate 2% (1 stroke), and the minor morbidity rate 25% (N = 36), which included transient facial pain, headaches and femoral problems related to access. Our results compare favourably with other published series. In conclusion, endovascular embolisation for intractable epistaxis is available locally as an alternative technique for the treatment of this difficult condition. Introduction Epistaxis is a common condition, affecting an estimated 60% of the gen- eral population of whom an estimat- ed 6% will seek or require medical assistance.1 Refractory or intractable epistaxis is defined as recurrent or persistent bleeding after appropriate conservative treatment, or multiple episodes of epistaxis over a short peri- od of time, each requiring medical attention.2 Intractable epistaxis usual- ly arises from the posterior or superi- or parts of the nasal cavity, and is therefore not readily controllable by direct pressure, topical cauterisation or anterior nasal packing. Arterial lig- ation has remained the mainstay of treatment for intractable posterior epistaxis in many centres.3-6 Percu- taneous embolisation of the internal maxillary artery for nasal haemor- rhage was first described by Sokoloff et al. in 1974.7 Several other reports describing the efficacy of endovascu- lar embolisation followed.8-11 Currently, endovascular embolisation is an accepted method of treatment for haemorrhage from the nasal cavity or other craniofacial lesions .12,13 Materials and methods A retrospective audit was done of 57 percutaneous endovascular embolisation procedures in 51 patients performed over the 4-year period July 1999 - June 2003 at the Unitas Interventional Unit in Centurion. All patients were referred by an otorhinolaryngologist after failed conventional treatment, gener- ally involving local cauterisation and/or nasal packing; 12 patients had also received a blood transfusion prior to embolisation. We reviewed our procedural data notes, with further clinical data obtained either from ini- tial referral letters or follow-up notes provided by referring clinicians. Long-term telephonic follow-up was obtained from 38 patients (respon- dents), with 13 patients being untraceable during the period of the audit. Of the 38 respondents, 2 had died of unrelated causes since the embolisation, with telephonic inter- views obtained with the remaining 36. The collection of data was flawed by incomplete clinical record keeping. The most complete data obtained ORIGINAL ARTICLE 9 SA JOURNAL OF RADIOLOGY • October 2004 Endovascular treat- ment of intractable epistaxis — results of a 4-year local audit I C Duncan FFRad (D) P A Fourie MMed Rad (D) C E le Grange Nat Dipl Rad H A van der Walt BSc (Verpl) Unitas Interventional Unit Centurion, Gauteng were for the 36 respondents, for whom much of the recorded data could be cross-checked and who could also provide missing informa- tion in addition to long-term follow- up. The long-term follow-up period varied from 1 to 47 months. All embolisation procedures were performed in the Unitas Interven- tional Unit vascular laboratory using a Phillips V5000 Integris digital mono- plane angiography unit (Phillips Medical Systems, Netherlands BV). Of the procedures 22 (38.6%) were performed under general anaesthesia and 35 (61.4%) under local anaesthe- sia and sedation. A co-axial micro- catheter technique was utilised in 56 procedures (98.2%), with embolisa- tion being performed through a stan- dard 4F diagnostic catheter in only 1 case (1.8%). The co-axial technique involved initial selective catheterisa- tion of the external carotid artery (ECA) with a 4F or 5F 0.038-inch lumen diagnostic catheter, followed by superselective catheterisation of the relevant ECA branches by place- ment of a microcatheter through the diagnostic catheter. The type or make of diagnostic catheter and micro- catheter/microguidewire system used varied according to operator prefer- ence, vascular anatomy and stock availability. Both the guiding catheter and microcatheter were continuously irrigated with heparinised saline (2000 u in 1 litre) using a pressure bag system via Y-connectors attached to each catheter. Systemic heparin was generally not given in uncomplicated cases. Initial diagnostic arteriograms of the internal carotid artery (ICA) and ECA were obtained on each side. The former were done in order to exclude an intracranial aneurysm, arteriove- nous shunt or frontal tumour as a possible cause of the bleeding as well as to identify any arterial supply to the nasal cavity from ethmoidal branches of each ophthalmic artery (Fig. 1). The ipsilateral internal maxillary artery (IMAX), defined as the one supplying the nasal cavity from which the bleeding was visualised or assumed to arise, was then superselec- tively catheterised and embolised in all cases except 1, in which the ipsilat- eral ECA origin was occluded due to atheromatous disease and a contralat- eral IMAX embolisation was per- formed. Other vessels superselectively catheterised and embolised included the ipsilateral facial artery (N = 29 (51%)), the contralateral IMAX (N = 27 (47.4%)), the contralateral facial artery (N = 8 (14%)), the ascending pharyngeal artery (N = 1 (1.7%)) and the accessory meningeal artery (N = 1 (1.7%)). The decision to embolise arteries other than the ipsi- lateral IMAX was based upon the rel- ative contributions of each vessel to the supply of the nasal cavity as well as the potential for collateral supply to the nasal cavity (Fig. 2a). During arte- riography the actual site of the bleed- ing can usually not be identified and often no abnormal vessels are seen in the nasal cavities, although in several cases a nonspecific generalised nasal mucosal ‘blush’ due to nasal mucosal congestion or arterial tortuosity may be seen (Figs 2b - 2d). The embolic agents used were microparticles in 56 procedures (98.2%), with cyanoacry- late (B Braun, Melsungen, Germany) and platinum microcoils (Target Therapeutics, Fremont, Calif., USA) used as the sole agents in 1. Of the 56 procedures performed using micro- particles, 47 (77.2%) were done using polyvinyl alcohol (PVA) microparti- cles (Trufill, Cordis Johnson and Johnson, Miami, Fla., USA) and 9 (15.8%) using trisacryl gelatine microspheres (Embospheres, Guerbet, Paris, France). Particle sizes ranged from 150 to 700 µm in diameter and were usually between 250 and 500 µm. Other adjunctive embolic mate- rials used included cyanoacrylate (N = 5 (8.8%)), platinum microcoils (N = 4 (7%)) and shredded Spongistan (Cordis, Johnson and Johnson, Miami, Fla., USA) (N = 4 (7%)). In all cases where no macroscopic cause of the bleeding such as a pseudo- aneurysm could be identified, and where microparticulate embolisation was performed, the desired end-point of embolisation was a significant visi- ble reduction or cessation of flow in the target vessel(s) (Fig. 3). The nasal packing was removed in theatre in 56% of cases in which this was docu- mented and afterwards in 44% (N = 36). Results The male/female ratio of our patients was 1.2: 1 (28 men and 23 women), and the mean age was 54.4 years (range 17 - 83 years). Only 15 patients were referred from the Pretoria area, 36 being transferred from other centres. Thirty two (63%) were referred between the months of May and September. The causes of epistaxis in our cases are summarised in Table I. Of the trauma-related cases 1 occurred shortly after a direct blow to the nose and 1 following a Le Fort fracture, whereas the 3rd patient (who suffered the intraprocedural stroke) had been severely assaulted 3 weeks before presentation. Of the 2 patients whose epistaxis was related to prior surgery, 1 had recently undergone ORIGINAL ARTICLE 10 SA JOURNAL OF RADIOLOGY • October 2004 removal of an osteoma from the sphe- noid sinus (with ipsilateral IMAX occlusion seen at angiography) and the other presented with severe bleed- ing from a large pseudo-aneurysm of the distal IMAX following a recent maxillary osteotomy. Identifiable risk factors in the respondent group (N = 36) are listed in Table II. None of the respondents volunteered any history of alcohol or illicit drug abuse. One patient had previously undergone radiation therapy for a maxillary tumour considered inactive at the time of the embolisation. One of the non-respondents developed severe epistaxis during the 25th week of pregnancy. No underlying cause for this was found. A 17-year-old girl with sideroblastic anaemia for which she had received multiple blood transfu- sions over a period of several years was referred for a semi-elective procedure, the only patient in our series not treat- ed on an emergency basis. Eight patients (15.7%) developed a rebleed between 1 and 33 days after the initial embolisation (Table III). Of these, 4 patients (7.8%) underwent a second embolisation procedure and 1 12 SA JOURNAL OF RADIOLOGY • October 2004 ORIGINAL ARTICLE Fig 1. Selective internal carotid digital subtraction arteriogram showing supply to the superior nasal cavity via the ethmoidal branches (black arrows) of the ophthalmic artery (white arrow). Fig 2a. Selective external carotid digital subtrac- tion arteriogram showing the arterial supply to the nasal cavity via terminal branches of the internal maxillary artery (black arrow) and facial artery (white arrow). Fig 2b. Selective internal maxillary arteriogram (same case as Fig. 2a) showing the typical appearance of the nasal arteries prior to emboli- sation. No bleeding site is identifiable and the arteries have a normal appearance. Fig 2c. In some cases a prominent nasal capillary blush may be seen in keeping with mucosal con- gestion. Fig 2d. In others tortuosity of the intranasal arter- ies may be seen. Fig 3. In the same case as shown in Figs 2a and 2b, a selective internal maxillary arteriogram fol- lowing microparticulate embolisation shows very little contrast opacification of the nasal branches, indicating a satisfactory angiographic end-point for embolisation. Table I. Causes of epistaxis Idiopathic 45 88.2% Trauma 3 5.9% Post surgery 2 3.9% HHT 1 2% Table II. Risk factors for epistaxis (36 respondents) Hypertension 19 52.8% Smoking 9 25% Anticoagulation/ASA 5 13.9% Radiation therapy 1 2.8% One patient had also received multiple blood transfusions for chronic sideroblastic anaemia. patient with hereditary haemorrhagic telangiectasia (HHT) underwent two further embolisation procedures in our unit and one at another centre. Two patients (3.9%) underwent addi- tional surgical ligation of the ethmoid arteries, after which no further bleed- ing was encountered. One of these was the patient with the Le Fort II fracture and the other had an idio- pathic-type bleed. One patient had a single post-procedural rebleed for which angiography was repeated but no further embolization performed. Forty-four patients (86.3%) therefore responded well to a single embolisa- tion procedure. No further rebleeds were noted in the 4 patients who underwent a second embolisation procedure, giving a cumulative suc- cess rate for embolisation alone of 94.1%. With the exception of the patient with HHT, none of the 36 liv- ing respondents reported a late rebleed after primary or secondary intervention. The mortality rate in our series was 0%, and we encoun- tered only one major complication (2%), being the development of a right-sided cerebral infarction during attempted guiding catheter replace- ment in a tortuous carotid artery. Minor complications are listed in Table IV. Those related to the femoral access included transient tenderness in 2 cases, a tender lump (non- aneurysmal) in 1 and prolonged numbness around the puncture site in 1. The total minor complication rate for the respondent group is therefore 25%. Discussion Most cases of epistaxis occur in the anterior nasal cavity in the region of 13 SA JOURNAL OF RADIOLOGY • October 2004 ORIGINAL ARTICLE Table III. Rebleeding after initial embolisation Patient Age (yrs) Risk factors Time of rebleed Cause of rebleed Further treatment Outcome 1 34 Smoker 2 days Unknown Repeat angiogram only No rebleed 2 58 Smoker, Multiple rebleeds HHT Total of 3 Eventually well HHT over many years embolisations performed palliated for (+ 1 at another centre) > 1 yr with in 2 years intralesional bleomycin 3 50 Warfarin and 1/2 day Unknown. Repeat embolisation No rebleed disprin (cardiac The PI at time of of ipsilateral IMAX valve the rebleed was only with replacement) 75% microparticles 4 25 Pregnant 33 days Unknown Repeat embolisation No rebleed (25 weeks) of ipsilateral IMAX only with microparticles 5 83 Warfarin 1 day Significant Repeat embolisation No rebleed (pulmonary collateral supply of ipsilateral IMAX embolism), PI via accessory and accessory on admission meningeal artery meningeal artery of 34% 6 36 Le Fort II 2 days Significant Surgical ligation of No rebleed fracture collateral supply ethmoid arteries via ethmoid arteries 7 55 Hypertension 1/2 day Significant collateral Surgical ligation of No rebleed supply via ethmoid ethmoid arteries arteries 8 18 Maxillary 10 days Coil migration and Repeat embolisation No rebleed osteotomy with recannalisation using particles, coils IMAX through coils and cyanoacrylate pseudo-aneurysm inserted previously in the IMAX PI = prothrombin index. the antero-inferior septum known as Little’s area. Underlying this is a con- fluence of arterial territories compris- ing those of the sphenopalatine artery, the greater palatine artery, the facial artery and the anterior and posterior ethmoidal arteries. This arterial con- fluence is known as Kisselbach’s plexus.14 Anterior epistaxis is usually easily controlled by conservative mea- sures including localised pressure, topical cauterisation and vasocontric- tion, local infiltration with antifibri- nolytic agents and anterior nasal packing.15 Posterior (and to a lesser degree superior) epistaxis accounts for about 5% of all cases and can be extremely difficult to manage. Posterior nasal packing can be done with gauze or balloon catheters. Nasal packing has a reported failure rate of 26 - 52% and a complication rate of 69%.14,16 Complications related to packing include nasal trauma, vaso- vagal response, aspiration, displace- ment of the packing, persistent bleed- ing, infection, toxic shock syndrome and hypoxia.15,17 Surgical approaches include transantral ligation of the dis- tal IMAX and ligation of the ethmoid arteries for superior epistaxis.3 More recently endoscopic cauterisation and arterial ligation techniques have been described, although these are techni- cally more demanding.18-20 Since the advent of nasal embolisation in 1974,7 the endovascular management of epistaxis has become an established alternative to surgical ligation. In a comparison of efficacy between transantral ligation and embolisation in intractable epistaxis, Strong et al.21 reported success rates from the litera- ture of 85% and 90% and average complication rates of 28% and 27% respectively for ligation and embolisa- tion, with success rates of 89% and 94% respectively from their own series. Cullen and Tami22 showed a failure rate of 21% for embolisation versus 27% for ligation (with or with- out ethmoid ligation) and an overall complication rate of 16% for emboli- sation and 18% for IMAX ligation.22 In their review of the literature, which expanded on that by Strong et al., they reported a slightly higher failure rate for embolisation (20%) than for IMAX ligation (18%) but a signifi- cantly higher complication rate for IMAX ligation (26%) than for embolisation (14%). No difference in major complications rates (5% v. 4%) was noted between the two methods. The goal of embolisation is simply to reduce the arterial pressure head to the affected region without causing any ischaemic damage to the nasal soft tissues,13 so allowing the body to heal itself. The posterior nasal cavity is supplied mainly via the sphenopala- tine artery and greater palatine artery, both of which are terminal branches of the IMAX. This means that the management of posterior epistaxis largely hinges on control of the sphenopalatine artery,23 and explains the equally high rate of success of ipsi- lateral IMAX embolisation alone. However, there is still a failure rate of 10 - 15% for both embolisation and IMAX/sphenopalatine ligation. In some cases embolisation may succeed where IMAX ligation fails.24 Furthermore, as shown by Vitek11 the technical success rate of embolisation increases significantly when addition- al embolisation of the ipsilateral facial and contralateral IMAX arteries is performed as well. This attests to the importance of collateral vessels in the facial region with collateral blood sup- ply to the posterior nasal cavity, which probably accounts for a significant percentage of failed IMAX ligation or embolisation procedures.25-27 The advantage of arteriography is that it can often identify these collateral sources, allowing them to be treated simultaneously. Collateral supply to the nasal cavity was important in 4 of our cases, leading to recurrent haem- orrhage. In 1 case this involved a col- lateral pathway via the accessory meningeal artery, a hitherto unde- scribed variant of importance in the treatment of epistaxis.28 Collateral supply via the ethmoid arteries led to secondary surgical intervention in 2 cases. Another potential complication related to collateral circulation is the presence of intracranial-extracranial arterial anastomoses, as inadvertent embolisation through these pathways can lead to ophthalmological or neu- rological complications.12 It is there- fore vital to identify these communi- cations during the initial angiograph- ic investigation. Although we routine- ly check both internal and external carotid arteries during each proce- 14 SA JOURNAL OF RADIOLOGY • October 2004 ORIGINAL ARTICLE Table IV. Complications of embolisation Major (N = 51) CVA 1 2% Minor (N = 36) Headache 3 8.3% Transient facial pain/ paresthesia 2 5.5% Local groin complications 4 11% dure, we do not follow a rigid treat- ment protocol with regard to the number of vessels embolised but rather tailor the approach in each patient on the basis of the vascular anatomy, ease or difficulty of selective and superselective catheterisation, and the presence or absence of other associated extracranial vascular disease. Nearly 50% of our cases involved single-vessel (ipsilateral IMAX) embolisation only. Two of our cases with a rebleed following initial embolisation of the ipsilateral IMAX underwent a second procedure involving a repeat micro- particulate embolisation of the same vessel, with good outcome. Inadequate embolisation, like incom- plete IMAX ligation, can therefore lead to recurrent bleeding. One patient who had a rebleed 2 days after embolisation underwent a repeat arteriogram that showed adequate occlusion of the ipsilateral distal IMAX branches. No significant col- lateral vessels were identified, so no further embolisation was performed. No further bleeding was experienced thereafter. False rebleeds following embolisation may occasionally be encountered and may be due to retained blood in and around the nasal packing or blood draining from the paranasal sinuses. We used microcatheter techniques in all cases but 1. Although leading to increased expense, procedural dura- tion and complexity, the use of micro- catheters has been reported to reduce the number of local cranial complica- tions although to date this has not been proven in any randomised study.29,30 In Table V we review four studies conducted during or after 1995 and reporting the routine use of microcatheter techniques and calcu- late a cumulative success rate of 90.2% and overall complication rate of 13.4% (11.4% minor and 2% major) with microcatheter use. Although the use of microcatheter techniques does not improve the overall success rate, there is a tendency towards a lower complication rate. This factor should be weighed up against the additional procedural costs involved. We have also noted that when microcatheters are used, arterial vasospasm, which can prolong and complicate a proce- dure, is less frequent. One problem apparent in all of the embolisations reported to date is inconsistency in the reporting of minor and major com- plications and hence variation in the reported figures. Other factors such as improvements in catheter and guidewire design and increased oper- ator experience have also probably contributed to the reduction in com- plication rates in more recent times. Other complications related to embolisation for epistaxis reported in other local institutions include ischaemic necrosis of the upper lip (facial arterial embolisation), unilater- al trismus (related to deep temporal arterial occlusion) and ischaemic sialadenitis (facial artery embolisa- tion).31 Further complications des- cribed in the literature include facial nerve paralysis, tongue necrosis, ton- sillar ulceration, facial atrophy and transient submandibular gland swelling.32 Other potential complica- tions can be related to the femoral access (pain, bruising, pseudo- aneurysm or arteriovenous fistula) or to the use of contrast media (allergic reaction, renal failure).33 Our single major complication was a stroke relat- ed to attempted replacement of a guiding catheter in a very tortuous carotid artery. Despite our recent suc- cess in treating hyperacute iatrogenic strokes during neuro-interventional procedures with intra-arterial abcix- imab, we were unable to prevent major cerebral infarction in this case.34 16 SA JOURNAL OF RADIOLOGY • October 2004 ORIGINAL ARTICLE Table V. Reported success and complication rates since 1995 Study No. of patients Success rate Minor complications Major complications Overall complication Elahi et al., 57 52 (96%) None reported 3 (6%) 3 (6%) 199532 Tseng et al., 114 101 (88%) 17 (15%) 2 (1.8%) 19 (16.8%) 19982 Leppanen et al., 37 33 (89%) 4 (8%) 0 (0%) 4 (8%) 199929 Oguni et al., 37 35 (94.6%) 7 (45%) 0 (0%) 7 (45%) 200033 Total 245 221 (90.2%) 28 (11.4%) 5 (2%) 33 (13.4%) All head and neck embolisation pro- cedures should therefore ideally be performed by a team capable of man- aging serious cerebrovascular compli- cations. One advantage of endovascular treatment is that it can be performed under local anaesthesia with sedation if required. Although only 38.6% of our cases were performed under gen- eral anaesthesia, we now routinely utilise general anaesthesia for two rea- sons arising from our accumulated experience. Firstly, patients are gener- ally uncomfortable, with nasal pack- ing in situ and occasionally also active bleeding during the procedure. Prolonged immobilisation on the angiography table may be required during difficult cases. This results in further patient discomfort and reduced co-operation with move- ment (voluntary and involuntary), rendering the use of electronic vascu- lar roadmapping useless, further pro- longing the procedure and adding to the risk of complications or an incom- plete or inadequate procedure. Secondly, we now insist on full airway protection by means of a cuffed endo- tracheal tube before commencing any embolisation procedure in the head and neck region where active bleeding is an issue.28 Regardless of whether or not a general anaesthetic is adminis- tered, an anaesthetist is always present for patient monitoring and adminis- tration of analgesic or sedative drugs as required. One subgroup of patients who develop recurrent epistaxis are those with HHT (Osler-Weber-Rendu dis- ease). HHT is a genetic multisystemic angiodysplasia. These patients devel- op fragile nasal mucosal telangiec- tasias and more than 90% are are prone to repeated and intractable epistaxis18 (Figs 4a and 4b). The ENT surgeon can miss the diagnosis of HHT during the acute presentation.35 Embolisation is not a definitive treat- ment for epistaxis in these patients, but can control an acute bleeding episode. Because of the known propensity for epistaxis to recur in these patients, Elden et al.30 found that their long-term success rate for embolisation increased from 82% to 90% once the HHT patients in their series were excluded. There is still no definitive treatment available for the nasal manifestations of HHT. Palliative treatment with intramucos- al injections of bleomycin (Blenoxane, Bristol-Myers Squibb) has been suc- cessful in our patient for more than 18 months.36 Although embolisation is a good alternative to surgical IMAX ligation (or related procedures), intervention- al expertise is only available in the major centres in South Africa. Of our patients 70% were referred from out- side of the Pretoria area, although most were from within a 150 km radius of the Unitas Interventional Unit. In their 1998 study of the atti- tudes of practising otorhinolaryngol- ogists in Ohio, Cullen and Tami22 found that only 16% had referred patients for embolisation; of these 75% had urban practices and the rest were from rural areas. They also found that more hospitals in urban areas than rural ones had embolisa- tion facilities. This situation is mir- rored and undoubtedly amplified in South Africa. In their comparison of the respective costs of IMAX ligation and embolisation, Strong et al.21 found the average cost per case in 1994 for antral ligation to be US$5 941 versus US$6 783 for embolisation.21 Cullen and Tami22 calculated the average costs in their institution in 1998 to be US$ 6 184.55 for IMAX ligation and US$ 4 544.85 for embolisation. These fig- ures include the combined costs of hospitalisation, treatment and con- sumable items. We were only able to calculate the radiological costs per case, which included the embolisation procedure and interventional theatre costs, as shown in Table VI. Not included in these figures are the costs of hospitalisation and private anaes- thetist and ENT specialist fees. The overall cost of hospitalisation would be extremely difficult to calculate, as many patients had already been treat- ed or hospitalised at other institutions before transfer to our own. In general, 17 SA JOURNAL OF RADIOLOGY • October 2004 ORIGINAL ARTICLE Fig 4a. Selective left facial arteriogram in our HHT patient showing multiple enhancing lesions repre- senting small nasal mucosal telangiectasias. Fig 4b. Endoscopic nasal view showing multiple small red telangiectasias seen through a perfora- tion of the nasal septum, a complication of repeat- ed surgical attempts at managing the recurrent epistaxis in this patient. uncomplicated cases would be admit- ted overnight for observation either in a high-care facility or more usually a general ward, with discharge or trans- fer back to the referring institution during the following day. Conclusion Intractable epistaxis is a debilitat- ing condition, the treatment of which can be extremely difficult. Percuta- neous transcatheter embolisation of the nasal arteries is an accepted alter- native to surgical intervention, with comparable major and minor compli- cation rates, success rates and overall costs. Most cases will respond well to a single embolisation procedure, with approximately 10% failing to respond due to factors such as collateral arteri- al supply and HHT. Success and com- plication rates for procedures per- formed at the Unitas Interventional Unit compare favourably with those reported in the literature to date. These procedures should be per- formed by suitably experienced inter- ventional radiologists, either under general anaesthesia or local anaesthe- sia with sedation, with full monitoring and anaesthetic backing. References 1. Small M, Murray J, Maran AG. A study of patients with epistaxis requiring admission to hospital. Health Bull (Edinb) 1982; 40: 20-29. 2. Tseng EY, Narducci CA, Willing SJ, Silliers MJ. Angiographic embolization for epistaxis. Laryngoscope 1998; 108: 615-619. 3. Chandler JR, Serrins AJ. Transantral ligation of the internal maxillary artery for epistaxis. Laryngoscope 1965; 75: 1151-1160. 4. Wang L, Vogel DH. Posterior epistaxis: Comparison of treatment. Otolaryngol Head Neck Surg 1981; 89: 1001-1006. 5. Small M, Maran AGD. Epistaxis and arterial lig- ations. J Laryngol Otol 1984; 98: 281-284. 6. Hunter K, Gibson R. Arterial ligation for severe epistaxis. J Laryngol Otol 1989; 83: 1099-1103. 7. Sokoloff J, Wickbom I, McDonald D, Brahme F, Goergen TG, Goldberger LE. Therapeutic percu- taneous embolization in intractable epistaxis. Radiology 1974; 111: 285-287. 8. Van Wyck LG, Vinuela F, Hoeneman H. Therapeutic embolization for severe epistaxis J Otolaryngol 1982; 11: 271-274. 9. Parnes LS, Hoeneman H, Vinuela F. Percutaneous embolization for control of nasal blood circulation. Laryngoscope 1987; 97: 1312- 1315. 10. Hicks JN, Vitek JJ. Transarterial embolization to control posterior epistaxis. Laryngoscope 1989; 99: 1027-1029. 11. Vitek JJ. Idiopathic intractable epistaxis: Endovascular therapy. Radiology 1991; 181: 113- 116. 12. Kagetsu NJ, Berenstein A, Choi IS. Interventional radiology of the extracranial head and neck. Cardiovasc Intervent Radiol 1991; 14: 325-333. 13. Connors JJ III, Wojak JC. Epistaxis. In: Connors JJ III, Wojak JC, eds. Interventional Neuro- radiology: Strategies and Practical Techniques. Philadelphia: WB Saunders, 1999: 147-156. 14. Koh E, Frazzini VI, Kagetsu NJ. Epistaxis: Vascular anatomy, origins and endovascular treatment. Am J Roentgenol 2000; 174: 845-851. 15. Tan LKS, Calhoun KH. Epistaxis. Med Clin North Am 1989; 83: 43-56. 16. Schaitken B, Strauss M, Houck JR. Epistaxis: medical versus surgical therapy- a comparison of efficacy, complications and economic considera- tions. Laryngoscope 1987; 97: 1392-1396. 17. Fairbanks DNF. Complications of nasal packing Otolaryngol Head Neck Surg 1986; 94: 412-415. 18. Elwany S, Abdel-Fatah H. Endoscopic control of posterior epistaxis. J Laryngol Otol 1996; 110: 432-434. 19. Winstead W. Sphenopalatine artery ligation: An alternative to internal maxillary ligation for intractable posterior epistaxis. J Laryngol 1996; 106: 667-669. 20. Pritikin JB, Caldarelli DD, Panje WR. Endoscopic ligation of the internal maxillary artery for treat- ment of intractable posterior epistaxis. Ann Otol Rhinol Laryngol 1998; 107: 85-91. 21. Strong EB, Bell DA, Johnson LP, Jacobs JM. Intractable epistaxis: Transantral ligation versus embolization: Efficacy review and cost analysis. Otolaryngol Head Neck Surg 1995; 113: 674-678. 22. Cullen MM, Tami TA. Comparison of internal maxillary artery ligation versus embolization for refractory posterior epistaxis. Otolaryngol Head Neck Surg 1998; 118: 636-642. 23. Simpson GT, Janfaza P, Becker GD. Transantral sphenopalatine artery ligation. Lar y ngos cope 1982; 92: 1001-1005. 24. Breda SD, Choi IS, Persky MS, Weiss M. Embolization in the treatment of epistaxis after failure of internal maxillary artery ligation. Laryngoscope 1989; 99: 809-813. 25. Hacien-Bay L, Rosenbloom JS, Pile-Spellman J, et al. Anastomoses in recurrent epistaxis. J Vasc Intervent Radiol 1997; 8: 535-538. 26. Lasjaunias P, Marsot-Dupuch K, Doyon D. The radio-anatomical basis of arterial embolization for epistaxis. J Neuroradiol 1979; 6: 45-53. 27. Lasjaunias P, Berenstein A. Surgical Neuroangiog- raphy: Functional Anatomy of Craniofacial Arteries. Vol 1. Berlin: Springer-Verlag, 1987. 28. Duncan IC, Dos Santos C. Accessory meningeal arterial supply to the posterior nasal cavity: Another reason for failed endovascular treat- ment of epistaxis. Cardiovasc Intervent Radiol 2003; 26: 488-491. 29. Leppanen M, Seppanen S, Loranne J, Kuoppala K. Microcather embolization of intractable idio- pathic epistaxis. Cardiovasc Intervent Radiol 1999; 22: 499-503. 30. Elden L, Montanera W, TerBrugge K, Willinsky R, Lasjaunias P, Charles D. Angiographic embolization for the treatment of epistaxis: A review of 108 cases. Otolaryngol Head Neck Surg 1994; 111: 44-50. 31. Duncan IC, Spiro FI, Van Staden D. Acute ischaemic sialadenitis following facial artery embolization. Cardiovasc Intervent Radiol 2004; 27: 300-302. 32. Elahi MM, Panes LS, Fox AJ, Pelz DM, Lee DM. Therapeutic embolization in the treatment of epistaxis. Arch Otolaryngol Head Neck Surg 1995; 121: 65-69. 33. Oguni T, Korogi Y, Yasunaga T, et al. Superselective embolization for intractable idio- pathic epistaxis. Br J Radiol 2000; 73: 1148-1153. 34. Duncan IC, Fourie PA. Catheter-directed intra- arterial abciximab administration for acute thrombotic occlusions during neurointerven- tional procedures. Interventional Neuroradio- logy 2002; 8: 159-168. 35. Haitjema T, Balder W, Disch FJ, Westermann CJ. Epistaxis in hereditary haemorrhagic telangiecta- sia. Rhinology 1996; 34: 176-178. 36. Duncan IC, Van der Nest L. Intralesional bleomycin injections (IBI) for the palliation of epistaxis in hereditary haemorrhagic telangiec- tasia. Am J Neuroradiol 2004; 25: 1144-1146. ORIGINAL ARTICLE 18 SA JOURNAL OF RADIOLOGY • October 2004 Table VI. Average costs per embolisation procedure Year Rands US dollars ($1 = R8) 1999 R 16 628 US$2 078 2000 R 15 993 US$1 999 2001 R 18 551 US$2 319 2002 R 22 761 US$2 845 2003 R 22 136 US$2 767 The above excludes all hospitalisation costs and professional private fees for the referring ENT specialist and anaesthetist. A shortened version of this article was published in the South African Medical Journal 2004; 94: 373-378.