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Eur Arch Otorhinolaryngol DOI 10.1007/s00405-011-1659-y RHINOLOGY Serious spontaneous epistaxis and hypertension in hospitalized patients Cyril Page • Aurélie Biet • Sophie Liabeuf Vladimir Strunski • Albert Fournier • Received: 25 February 2011 / Accepted: 25 May 2011 Springer-Verlag 2011 Abstract The aim of the study was to evaluate the role of hypertension in patients hospitalized for serious spontaneous epistaxis. This 6-year retrospective study was based on 219 patients hospitalized in a University Hospital ENT and Head and Neck surgery department for serious spontaneous epistaxis. The following parameters were recorded: length of hospital stay, history of hypertension, blood pressure (BP) recordings (on admission, during hospitalization and on discharge), epistaxis severity criteria, including medical and/or surgical management of epistaxis (blood transfusion depending on blood count, embolization, surgery), medications affecting clotting. Epistaxis was classified into two groups: serious and severe. No significant differences were observed between the two groups in terms of age, sex ratio, history of epistaxis and BP characteristics including history of hypertension, mean BP on admission, mean arterial pressure on discharge and number of patients in whom BP was difficult to control. Patients with more severe epistaxis had a similar exposure to anticoagulant and platelet antiaggregant medications as patients with less severe epistaxis. Overall, on univariate logistic regression analysis, no factors were independently associated with severity C. Page (&) A. Biet V. Strunski ENT and Head and Neck Surgery Department, C.H.U Amiens, Centre Hospitalier Nord, Place Victor Pauchet, 80054 Amiens cedex, France e-mail: [email protected] S. Liabeuf Clinical Pharmacology Department, CHU AMIENS - Hopital Sud, Avenue Laënnec, Salouel, 80054 Amiens cedex, France A. Fournier Nephrology Department, CHU AMIENS - Hopital Sud, Avenue Laënnec, Salouel, 80054 Amiens cedex, France of epistaxis. The pathophysiology of serious spontaneous epistaxis remains to be unclear. It concerns elderly patients ([60–70 years old) with a history of hypertension in about 50% of cases. Serious spontaneous epistaxis may also be the presenting sign of underlying true hypertension in about 43% of patients with no history of hypertension. However, hypertension per se does not appear to be a statistically significant causal factor and/or a factor of severity of serious spontaneous epistaxis. Keywords Epistaxis Hypertension Introduction Epistaxis is one of the commonest ENT emergencies requiring hospital admission (15% of cases according to Timsit) [1]. Although predominantly a benign condition regardless of its etiology, epistaxis can be severe, particularly in elderly and/or frail patients, requiring hospitalization and ‘‘aggressive’’ management including repeated nasal packing, blood transfusion, arterial embolization or surgery [2–6]. Epistaxis can be posttraumatic, iatrogenic (nose surgery, particularly endonasal procedures) or ‘‘spontaneous’’, resulting from numerous possible causative factors including local nasal factors (inflammation, infection…), medications, and systemic factors such as platelet and coagulation abnormalities, alcoholism, hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) and hypertension [1–6]. Hypertension has been considered to be a major cause of spontaneous epistaxis for a long time [7, 8]. However, particularly in the recent medical literature, the relationship between hypertension and epistaxis appears to be more controversial [9–16]. 123 Eur Arch Otorhinolaryngol This retrospective study concerning 219 patients hospitalized for serious spontaneous epistaxis was designed to elucidate the role of hypertension in these patients managed in a university hospital ENT and Head and Neck Surgery department. Materials and methods This retrospective study was performed over a 6-year period from January 2004 to December 2009 in the University Hospital of Amiens, France. This study was approved by the Amiens University Medical Center’s institutional review board. Patient selection A total of 219 patients were included in the study. The study inclusion criteria were: – – male and female patients of any age patients admitted to the ENT and Head and Neck surgery department with a diagnosis of serious spontaneous epistaxis requiring at least one nasal pack. The exclusion criteria were: patients with minor epistaxis easily managed by first aid measures and/or immediately successful local treatment (cauterization), posttraumatic epistaxis (including iatrogenic epistaxis after nasal surgery) and patients usually followed for Hereditary Hemorrhagic Telangiectasia. Four patients hospitalized for epistaxis (two patients followed for nasal cancer, one patient with leukemia and chemotherapy-induced pancytopenia and one patient with Child-Pugh C cirrhosis were also excluded from the study. Management of epistaxis Management of epistaxis ranged from unilateral nasal packing to endoscopic surgery or embolization depending on the severity of epistaxis. Patients with systolic blood pressure (BP) higher than 160 mmHg also received nicardipine intravenous infusion (syringe pump) to control BP. Anterior nasal packing was performed with Polyvinyl Alcohol sponge (MEROCEL Standard nasal dressing); anterior and posterior nasal packing was performed with a double balloon nasal catheter (BIVONA). Nasal packs were removed after 24–48 h if the patient did not re-bleed. In cases of re-bleeding after removal of nasal packs, nasal packing was repeated. Embolization or surgery was only indicated in the case of anemia or persistent bleeding after 2 or 3 nasal packs. 123 Study protocol A history of hypertension was defined as patients treated with antihypertensive drugs. Patients with a self-reported history of epistaxis or who had been already hospitalized for at least one episode of epistaxis were considered to have a history of epistaxis. The mean of all BP measurements during hospitalization was determined, and BP that was difficult to control was defined as BP higher than 140/80 mmHg. International Normalized Ratio (INR) for prothrombin time was evaluated for 72 patients treated with vitamin K antagonists. Epistaxis was classified as grade 1 (serious) or grade 2 (severe). Serious epistaxis was defined by the need for medical management requiring hospitalization of the patient for epistaxis. Severe epistaxis (grade 2) was defined as follows: – – – – – length of hospital stay [3 days nasal packing using double balloon nasal catheter two or more nasal packs presence of hematologic consequences: anemia (hemoglobin \10 g/dl) and/or blood transfusion patients treated by embolization or surgery Statistical analysis Data were expressed as mean ± S.D., and range or frequency, as appropriate. For descriptive and analytical purposes, patients were stratified by severity of epistaxis, defined as Grade 1 or Grade 2. Between-group comparisons were performed with a v2 test for categorical variables and Student’s t test or Mann–Whitney test for continuous variables. Univariate logistic regression analysis was then performed to identify the variables independently associated with severity of epistaxis. A p B 0.05 was considered to be statistically significant. All statistical analyses were performed using SPSS (SPSS Inc, Chicago, IL), version 13.0 for Windows (Microsoft Corp, Redmond, WA). Results A total of 219 patients admitted to the ENT and Head and Neck Surgery Department were included. Table 1 shows the clinical characteristics of the patients according to the severity of epistaxis. No significant differences were observed between the two groups in terms of age, sex ratio, history of epistaxis and BP characteristics including history of hypertension, mean BP on admission, mean BP on discharge and number Eur Arch Otorhinolaryngol Table 1 Clinical and demographic characteristics of the study population Severity of epistaxis All n = 219 Grade 1 n = 94 Grade 2 n = 125 p 0.6 Age (years) 70 ± 15 70 ± 15 69 ± 15 Male gender, n (%) 123 (57) 48 (53) 75 (60) 0.3 Systolic blood pressure on admission (mmHg) Diastolic blood pressure on admission (mmHg) 147 ± 2.9 80 ± 16 147 ± 2.5 80 ± 15 146 ± 3.2 80 ± 16 0.7 0.9 Number of patients in whom blood pressure as difficult to control, n (%) 127 (59) 51 (57) 76 (60) 0.5 Systolic blood pressure on discharge (mmHg) 128 ± 16 129 ± 17 127 ± 16 0.3 Diastolic blood pressure on discharge (mmHg) 71 ± 11 72 ± 11 70 ± 11 0.2 History of hypertension, n (%) 118 (55) 48 (53) 70 (56) 0.7 History of epistaxis, n (%) 72 (34) 29 (32) 43 (34) 0.7 Vitamin K antagonist n (%) 72 (34) 29 (32) 43 (34) 0.7 INR (n = 72) 3±1 2.9 ± 1.1 3 ± 1.6 0.6 Aspirin, n (%) 59 (27) 27 (30) 32 (26) 0.5 Clopidogrel, n (%) 11 (5) 4 (4) 7 (6) 0.7 Length of hospital stay (days) 3.1 ± 1.9 2.1 ± 0.8 3.9 ± 2 NA Hemoglobin (g/dl) 11.7 ± 2.4 13 ± 1.4 11 ± 2.7 NA Treatment with sphenopalatine artery surgical ligation or embolization n (%) 13 (3) 0 (0) 13 (4) NA Treatment with double-cuffed nasal tamponade balloon n (%) 65 (30) 0 (0) 65 (52) NA Treatment with more than 2 nasal packs n (%) 44 (20) 0 (0) 44 (35) NA of patients in whom BP was difficult to control. Patients with more severe epistaxis had a similar exposure to anticoagulant and platelet antiaggregant medications as patients with less severe epistaxis. On univariate logistic regressions, no factors were independently associated with severity of epistaxis (data not shown). (Osler-Weber-Rendu disease), the cause of epistaxis can be identified in only about 15% of patients [4]. In the absence of documented evidence (a visible bleeding vessel on the nasal septum for example), no obvious cause-and-effect relationship can be confirmed, especially concerning hypertension. Only statistical associations between hypertension and epistaxis have been reported [7–16]. Discussion Definition of serious spontaneous epistaxis Serious spontaneous epistaxis is a challenging medical problem in otorhinolaryngology, particularly concerning its physiopathology and its relationship with hypertension. Etiologies of epistaxis Classical teaching and medical literature highlight many possible etiologic factors for epistaxis; including environmental factors (humidity, temperature), local factors (inflammation, deviated septum and/or perforation, tumors, foreign bodies, aneurysm), systemic factors (hypertension, platelet and coagulation abnormalities, renal failure, alcoholism, arteriosclerosis, hereditary hemorrhagic telangiectasia), and medications affecting clotting (anticoagulants, nonsteroidal anti-inflammatory drugs) [3]. Although some etiologies of epistaxis are obvious such as trauma (iatrogenic or non-iatrogenic), nasal inflammation and/or infection or tumors and hereditary hemorrhagic telangiectasia Epistaxis is a benign condition in the majority of cases, but can sometimes be sufficiently serious (6% of cases according to Pollice) [6] to require emergency hospitalization for medical and/or surgical management and close follow-up, especially in patients older than 65 years [2]. However, in the majority of cases, patients present themselves (often to the emergency department) with ‘‘spontaneous’’ epistaxis with no obvious cause and emergency management must be performed before determining the etiology of the nose-bleed. Classical textbooks and the medical literature do not provide a precise definition for the severity of epistaxis which is often based on subjective impressions (subjective evaluation of the volume of bleeding) or anatomic features, essentially posterior epistaxis [5]. Hoag et al. recently proposed an epistaxis severity score but specifically for hereditary hemorrhagic telangiectasia [16]. In our opinion, epistaxis should be 123 Eur Arch Otorhinolaryngol considered to be serious when it requires specific medical and/or surgical management including at least one nasal pack and hospitalization for close follow-up. The complete criteria used to classify the severity of epistaxis as serious or severe in the present study are shown in Table 1. Finally, most articles in the medical literature concerning the association between epistaxis and hypertension do not clearly define the severity of epistaxis, which, in our opinion, constitutes a major problem: is hypertension related to serious spontaneous epistaxis? In another study concerning 372 patients, Herkner et al. [14] concluded that active epistaxis in the emergency department was associated with hypertension, suggesting that hypertension was a predisposing factor for acute nosebleed. Knopfholz et al. [15] in a series of 36 patients, concluded that the incidence of epistaxis in hypertensive patients was not associated with the severity of hypertension. Moreover, BP readings in the setting of epistaxis were similar to those obtained in routine settings. Association between epistaxis and hypertension Comparison of the present series with the medical literature Epistaxis has been considered to be related to hypertension for a long time. In 1959, Mitchell [7] statistically compared two groups of patients (one group of 374 patients with a history of hypertension and another group of 162 patients with acute epistaxis but with no history of hypertension) and concluded that, in the absence of local nasal disease, epistaxis was associated with high BP. In 1977, Charles and Corrigan [8] confirmed this conclusion in a series of 194 patients and, more recently, Isezuo et al. [9] also showed a statistically significant association between epistaxis and hypertension in a series of 62 patients. However, Fuchs et al. [10] in a sample of 1,174 subjects over the age of 18 years representative of Porto Allegre general population, found no association between epistaxis and hypertension. The same group, however, [11] in a study based on 323 adults with hypertension, pointed out however that duration of hypertension and left ventricular hypertrophy were associated with epistaxis, suggesting that epistaxis might be a consequence of long-lasting hypertension. In another study of 121 hypertensive patients, Lubianca Neto et al. tried to evaluate the association between severity of hypertension and history of epistaxis. They concluded that the severity of hypertension was not associated with a history of epistaxis, but they found a statistically significant tendency towards an association between history of epistaxis with duration of hypertension and left ventricular hypertrophy, in addition they noticed that among the abnormalities detected at rhinoscopy, only the presence of enlarged septal vessels was associated with a history of epistaxis. They concluded that long lasting hypertension might contribute to epistaxis but the role of septal vessel abnormalities needed further work to be established [12]. Herkner et al. [13] in a series of 426 patients admitted at the emergency room, demonstrated that patients with epistaxis had higher BP than control patients. 79% of patients with elevated BP during epistaxis had sustained hypertension and 27% of these patients were unaware of their hypertension, indicating that epistaxis may be the presenting sign of hypertension. 123 The present series is fairly similar to other series of patients hospitalized for epistaxis published in the medical literature, but the patients of this series were slightly older with a mean age of 70 years versus 64.3 years for Viducich [5] and 60 years for Pollice (with 70% of patients [50 years) [6]. 55% of the patients in the present series had a history of hypertension versus 48% for Viducich [5] and 47% for Pollice [6]. The main bias of this retrospective series was that this study only concerned patients hospitalized for serious spontaneous epistaxis requiring medical and/or surgical management and close follow-up in hospital. The majority of cases of benign epistaxis were not considered in this study, and it would have possibly been interesting to compare the clinical features and concomitant diseases of patients with benign epistaxis versus patients with serious epistaxis. However, this study reveals interesting results, as no significant differences were observed between the two patient groups concerning the role of hypertension. A history of hypertension was not associated with severe epistaxis versus serious epistaxis. No statistically significant difference was observed between patients with a history of epistaxis in the two patient groups (with or without a history of hypertension). No statistically significant difference was observed between BP recordings on admission between the two patient groups (with or without a history of hypertension). The severity of hypertension (BP [160/100 mmHg) was not associated with severe epistaxis versus serious epistaxis. Blood pressure recordings were also not significantly different between the two groups of hypertensive versus non-hypertensive patients, which may indicate that, as suggested by Tan and Calhoun [3], hypertension at the time of treatment of epistaxis may be anxiety-related, and BP returns to normal after control of epistaxis and reassurance. However, 43 of the 127 patients with abnormal BP recordings during hospitalization had no history of hypertension. True hypertension was diagnosed in these patients, i.e 42.57% of patients with no Eur Arch Otorhinolaryngol previous history of hypertension. However, we have recorded BP only during their hospitalization and not weeks after discharge as appropriately did Herkner et al. [13] for confirming or excluding sustained hypertension with a 24-h ambulatory BP recording. In contrast to Lubianca Neto, in the present series, we found only a dozen patients who underwent septal cauterization 3 weeks after the episode of epistaxis and no local nasal factor was found on rhinoscopy performed at the D21 follow-up visit in the other patients. Overall, the very local nasal origin of epistaxis remains to be unclear in the majority if not all cases. We can conclude like Celik et al. [16] that: the debate on BP and epistaxis will continue. The potential influence of BP levels on acute episodes of epistaxis still requires investigations. Our clinical data are not sufficient to support or dismiss the idea that epistaxis is secondary to end-organ damage caused by hypertension. This is corroborated by nasal examinations after the episode of epistaxis, since they were normal in almost all cases in our ENT experience. 3. 4. 5. 6. 7. 8. 9. 10. Conclusion The pathophysiology of serious spontaneous epistaxis remains to be unclear. It mainly occurs in elderly patients ([60–70 years old) with a history of hypertension in about 50% of cases. Serious spontaneous epistaxis may reveal underlying true hypertension in about 43% of patients (in this series) with no previous history of hypertension. Serious spontaneous epistaxis probably results from a combination of several local and systemic causal factors or diseases. Further prospective studies are required to elucidate the pathophysiology and the exact role played by hypertension. Conflict of interest 2. 11. 12. 13. 14. The authors declare no conflict of interest. 15. References 16. 1. Timsit CA, Bouchène K, Olfatpour B, Tsigaridis P, Herman P, Tran Ba Huy P (2001) Etude épidémiologique et clinique portant sur 20 563 patients accueillis à la grande garde d’urgence ORL adulte de Paris Ile de France (Epidemiology and clinical findings in 20, 563 patients attending the Lariboisière Hospital ENT Adult Emergency Clinic, French). Ann Otolaryngol Chir Cervicofac 118:215–224 Klossek JM, Dufour X, de Montreuil CB, Fontanel JP, Peynègre R, Reyt E, Rugina M, Samardzic M, Serrano E, Stoll D, Chevillard C (2006) Epistaxis and its management: an observational pilot study carried out in 23 hospital centres in France. Rhinology 44:151–155 Tan LK, Calhoun KH (1999) Epistaxis. Med Clin North Am 83:43–56 Kotecha B, Fowler S, Harkness P, Walmsley J, Brown P, Topham J (1996) Management of epistaxis: a national survey. Ann R Coll Surg Engl 78(5):444–446 Viducich RA, Blanda MP, Gerson LW (1995) Posterior epistaxis: clinical features and acute complications. Ann Emerg Med 25:592–596 Pollice PA, Yoder MG (1997) Epistaxis: a retrospective review of hospitalized patients. Otolaryngol Head Neck Surg 117:49–53 Mitchell JR (1959) Nose-bleeding and high blood pressure. Br Med J 1:25–27 Charles R, Corrigan E (1977) Epistaxis and hypertension. Postgrad Med J 53:260–261 Isezuo SA, Segun-Busari S, Ezunu E, Yakubu A, Iseh K, Legbo J, Alabi BS, Dunmade AE, Ologe FE (2008) Relationship between epistaxis and hypertension: a study of patients seen in the emergency units of two tertiary health institutions in Nigeria. Niger J Clin Pract 11:379–382 Fuchs FD, Moreira LB, Pires CP, Torres FS, Furtado MV, Moraes RS, Wiehe M, Fuchs SC, Lubianca Neto JF (2003) Absence of association between hypertension and epistaxis: a population-based study. Blood Press 12(3):145–148 Lubianca Neto JF, Fuchs FD, Facco SR, Gus M, Fasolo L, Mafessoni R, Gleissner AL (1999) Is epistaxis evidence of endorgan damage in patients with hypertension? Laryngoscope. 109:1111–1115 Lubianca-Neto JF, Bredemeier M, Carvalhal EF, Arruda CA, Estrella E, Pletsch A, Gus M, Lu L, Fuchs FD (1998) A study of the association between epistaxis and the severity of hypertension. Am J Rhinol 12:269–272 Herkner H, Laggner AN, Müllner M, Formanek M, Bur A, Gamper G, Woisetschläger C, Hirschl MM (2000) Hypertension in patients presenting with epistaxis. Ann Emerg Med 35: 126–130 Herkner H, Havel C, Müllner M, Gamper G, Bur A, Temmel AF, Laggner AN, Hirschl MM (2002) Active epistaxis at ED presentation is associated with arterial hypertension. Am J Emerg Med 20:92–95 Knopfholz J, Lima-Junior E, Précoma-Neto D, Faria-Neto JR (2009) Association between epistaxis and hypertension: a one year follow-up after an index episode of nose bleeding in hypertensive patients. Int J Cardiol 134:e107–e109 Celik T, Iyisoy A, Yuksel UC, Karahatay S, Tan Y, Isik E. A new evidence of end-organ damage in the patients with arterial hypertension: epistaxis? Int J Cardiol 2009; doi:10.1016/j.ijcard. 2008.11.090 123 Turkish Journal of Medical Sciences http://journals.tubitak.gov.tr/medical/ Research Article Turk J Med Sci (2014) 44: 133-136 © TÜBİTAK doi:10.3906/sag-1301-58 Epistaxis in geriatric patients Alper YÜKSEL*, Hanifi KURTARAN, Ekrem Said KANKILIÇ, Nebil ARK, Kadriye Şerife UĞUR, Mehmet GÜNDÜZ Department of Otolaryngology - Head and Neck Surgery, Faculty of Medicine, Fatih University, Ankara, Turkey Received: 14.01.2013 Accepted: 22.02.2013 Published Online: 02.01.2014 Printed: 24.01.2014 Aim: Epistaxis is a common emergency in otolaryngology. The aim of this study is to analyze the etiology, management, and accompanying disorders of epistaxis in geriatric patients by reviewing the literature Materials and methods: Data of 117 patients 65 years old and older who presented to the Department of Otorhinolaryngology with active epistaxis between 2004 and 2010 were retrospectively reviewed. Records were evaluated for age, sex, accompanying disorders, drug medication, detailed otorhinolaryngological findings, and management of epistaxis. Results: There were 67 women (57.26%) and 50 men (42.74%) with a mean age of 73.51 years (range: 65–90). Ninety-four (80.34%) patients had accompanying disorders such as hypertension, diabetes mellitus, cerebrovascular disease, sinusitis, chronic obstructive lung disease, nasal polyp, and drug treatment. The bleeding site was anterior in 90 patients (76.92%) and posterior in 16 (13.67%). In 11 patients (9.4%), the bleeding site was not identified. Fifty-seven patients (48.71%) were treated with cauterization, 17 patients (14.52%) with nasal packing, 12 patients (10.25%) with medical treatment, 1 patient (0.85%) with mass excision and nasal packing, and 19 patients (16.23%) with more than 1 treatment method. Six patients (5.12%) were untreated because of the unidentified bleeding point. Bleeding control was performed under local anesthesia in 113 patients (96.58%) and under general anesthesia in 4 patients (3.41%). Twenty-one patients (17.94%) were hospitalized and 3 patients (2.56%) required a blood transfusion. Conclusion: Epistaxis is the most common otorhinolaryngological emergency. It must be evaluated carefully to avoid the potential complications resulting from both epistaxis and its associated disorders, especially in geriatric patients. Key words: Epistaxis, cauterization 1. Introduction Epistaxis is one of the most common nasal emergencies, with an incidence ranging from 30 to 100 per 100,000 each year (1). The lifetime occurrence rate of epistaxis is approximately 60% (2). However, most bleeding episodes are minor and require no medical treatment. Minor bleeding episodes occur more frequently in children and adolescents, whereas severe bleeds requiring otolaryngological intervention often occur in patients older than 50 years (3). Anterior nosebleeds are observed in approximately 80% patients with epistaxis (4). They arise from an anastomosis called Kiesselbach’s plexus in the lower portion of the anterior septum, called Little’s area. Conservative treatment methods are often sufficient for most patients with anterior epistaxis. These methods include local pressure, chemical cautery, and anterior nasal packing (5). Posterior bleeding originates primarily from the posterior septal nasal artery, a branch of the sphenopalatine artery, and tends to be more serious compared with anterior *Correspondence: [email protected] bleeding. Conservative methods are generally insufficient for the treatment of patients with posterior epistaxis, who often require further otolaryngological intervention (6). Further treatment options include posterior packing, arterial ligation, and embolization. Treatment modalities differ because of factors such as site and severity of bleeding, predisposing conditions, and experience of the otolaryngologist. Various local and systemic factors cause epistaxis. Common local factors include digital trauma, nasal septal deviation, neoplasia, inflammation, and chemical irritants, whereas coagulopathies, renal failure, alcoholism, and vascular abnormalities are common systemic factors (7,8). Patients presenting with epistaxis in the geriatric population must be evaluated carefully. The clinical status of geriatric patients may deteriorate quickly; therefore, rapid evaluation and treatment of these patients must be performed (4). In this study, the etiology, management, and accompanying disorders of epistaxis were analyzed in 133 YÜKSEL et al. / Turk J Med Sci geriatric patients. A review of the relevant literature is also presented. 2. Material and methods The data of 156 patients aged ≥65 years, who presented to the Department of Otorhinolaryngology with active epistaxis between 2004 and 2010, were retrospectively reviewed. Patients were identified by a search of the electronic data record system of the hospital. In total, 39 patients were excluded, 22 because they presented with epistaxis caused by trauma and 17 because of insufficient data. Therefore, 117 patients with a diagnosis of epistaxis as confirmed by chart review were eligible for the study. Epistaxis was defined as bleeding from the nasal cavity as confirmed by nasal inspection on initial evaluation. The condition of active or inactive epistaxis was determined on the basis of the nasal inspection results. The localization of epistaxis was classified as diffuse or limited and unilateral or bilateral. The bleeding site was identified as anterior or posterior after nasal endoscopic examination using 0° and 30° rigid endoscopes. Anterior epistaxis was identified in cases in which the bleeding site was visible on anterior rhinoscopy (9). Patients were labeled positive for hypertension if this condition was stated in their medical charts or if they were on antihypertensive medication. Treatment with anticoagulant medication such as Coumadin, heparin, Fraxiparine, or aspirin was ascertained during evaluation. Records were examined to obtain information regarding age, sex, accompanying disorders, detailed otorhinolaryngological findings, and management of epistaxis. This study was approved by the local ethics committee of the hospital. 3. Results This study included 67 women (57.26%) and 50 men (42.74%) with a mean age of 73.51 years (range: 65–90 years). Ninety-four (80.34%) patients had accompanying disorders such as hypertension, diabetes mellitus, cerebrovascular disease, sinusitis, coronary artery disease, nasal polyp, or a history of drug medication (Table 1). Table 1. Underlying disorders. Hypertension 91 (77.7%) Diabetes mellitus 69 (58.9%) Coronary artery disease 17 (14.5%) Anticoagulant medication 13 (11.1%) Sinusitis 11 (9.4%) Nasal polyp 9 (7.6%) Cerebrovascular disease 3 (2.5%) 134 The bleeding site was anterior in 90 patients (76.92%) and posterior in 16 (13.67%). In 11 patients (9.4%), the bleeding site was not identified. Treatment modalities used for the management of epistaxis in the patients included in this study are shown in Table 2. No bleeding points were identifiable in 6 patients (5.12%). Epistaxis healed spontaneously in all patients, with no evidence of recurrence on follow-up. Bleeding control was performed under local anesthesia in 113 patients (96.58%) and under general anesthesia in 4 (3.41%). Twenty-one patients (17.94%) were hospitalized and 3 (2.56%) required a blood transfusion. 4. Discussion Bleeding from the nose is a common complaint, and it occurs in approximately 10% of the population at any given time (10). Epistaxis may lead to mortality and morbidity in vulnerable groups such as children and the elderly and in patients with additional systemic disorders. The interaction of several local and systemic factors results in nosebleeds. These factors damage the nasal mucosa, affect the vascular structure, and/or disrupt blood clotting. They include environmental conditions, trauma, nasal septal deviation, tumors, inflammation, bleeding disorders, anticoagulant medications, hypertension, and age. In geriatric patients, systemic factors such as hypertension, advanced age, and bleeding disorders are the most common causes of serious epistaxis (7,8). Vascular wall changes associated with ageing, such as fibrosis of the arterial tunica media, have been implicated in the development of epistaxis. Therefore, elderly patients are at higher risk of epistaxis (11). The prevalence of hypertension in patients with epistaxis reportedly ranges from 24% to 64% (12). Another controlled study provided a relationship between epistaxis and high blood pressure (13). In contrast, a crosssectional study in patients with hypertension found no independent association between the severity of epistaxis and hypertension (14). Other studies have suggested that hypertension in patients with epistaxis may be related to anxiety (15). Ninety-one (77.7%) of the 117 patients in our study group had a history of epistaxis. The role of hypertension in epistaxis is controversial, and the evidence available is insufficient to prove a significant association between hypertension and epistaxis. However, the control of epistaxis may be more difficult in patients with hypertension (7). In rare cases, epistaxis may be a life-threatening emergency, especially in elderly patients with hypertension and severe hemorrhage (10). In our study group, none of the patients required resuscitation despite old age (>65 years old) and underlying disorders (80.34% patients). Coagulation screening is not routinely used in our institution. Studies have shown that routine coagulation YÜKSEL et al. / Turk J Med Sci Table 2. Treatment modalities. Anterior Posterior SN EC AP 48 2 10 7 5 PP 2 MT SN + AP ME + AP 12 17 1 2 SN = silver nitrate, EC = electrocautery, AP = anterior packing, PP = posterior packing, MT = medical treatment, ME = mass excision. studies such as prothrombin time and activated partial thromboplastin time are not necessary in patients with epistaxis. Coagulation screening should be used in patients with suspected clotting disorders or in patients who receive anticoagulation treatment (16,17). The first step in the treatment of acute epistaxis is identification of the bleeding point. In our study, 90 (76.92%) of the patients had anterior epistaxis. This incidence rate is compatible with the rates reported in the literature (4). After localization of the bleeding point, chemical cautery or electrocautery can be performed. Silver nitrate can be used as a chemical cauterization agent, especially for minor bleeding, with minimal discomfort. Electric cauterization must be performed for more aggressive bleeding from the anterior septum. Cauterization should be one-sided in order to prevent septal perforation (18). There is no evidence to prove that electrocautery has any advantage over silver nitrate cautery (10). In our study group, 90 (76.92%) patients had anterior epistaxis, 48 (41.02%) of whom were successfully treated with silver nitrate cautery. Only 2 patients were treated with electrocautery because of severe epistaxis from the anterior septum. In the case of cauterization failure, nasal packing must be considered as the next treatment option. Many different types of packs are available, including absorbable, nonabsorbable, anterior, and posterior packs. Common absorbable materials used for anterior packing include oxidized cellulose (e.g., Surgicel, Johnson & Johnson, New Brunswick, NJ, USA) and gelatin foams (e.g., Gelfoam, Pfizer, New York, NY, USA). Another product that combines thrombin with gelatin (e.g., Floseal, Baxter Health Care Corp, Deerfield, IL, USA) is used as a highviscosity gel for hemostasis (19). All these absorbable products are easily used and cause minimal pain and discomfort. Various kinds of nonabsorbable packing materials are also available, including inflatable balloons, calcium alginate, polyvinyl alcohol (e.g., Merocel, Medtronic XOMED, Jacksonville, FL, USA), and petroleum jellyimpregnated gauze. The major disadvantage of anterior packing with these materials is the need for removal of the material and the pain associated with placement and removal. Complications caused by anterior packs include ulcerations, septal perforation, sinusitis, synechia, hypoxemia, and arrhythmias (20). Contrarily, Kurtaran et al. reported that nasal packing with airway tubes is not a cause for postoperative respiratory dysfunction and hypoxia (21). Merocel is most commonly used for anterior packing in our institution. None of the complications mentioned above were observed in this study, although our study group comprised geriatric patients. Approximately 10% of all nosebleeds arise from the posterior part of the nose (22). Posterior epistaxis is often encountered in elderly individuals (23). This condition may be associated with diseases such as hypertension and arterial degeneration (24). In our study group, 16 (13.67%) patients had posterior epistaxis. Although no research on epistaxis in geriatric patients is available, the incidence of posterior epistaxis in this study was not significantly higher than that in the normal population. In this study, a formal posterior pack made of ribbon gauze was used in 2 patients, although balloon catheters are more commonly used. However, posterior packing is associated with increased risk of mortality and morbidity. Nasal packing may cause significant hypoxia, especially in patients with chronic systemic disorders (10). In some cases, traditional nasal packing fails to control the epistaxis. Angiographic embolization or endoscopic techniques for sphenopalatine artery ligation can be used for the control of intractable bleeding. Angiographic embolization for posterior epistaxis was first described in 1974 (25), with success rates ranging from 79% to 96% (26). Complications of embolization include rebleeding, stroke, blindness, facial numbness, skin sloughing, and groin hematoma. A success rate of 98% was reported for endonasal ligation of the sphenopalatine artery to control bleeding in 127 patients; no significant treatment-related complications were reported in that study (27). In our study, all patients with epistaxis were treated using conventional methods. No further interventions such as embolization or sphenopalatine artery ligation were required. Some authors recommend a formal nasal examination under general anesthesia in patients with posterior epistaxis (23). In our study group, only 4 (3.41%) of the 16 (13.6%) patients with posterior epistaxis were treated under general anesthesia. In fact, treatment of epistaxis under general anesthesia is easier than treatment under 135 YÜKSEL et al. / Turk J Med Sci local anesthesia for both the surgeon and the patient; however, general anesthesia can be dangerous for geriatric patients with systemic disorders. Bleeding control was performed under local anesthesia in 113 patients (96.58%). Twenty-one patients (17.94%) were hospitalized and 3 (2.56%) required a blood transfusion. In conclusion, epistaxis, which is the most common otorhinolaryngological emergency, must be evaluated carefully to avoid the potential complications resulting from both epistaxis and its associated disorders, especially in geriatric patients. Multiple methods for treating anterior and posterior epistaxis are available, and occasionally more than one treatment is used. Otolaryngologists must be prepared to deal with severe bleeding through the use of medications, packing materials, and radiological or surgical interventions, especially in geriatric patients. References 1. O’Donnell M, Robertson G, McGarry GW. A new bipolar diathermy probe for the outpatient management of adult acute epistaxis. Clin Otolaryngol 1999; 24: 537–541. 2. Weiss NS. Relation of high blood pressure to headache, epistaxis, and selected other symptoms — The United States Health Examination Survey of Adults. N Engl J Med 1972; 287: 631–633. 3. Massick D, Tobin EJ. Epistaxis. In: Cummings C, Haughey B, Thomas R, Harker L, Robbins T, Schuller D, Flint P, editors. Cummings Otolaryngology: Head and Neck Surgery. Philadelphia, PA, USA: Mosby; 2005. pp. 942–961. 4. Pope LE, Hobbs CG. Epistaxis: an update on current management. Postgrad Med J 2005; 81: 309–314. 14. Lubianca Neto JF, Fuchs FD, Facco SR, Gus M, Fasolo L, Mafessoni R, Gleissner AL. Is epistaxis evidence of end-organ damage in patients with hypertension? Laryngoscope 1999; 109: 1111–1115. 15. Alvi A, Joyner-Triplett N. Acute epistaxis: how to spot the source and the flow. Postgrad Med 1996; 99: 83–96. 16. Thaha MA, Nilssen EL, Holland S, Love G, White PS. Routine coagulation screening in the management of emergency admission for epistaxis-is it necessary? J Laryngol Otol 2000; 114: 38–40. 17. Awan MS, Iqbal M, Imam SZ. Epistaxis: when are coagulation studies justified? Emerg Med J 2008; 25: 156–157. 5. Shaw CB, Wax MK, Wetmore SJ. Epistaxis: a comparison of treatment. Otolaryngol Head Neck Surg 1993; 109: 60–65. 18. Hanif J, Tasca RA, Frosh A, Ghufoor K, Stirling R. Silver nitrate: histological effects of cautery on epithelial surfaces with varying contact times. Clin Otolaryngol Allied Sci 2003; 28: 368–370. 6. Monte ED, Belmont MJ, Wax MK. Management paradigms for posterior epistaxis: a comparison of costs and complications. Otolaryngol Head Neck Surg 1999; 121: 103–106. 19. Mathiasen RA, Cruz R. Prospective, randomized, controlled clinical trial of a novel matrix hemostatic sealant in patients with acute anterior epistaxis. Laryngoscope 2005; 115: 899–902. 7. Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin N Am 2008; 41: 525–536. 8. Genç S, Kürkçüoğlu ŞS, Karabulut H, Acar B, Tunçel Ü, Değerli S. Giant lobular capillary hemangioma of the nasal septum. Turk J Med Sci 2009; 39: 325–328. 20. Klotz DA, Winkle MR, Richmon JBS, Hengerer AS. Surgical management of posterior epistaxis: a changing paradigm. Laryngoscope 2002; 112: 1577–1582. 9. El-Guindy A. Endoscopic transseptal sphenopalatine artery ligation for intractable posterior epistaxis. Ann Otol Rhinol Laryngol 1998; 107: 1033–1037. 10. Middleton MP. Epistaxis. Emergency Medicine Australasia 2004; 16: 428–440. 11. Santos PM, Lepore ML. Epistaxis. In: Bailey BJ, Calhoun KH, Derkay CS, Friedman N, Gluckman J, Healy GB, Jackler RK, Johnson JT, Lambert PR, Newlands S et al., editors. Bailey’s Head and Neck Surgery-Otolaryngology. Philadelphia, PA, USA: Lippincott, Williams & Wilkins; 2001. pp. 513–529. 12. Herkner H, Havel C, Müllner M, Gamper G, Bur A, Temmel AF, Laggner AN, Hirschl MM. Active epistaxis at ED presentation is associated with arterial hypertension. Am J Emerg Med 2002; 20: 92–95. 13. Herkner H, Laggner AN, Müllner M, Formanek M, Bur A, Gamper G, Woisetschläger C, Hirschl MM. Hypertension in patients presenting with epistaxis. Ann Emerg Med 2000; 35: 126–130. 136 21. Kurtaran H, Ark N, Sadıkoğlu F, Uğur KŞ, Yılmaz T, Yıldırım Z, Aktaş D. The effect of anterior nasal packing with airway tubes on pulmonary function following septoplasty. Turk J Med Sci 2009; 39: 537–540. 22. Bhatnagar RK, Berry S. Selective surgicel packing for the treatment of posterior epistaxis. Ear Nose Throat J 2004; 83: 633–634. 23. Thornton MA, Mahesh BN, Lang J. Posterior epistaxis: identification of common bleeding sites. Laryngoscope 2005; 115: 588–590. 24. Shaheen OH. Arterial epistaxis. J Laryngol Otol 1975; 89: 17–34. 25. Sokoloff J, Wickborn I, McDonald D, Brahme F, Goergen TG, Goldberger LE. Therapeutic percutaneous embolization in intractable epistaxis. Radiology 1974; 111: 285–287. 26. Smith TP. Embolization in the external carotid artery. J Vasc Interv Radiol 2006; 17: 1897–1912. 27. Kumar S, Shetty A, Rockey J, Nilssen E. Contemporary surgical treatment of epistaxis. What is the evidence for sphenopalatine artery ligation? Clin Otol 2003; 28: 360–363. The Laryngoscope C 2010 The American Laryngological, V Rhinological and Otological Society, Inc. An Epistaxis Severity Score for Hereditary Hemorrhagic Telangiectasia Jeffrey B. Hoag, MD, MS; Peter Terry, MD, MA; Sally Mitchell, MD; Douglas Reh, MD; Christian A. Merlo, MD, MPH Objectives/Hypothesis: Hereditary hemorrhagic telangiectasia (HHT)-related epistaxis leads to alterations in social functioning and quality of life. Although more than 95% experience epistaxis, there is considerable variability of severity. Because no standardized method exists to measure epistaxis severity, the purpose of this study was to determine factors associated with patient-reported severity to develop a severity score. Study Design: Prospective, survey-based study. Methods: HHT care providers and a focus group of patients were interviewed to determine epistaxisassociated factors. From this, an electronic survey was developed and administered to patients with HHT. Descriptive analyses were performed with calculations of means and medians for continuous and proportions for categorical variables. Multiple ordinal logistic and linear regression models were developed to determine risk factors for epistaxis severity. Results: Nine hundred respondents from 21 countries were included. Eight hundred fifty-five (95%) subjects reported epistaxis. The mean (standard deviation) age was 52.1 (13.9) years, and 61.4% were female. Independently associated risk factors for self-reported epistaxis severity included epistaxis frequency (odds ratio [OR] 1.57), duration (OR 2.17), intensity (OR 2.45), need for transfusion (OR 2.74), anemia (OR 1.44), and aggressiveness of treatment required (OR 1.53, P < .001 for all). Conclusions: Risk factors for increasing epistaxis severity in patients with HHT include frequency, duration, and intensity of episodes; invasive- From the Department of Medicine (J.B.H.), the Drexel University College of Medicine, Philadelphia, Pennsylvania; and Department of Medicine (P.T., C.A.M.), Department of Interventional Radiology (S.M.), and Department of Otolaryngology (D.R.), The Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A. Editor’s Note: This Manuscript was accepted for publication December 2, 2009. This project was provided by the HHT Foundation International, Inc. The authors have no other funding, financial relationships, or conflicts of interest to disclose. Send correspondence to Jeffrey B. Hoag, MD, Division of Pulmonary, Critical Care, and Sleep Medicine, Drexel University College of Medicine, 245 N. 15th St., Mail Stop 107, NCB 12th Floor, Philadelphia, PA 19102. E-mail: [email protected] DOI: 10.1002/lary.20818 Laryngoscope 120: April 2010 838 ness of prior therapy required to stop epistaxis; anemia; and the need for blood transfusion. From these factors, an epistaxis severity score will be presented. Key Words: Epistaxis, hereditary hemorrhagic telangiectasia, Osler-Rendu-Weber severity score. Level of Evidence: 1b. Laryngoscope, 120:838–843, 2010 INTRODUCTION Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disease characterized by epistaxis, telangiectases, and visceral arteriovenous malformations that has nearly 100% penetrance by age 40 years. As this disease afflicts an estimated one in 10,000 to 15,000 individuals,1 it represents a significant health burden. Epistaxis related to HHT is a major complaint in up to 90% of patients with HHT,2 and has a significantly negative impact on quality of life.3,4 Many studies5–7 have described methods of assessing epistaxis severity (Table I), although none have directly addressed the validity of the scoring system itself. These instruments share several factors, such as epistaxis frequency measured as number of bleeds per unit time as well as the need for blood transfusions specifically related to epistaxis. Similarly, duration of bleeding episodes, intensity, and changes in quality of life have served as factors to calculate epistaxis severity. Al-Deen and Bachmann-Harildstad7 published a study in which experts in the field of HHT-related epistaxis were polled as to their impressions of factors that best correlated with epistaxis severity. They determined that a need for blood transfusions, ease of comprehension by both patients and care providers, and frequency of bleeds were the most important factors to calculate severity of bleeding in this patient population. Although HHT care providers have extensive experience treating epistaxis in these complex patients, and individual HHT centers of excellence utilize their particular systems for grading epistaxis severity, there has been resistance to adopt any particular severity scoring system as a universal, standardized system. Some of this resistance may be due to particular care providers’ comfort with their own systems. Another possible reason Hoag et al.: Epistaxis Severity Score for HHT TABLE I. Summary of HHT-Related Epistaxis Factors Used to Assess Overall Severity Published in the Literature.5–7 Frequency Duration Intensity Need for blood transfusion Anemia and/or iron replacement therapy Quality of life Patient satisfaction with therapy Duration of therapeutic effect Side effects of therapy Subject Recruitment The survey was compiled and distributed using an internet-based tool (SurveyMonkey, www.surveymonkey.com). Subjects were recruited from the membership registry of the HHT Foundation International, Inc. through an email blast advertisement of the project and through posting of the survey on the HHT Foundation International, Inc.’s website (www.HHT.org). The survey was anonymous and deidentified. Imbedded in the survey were questions to confirm the diagnosis of HHT by the Curaçao Criteria as described by Shovlin et al.9 Subjects were included in the analysis if they completed a series of mandatory response questions that included those used to confirm the diagnosis of HHT, information about epistaxisrelated clinical factors, and treatments received for epistaxis. See also online supplemental references. Statistical Analysis for not adopting a single system of grading may stem from a lack of statistical support for any given system. Several lines of evidence support the need for a standardized severity scoring system in HHT. First, in an informal survey of 100 patients with HHT (Terry 2007, unpublished data), epistaxis was the primary issue that the patients wanted improvement in therapy. Second, the Scientific Medical Advisory Board (SMAB) of the HHT Foundation International, Inc. came to the conclusion that epistaxis treatment is the highest priority for future research. Finally, the SMAB issued a consensus statement from the recent International HHT Clinical Guidelines Conference8 that there is insufficient evidence on how to measure the severity of HHT-related epistaxis. Therefore, the purpose of this investigation was to determine factors associated with epistaxis severity, and to utilize these factors to develop a standardized, validated epistaxis severity score (ESS). Data are presented as absolute numbers, percentages, and means (6 standard deviation) where appropriate. A descriptive analysis was performed with calculation of mean and medians for continuous variables and percentages for categorical variables. Multiple ordered logistic regression models and linear regression models were constructed to evaluate the association between covariates and epistaxis severity. Analysis of variance and Fisher exact testing were used where appropriate. Values were considered statistically significant for P < .05. All statistical calculations were performed using STATA SE version 10 statistical software (STATA Corp., College Station, TX). Validation Internal validation was performed through bootstrapping methods.10 External validation was performed by comparing ESS calculations with invasiveness of treatment received for epistaxis. Treatments were divided into minimally invasive (topical or oral medications, nasal packing), moderately invasive (endoscopic procedures including laser therapy, electrocautery, argon plasma coagulation), and most invasive (Young’s Procedure, septal dermoplasty, arterial ligation, or embolization). MATERIALS AND METHODS This study was approved by the institutional review boards of both Johns Hopkins University School of Medicine and Drexel University College of Medicine. Development of Survey A comprehensive list of covariates including demographics and clinical characteristics related to epistaxis severity was obtained through discussions with care providers from HHT centers of excellence, informal discussions with HHT patients, and review of previously published studies utilizing measures of epistaxis severity. From this comprehensive list, a cross-sectional survey was developed that utilized 120 questions to gather demographic information, disease specific data, and treatments received for epistaxis. The survey also contained 19 open-ended questions to allow for more detailed responses and clarifications by the participants. Only respondents with HHT were included in the analysis. Diagnosis of HHT was determined using the Curaçao Criteria,9 in which subjects with three or four criteria have a definite diagnosis. In those patients with two criteria (possible HHT), specific survey responses and open-ended questions were evaluated for potentially omitted diagnostic criteria. From these 253 respondents, more than 90% had other corroborating evidence for the diagnosis of HHT and were thus included in the analysis of factors correlating to epistaxis severity. Table II describes the diagnostic criteria to support HHT in the subject cohort. Laryngoscope 120: April 2010 RESULTS Demographics and HHT Diagnostic Criteria Nine hundred fifteen survey responses were collected for a 6-month period of time from March 2008 through August 2008. Fifteen subjects were excluded due to age outside the range approved by the TABLE II. Distribution of Study Subject Curaçao Criteria for Diagnosis of HHT and Specific Factors Leading to Diagnosis. Description of HHT Criteria No. % 4 3 229 386 25.7 43.4 2 Curaçao Criteria 253 28.4 1 Epistaxis 21 855 2.4 98.5 Visceral AVMs (diagnosed) 505 58.1 Family history Telangiectasia 763 382 87.9 44.0 HHT ¼ hereditary hemorrhagic telangiectasia; AVMS ¼ arteriovenous malformations. Hoag et al.: Epistaxis Severity Score for HHT 839 TABLE III. Demographic Data of Respondents. Descriptions of Respondents TABLE IV. Correlation of Factors With Self-Reported Severity of Epistaxis. No. (%) Variable Coefficient SE P Value Intensity 0.25 0.07 <.001 Frequency 0.14 0.02 <.001 353 (38.6) Duration Need for medical attention 0.25 0.30 0.02 0.07 <.001 <.001 Age, yr Diagnosis Transfusion related to epistaxis 0.31 0.07 <.001 32.0616 Anemia 0.20 0.06 .001 Current 52.6613.9 No. 894 Gender Female 561 (61.4) Male Location of respondents North America 813 (89) Europe 46 (5) Australia Asia 37 (4) 9 (1) South America 7 (0.8) Africa 2 (0.2) institutional review board protocol (age <18 or >89). Table III shows the demographic data of the cohort of respondents. The average age of the cohort was 52.6 (613.9) years, and there were more female respondents (61.4%) than male. Most of the respondents from this cohort were from North America, with approximately 80% from the United States, reflecting the membership of the HHT Foundation International, Inc. Descriptive Distribution of Epistaxis-Related Factors Approximately 45% of the cohort self-reported epistaxis severity in the moderate range, with 29.9% selfclassifying above and 26.2% below (Fig. 1). Factors leading to particular self-classification were similar to factors previously described in the literature as being important predictors of epistaxis. Epistaxis episode duration ranged from <1 minute to >30 minutes, with a mean duration of about 6 to 15 minutes of bleeding per epistaxis episode. There was considerable variability in the frequency of epistaxis episodes ranging from several per day to more than a month between episodes of bleeding. Of the patients, 13.7% described their epistaxis SE ¼ standard error. intensity as either gushing or pouring. Of notable interest, 17.5% of this cohort had never sought medical attention related specifically to epistaxis. Furthermore, more than 30% of respondents had never seen an otolaryngologist, suggesting that a significant percentage of these individuals are seeking epistaxis therapy from other types of care providers. Of the study subjects, 59.8% reported a prior history of anemia, whereas 35.9% reported anemia at the time of the survey. Red cell transfusions were also common, with 26.6% receiving a blood transfusion related to blood loss from epistaxis at some point in life; however, only 22.6% of study subjects knew their current hemoglobin (9.9 6 2.1 mg/dL; range, 3.5–16.5). Epistaxis Severity Score Six factors were independent predictors of selfdescribed epistaxis severity (Table IV). Using these six predictors of epistaxis severity, we developed an ESS (Table V). The responses are weighted by respective TABLE V. Data Sheet for the Calculation of the Epistaxis Severity Score for Hereditary Hemorrhagic Telangiectasia. How often do you TYPICALLY have nose bleeding? (coefficient 0.14) 0 — Less than monthly 1 — Once per month 3 — Several per week 4 — Once per day 2 — Once per week 5 — Several each day How long do your TYPICAL nose bleeds last? (coefficient 0.25) 0 — <1 minute 3 — 16–30 minutes 1 — 1–5 minutes 4 — >30 minutes 2 — 6–15 minutes How would you describe your TYPICAL nose bleeding intensity? (coefficient 0.25) 0 — Not typically gushing 1 — Typically gushing or pouring Have you every sought medical attention for nose bleeding? (coefficient 0.30) 0 — No 1 — Yes Are you anemic (low blood count) currently? (coefficient 0.20) 0 — No 1 — Yes Have you ever received a red blood cell transfusion specifically because of nose bleeding? (coefficient 0.31) 0 — No 1 — Yes Fig. 1. Self-reported epistaxis severity and general factors leading to severity characterization. Laryngoscope 120: April 2010 840 Six questions are answered, the number of the response is multiplied by the respective coefficient, and the sum of these gives the raw epistaxis severity score. Hoag et al.: Epistaxis Severity Score for HHT Fig. 2. Calculation of the raw and normalized epistaxis severity score (ESS). The responses to each of the six questions are assigned a weighted integer that is multiplied by the question’s coefficient. These are added to yield the raw score. The raw score is then normalized by dividing the raw score by the maximum possible score (2.71), then multiplied by 10 to give the normalized ESS. HHT ¼ hereditary hemorrhagic telangiectasia. coefficients from the model, and these are added together yielding a raw ESS. This is then divided by the range of the raw score (2.71) and multiplied by 10 to give the normalized ESS within a range of 0 (no epistaxis) to 10 (most severe epistaxis) (Fig. 2). Validation of the ESS Bootstrapping resampling using 1,000 replications was performed to obtain variance of the independent predictor variables in the final ESS model to ensure internal model validation.10 The standard errors of the predictor variables presented in the final ESS are those obtained through bootstrapping resampling. Logistic regression models were also fit to evaluate the association between ESS and prior invasiveness of treatment for epistaxis as a means of external validation. The ESS was found to be a significant predictor of invasiveness of treatment (Fig. 3), as patients with higher ESS had a much greater risk of requiring surgical procedures for epistaxis (odds ratio, 1.61; 95% confidence interval, 1.461.78). with HHT, we were able to identify six factors with the highest correlation to epistaxis severity. The resulting ESS questionnaire is easy to administer and comprehend, and it should provide an effective tool in assessing epistaxis severity. We sought to develop a scoring system that can be administered by either care providers or self-administered by patients. The questions are easy to understand by both medical and lay persons. Because of this it may serve as an adjunct for therapeutic algorithms. Treating physicians may utilize the questionnaire or individual DISCUSSION This is the first paper to propose a statistically validated ESS based on a comprehensive survey of a large cohort of HHT patients. Through review of a comprehensive list of possible related factors derived from information obtained from otolaryngologists with extensive experience with HHT, non-ear, nose, and throat HHT center of excellence care providers, and patients Laryngoscope 120: April 2010 Fig. 3. Correlation between invasiveness of therapy and normalized epistaxis severity score (ESS). Trends were statistically significant (P < .0001; Fisher exact test). Hoag et al.: Epistaxis Severity Score for HHT 841 scores to gauge patient responses to various epistaxis therapies. This scoring system is not meant to supplant expert evaluation; however, as we demonstrated in this survey, a significant number of HHT patients are not seeing experienced otolaryngologists (40%). Many of these patients are frequently visiting emergency rooms and primary care providers. Such a score may help to identify unrecognized epistaxis severity that should be referred to more appropriate providers. Second, this scoring system, through its ease of interpretation, may help patients to monitor their own symptoms with an objective measurement. Many patients with chronic disease have improved outcomes through utilization of patient-centered treatment aids.11,12 This may serve as a benchmark for epistaxis in this group of patients who have a lifetime of experience caring for the nasal bleeding complications of the illness. Finally, this ESS fills an unmet need as an accurate, reproducible, and validated objective measure of epistaxis severity to be used to compare existing and new therapeutics. Several reports5–7 have utilized epistaxis severity scoring systems to assess treatment efficacy; however, they all suffer from an important limitation, a lack of systematic evaluation of validity of the score itself. Nevertheless, it is important to point out that our system was derived, in part, by the tremendous experience compiled by these earlier investigators. Very few randomized clinical trial have been performed in HHT, and moreover, almost no multicenter trials have been undertaken. Part of the inability to pool patients from multiple centers and conduct these necessary trials comes from the lack of standardized measurement tools for standardization among centers. Al-Deen and Bachmann-Harildstad determined that ease of understanding for both care providers and patients, inclusion of transfusion needs, and association for a fixed time interval were important attributes of an epistaxis severity survey.7 Their proposed scoring scale shares measures of intensity, frequency, and transfusion needs, although their scale was not been systematically validated. Despite the many strengths of this investigation, there are several limitations that warrant mentioning. First, data included in the project were derived from survey responses to an anonymous, deidentified survey. This adds potential misclassification of study subjects without disease. We believe that we overcame this limitation by targeting membership of the disease-specific foundation for inclusion and by using questions embedded into the questionnaire that accurately predict the diagnosis of HHT.13 Another piece of information that is lacking from this analysis stems from the cross-sectional nature of the data used to calculate the ESS. Future studies could collect data longitudinally from this patient group to determine measures such as minimum clinically relevant changes. A possible criticism to this scoring system may center on the ease of calculation. With the inclusion of weighted factors, on-the-spot calculations may be difficult without a computer program or calculator. Although Laryngoscope 120: April 2010 842 this is a valid argument, as the ease of calculation is improved, the robust, statistically supported nature of this score is weakened. This score is analogous to other clinical scoring systems, like the lung allocation score, used for lung transplantation listing.14 Although a computerized method of calculating the score may be necessary, we believe the fear of using a labor-intensive system can be overcome with only six questions requiring single selection responses. Finally, this ESS has not yet been correlated with existing grading of nasal telangiectases. Mahoney and Shapshay15 developed objective grading of nasal involvement of telangiectases, which described a range from small, punctuate telangiectases to confluent, large nasal arteriovenous malformations. Although this grading system did not correlate epistaxis severity with the particular lesions, there could be a linear correlation that could be corroborated with further analysis using this study’s proposed ESS. CONCLUSION Through the evaluation of a comprehensive list of factors related to epistaxis severity in patients with hereditary hemorrhagic telangiectasia, we determined six factors associated with self-reported severity, including: frequency, duration, intensity, need for medical attention, anemia, and need for transfusion. By compiling responses to six questions focused on these factors, an ESS can be generated that is accurate and validated. This ESS can serve as a clinical and therapeutic outcome measure for epistaxis in HHT. Acknowledgments This project was supported by a generous grant from the Hereditary Hemorrhagic Telangiectasia Foundation International, Inc. We would like to thank Dr. Douglas Ross and Dr. Urban Geisthoff, who led the section for epistaxis at the 2009 International HHT Conference in Santander, Spain for their insights into the topic. We would also like to thank the HHT center of excellence care providers from around the world for their support and assistance with this project. BIBLIOGRAPHY 1. Westermann CJJ, Rosina AF, de Vries V, de Coteau PA. The prevalence and manifestations of hereditary hemorrhagic telangiectasia in the Afro-Caribbean population of the Netherlands Antilles: a family screening. Am J Med Genet A 2003;116:324–328. 2. Guttmacher AE, Marchuk DA, White RI Jr. Hereditary hemorrhagic telangiectasia. N Engl J Med 1995;333: 918–924. 3. Pasculli G, Resta F, Guastamacchia E, Di Gennaro L, Suppressa P, Sabba C. Health-related quality of life in a rare disease: hereditary hemorrhagic telangiectasia (HHT) or Rendu-Osler-Weber disease. Qual Life Res 2004;13: 1715–1723. 4. Lennox PA, Hitchings AE, Lund VJ, Howard DJ. The SF-36 health status questionnaire in assessing patients with epistaxis secondary to hereditary hemorrhagic telangiectasia. Am J Rhinol 2005;19:71–74. 5. Levine CG, Ross DA, Henderson KJ, Leder SB, White RI Jr. Long-term complications of septal dermoplasty in Hoag et al.: Epistaxis Severity Score for HHT 6. 7. 8. 9. 10. patients with hereditary hemorrhagic telangiectasia. Otolaryngol Head Neck Surg 2008;138:721–724. Geisthoff UW, Heckmann K, D’Amelio R, et al. Healthrelated quality of life in hereditary hemorrhagic telangiectasia. Otolaryngol Head Neck Surg 2007;136:726–733. Al-Deen S, Bachmann-Harildstad G. A grading scale for epistaxis in hereditary haemorrhagic telangiectasia. Rhinology 2008;46:281–284. Faughnan ME, Palda VA, Garcia-Tsao G, et al. International Guidelines for the Diagnosis and Management of Hereditary Hemorrhagic Telangiectasia. J Med Genet. In press. Shovlin CL, Guttmacher AE, Buscarini E, et al. Diagnostic criteria for hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber Syndrome). Am J Med Genet 2000; 91:66–67. Efron B. Bootstrap methods: another look at the jackknife. Ann Stat 1979;7:1–26. Laryngoscope 120: April 2010 11. Lorig KR, Sobel DS, Stewart AL, et al. Evidence suggesting that a chronic disease self-management program can improve health status while reducing hospitalization: a randomized control trial. Med Care 1999;37:5–14. 12. Institute of Healthcare Improvement. Partnering with patients and families to design a patient- and family-centered health care system: recommendations and promising practices (April 2008). Available at: www.IHI.ORG. Accessed October 1, 2008. 13. Van Gent MWF, Post MC, Mager JJ, et al. Diagnostic Curacao criteria for HHT; are they still valid? Haematol Meet Rep 2009;3;C13–C25. 14. United Network for Organ Sharing. Lung transplantation allocation score. Available at: www.unos.org/resources/ frm_LAS_Calculator.asp. Accessed August 20, 2009. 15. Mahoney EJ, Shapshay SM. New classification of nasal vasculature patterns in hereditary hemorrhagic telangiectasia. Am J Rhinol 2006;20:87–90. Hoag et al.: Epistaxis Severity Score for HHT 843 ACTA otorhinolaryngologica italica 2014;34:1-8 Review Endoscopic management of posterior epistaxis: a review Il trattamento endoscopico delle epistassi posteriori: revisione della letteratura S.W. McClurg, R. Carrau Department of Otolaryngology-Head and Neck Surgery, The Ohio State University, Columbus, OH, USA Summary The paradigm for the management of epistaxis, specifically posterior epistaxis, has undergone significant changes in the recent past. Recent prospective and retrospective data has shown that the endonasal surgical management of posterior epistaxis is superior to posterior nasal packing and angiography/embolization with regards to various factors including pain, cost-effectiveness, risk and overall control of bleeding. Endonasal endoscopic surgical techniques for posterior epistaxis include direct cauterization and transnasal endoscopic sphenopalatine/posterior nasal artery ligation or cauterization with or without control of the anterior ethmoidal artery. Despite the evidence provided by the current literature, a universal treatment protocol has not yet been established. This review article provides an up-to-date assessment of the available literature, and presents a structured paradigm for the management of posterior epistaxis. Key words: Epistaxis • Endoscopic sphenopalatine artery ligation • Posterior epistaxis • Sphenopalatine artery Riassunto Il trattamento delle epistassi posteriori ha subito significativi cambiamenti negli ultimi anni. I recenti dati prospettici e retrospettivi hanno dimostrato che il trattamento chirurgico endoscopico delle epistassi posteriori presenta dei vantaggi rispetto al tamponamento nasale e/o all’embolizzazione previa angiografia ed in particolare in termini di dolore, rapporto costo-beneficio, effetti collaterali, e infine in termini di controllo di sanguinamento. Il trattamento endoscopico chirurgico delle epistassi posteriori include la cauterizzazione diretta e la legatura dell’arteria sfeno-palatina e/o cauterizzazione dell’arteria etmoidale anteriore. Nonostante le evidenze presenti in letteratura un protocollo universale non è stato ancora realizzato. Questa revisione della letteratura offre un aggiornamento sui dati attuali sull’argomento, proponendo un algoritmo per il trattamento delle epistassi posteriori. Parole chiave: Epistassi • Legatura endoscopica della arteria sfeno palatina • Epistassi posteriore • Arteria sfeno-palatina Acta Otorhinolaryngol Ital 2014;34:1-8 Introduction Epistaxis is a very common presenting complaint and the most common emergency for the OtolaryngologistHead and Neck Surgeon. The distribution of epistaxis is bimodal. It is most common before age 10, and then peaks again between ages 45 and 65 years of age 1 2. Many factors including seasonal variation, concomitant inhalational allergy, oestrogens (extraneous and endogenous), environmental humidity and upper respiratory tract infections affect the incidence of epistaxis. Epistaxis can be divided into anterior and posterior based upon the arterial supply and location of the offending vessel. Most cases of epistaxis are anteriorly located (90-95%), and are usually treated effectively after visual localization with local chemical or electrical cauterization via anterior rhinoscopy 3. Approximately 5-10% of epistaxis arises posteriorly 3, and requires more aggressive measures for control. It has been prospectively shown that patients with posterior epistaxis are more likely to require hospitalization, are twice as likely to require nasal packing and require a longer hospital stay 4. The sphenopalatine (SPA) and posterior nasal (PNA) arteries, terminal branches of the internal maxillary artery (IMA), provide blood supply to the lateral nasal wall below the middle turbinate, rostrum of the sphenoid sinus and posterior nasal septum. Therefore, a majority of posterior epistaxes arise from these two vessels. Measures to control posterior epistaxis include direct cauterization, posterior nasal packing, embolization or surgery. Many studies have shown surgical control to be superior to angiography/embolization 3 5 as well as posterior packing 3. Intervention for posterior epistaxis is direct endonasal endoscopic cauterization of the offending site. However, in a significant number of patients, if not most, with posterior epistaxis, the site will remain undefined. Recent reports suggest that ligation of the sphenopalatine and posterior nasal arteries seems to be the best option for patients with 1 S.W. McClurg, R. Carrau posterior epistaxis and without comorbidities that would of the palatine bone (Fig. 1), usually lies at the posterior preclude a surgical intervention 3 5. end of the middle turbinate, in the lower part of the supeThe surgical management of epistaxis has undergone rior meatus, and at the junction between the palatine and significant transitions and changes. Carnochan 6 de- sphenoid bone on the lateral nasal wall. Simmen reported scribed the first surgical technique to the pterygopala- that the mean vertical and horizontal diameters of the SPF tine fossa (PTPF) in 1858, using a transfacial-transantral are 6.2 and 5.1 mm, respectively 7. From an endoscopic approach to the pterygopalatine fossa (PTPF). In 1890, standpoint, the foramen can be found just posterior to the Segond introduced a lateral transfacial approach to the superior one-third of the posterior wall of the antrum. Anpterygopalatine fossa 6. Subsequently, Hide introduced other reliable landmark is the crista ethmoidalis, which is the ligation of the external carotid artery for the manage- a small spur of bone just anterior to the sphenopalatine ment of epistaxis. In 1948, Silverblatt first described the foramen (Fig. 2). ligation of the anterior ethmoid artery. These techniques The arterial configuration within the pterygopalatine are still utilized around the world to manage patients fossa is also highly variable and complex. In a cadaveric with refractory epistaxis. In 1929, Seiffert described the study of 128 tissue blocks by Chiu 8, it was found that sublabial-transantral approach for ligation of the max- the internal maxillary artery bifurcates before reaching illary artery, which was subsequently standardized and the sphenopalatine foramen in 89% of cases, splitting off popularized by Chandler (1956); and, further improved into two (69%), three (19%) or four branches (2%). In a upon by Simpson (1982) by focusing on its terminal similar anatomical study, Simmen documented that there branches (i.e. sphenopalatine and posterior nasal arter- may even be up to 10 arterial branches 7. This study also ies) 6. In 1976, Prades described an endonasal micro- demonstrated that in 58% of cases the SPF lies in both the scopic ligation of the sphenopalatine artery, which was superior and middle meati. emulated by Borgstein who introduced the endoscope as Variability of the vascular anatomy within the pterygopalaa visualization tool in 1987 6. tine fossa is remarkable and ranges from a relatively simple A thorough knowledge of the anatomy of the posterior or “classic” pattern to one that is highly complex 9. In turn, nasal cavity and pterygopalatine fossa is essential for the the branching pattern of the sphenopalatine artery is also proper surgical management of posterior epistaxis. Arte- striking. Schartzbauer showed that in fresh cadavers, aprial supply to the nasal cavity is both robust and variable, proximately 16% of the terminal branches split off from with contributing arteries deriving from both the internal the maxillary artery distal to the sphenopalatine foramen, and external carotid arteries. Contributions from the ex- 42% branch proximally and 42% branch through separate ternal carotid artery include the sphenopalatine, posterior foramina 10. In 75 cadaveric specimens, Simmen showed nasal, superior labial, greater palatine, angular and as- that in 97% of the samples the sphenopalatine artery had cending pharyngeal arteries. The internal carotid artery 2 or more branches exiting the lateral nasal wall, 67% had furnishes the anterior ethmoid and posterior ethmoid ar- 3 or more branches, 35% had 4 or more branches, 3% had teries via the ophthalmic artery. Branches of the ethmoi- 1 single trunk and 1% had 10 branches 7. A representative dal arteries supply the lateral nasal wall above the level example of the sphenopalatine artery is shown in Fig. 1. of the middle turbinate. It must be noted that there is ample communication between the two systems. The vidian artery and the artery that accompanies V2 (artery of the foramen rotundum) are robust examples of these communications that can lead to collateral blood flow, thus causing re-bleeding and which must be considered when embolizing the internal maxillary artery. The sphenopalatine foramen (SPF), which is a notch between the orbital and sphenoidal processes Fig. 1. Right pterygopalatine fossa. of the ascending aspect PF: pterygopalatine fossa; SPA: sphenopalatine artery; MAX: posterior wall of maxillary sinus. 2 Endoscopic management of posterior epistaxis considered. If the airway is deemed stable, nonsurgical approaches for haemostasis should first be attempted. Local vasoconstrictors (i.e. epinephrine), either topical and/or injected, may assist with haemostasis. If the site of bleeding is visible, its cauterization may be possible. Posterior epistaxis is usually quite brisk, and also due to its inherent position in the posterior nasal cavity, it is often difficult to pinpoint the location of bleeding. In the surgical theatre, however, Thornton et al. 13 were able to identify the location of posterior epistaxis in 36 of 43 cases. Of these, 20% were located on the Fig. 2. Right ethmoid crest. Yellow arrow pointing to crista ethmoidalis. Red dashed arrow showing the path of the posterior nasal septum, internal maxillary before it divides in to the sphenopalatine and posterior nasal arteries. and 80% of those were located on the lateral aspect of the middle or inferior Another common and useful landmark for the identi- turbinates or the lateral aspect of the middle or inferior fication of the sphenopalatine foramen is the ethmoid meatus. It should be noted that all identified sites were locrest or crista ethmoidalis (CE), (Fig. 2). In a study by cated within the distribution of the sphenopalatine artery. Rezende, the crista ethmoidalis was found in 96% of ca- Intraoperatively, anaesthesia-induced hypotension and/or daveric specimens, and was located just anterior to the elevation of the head of the bed may decrease bleeding; SPF in most cases 11. Similar to other aforementioned thus, potentially facilitating the identification and control studies, they found that 43% of specimens had accessory of the bleeding site. foramina. Similarly, Padua showed that the crista ethmoi- Any surgical intervention requires prior stabilization of dalis was anterior to the sphenopalatine foramen in 98% the patient and control of bleeding. If the patient had preof specimens 12. In this latter study, the SPF was located viously been treated (commonly by a non-otolaryngolobetween the middle meatus and the superior meatus in gist), the patient may present with posterior packing al87% of specimens, and at the superior meatus in 13%. In ready in place. In the hands of a non-specialist, posterior Padua’s study accessory foramina were present in 10% of packing is efficacious in approximately 70% of cases 14. specimens. These studies suggest that, in fact, the most re- In the untreated patient, a posterior nasal pack using traliable localizer for the SPF is the crista ethmoidalis; how- ditional tonsil packs with ribbon-gauze coated with antiever, the frequency of multiple foramina and branches is biotic ointment, expandable sponges such as the Merocel significant; thus, the surgeon should anticipate their pres- Pope nasal packing (Medtronic ENT, Jacksonville, FL, USA), Rapid Rhino (Applied Therapeutics, Tampa, FL, ence 12. USA) Epistat, Postpac (Medtronic ENT, Jacksonville, FL, USA) or any of the multiple available balloon-packing deInitial management vices may be effective. Topical haemostatic compounds The initial evaluation of the patient presenting with such as a mixture of gelatin and thrombin (e.g. Floseal, epistaxis should focus on evaluating the stability of the Baxter Healthcare Corp., Deerfield, IL, USA) has been airway, initial control of the bleeding and stabilization of shown to be effective in anterior epistaxis 15, but it has not vital signs with fluid replacement or blood transfusions. In been properly assessed for posterior bleeds; thus, it is not a patient with severe uncontrolled epistaxis, the need for advocated in the setting of posterior epistaxis where a speintubation or even a surgical airway, albeit rare, must be cific site of bleeding cannot be identified. 3 S.W. McClurg, R. Carrau There have been multiple studies comparing the various types of nasal packing for anterior bleeds, but unfortunately, there are relatively few studies looking at comparisons between various posterior nasal packings. In a comparison study by Callejo 16, classic tetracaine-coated gauze packing was compared to a bi-chambered pneumatic packing device. They found that the classic packing was less expedient, and less comfortable, but was associated with fewer episodes of re-bleeding (17% against 28%, respectively) and less expensive (€ 1327 vs. € 1648). Posterior packing is associated with its own set of specific complications, such as the naso-vagal reflex that can trigger cardiac dysfunction or respiratory arrest 17. In addition, packing may be inadvertently swallowed or aspirated if not adequately secured 18. Conversely, if the packing is secured too tightly, it may lead to alar, columellar or septal necrosis 19. Due to the possible compressive ischaemia of nasal structures, we advocate to avoid bilateral posterior packing whenever possible, and to routinely deflate the cuff of balloon occlusive devices to allow septal blood flow. If a Foley balloon-type device (i.e. any inflatable balloon) is used for posterior packing, air is not suitable for inflating the balloon. Rashid showed that Foley catheters inflated with air deflated within approximately 48 hr 20; therefore, saline or sterile water should be utilized for balloon inflation. We recommend utilizing antibiotics while the posterior packing is in place, even though prophylactic antibiotics have not been shown to decrease infectious complications 21. However, rare complications such as infective endocarditis and spondylodiscitis have been reported in patients with posterior nasal packing who were not covered with systemic antibiotic prophylaxis 22. Once the bleeding is controlled, all contributing factors that may be exacerbating the epistaxis should be addressed. These may include co-morbidities such as coagulopathies (congenital or acquired), hypertension, maxillofacial trauma, recent endonasal or orthognathic surgery and history of hereditary hemorrhagic telangiectasia (HHT). Basic laboratory studies (including complete blood count, chemistry panel, platelet count, prothrombin time and partial thromboblastin time) should be obtained during initial workup. Consider blood transfusion if haemoglobin is noted to be significantly low (this varies according to patient’s cardiovascular reserve, comorbidities, symptoms and regional practices). These contributing factors should be addressed prior to any operative intervention whenever feasible. There are specific clinical scenarios that deserve special consideration. In patients with hereditary hemorrhagic telangiectasia (HHT), an autosomal dominant disorder resulting in localized vascular malformations, these malformations may extend posteriorly, and their acute management includes surgical cauterization or angiography and 4 embolization. Ligation of the arteries is rarely performed as this precludes the possibility of angiography and embolization and due to the nature of the disease, and the benefits of the surgery are short-lived. The possibility of a primary or metastatic tumour causing the epistaxis may also need to be addressed with thorough history and physical examination and possibly further imaging studies. In any adolescent male patient, the possibility of a juvenile nasopharyngeal angiofibroma should also be considered. A history of recent maxillofacial trauma, or recent endonasal or orthognathic surgery, poses the possibility of an arterial injury or a pseudoaneurysm. This latter lesion results from an incomplete tear a major artery, causing bleeding from the artery into the arterial adventitia, resulting in a localized haematoma with a continued connection to the offending artery. Pseudoaneurysms are usually unresponsive to nasal packing (immediate re-bleeding upon packing removal). They may arise from any sinonasal artery, but the arteries most commonly involved after orthognathic surgery are the internal maxillary artery and the sphenopalatine artery 2. The treatment for a pseudoaneurysm is arterial selective embolization 2. Surgery After haemodynamic stabilization, the patient is taken to the operative suite. As previously discussed, anaesthesiacontrolled hypotension and/or elevation of the head of the bed decreases the bleeding, and potentially facilitates localization of the offending bleeding site. Any previous nasal packing is removed and a thorough nasal endoscopy is performed to identify the specific site of bleeding. Some common locations for bleeding include the spheno-ethmoid recess, turbinates, middle meatus and the septum. If a bleeding site is identified, it may be directly cauterized. Local cauterization has the advantage of requiring no packing, and is associated with shorter hospital stay and greater patient comfort 23. Direct cauterization may also be conducted under topical or local anaesthesia. A potential disadvantage of this technique include a lower success rate than formal sphenopalatine artery ligation (mostly due to inadequate identification of the bleeding site). Some propose attempting a local cauterization of bleeding sites in cases of posterior epistaxis 23 under general or local anaesthesia, by first visualizing the various sites of possible bleeding including the posterior aspect of the lateral wall of inferior meatus; posterior part of lateral nasal wall near the sphenopalatine foramen; posterior end of inferior turbinate; the middle turbinate and its medial surface; middle and posterior part of septum and floor of nose beneath the inferior turbinate 23. However, the preferred approach for surgical management of posterior epistaxis, in which a specific site is indisputably identified, is endonasal endoscopic ligation of the sphenopalatine and pos- Endoscopic management of posterior epistaxis terior nasal arteries. The efficacy of this technique is de- tine fossa. It is important to dissect the sphenopalatine and pendent on controlling the multiple, robust branches that posterior nasal arteries free from the posterior aspect of the sphenopalatine and posterior nasal arteries give rise the SPF, as this will allow a complete clipping or cauterito. Indications for surgical ligation include the inability to zation of the arteries. place packing effectively due to an anatomical deformity, A concurrent anterior ethmoid artery (AEA) ligation failure of non-surgical therapy, recurrent epistaxis, con- along with the endonasal endoscopic ligation of the sphetraindications for embolization and patient preference. nopalatine and posterior nasal arteries should be considContraindications for embolization include severe carotid ered, if the site of bleeding is not known pre-operatively, atherosclerosis, prior external carotid or internal maxil- if the patient’s history is unreliable, if packing was placed lary artery ligation or bleeding from the anterior ethmoid at an outside institution, or if there is no evidence of artery (which arises from the ophthalmic artery, a branch bleeding at the time of surgery (unidentified site of bleeding). AEA ligation has a low morbidity, and should be of the ICA). A cost analysis study by Dedhia 24, showed that first-line strongly considered if the patient has been referred for endonasal endoscopic sphenopalatine/posterior nasal definitive treatment from a region distant from the hosarteries ligation results in a significant overall cost sav- pital. Approaches for AEA ligation include an external ings if ≥ 3 days of posterior nasal packing were required incision and dissection between the lamina papyracea and ($ 6,450 vs. $ 8,246, respectively). Therefore, it is rec- the periorbita with endoscopic assistance, and endonasal ommended that endonasal endoscopic sphenopalatine approach with bipolar cauterization of the AEA (Fig. 3). and posterior nasal artery ligation should be offered as an Identification of the anterior ethmoidal artery on coronal initial treatment option for medically stable patients diag- computed tomography is assisted with its location at the retro-bulbar level, or by utilizing the “nipple or pyramidal nosed with posterior epistaxis 24. Our preferred technique for endonasal endoscopic sphe- sign” (a triangular evagination of the lamina papyracea nopalatine and posterior nasal artery ligation 25 26 involves between the superior oblique and medial rectus muscles) performing a standard uncinectomy, with identification of (Fig. 4). It has been shown that 36% of anterior ethmoidal the natural maxillary sinus ostium and its enlargement in- arteries were located in a mesentery, and 20% could be feriorly (to the level of the inferior turbinate), superiorly clipped endoscopically 27. However, an external approach (to the level of the orbit) and posteriorly (to be flush with is safer to access the AEA. A small naso-orbital incision the back wall of the antrum). Next, the sphenopalatine provides access to the periorbita, which is incised and foramen is identified using all the previously discussed elevated under endoscopic visualization. Following the anatomical landmarks (posterior wall of the antrum, mid- frontoethmoidal suture leads to the ethmoidal foramina, dle turbinate root, and crista ethmoidalis). Using a Freer located an average of 24 mm from the lacrimal crest. In or Cottle periosteal elevator, the mucoperiosteum over the turn, the posterior ethmoid artery (PEA) is located 12 mm ascending process of the palatine bone is widely elevated to expose the sphenopalatine foramen and the sphenopalatine and posterior nasal arteries. Wide elevation is important to identify anatomical variants such as multiple foramina and/or multiple vessels traversing the lateral nasal wall from the pterygopalatine fossa. The vessels can frequently be controlled at this point either with haemostatic clips or bipolar electrocautery. If necessary a longer segment of the arteries can be exposed by removing the anterior aspect of the sphenopalatine foramen (i.e. posterior nasal wall) using a Kerrison or Citelli Fig. 3. Endoscopic view of left nasal cavity. Orbital decompression with lamina papyracea bone (LP) removed. rongeur; thus, following the This specimen shows a middle ethmoidal artery. arteries into the pterygopala- AE: anterior ethmoid artery; ME: middle ethmoid artery; PE: posterior ethmoid artery/ 5 S.W. McClurg, R. Carrau Fig. 4. Coronal cut of CT image showing “nipple sign” at the level of entry (white arrow) of the anterior ethmoid artery into the nasal cavity. posterior to the anterior ethmoidal artery, and the optic canal is located 6 mm posterior to the posterior ethmoid artery. After surgical control is achieved, silicone septal splints are placed if there was excessive trauma to the mucosa or if there is a possibility of post-operative nasal synechiae. In a retrospective review, Kumar showed that the overall mean success rate of sphenopalatine artery ligation in 11 case series including 127 patients was 98% (range 92100%) 28. In a retrospective study of 678 patients, Soyka 5 showed that the successful treatment in patients with posterior epistaxis could be achieved in 62% by packing (Foley + fat-gauze), and in 97% by surgery. Despite the high success rate of arterial ligation, there is still the possibility of failure. Possible reasons for recurrent bleeding include failure to ligate all terminal branches of the sphenopalatine artery, dislodged clips, bleeding diatheses, the development of collateral blood vessels or unrecognized AEA bleeding sites. In a recent prospective study by Nikolaou 29, it was shown that surgery was the most cost effective and least painful treatment regimen for posterior epistaxis. Their treatment regimen consisted of placement of either a Rapid Rhino 7.5 cm packing or balloon packing for posterior epistaxis, followed by endonasal endoscopic sphenopalatine and posterior nasal artery ligation for patients that had further bleeding upon removal of the packing. In this study of 61 patients (45 with anterior epistaxis, 16 with posterior epistaxis), they showed that the median visual analogue scale for the evaluation of pain (VAS score) for Rapid Rhino packing, surgery and balloon packing was 6.0, 3.0 and 7.5, respectively. The median costs of treat6 ment for 96 patients were calculated, and were found to be approximately the same for patients with Rapid Rhino packing and surgery (10,192 Swiss Francs), balloon packing and surgery (10,192 Swiss Francs) and surgery alone (10,269 Swiss Francs). Overall, their findings suggested that surgery is less troublesome to the patient, and does not increase the costs of treatment. This technique has also been shown to be efficacious and safe in the paediatric population 30. After control of the posterior epistaxis is achieved, appropriate postoperative care is needed. Elevate the head of the bed, avoid hypertension, provide appropriate analgesia and promote aggressive nasal hygiene. Nasal hygiene includes saline nasal sprays, saline irrigations, use of oxymetazoline and/or a nasal sling. The patient should follow-up in clinic 5-7 days after surgical intervention for removal of silicone splints, if they were placed. If endonasal endoscopic sphenopalatine and posterior nasal arteries ligation is not successful, a transantral internal maxillary artery (IMAX) ligation or angiography with embolization may be considered. Further, if IMAX ligation is not successful or angiography with embolization is not available, an external carotid artery ligation may be considered. It should be noted that this is a last resort, as a retrospective review conducted by Spafford 31 showed a high rate of re-bleeding with external carotid artery ligation (45%), but showed that IMAX ligation was successful in 90% of patients. Embolization is an alternative option for posterior epistaxis, and is our preferred intervention for recurrent epistaxis after a seemingly adequate endonasal endoscopic sphenopalatine and posterior nasal artery ligation. Angiographic embolization was first described for posterior epistaxis in 1974 by Sokolof 32. Possible candidates for embolization include patients with HHT (Osler-Weber-Rendu) syndrome, bleeding tumours, poor surgical candidates or if the patient chooses it. Bleeding during transphenoidal or maxillofacial surgery should be considered for endovascular management due to possible internal carotid artery injury or pseudoaneurysm formation 33. Possible minor complications of angiography include trismus, facial pain, facial paresthesia or haematoma. Possible major complications include cerebrovascular accident, internal carotid artery dissection, blindness, necrosis or facial paralysis. In a retrospective review of 70 patients, Christensen found that 86% of their cases had minor or no complications after embolization, and were discharged within 24 hours 34. A major re-bleed, requiring surgical intervention, occurred within 6 weeks of embolization in 13% of these patients, and one patient had a significant cerebrovascular accident. Also of note, this study showed that the average cost of hospitalization in the respective institution was $ 18,000 per patient with epistaxis, and the cost Endoscopic management of posterior epistaxis of embolization was an average of $ 11,000 34. In a retrospective study by Cohen, 19 patients underwent endovascular embolization with no minor or major complications, and an average hospital stay of 11.1 days 35. As previously mentioned, in any adolescent male patient, the possibility of a juvenile nasopharyngeal angiofibroma should also be assessed. In these patients, embolization via angiography is usually utilized prior to surgical resection 33. Given the various presentations and possible sources of bleeding in a patient with posterior epistaxis, we propose the following diagnostic workup and treatment (Fig. 5) to optimize the management of posterior epistaxis. Conclusion Fig. 5. Flow diagram for management of posterior epistaxis. Note that this diagram should be used for patients that have failed conservative management and local cauterization in the non-operative setting. AE: anterior ethmoid artery; A&E: angiography and embolization; SPA: sphenopalatine artery; PNA: posterior nasal artery. Ligation of the sphenopalatine and posterior nasal arteries is a very effective treatment for severe posterior epistaxis. Concomitant anterior ethmoidal artery ligation may be more effective than sphenopalatine artery/posterior nasal artery ligation alone. Surgical intervention of posterior epistaxis provides a low-morbidity and cost-effective treatment. We present a flow diagram for management of posterior epistaxis. References 1 Tomkinson A, Roblin DG, Flanagan P, et al. Patterns of hospital attendance with epistaxis. Rhinology 1997;35:129-31. 9 Fortes FS, Sennes LU, Carrau RL, et al. Endoscopic anatomy of the pterygopalatine fossa and the transpterygoid approach. Laryngoscope 2008;118:44-9. 10 Schartzbauer HR, Shete M, Tami TA. Endoscopic Anatomy of the sphenopalatine and posterior nasal arteries: Implications for the endoscopic management of epistaxis. Am J Rhinol 2003;17:63-6. 11 Rezende GL, Soares VY, Moraes WC, et al. The sphenopalatine artery: a surgical challenge in epistaxis. Braz J Otorhinolaryngol 2012;78:42-7. 12 Padua FG; Voegels RL. Severe posterior epistaxis - endoscopic surgical anatomy. Laryngoscope 2008;118:156-61. 13 Thornton MA, Mahesh BN, Lang J. Posterior epistaxis: identification of common bleeding sites. 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Operative Techniques in Otolaryngology - Head and Neck Surgery 1997;8:85-9. Abruzzo TA, Heran MK. Neuroendovascular therapies in pediatric interventional radiology. Tech Vasc Interv Radiol 2011;14:50-6. 34 Snyderman C, Goldman S, Carrau R, et al. Endoscopic sphenopalatine artery ligation is an effective method of treatment for posterior epistaxis. Am J of Rhinol 1999;13:137-40. Christensen NP, Smith DS, Barnwell SL, et al. Arterial embolization in the management of posterior epistaxis. Otolaryngol Head Neck Surg 2005;133:748-53. 35 Cohen JE, Moscovici S, Gomori JM, et al. Selective endovascular embolization for refractory idiopathic epistaxis is a safe and effective therapeutic option: technique, complications, and outcomes. J Clin Neurosci 2012;19:687-90. Gungor H, Ayik MF, Gul I, et al. Infective endocarditis and spondylodiscitis due to posterior nasal packing in a patient with a bioprosthetic aortic valve. Cardiovasc J Afr 2012;23:e5-7. Paul J, Kanotra SP, Kanotra S. Endoscopic management of posterior epistaxis. Indian J Otolaryngol Head Neck Surg 2011;63:141-4. Dedhia RC, Desai SS, Smith KJ, et al. Cost-effectiveness of endoscopic sphenopalatine artery ligation vs. nasal packing as first-line treatment for posterior epistaxis. Int Forum Allergy Rhinol 2013;3:563-6. Floreani SR, Nair SB, Switajewski MC, et al. Endoscopic anterior ethmoidal artery ligation: a cadaver study. Laryngoscope 2006;116:1263-7. Received: June 21, 2013 - Accepted: June 27, 2013 Address for correspondence: Ricardo L. Carrau, Department of Otolaryngology-Head & Neck Surgery, The Ohio State University Medical Center, Starling Loving Hall – Room B221, 320 West 10th Avenue, Columbus, OH 43210, USA. E-mail: Ricardo.Carrau@ osumc.edu 8 World J Gastroenterol 2014 October 14; 20(38): 13993-13998 ISSN 1007-9327 (print) ISSN 2219-2840 (online) Submit a Manuscript: http://www.wjgnet.com/esps/ Help Desk: http://www.wjgnet.com/esps/helpdesk.aspx DOI: 10.3748/wjg.v20.i38.13993 © 2014 Baishideng Publishing Group Inc. All rights reserved. OBSERVATIONAL STUDY Epistaxis in end stage liver disease masquerading as severe upper gastrointestinal hemorrhage Marine Camus, Dennis M Jensen, Jason D Matthews, Gordon V Ohning, Thomas O Kovacs, Rome Jutabha, Kevin A Ghassemi, Gustavo A Machicado, Gareth S Dulai Marine Camus, Dennis M Jensen, Gordon V Ohning, Thomas O Kovacs, Rome Jutabha, Kevin A Ghassemi, Gustavo A Machicado, Gareth S Dulai, CURE Hemostasis Research Group, CURE Digestive Diseases Research Center, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095, United States Marine Camus, Dennis M Jensen, Thomas O Kovacs, Rome Jutabha, Kevin A Ghassemi, Gustavo A Machicado, Gareth S Dulai, Division of Digestive Diseases at University of California, Los Angeles, Ronald Reagan Medical Center, Los Angeles, CA 90095, United States Marine Camus, University Paris 7, Department of Gastroenterology, Lariboisiere Hospital, APHP, Paris 75010, France Dennis M Jensen, Gordon V Ohning, Thomas O Kovacs, Gustavo A Machicado, Gareth S Dulai, Gastroenterology Division at VA Greater Los Angeles Healthcare System, Los Angeles, CA 90095, United States Jason D Matthews, Hunterdon Gastrointestinal Associates, Flemington, NJ 08822, United States Author contributions: Jensen DM and Matthews JD designed research; Ohning GV, Kovacs TO, Jutabha R, Ghassemi KA, Machicado GA and Dulai GS performed research; Camus M contributed new reagents/analytic tools; Camus M and Jensen DM analyzed data; Camus M, Matthews JD and Jensen DM wrote the paper. Supported by National Institutes of Health, No. 41301; Veteran Administration Clinical Merit Review Grant, to Dr Dennis M Jensen; and Philippe Foundation Grant, to Dr. Marine Camus Correspondence to: Marine Camus, MD, Assistant Professor, Department of Gastroenterology, Lariboisiere Hospital, APHP, 2 rue Ambroise Pare, 75010 Paris, France. [email protected] Telephone: +33-6-81933140 Fax: +33-1-49952577 Received: April 9, 2014 Revised: June 8, 2014 Accepted: July 11, 2014 Published online: October 14, 2014 Abstract AIM: To describe the prevalence, diagnosis, treatment, and outcomes of end stage liver disease (ESLD) WJG|www.wjgnet.com patients with severe epistaxis thought to be severe upper gastrointestinal hemorrhage (UGIH). METHODS: This observational single center study included all consecutive patients with ESLD and epistaxis identified from consecutive subjects hospitalized with suspected UGIH and prospectively enrolled in our databases of severe UGIH between 1998 and 2011. RESULTS: A total of 1249 patients were registered for severe UGIH in the data basis, 461 (36.9%) were cirrhotics. Epistaxis rather than UGIH was the bleeding source in 20 patients. All patients had severe coagulopathy. Epistaxis was initially controlled in all cases. Fifteen (75%) subjects required posterior nasal packing and 2 (10%) embolization in addition to correction of coagulopathy. Five (25%) patients died in the hospital, 12 (60%) received orthotopic liver transplantation (OLT), and 3 (15%) were discharged without OLT. The mortality rate was 63% in patients without OLT. CONCLUSION: Severe epistaxis in patients with ESLD is (1) a diagnosis of exclusion that requires upper endoscopy to exclude severe UGIH; and (2) associated with a high mortality rate in patients not receiving OLT. © 2014 Baishideng Publishing Group Inc. All rights reserved. Key words: Epistaxis; Upper gastrointestinal bleeding; End stage liver disease; Cirrhosis; Nasogastric tube; Liver transplantation; Digestive bleeding; Nasal packing; Coagulopathy Core tip: Severe posterior nasopharyngeal epistaxis in hospitalized patients with end stage liver disease (ESLD): (1) is a diagnosis of exclusion that requires upper endoscopy to rule out common causes of upper gastrointestinal hemorrhage (UGIH); (2) can usually be effectively treated with nasal packing and correction of coagulopathy; (3) was the diagnosis of the bleeding 13993 October 14, 2014|Volume 20|Issue 38| Camus M et al . Epistaxis in end stage liver disease source in 4.3 % of cirrhotic patients with a suspected UGIH; and (4) is associated with a high rate of mortality (63%) in those not receiving liver transplantation. Physicians managing patients with ESLD should be aware that epistaxis can masquerade as massive UGIH, particularly in those with severe coagulopathy. Camus M, Jensen DM, Matthews JD, Ohning GV, Kovacs TO, Jutabha R, Ghassemi KA, Machicado GA, Dulai GS. Epistaxis in end stage liver disease masquerading as severe upper gastrointestinal hemorrhage. World J Gastroenterol 2014; 20(38): 13993-13998 Available from: URL: http://www.wjgnet. com/1007-9327/full/v20/i38/13993.htm DOI: http://dx.doi. org/10.3748/wjg.v20.i38.13993 INTRODUCTION Massive upper gastrointestinal hemorrhage (UGIH) in patients with end stage liver disease (ESLD) is often fatal[1,2]. Concomitant coagulopathy is a common comorbidity in cirrhotics and it frequently worsens the outcome. Expedient diagnosis and intervention are therefore imperative when encountering such cases. Although rare, severe epistaxis is a diagnosis that must be considered in patients presenting with signs and symptoms of severe UGIH, in order to avoid delays in the provision of potentially life-saving therapy[3]. About 5% of epistaxis originates from a posterior nasal source[4]. Bleeding in these cases can be especially severe. Local therapy such as nasal packing or cauterization is usually sufficient, but continued or intractable hemorrhage may require arterial ligation, embolization or more recently endoscopic ligation[4]. Delayed treatment may lead to excessive blood loss and increased morbidity and mortality. Literature about epistaxis and cirrhosis is limited as few case reports[5]. Our aims were (1) to describe the diagnosis, treatment, and outcomes of ESLD patients with severe epistaxis whose initial clinical diagnosis prior to endoscopy was severe UGIH probably secondary to esophageal varices; and (2) to estimate the prevalence of epistaxis as the final diagnosis in cirrhotics who present with signs of severe UGIH. MATERIALS AND METHODS University of California, Los Angeles Center for Health Sciences (UCLA-CHS) is an urban, academic, tertiary care referral medical center. Nearly 30000 patients are discharged from this facility yearly. Attending gastroenterologists from the Center for Ulcer Research and Education (CURE) Hemostasis Research Group are available 24 h a day for the evaluation and treatment of patients hospitalized with severe gastrointestinal (GI) hemorrhage. The UCLA Ronald Reagan Medical Center (RRMC) also has a liver transplant program that is one of the largest in the world by volume. As the most experienced WJG|www.wjgnet.com liver transplantation program in the western United States, UCLA serves the area from California, Oregon, Washington, and throughout the Southwest. Cases in this report were retrospectively identified from consecutive hospitalized subjects with severe UGIH who were enrolled in our studies of severe UGIH in ESLD between September 26, 1998 and June 1, 2011. This observational study was approved by the UCLA Office for the Protection of Research Subjects. Informed consent for endoscopy was obtained before each clinically indicated procedure. ESLD disease was diagnosed based upon clinical parameters, radiologic imaging, and/ or liver biopsy results. Suspected severe UGIH was defined as (1) signs or symptoms of UGI hemorrhage (hematemesis and/or melena); (2) decrease in hemoglobin from baseline of ≥ 2 g/dL; and (3) and/or transfusions of ≥ 2 units of packed red blood cell (PRBC). All upper endoscopies were performed by experienced endoscopists using therapeutic sized video endoscopes. Patients underwent emergency endoscopy after resuscitation. Careful examination of the esophagus, stomach (including retroflex views), and duodenum was performed in each case. Members of the CURE Hemostasis Group and a skilled research coordinator collected prospective data from the time of presentation using standardized data forms. All patients underwent clinical evaluation about bleeding symptoms: hematemesis, melena, hematochezia; bleeding severity: hypotension, shock, need for pressors; and cirrhosis data: etiology of cirrhosis, severity of cirrhosis (Child-Pugh class and Model of End Stage Liver Disease - MELD score) from the time of presentation. Laboratory data (creatinine, hematocrit, hemoglobin and coagulation tests) and endoscopic findings were also recorded from the time of presentation. The patients were prospectively followed-up from the date of diagnosis to hospital discharge, death, or liver transplantation. Coagulopathy was defined as values of prothrombin time (PT), international normalized ratio (INR), or platelet count outside the institutional normal ranges. ChildPugh class and MELD score were calculated according to a well-accepted classification[6-8]. Hypotension was defined as a systolic blood pressure persistently less than 100 mmHg despite adequate volume resuscitation. Rebleeding was defined as recurrent severe epistaxis (or signs of UGI bleeding) at least 24 h after observed complete cessation of pharyngeal bleeding following appropriate treatment, with decrease in hemoglobin of ≥ 2 g/dL after resuscitation and initial diagnosis and/or ≥ 2 units of PRBC. Follow-up time was calculated from the time of presentation to the GI Hemostasis Team until death, liver transplantation, or discharge from the hospital. Statistical analysis All data were de-identified and entered onto data files. SAS software, version 9.1 (SAS Institute, Cary, NC) was used for data management. Missing or inconsistent data were resolved by a joint review of the medical record and discussion with program instructor (DMJ) and co-investigators 13994 October 14, 2014|Volume 20|Issue 38| Camus M et al . Epistaxis in end stage liver disease Table 1 Characteristics of patients n (%) Characteristic Data Age (yr, mean ± SD, range) 54.4 ± 9.7 (40-75) Sex (Male/Female) 12/8 (60/40) Child Pugh class A: 0; B: 1 (5); C: 19 (95) MELD score, (mean ± SD, range) 29.6 ± 7.5 Etiology HCV + Alcoholic 5 (25) Alcoholic 5 (25) Cryptogenetic 5 (25) HCV 4 (20) PBC + AIH 1 (5) Inpatient start of bleeding 18 (90) Nasogastric tube placed prior to bleeding 16 (80) Hematemesis 15 (75) Melena and/or Hematochezia 9 (45) PT (s, mean ± SD, range) 20.7 ± 6.8 (13.4-42.6) INR (mean ± SD, range) 2.3 ± 1.4 (1.4-7.8) Platelet count (/mm3, mean ± SD, range) 51000 ± 32082 (11000-120000) Hematocrit (mean ± SD, range) 23.5% ± 2.9% (18.5%-29.9%) AIH: Autoimmune hepatitis; HCV: Hepatitis C virus; INR: International normalized ratio; MELD: Model for end stage liver disease; PBC: Primary biliary cirrhosis; PT: Prothrombin time; SD: Standard deviation. (JM or MC). RESULTS A total of 1249 patients were registered for severe UGIH in the data basis, 461 (36.9%) were cirrhotic patients. Epistaxis was determined to be the source of severe hemorrhage in 20 patients with ESLD hospitalized for severe UGIH. Based on the number of cirrhotic patients evaluated for severe UGIB during the same period of time, we estimated that the epistaxis diagnosis represented 4.3% (20/461) of all cirrhotic patients hospitalized for suspected severe UGIH. Most patients (18/20 = 90%) developed what was clinically diagnosed as inpatient UGIH after hospitalization for worsening liver disease and did not have signs of UGIH on admission. In this particular subgroup of inpatients with cirrhosis and severe UGI hemorrhage, the prevalence of epistaxis was higher and was estimated to be 15.3% (18/117) (Table 1). The age (mean ± SD) of the subjects with epistaxis was 54.4 ± 9.7 year with men comprising 12/20 (60%). Etiologies of ESLD were hepatitis C and alcohol in 5 (25%), cryptogenic cirrhosis in 5 (25%), alcohol alone in 5 (25%), hepatitis C alone in 4 (20%), and primary biliary cirrhosis plus autoimmune hepatitis in 1 (5%). Most patients (19/20 = 95%) were Child-Pugh class C. The majority (16/20 = 80%) had a nasogastric (NG) tube placed prior to the onset of bleeding. The reasons of NG tube placement were intubation, decompression or suctioning the stomach, checking for bright red bleeding (BRB) in stomach to establish the acuity of bleeding, and assisting of esophagogastroduodenoscopy (EGD) by clearing of blood, clots, or gastric contents. Seventeen (85%) patients required endotracheal intubation for airway protection. WJG|www.wjgnet.com All patients had clinically severe bleeding presenting as hematemesis (15/20; 75%) or hematochezia/melena (9/20; 45%). In 9 (45%) patients, bleeding was accompanied by shock or persistent hypotension requiring administration of intravenous pressor agents. All patients had concurrent severe coagulopathy with a mean PT ± SD of 20.7 ± 6.8 s (range: 13.4-42.6), INR (mean ± SD) of 2.3 ± 1.4 (range: 1.4-7.8), and platelet count (mean ± SD) of 51000 ± 32082/mm 3 (range: 11000-120000). The hematocrit (mean ± SD) before resuscitation was 23.5% ± 2.9% (range: 18.5-29.9). Most (14/20; 70%) patients had esophageal varices but none had active bleeding, platelet plugs, or other stigmata of recent hemorrhage[9]. No other upper GI lesions with active bleeding, visible vessels, or adherent clots were found. Upon withdrawal of the endoscope, fresh red blood (indicating active bleeding) was found in the proximal esophagus coming down from the posterior nasopharynx in each case. Once diagnosed by endoscopy, epistaxis was initially controlled in all cases. Fifteen (75%) patients required posterior nasal packing by an otolaryngologist in addition to correction of coagulopathy. Two (10%) patients had angiographic embolization of branches of the splenopalatine artery after failure of nasal packing. Five (25%) patients rebled during follow-up. During follow-up, the number of RBC units transfused (mean ± SD) was 9.8 ± 11.7, the number of FFP units transfused (mean ± SD) was 14.7 ± 21.8, and the number of platelets units transfused (mean ± SD) was 8 ± 9.9. Patients’ outcomes were summarized in Table 2. Five (25%) patients died in the hospital, 12 (60%) received orthotopic liver transplantation (OLT) during the hospitalization, and 3 (15%) were discharged without OLT. The mortality rate was 63% (5/8) in patients who did not undergo OLT. The mean ± SD length of time until death, liver transplantation, or discharge from the hospital was 13.6± 18.3 d. Among the 5 deaths in the hospital, one was due to uncontrolled recurrent epistaxis and very severe hemorrhage and all others were from ESLD or severe co-morbiditis. The patient who died of uncontrolled epistaxis was a 75-year-old male with hepatitis C and alcoholic cirrhosis who was maintained on oral anticoagulation with warfarin for a St. Judes mitral valve replacement. He developed epistaxis after an increase in his outpatient warfarin dose and was admitted with an INR of 7.7. The epistaxis was controlled after correction of his coagulopathy and posterior nasal packing but recurred 8 d later days after the packing was removed. At the time of the rebleed, the INR was 1.5 and platelet count was above 100000/mm. Bleeding continued despite repeat posterior nasal packing and transfusion with fresh frozen plasma and platelets, and the patient subsequently developed a myocardial infarction and cardiogenic shock. The patient’s family chose to withdraw care given his very poor prognosis and he expired soon after. Among the four other deaths, one patient died during OLT pro- 13995 October 14, 2014|Volume 20|Issue 38| Camus M et al . Epistaxis in end stage liver disease Table 2 Outcomes of patients n (%) OLT Death in hospital Discharge without OLT No. of patients Age (yr) PT (s) INR Platelet count 3 (/mm ) MELD score Time between diagnosis and death, OLT or discharge (d) Rebleeding before death, OLT or discharge 12 (60) 5 (25) 51.5 ± 8.7 57.6 ± 10.1 22.6 ± 7.9 17.7 ± 5.5 2.7 ± 1.7 1.8 ± 0.5 43333 ± 27955 54400 ± 41578 31.8 ± 6.4 30.8 ± 9.5 8.4 ± 8.2 10.8 ± 6.0 3 (25) 1 (20) 3 (15) 60.3 ± 11.7 18.6 ± 0.7 1.8 ± 0.1 76000 ± 26514 20.5 ± 2.1 39.0 ± 39.9 1 (33) MELD: Model for end stage liver disease; OLT: Orthotopic liver transplantation; PT: Prothrombin time; INR: International normalized ratio; SD: Standard deviation. cedure and the tree other patients died in intensive care unit (ICU) because of multiorgan failure due ESLD. DISCUSSION Patients with ESLD presenting with massive hematemesis, hematochezia, and/or melena require rapid diagnosis and intervention to reduce the high mortality associated with cirrhosis[2]. Many of these patients have coexisting coagulopathies that can worsen their outcomes. In patients, with ESLD, epistaxis can be a cause of severe hemorrhage which may be overlooked and usually masquerades as UGIH, because of the clinical presentation[5]. We estimated that in cirrhotic patients hospitalized for severe UGIH symptoms, epistaxis was the diagnosis in 4.3% of cases. This prevalence increased more than three times when cirrhotic patients were already hospitalized before they started bleeding (15.3%). Few data have been reported about the prevalence of epistaxis in patients presenting with signs of severe UGIH. Hutchison et al[3] reported 10 cases with apparent upper gastrointestinal bleeding, comprising a 0.55% incidence of hematemesis and melena in the population studied of patients referred for UGIH without information on their liver function. In ambulatory patients without cirrhosis, epistaxis most commonly arises from the vessels located in the anterior nasopharynx (Kiesselbach’s plexus), especially in children and young adults. The source of bleeding is usually obvious, often related to local trauma, and rarely is clinically severe[10]. In contrast, posterior nasopharyngeal epistaxis may be occult, large volume, and associated with high mortality[11]. It is reported to be more common in older patients, less likely trauma-related given its anatomic location, and more likely the result of spontaneous bleeding from a sclerotic vessel. In contrast to published figures that only 5% of all epistaxis is from a posterior nasopharyngeal source, all of our patients with epistaxis had posterior hemorrhage and most 15 (75%) required posterior nasal packing. Although ESLD is now more often considered as a procoagulant state, in our cirrhotic patients with epistaxis, portal hypertension and coagulopathy were risk factors in all patients. These risk factors predisposed them to severe posterior nasopharyngeal hemorrhage. One of the most common causes of epistaxis is trau- WJG|www.wjgnet.com ma. Most patients (80%) in this study had epistaxis after a recently placed nasogastric tube. Nasogastric tube placement may initiate or exacerbate pharyngeal bleeding, especially in patients with ESLD. Altered mental status from hepatic encephalopathy, shock, or mechanical ventilation related sedation might increase the risk of pharyngeal trauma during nasogastric tube placement by blunting a patient’s natural response to pain or discomfort. Abnormal coagulation may also increase the risk of epistaxis arising from minimal pharyngeal trauma. Therefore, NG tube placement should be avoided as often as possible especially forceful or traumatic insertion in the patients with ESLD. However by clearing the stomach of blood, clots, or gastric contents and helping establish the acuity of bleeding, these devices may help localize a bleeding source, decrease the risk of massive aspiration, and increase the amount of gastric mucosa seen during endoscopy[12-14]. NG or orogastric tubes are also useful for enteral delivery of medications and nutrition in ESLD patients with severe encephalopathy. If there is concern about inducing epistaxis in patients with ESLD and coagulopathy and a gastric tube is required, an orogastric tube can be considered instead of a nasogastric tube. Most patients with ESLD without epistaxis tolerate such tubes well and do not have complications in current practice. However it would be interesting to know the prevalence of epistaxis in population of patients with ESLD who underwent ng tube placement and further studies are warranted. Mortality rates approaching 5% have been reported for all patients with posterior epistaxis[3]. Given associated coagulopathy and other factors, it is expected that patients with ESLD who develop a severe posterior nasopharyngeal bleed would have significantly higher mortality. Our overall mortality rate of 25% (5/20) supports this idea, and the rate in those not receiving liver transplantation was even higher (5/8, 63%). Epistaxis as a source of severe bleeding must be included in the differential diagnosis of inpatient hemorrhage for patients with ESLD and nasogastric tubes or nasotracheal intubation. However, this is still a diagnosis of exclusion. Especially in cirrhotic patients who often have variceal hemorrhage, upper endoscopy should always be performed to rule out more common causes of UGIH, and in the absence of an actively bleeding lesion on esophagogastroduodenoscopy, careful examination 13996 October 14, 2014|Volume 20|Issue 38| Camus M et al . Epistaxis in end stage liver disease of the mouth and nasopharynx should be performed. Delayed diagnosis of severe epistaxis from posterior pharyngeal sources can lead to significant blood loss and resulting hypovolemia, shock, and death[5]. Once the diagnosis of posterior nasopharyngeal epistaxis is established, an otolaryngologist should be consulted about treatment options, which include posterior nasal packing, possible embolization of arteries supplying that region, and/or endoscopic ligation[10,15]. Posterior nasal packing is not without potential complications, including aspiration, hypoxia, and toxic shock as the most serious. Supplemental oxygen should be provided and, whenever necessary, intubation and mechanical ventilation should be considered to help prevent aspiration and hypoxia. Nonetheless, despite rapid diagnosis and treatment, the outcome for these patients is poor, most likely influenced by their significant comorbidities, particularly ESLD and coagulopathy. In the absence of an early otolarygoscopic exam, turning the patient onto the side and looking for nasal blood loss may help suggest an occult posterior pharyngeal hemorrhage as well as facilitate drainage. Other measures that might influence diagnosis, treatment, and outcome include oral passage of a gastric lavage tube and early referral for liver transplantation. In conclusion, severe posterior nasopharyngeal epistaxis in hospitalized patients with ESLD: (1) is a diagnosis of exclusion that requires upper endoscopy to rule out common causes of UGIH; (2) can usually be effectively treated with nasal packing and correction of coagulopathy; (3) was the diagnosis of the bleeding source in 4.3% of cirrhotic patients with a suspected UGIH and this prevalence increased to 15.3% in the subgroup of cirrhotic patients in whom the hemorrhage started after hospitalization for worsening liver disease and did not have signs of UGIH on admission; and (4) is associated with a high rate of mortality (63%) in those not receiving liver transplantation. Physicians managing patients with ESLD should be aware that posterior nasopharyngeal epistaxis can masquerade as massive UGIH, particularly in those with severe coagulopathy. ACKNOWLEDGMENTS The authors are grateful to Nan Sun, MS and Mary Ellen Jensen, MLS for data management, and Martha Carrico, RN, as the research coordinator. COMMENTS COMMENTS Background Severe epistaxis is a rare cause of massive bleeding which can masquerade as upper gastrointestinal hemorrhage (UGIH) in patients with end stage liver disease (ESLD). Research frontiers Little is known about prevalence, treatment and outcomes of patients suffering from epistaxis in case of ESLD. Only few cases series are available in literature. Innovations and breakthroughs The authors described that epistaxis was the diagnosis of the bleeding source in 4.3% of cirrhotic patients with a suspected UGIH and this prevalence in- WJG|www.wjgnet.com creased to 15.3% in the population of cirrhotic patients in whom the hemorrhage occurred after hospitalization for worsening liver disease and did not have signs of UGIH on admission. The authors found that epistaxis in such cases could usually be effectively treated with nasal packing and correction of coagulopathy. This treatment should not be delayed. In fact, epistaxis in ESLD was associated with a high rate of mortality (63%) in those not receiving liver transplantation. Applications Physicians managing patients with ESLD should be aware that posterior nasopharyngeal epistaxis can masquerade as massive UGIH, particularly in those with severe coagulopathy. Peer review Well written and discussed study. The authors described the prevalence, diagnosis, treatment, and outcomes of ESLD patients with severe epistaxis masqueraded as upper gastrointestinal hemorrhage. We have limited knowledge in this subject and the authors made an important observation. REFERENCES 1 Cholongitas E, Senzolo M, Patch D, Kwong K, Nikolopoulou V, Leandro G, Shaw S, Burroughs AK. Risk factors, sequential organ failure assessment and model for end-stage liver disease scores for predicting short term mortality in cirrhotic patients admitted to intensive care unit. Aliment Pharmacol Ther 2006; 23: 883-893 [PMID: 16573791 DOI: 10.1111/j.1365-2036.2006.02842.x] Das V, Boelle PY, Galbois A, Guidet B, Maury E, Carbonell 2 N, Moreau R, Offenstadt G. Cirrhotic patients in the medical intensive care unit: early prognosis and long-term survival. Crit Care Med 2010; 38: 2108-2116 [PMID: 20802324 DOI: 10.1097/CCM.0b013e3181f3dea9] Hutchison SM, Finlayson ND. Epistaxis as a cause of he3 matemesis and melena. J Clin Gastroenterol 1987; 9: 283-285 [PMID: 3497188] Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North 4 Am 2008; 41: 525-536, viii [PMID: 18435996 DOI: 10.1016/ j.otc.2008.01.003] Johal SS, Austin AS, Ryder SD. Epistaxis: an overlooked 5 cause of massive haematemesis in cirrhosis. BMJ 2003; 326: 440-441 [PMID: 12595387 DOI: 10.1136/bmj.326.7386.440] D'Amico G, Garcia-Tsao G, Pagliaro L. Natural history and 6 prognostic indicators of survival in cirrhosis: a systematic review of 118 studies. J Hepatol 2006; 44: 217-231 [PMID: 16298014 DOI: 10.1016/j.jhep.2005.10.013] Kamath PS, Wiesner RH, Malinchoc M, Kremers W, Ther7 neau TM, Kosberg CL, D’Amico G, Dickson ER, Kim WR. A model to predict survival in patients with end-stage liver disease. Hepatology 2001; 33: 464-470 [PMID: 11172350 DOI: 10.1053/jhep.2001.22172] Kremers WK, van IJperen M, Kim WR, Freeman RB, Harper 8 AM, Kamath PS, Wiesner RH. MELD score as a predictor of pretransplant and posttransplant survival in OPTN/UNOS status 1 patients. Hepatology 2004; 39: 764-769 [PMID: 14999695 DOI: 10.1002/hep.20083] Jensen DM. Endoscopic screening for varices in cirrhosis: 9 findings, implications, and outcomes. Gastroenterology 2002; 122: 1620-1630 [PMID: 12016427] 10 Douglas R, Wormald PJ. Update on epistaxis. Curr Opin Otolaryngol Head Neck Surg 2007; 15: 180-183 [PMID: 17483687 DOI: 10.1097/MOO.0b013e32814b06ed] 11 Tan LK, Calhoun KH. Epistaxis. Med Clin North Am 1999; 83: 43-56 [PMID: 9927959] 12 Pallin DJ, Saltzman JR. Is nasogastric tube lavage in patients with acute upper GI bleeding indicated or antiquated? Gastrointest Endosc 2011; 74: 981-984 [PMID: 22032314 DOI: 10.1016/j.gie.2011.07.007] 13 Perng CL, Lin HJ, Chen CJ, Lee FY, Lee SD, Lee CH. Characteristics of patients with bleeding peptic ulcer requiring emergency endoscopy and aggressive treatment. Am J Gastroenterol 1994; 89: 1811-1814 [PMID: 7942673] 13997 October 14, 2014|Volume 20|Issue 38| Camus M et al . Epistaxis in end stage liver disease 14 Stollman NH, Putcha RV, Neustater BR, Tagle M, Raskin JB, Rogers AI. The uncleared fundal pool in acute upper gastrointestinal bleeding: implications and outcomes. Gastrointest Endosc 1997; 46: 324-327 [PMID: 9351035] 15 Tateshima S, Froehler M, Cramer R, Rastogi S, Viñuela F. Trans-radial embolization of epistaxis in patients with endstage liver disease. Neuroradiology 2012; 54: 1241-1244 [PMID: 22205340 DOI: 10.1007/s00234-011-0999-z] P- Reviewer: Celikbilek M, Ding SG, Malnick SDH S- Editor: Nan J L- Editor: A E- Editor: Liu XM WJG|www.wjgnet.com 13998 October 14, 2014|Volume 20|Issue 38| Published by Baishideng Publishing Group Inc 8226 Regency Drive, Pleasanton, CA 94588, USA Telephone: +1-925-223-8242 Fax: +1-925-223-8243 E-mail: [email protected] Help Desk: http://www.wjgnet.com/esps/helpdesk.aspx http://www.wjgnet.com I S S N 1 0 0 7 - 9 3 2 7 3 8 9 7 7 1 0 0 7 9 3 2 0 45 © 2014 Baishideng Publishing Group Inc. All rights reserved. Seediscussions,stats,andauthorprofilesforthispublicationat:http://www.researchgate.net/publication/7407797 Guidelinestothemanagementofepistaxis. ARTICLEinB-ENT·FEBRUARY2005 ImpactFactor:0.08·Source:PubMed CITATIONS DOWNLOADS VIEWS 3 745 618 6AUTHORS,INCLUDING: PhilippeEloy StéphanieCollet CatholicUniversityofLouvain CliniquesUniversitairesSaint-Luc 101PUBLICATIONS562CITATIONS 37PUBLICATIONS222CITATIONS SEEPROFILE SEEPROFILE Availablefrom:PhilippeEloy Retrievedon:04August2015 B-ENT, 2005, 1, Suppl. 1, 27-43 Guidelines to the management of epistaxis B. Bertrand*, Ph. Eloy*, Ph. Rombaux*, C. Lamarque**, J. B. Watelet***, S. Collet*. * ENT and HNS Department, Catholic University of Louvain, Cliniques Universitaires UCL de Mont-Godinne, Yvoir, Cliniques Universitaires Saint-Luc, Brussels; ** ORL Department, Cliniques Saint-Luc, Bouge; *** ENT and HNS Department, University of Ghent, UZ Gent, Ghent Key-Words. Epistaxis; nose bleeding; management; conservative treatment; surgery; endoscopic surgery; medical treatment; cost analysis Abstract. This article is a review of the literature on epistaxis and its treatment. Data were collected from MedLine until mid September 2005, and from others readings and books. Its first goal was to present to the Belgian ENT practitioners an overview, as complete as possible, of the modern concepts in etiologies, medical, conservative, surgical (including embolization), and adjunctive therapies of epistaxis. All these topics are discussed and commented, from a medico-surgical point of view, and also from a cost effectiveness one. Foreword First of all, it has to be stressed on that this topic on epistaxis – or nose bleed – is presented to you as a guideline only and no more. The elements of history, discussion of pathophysiology, and details of manoeuvres are presented to help the physician best assess which patients are likely to benefit from this guideline, and which are most likely to need surgical therapy. The suggested studies, physical examination – of the nasal cavities and of the total body –, medical material including rigid endoscope and fiberscope, plain X-ray, CT, MRI, lab exams, and others, are intended to maximize the adherence process to these guideline, they will not ensure successful treatments in every patient nor in every situation. The present guideline should not be considered inclusive of all accepted methods of caring nose bleeds or exclusive of other cares that can be assumed as reasonably aimed toward gaining the same results. The ultimate decision regarding the appropriateness of any specific procedure, therapy, or referral must be made by the physician him or herself in lights of – and depending on – all the circumstances presented by the patient as an individual and all surroundings. Furthermore, medicine is a permanently changing science and not all therapies are clearly and definitely established. Obviously, new researches and discoveries are modifying medical and surgical treatments daily. That is why the reader should confirm the information in this guideline from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. Background Bleeding from the nose, or epistaxis – Greek for nosebleed that means “which is leaking on, drop by drop” –, is a problem that has been a part of the human experience from earliest times. It was the subject for folklore and myth, and has been treated by physicians – and others – from the earliest times. Centuries ago, Hippocrates reported that pinching the nose may help to stop bleeding. His technique is still in use today. Writing magical words on the forehead with the patient’s own blood, having the patient sniff his/her own fried blood into their nose, wearing amulets preferably tinted in red, have also been tried with more or less success obviously. Carl Michel (1871), James Little (1879), and Wilhelm Kiesselbach were the first to identify the nasal septum’s anterior plexus as a source of nasal bleeding. Pilz was the first to treat epistaxis with ligature of the common carotid artery (1869). This was 28 followed by Seiffert who was doing the same with the internal maxillary artery via the maxillary sinus in 1928. Henry Goodyear performed the first anterior ethmoid artery ligature in the treatment of epistaxis. The medical community’s understanding of epistaxis has increased dramatically. Our treatment, though somewhat modified over the years, has continued to include techniques first noted several thousand years ago. Epistaxis is very common in its frequency and varied in its presentation. The true incidence of epistaxis is not known in the literature because most episodes are selftreated and thus are not reported. Most nose bleeds are mere nuisances, but some are quite frightening, and a few are even life threatening. The site of a patient covered in blood surrounded by a hoard of anxious family members can make even the most experienced emergency physician feel a sense of dread. When medical cares are needed, it is usually because of the problem is either recurrent or severe. Treatment depends on the clinical picture, the experience of the physician, the availability of ancillary services and for some cases, the hospital medical equipment and the expertise and skill of members of the staff.1 In children, nosebleeds occurs also very commonly, especially in those between the ages of 2 and 10 years old. In most cases, they are secondary to local trauma and can be cared for by primary care physicians. In rare instances, however, a nosebleed may be difficult to control or may be a manifestation of a serious systemic illness. Referral to an otorhinolaryngologist or hematologist/oncologist is B. Bertrand et al. usually not required except in these situations, and hospitalization is generally unnecessary. Pathophysiology The blood supply of the nose is complex and particularly rich with contribution from both internal and external carotid arteries. The external carotid system supplies blood to the nose via the facial and internal maxillary arteries. The superior labial artery one of the terminal branches of the facial artery - contributes to the blood supply of the anterior part of the nasal floor and of the septum through a septal branch. The internal maxillary artery enters the pterygomaxillary fossa and divides into 6 branches: posterior superior alveolar, descending palatine, infraorbital, sphenopalatine, pterygoid canal, and pharyngeal. The descending palatine arteries are running down through the greater palatine canals and supply the lateral walls of the nasal cavities. They go back to the nose via a branch in the incisive foramen to irrigate the anterior septum. The sphenopalatine arteries enter the nose through the sphenopalatine foramen which is situated approximately 10 mm dorsally to a theoretical line drawn between both the posterior attachments of the middle and lower turbinates to supply the lateral nasal walls. It also gives a branch to the septum. The internal carotid artery irrigates the nose through the ophthalmic artery that enters the bony orbit via the superior orbital fissure and divides into several branches. One of which – the posterior ethmoid artery – exits the orbit for the nose through the posterior ethmoid foramen, located 2 mm to 9 mm anterior to the optic canal. The anterior ethmoid artery exits the orbit through the anterior ethmoid foramen. Both of the vessels cross the ethmoid roof to enter the anterior cranial fossa and then descend into the nasal cavity wherein they divide into lateral and septal branches to supply the lateral wall of the nose and the nasal septum. The Kiesselbach plexus, or Little area, is located on the lower third of the septal cartilage and is a very common spring for most anterior epistaxis. Many of the arteries supplying the septum have anastomotic connections in this plexus. The mucosa covering the area is thin and friable and the small vessels supplying the nasal mucous membrane have little structural support. Congestion of the vessels caused by conditions such as a URI or drying of the mucosa from low environmental humidity makes this area susceptible to bleeding. Sensory nerves follow the anatomical general pattern of the vessels. Trigeminal cranial nerves V1 and V2 supply the interior nose (anterior ethmoidal nerve and nasopalatine nerve respectively). Clinical presentation Nosebleeds may be either anterior or posterior in origin. Of the two categories of epistaxis, mundane and severe, the mundane, usually anterior epistaxis is the more common. All individuals suffer occasional nose bleeds, of which the great majority are minor and occur on the anterior septum where they are easily managed. Occasionally patients present with severe, life-threatening epistaxis arising from the larger vessels in the posterior and superior Guidelines to the management of epistaxis nasal cavity. Such bleeds occur primarily in older patients, often with significant comorbidities. Then the bleeding compromises the patient’s airway and results in hemodynamic instability. Management can be complex and severely tax the health care provider especially if he is not an otolaryngologist. With anterior nosebleeds blood exits almost entirely from the anterior portion of the nose. With posterior nosebleeds, most of the bleeding occurs in the nasopharynx and mouth, although some blood exits through the anterior nose as well. Posterior epistaxis are often more severe and more difficult to control, and patients may present in a hemodynamically unstable condition as written before. Patients with bleeding disorders may have recurrent nosebleeds and a history of prolonged bleeding, easy bruisability, or multiple bruises in unlikely locations. Alternatively, some patients who present with hematemesis have vomited swallowed nasal blood. In children, most have a history of bleeding at home and minimal or no bleeding at all at the time of presentation. Parents and children, who are often frightened by nosebleeds, frequently overestimate the amount of blood lost. Understanding and reassurance are important in dealing with patient anxiety.2 Epidemiology Epistaxis is the second most common cause of spontaneous bleedings. Sixty per cent of patients may experience at least one episode of epistaxis during their lifetime. Eighty per cent of epis- taxis occurs in Kiesselbach’s plexus.3 In children, one can estimate that thirty percent have one nosebleed by the time they are 5 years of age. In children between 6 and 10 years old, frequency increases to 56%. Nosebleeds are rare in early infancy and infrequent after puberty. They occur much more frequently in the late fall and winter months, when URIs are common, environmental humidity is relatively low, and the use of heating systems results in dryness. Nosebleeds are also more common in children who live in dry climates, especially if they have a URI or allergic rhinitis. Frequency The true frequency of epistaxis is quite impossible to determine because most episodes resolve either spontaneously or with selftreatment, and therefore, are not reported. Age The general distribution is bimodal, with peaks in young children and elderly individuals. Sex ratio Incidence of epistaxis is a little bit higher in males than in females. Mortality/Morbidity For most people, epistaxis is a kind of a nuisance only. However, the problem can be life threatening, especially in elderly patients and among those with underlying additional medical problems. Etiology A sum up of etiologies can be displayed as follows below; they have been divided in local and systemic causes for more clarity. 29 Most etiologies are evident and commonly accepted. Some are not and/or are matter of discussions in the literature. That is why immediately after this synthetic paragraph a special discussion is done of some particular etiologies on which there is no definite consensus or clues. Some others are simply requesting further explanation and comments. 1. Local causes 1. Trauma (most common) • Fracture(s): facial and nasal, of bone(s) and / or cartilage(s) • Self-induced digital trauma, foreign body • Iatrogenic: nasal / sinus / orbital / skull base surgery 2. Barometric changes 3. Nasal dryness - combination of dry air, septal deformities 4. Septal perforation 5. Chemical • Cocaine abuse • Nasal sprays (both steroids and decongestants) • Ammonia • Others: gasoline, phosphorus, chromium salts, sulfuric acid, etc. 6. Tumours • Benign: polyps, inverting papilloma, juvenile nasal angiofibroma, septal angioma • Malignant: squamous cell carcinoma, esthesioneuroblastoma 7. Inflammation • Rhinitis: allergic, non allergic • Sinusitis • Infections: bacterial, viral, fungal 2. Systemic causes 1. Coagulopathies • Anticoagulant use: coumadin, 30 heparin • NSAIDS, aspirin • Hemophilia • Von Willebrandt disease • Platelet defects • Catamenial and pregnancy • Hepatic insufficiency and alcohol4 • Scurvy • Hemorragic fever (Dengue, Ebola, …)5,6 2. Granulomatous disorders • Wegener’s disease • Mid face granuloma • Sarcoidosis • Syphilis • Tuberculosis • Rhinoscleroma • Systemic lupus erythematosis • Periarteritis nodosa 3. Intoxications: cobalt, phosphorus, arsenic, lead 4. Vascular • Hypertension • Circadian onset • Atherosclerosis • Osler-Weber-Rendu disease or hereditary hemorrhagic telangiectasia (HHT) 3. Idiopathic causes 4. Discussion of some etiologies 1. Trauma Self-induced trauma from repeated nasal picking can cause anterior septal mucosal ulceration and bleeding. This scenario frequently is observed in young children. Acute facial and nasal trauma commonly leads to epistaxis. If the bleeding is from minor mucosal laceration, it is usually limited. However, extensive facial trauma can result in severe bleeding requiring nasal packing. In these patients, delayed epistaxis may signal the presence of a traumatic aneurysm. B. Bertrand et al. Patients undergoing nasal surgery should be warned of the potential for epistaxis. As with nasal trauma, bleeding can range from minor (due to mucosal laceration) to severe (due to transection of a major vessel). 3. Inflammatory diseases Bacterial, viral, fungal and allergic rhinosinusitis cause mucosal inflammation and may lead to epistaxis. Bleeding in these cases is usually minor and frequently manifests as bloodstreaked nasal discharge. Granulomatosis diseases such as sarcoidosis, Wegener granulomatosis, tuberculosis, syphilis, and rhinoscleroma often lead to crusting and friable mucosa and may be a cause of recurrent epistaxis. trauma or surgery. Acquired coagulopathies can be primary or secondary. Among the more common acquired coagulopathies are thrombocytopenia and liver disease with its consequential reduction in coagulation factors. Even in the absence of liver disease, alcoholism also has been associated with coagulopathy and epistaxis. For those patients on anticoagulants, the altered coagulation should be carefully checked and monitored. For those on aspirin as a general prophylaxis 80 mg/d of aspirin is sufficient. Most use 300 mg daily or even more, as the adult aspirin tablets are easier to find and cheaper to purchase; 80 mg P.O. daily are enough to protect the heart and free the nose from an increased epistaxis risk. In the pediatric age group, about one third of children with recurrent epistaxis have a diagnosable coagulopathy. In those cases, together with a positive family history, a prothrombin time (PT) and a partial thromboplastin time (PTT) are giving the most useful and cost-effective data.7 4. Blood dyscrasias There is a caveat for epistaxis. While most are simple, straightforward problems, they also can be the heralding sign of underlying coagulopathy. Hemophilia, von Willebrandt disease, thrombocytopenia, all may have epistaxis as their initial symptom. Congenital coagulopathies should be suspected in individuals with a positive family history, easy bruising, or prolonged bleeding from minor 5. Scurvy In western countries the incidence of scurvy appears to be on the rise. Populations at risk include the elderly, chronic alcoholics, diet faddists, the mentally ill, and patients with cancer, malabsorption, or who are on renal dialysis. The symptoms of scurvy are weakness, lassitude, depression, arthralgias, petechiae, perifollicular hemorrhage, follicular hyperkeratosis, corkscrew hairs, purpura, ecchymoses, gingival 2. Septal deformities and perforations Septal deviations and spurs may disrupt the normal nasal airflow, leading to dryness and epistaxis. The bleeding sites usually are located anterior to the spurs in most patients. The edges of septal perforations frequently harbor crusting and are common sources of epistaxis. Guidelines to the management of epistaxis swelling, hemorrhage, halitosis, poor wound healing, and loss of teeth. Adults should receive 100 mg of vitamin C 3-5 x a day up to 4 gr followed by 100 mg/day. Infants and children should receive 10-25 mg 3 times a day. Symptoms disappear within 3-5 days. 6. Hypertension Beran et al.8 reported that the distribution of blood pressure of habitual nose bleeders did not differ from that of the control group. This is in concordance with the data of Lubianca Neto et al.9, who also could not establish a definite association between blood pressure and history of adult epistaxis in hypertensive patients, although they found a link to left ventricular hypertrophy. The evidence for an association of duration of hypertension and left ventricular hypertrophy with epistaxis suggests that epistaxis might be a consequence of long term hypertension. They observed also the presence of enlarged vessels at rhinoscopy in hypertensive patients with a history of epistaxis. Herkner et al.10 found higher blood pressure values in bleeding patients compared with controls. Padgham et al.11 found a positive correlation between hypertension and bleeding from the middle meatus, but not with the severity of bleeding. The discussion on blood pressure and epistaxis will continue.12 7. Circadian variation of onset Several physiopathological phenomena show two peaks during the day. In epistaxis, the time between the two peaks is about 12 hours. Globally, all circadian rhythms in the cardiovascular system and the blood parameters enhance blood coagulation and formation of thrombus in the morning, whereas blood coagulation decreases in the afternoon. In a clinical study, Manfredini et al.13 suggest that blood pressure might trigger or be conductive to epistaxis and that might show circadian variation. A circadian rhythm of epistaxis was significantly found with a primary peak in the morning (8:00) and a smaller secondary peak in the evening (20:00). This is quite similar with hypertension, subarachnoid hemorrhage and rupture of aortic aneurysms. This deserves further investigation. 8. Arteriosclerosis Atherosclerotic vascular disease is considered a reason for the higher prevalence of epistaxis in elderly individuals. 9. Hereditary hemorrhagic telangiectasia (HHT) Hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber disease) is an autosomal dominant disease associated with recurrent bleeding from vascular anomalies. The condition can affect vessels ranging from capillaries to arteries, leading to the formation of telangiectasias and arteriovenous malformations. Histopathologic examination of these lesions reveals a lack of elastic or muscular tissue in the vessel wall. As a result, epistaxis can occur from minor trauma and tends not to stop spontaneously. Various organ systems such as the respiratory, gastrointestinal, brain and genitourinary systems may be in- 31 volved. The epistaxis in these individuals is variable in severity but is almost universally recurrent. 10. Idiopathic causes Approximately 10% of patients with epistaxis have no identifiable causes even after a thorough evaluation. Management and work up 1. History • Specific questions about the severity, frequency, duration, and laterality of the epistaxis have to be asked. • Inquiries about precipitating and aggravating factors and methods previously used to stop the bleeding must be made. • A head and neck history with an emphasis on nasal symptoms has to be obtained. • In addition, a general medical history concerning relevant medical conditions (e.g., hypertension, arteriosclerosis, coagulopathies, liver disease), current medications (e.g., coumadin, nonsteroidal antiinflammatory drugs), smoking and drinking habits must be elicited. 2. General Assessment • Airway patency has to be controlled and restored when necessary. • Vital signs, pulse, respiration have to be checked. • Pressure on nose has to be maintained (patient pinches anterior nose and leans forward). A swimmer’s nose clip14 can be a very useful adjunct when treating patients with spontaneous, anterior epistaxis. This clip is efficient at providing constant, local- 32 ized pressure over the bleeding vessel, and alleviates the need to pinch the nose. • Assessment of blood loss and side of bleeding (ask patient to quantify blood loss). • Important and relevant medical problems: cardiac, cancer, previous epistaxis, allergies to medications (i.e.: local anaestetics). See details on drug safety in Table 1. • Intravenous access has to be set up in place if indicated. • Communication with patient can obtain consent and cooperation by explaining what is going to be done. 3. Examination • Preparation The patient has to blow his or her nose and all packing have to be removed even if bleeding is not active. • Hardware Before evaluating a patient with epistaxis, all the necessary topical medications, cauterization and packing materials should be ready. A good light is mandatory as well as an appropriate suction device, in order to clean up the nasal fossa from any cloths. • Head and neck examination A thorough head and neck examination must be performed if the patient’s condition permits as well as anterior rhinoscopy before and after topical administration of medication. • Anaestesia +/- vasoconstrictors See Table 1 for details on use, doses, safety in both adult and pediatric groups. A good local anaestesia allows further examination and pot- B. Bertrand et al. ential treatments to be done in cozy conditions both for patient and physician. A topical anaestetic, such as 4% aqueous lidocaine, and a vasoconstrictor, such as 0.05% oxymetazoline or 0.0002% epinephrine or another decongestant if not contraindicated, may be used. They can be applied via aerosolizing spray or cotton pledgets inside the nose for 7-10 minutes. With sprays topical medication may not stay in place long enough to be effective due to the blood flow. Some epistaxis will stop at this early step. • Endoscopy Finally, endoscopy has to be performed using a flexible or preferably a rigid endoscope to inspect the entire nasal cavity, including the nasopharynx. The rigid endoscope is generally preferred because of its superior optic resolution and its ability to allow endoscopic suction and cauterization. 4. Conservative Treatment 1. Anterior Epistaxis 1. With patient in a sitting up position to squeeze anterior (compressible cartilaginous part) nose for 10 minutes. 2. Nasal cream In children an antiseptic nasal cream can be very effective and avoids further manipulations in most cases.15 3. Cautery Bleeding from the Kiesselbach plexus often is treated with silver nitrate cauterization. Other cauterizing agents are also used: chromic acid, acetic acid, etc. Silver nitrate should be preferred because of the absence of any demonstrated carcinogenesis. The vessels leading to the site have to be treated first before treating the actual bleeding site. Random and aggressive cautery and cautery on opposing surfaces of the septum which is potential for septum perforation must be avoided. Silver nitrate doesn’t work very well in active bleeding. Thirty seconds of exposure allowed silver nitrate to penetrate to a depth of approximately 1 mm penetration in a study by Lloyd et al.16 Longer exposure resulted in no significant additional. There was also no direct evidence that silver nitrate damaged directly the septal cartilage. Sseptal perforations in patients treated by means of topical silver nitrate may be attributable to necrosis of the septal cartilage due to damage to the perichondrium, from which it receive its blood supply. 4. Electrocautery using an insulated suction cautery unit also can be used. This method usually is reserved for more severe bleedings and for bleedings which are more posteriorly located. It requires local anaesthesia.17 The effectiveness of both cauterization methods can be enhanced by using rigid endoscopes, especially in the case of more posteriorly located bleeding sites.18 After the bleeding has been controlled, the patient is Guidelines to the management of epistaxis 33 Table 1 Drugs and material of epistaxis managment Drug category Vasoconstrictor ; Act on alphaadrenergic receptors in the nasal mucosa Anesthetics ; see under (c) Proof Name Adult Dose Level Ia Oxymetazoline 2-3 sprays in 0.05% each nostril q12h Pediatric Contraindications Pregnancy Dose 6-12 years : Hypersensitivity ; Safety not 1-2 sprays MAOIs established each nostril q12h III Not Hypersensitivity ; Usually established Adams-Stokes safe syndrome ; Wolf-ParkinsonWhite syndrome Antibiotic ointments ; prevent local infection ; local moisturization Ib Cauterizing Ia agents ; coagulate cel lular proteins ; antibacterial effects Packing ; III mechanical effect Thrombin ; as local hemostatic Ib Adrenochromazo III ne; enhance capillary resistance Terlipressin Ib Interactions Precautions Guanethidine ; Do not use Phenothiazine ; topical see under (a) decongestants for >3-5 d ; see under (b) None reported Mucous membrane use only Lidocaine 2 or 4%; Xylocaine 2 or 4%; Pantocaine 2 or 4%; Cocaine 2 or 4% : see under (d) (use not permitted in some countries) Mupirocin ointment 2% (Bactroban®); Bacitracin ointment Spray or cotton pledgets 0.5 g in each Not Hypersensitivity nostril bid formally for 5 d established Usually safe None reported Prolonged use may result in growth of resistant organisms Silver nitrate ; cautery sticks and pearls Not formally Not Hypersensitivity established formally established, but commonly used NA NA NA Not Decreases established effects of sulfacetamide preparations Not for oral use ; Cauterize vessels one side at a time Safe None reported Mouth breathing, hypoventilation FloSeal® Not forNot formally mally established established Unknown None reported None reported Potential abortion effect before the 4th month Monitoring of blood pressure and electrocardiogram Gauze; Surgicel® ; Meroce®l ; Oxycel® Thrombase® ; Cotton pledgets Gel adrenochrome Per Os: 10 Per Os : 5 semicarbazone ; to 30 mgr to 10 mgr AC-17® ; Also IM and Also IM Adona® ; IV – check and IV – Adrenosem® ; package check Adrenoxyl® ; insert package Emex® ; insert Ibioxyl® ; carbazochrome salicylate ; carbazochrome sodium sulfonate ; adrenochrome semicarbazone sodium sulfonate Glypressine® ; Gel; Not Glypressin® IV: 20 to 30 formally microgr/kg; established check package insert Not formally established Hypersensitivity Hypersensitivity, asthma, hypertension, renal insufficiency, epilepsy 34 B. Bertrand et al. Table 1 (continuation) Drug Proof Name category Level Tranexamic acid III Exacyl® Vitamin K, III Phytonadione (Vitamin K1) ; Treat vitamin K deficiency Etamsylate ; II Benzenesulfonate derivative used as a systemic hemostatic. EstrogenII progesterone ; Ethynil-estradiol ; Hormonotherapy of HTT Snake venoms II Synkavit® ; Konakion® ; Vitamon K® Adult Dose Pediatric Dose PO : 1 to 20 1.5 gr/3/d ; mgr/kg/d ; check packIV : 0.5 to age insert 1 gr/2 to 4/d ; Nose gel PO, IM, IV PO, IM, IV ContraPregnancy indications Hypersensitivit ; To be history of avoided thrombosis ; renal insufficiency Interactions Precautions Hormonal contraception Chronic renal insufficiency : check creatinin level Hypersensitivity Unknown Warfarin (Coumadin) ; Cholestyramin ; Aspirin ; NSAID Cyclonamine ; 2-3 amp(of Half of the Acute porphyria. Unknown No interaction As a precauEtamsylate ; 250mgr)/day adult dose is known up to tion should Altodor® ; IM or IV now not be adminthen 6 co/d istered during Dicynone® for 10 days the first trimester of pregnancy, whereas during the second and third trimesters, it should be administered only if the expected therapeutic benefit is judged as superior to the potential risk for the foetus. Prémarin® IM or IV Not Check package Check pack- Check package Check pack20 mgr ; as established insert age insert insert age insert for hormonal contraception Reptilase® 1 U 1 amp IM 1 amp IM Check package Check pack- Check package Check packKlobusitzky / insert age insert insert age insert amp IM ; Reptilase® -R, 20 BU®, 1 ml/amp Table 1 comments. a) Hypotensive action of may be reversed; concurrent administration with methyldopa may increase vasopressor response; concurrent use of MAOIs and ephedrine may result in hypertensive crisis. Pressor sensitivity to mixed-acting agents such as ephedrine may be increased. Guanethidine potentiates epinephrine and inhibits ephedrine. may reverse action of nasal decongestants such as oxymetazoline. TCAs potentiate vasopressor response and may result in dysrhythmias. b) Caution in: hyperthyroidism, coronary artery and ischemic heart disease, diabetes mellitus, glaucoma and in patients with an increased intraocular pressure, and prostatic hypertrophy. Hypertensive patients may experience change in blood pressure. c) Together with vasoconstrictors and b-adrenergics, their effect is prolonged and the pain threshold is increased (Oxymetazoline 0.05%; Ephedrine, Epinephrine, Adrenaline 1/50.000 or 1/100.000). d) Pantocaine and cocaine have additional vasoconstrictive effects on the blood vessels, and a particularly high affinity for fat tissues. Guidelines to the management of epistaxis instructed to use saline spray and antibiotic ointment in his/her nose and to avoid strenuous activities for 7-10 days. NSAIDs are not to be used if at all possible. Digital manipulation of the nose is to be avoided. A topical vasoconstrictor may be used if minor bleeding recurs when eschars dislodge. 5. Gelfoam or Surgicel Local resorbable hemostatic agents can be placed against the bleeding site. Absorbable materials may be used in patients with coagulopathy to avoid trauma upon packing removal. 6. Thrombin locally applied On pledgets in the nose or more recently under the form of a gel. Floseal, a hemostatic sealant composed of collagenderived particles and topical bovine-derived thrombin, has been used as a high-viscosity gel for hemostasis in anterior epistaxis and as an easy alternative to nasal packing in patients suffering from acute anterior epistaxis in a study by Mathiasen and Cruz.19 A former work was done with this compound in ESS by Chandra et al.20 7. Conventional packing Nasal packing can be used to treat epistaxis that is not responsive to cautery. Two types of packing, anterior and posterior, can be placed. In both cases, adequate anaesthesia and vasoconstriction are necessary. For anterior packing, various packing materials are avail- able. They could be coated with an antibiotic and can be moisturized with a topical vasoconstrictor. Anterior packs stay in 2-5 days, and patients may require analgesics. They also should be given an antibiotic to prevent rhinosinusitis and possible toxic shock syndrome. Here are going some examples of material: 1. Nasal catheter – Epistat® (Xomed) • Anaesthetize nose then before inserting • Place ports horizontally so patient can eat/talk • Inflate balloons with saline 2. Nasal tampon/sponge Merocel® sponges can be placed relatively easily and quickly but may not provide adequate pressure. • The nose has to be anaesthetized and sponge lubricated before inserting. • Once inserted, sterile saline is injected into the sponge. • Rewet prior to removal, check that none has broken off after removal. 3. Vaseline gauze Petroleum jelly gauze with or without an antibiotic ointment traditionally is used. Layer it tightly and far enough backwards to provide adequate pressure. Blind packing with loose gauze is to be avoided. • Leave ends protruding from anterior nose and don’t let them dangle down pharynx. 35 • Packing has to be made in layers from nasal floor up. 2. Pediatric group Most pediatric epistaxis can be effectively managed with a single out-patient consultation (91%) using a topical chlorhexidine and neomycin cream in addition in some case with a chemical nasal cautery with silver nitrate.15,21 3. Posterior Epistaxis Epistaxis that cannot be controlled by anterior packing can be treated with a posterior pack. Classically, rolled gauzes are used, but medium tonsil sponges can be substituted. Inflatable balloon devices, such as 12F or 14F Foley catheters, or specially designed (eg, Storz Epistaxis Catheter®, Xomed Treace Nasal Post Pac®) have become popular because they are easier to place. Avoiding overinflation of the balloon is important because it can cause pain and displacement of the soft palate inferiorly, interfering with swallowing. Regardless of the type of posterior pack, an anterior pack also should be placed. Patients with posterior packing should be admitted for close monitoring of oxygenation, fluid status, and adequate pain control. Need of adequate pain control has to be balanced with the concern over hypoventilation in the patient with posterior pack. They also should be given an antibiotic to prevent rhinosinusitis and possible toxic shock syndrome. In a double blind placebo controlled study about antibiotherapy and nasal packing, Derkay et al. demonstrated that the 36 B. Bertrand et al. packing in the placebo group were foul smelling and heavily colonized with gram – while those from the antibiotic group were odor-free and lightly colonized by gram +. But no infectious complications were noted in both groups.22 5. Surgical cares Among most patients, the bleeding responds to cautery and/or packing. For those who have recurrent or severe bleeding for which medical therapy has failed, various surgical options are available. Packing failure can be caused by inadequate placement from either lack of cooperation by the patient (especially those in the pediatric age group) or from anatomic factors such as a deviated septum. In these patients, a careful endoscopic examination under general anaesthesia may be considered. 1. Examination under general anaesthesia and septoplasty Bleeding sites can be cauterized under endoscopic guidance, a deviated septum can be straightened, spurs can be removed, and meticulous packing can be placed. In addition, arterial ligation may be performed during the same setting if these steps fail to control the bleeding. 2. Fibrin glue Topical use of fibrin glue especially in coagulopathies has been advocated.23 3. Arterial ligation The specific vessel(s) to be ligated depend on the location of the epistaxis. In general, the closer the ligation is to the bleeding site, the more effective the procedure tends to be. 1. External carotid artery ligation Ligation of the external carotid artery can be performed with the patient under local or general anaesthesia. A horizontal skin incision is made between the hyoid bone and the superior border of the thyroid cartilage. Subplatysmal skin flaps are then raised, and the sternocleidomastoid muscle is retracted posteriorly. Next, the carotid sheath is opened, and its contents exposed. The external carotid artery is identified by following the internal carotid for a few centimeters and dissecting the external carotid beyond its first few branches. After the external carotid has been positively identified, it usually is ligated just distal to the superior thyroid artery. Continued bleeding after ligation may be from anastomoses with the opposite carotid system or the ipsilateral internal carotid artery. 2. Internal maxillary artery ligation This procedure has a higher success rate than external carotid artery ligation because of the more distal site of intervention. Traditionally, the internal maxillary artery was accessed transantrally through a Caldwell-Luc approach.24 The posterior sinus wall is removed, and the posterior periosteum opened. The internal maxillary artery and 3 of its terminal branches (i.e., sphenopalatine, descending palatine, pharyngeal) are elevated and clipped. The posterior sinus wall is then packed with gelfoam, and the Caldwell-Luc incision is closed. Transoral and transnasal endoscopic approaches have been described. The transoral approach is useful in patients with midface trauma, hypoplastic antra, or maxillary tumours.25 The buccinator space entered through a gingivobuccal incision. The buccal fat pad is removed, and the attachment of the temporalis muscle to the coronoid process is identified next. This process facilitates the identification of the internal maxillary artery which is clipped. This procedure has a higher failure rate because the site of ligation is more proximal than in the transantral approach. The endoscopic method requires high skills with endoscopes and endoscopic instruments. A large middle meatal antrostomy is made to expose the posterior sinus wall. The middle turbinate can be resected partially to ensure adequate exposure. The remaining steps are similar to the traditional transantral approach. 3. Endoscopic sphenopalatine artery ligation (ESAL) Guidelines to the management of epistaxis or transnasal endoscopic sphenopalatine artery ligation (TESPAL) Endoscopic technique also can be used to ligate the sphenopalatine artery at its exit from the sphenopalatine foramen, results are good and abundantly reported in the literature.26-30 An incision is made just dorsally to the posterior attachment of the middle turbinate. The mucosal flap is elevated to reveal the sphenopalatine artery, which is clipped and ligated. A recurrent bleed rate of 3/10 was found, which is higher than previously published results, in a study published by Rockey and Anand.31 4. Ethmoid artery ligation If bleedings occur high in the nasal vault, consider ligation of the anterior and/or posterior ethmoid arteries. These arteries are approached through an external ethmoidectomy incision. The anterior ethmoid artery usually is found 22 mm (range, 1629 mm) from the anterior lacrimal crest. If clipping the artery does not stop the bleeding, then the posterior ethmoid artery may be ligated. This artery is found approximately 12 mm posterior to its anterior counterpart. It should be clipped, not cauterized, because it is only 4-7 mm anterior to the optic nerve. A description of an endoscopic, intranasal tech- 37 nique for ligation of the anterior ethmoid artery in a single case report was made by Woolford and Jones.32 4. Embolization / Interventional radiology Bleeding from the external carotid system may be treated with embolization, either as a primary modality in poor surgical candidates or as a second-line treatment in those for whom surgery has failed.33-35 Preembolization angiography is performed to check for the presence of any unsafe communications between the internal and external carotid systems. Selective embolization of the internal maxillary artery and sometimes the facial artery may be performed. Ligature of the internal maxillary artery and selective percutaneous embolization gave similar results in a study performed by Romagnoli et al. among 203 patients.36 Superselective embolization with gelatin sponge for intractable epistaxis report no complication in 37 patients with a success rate of 94.6% after 7 days , remaining stables after 21 months.37 Postprocedure angiography can be used to evaluate the degree of occlusion. The most common reason for failure is continued bleeding from the ethmoid arteries. As the anterior ethmoid arteries arise from the ophthalmic which itself comes from the internal carotid, they must not be embolized. The disadvantages of arteriography and embolization are the expense and the small - risk of a stroke (CVA is quoted as 1 in 100) even among skilled and long trained radiology teams. For the most part angiography and embolization are reserved for very sick individuals and for whom surgery is an unsafe option. Embolization works best in active bleeding as one can see which artery is involved. 5. Treatment of hereditary hemorrhagic telangiectasia (HHT)38 Treatment of this disease is palliative because the underlying defect is not curable. Options include coagulation with potassium-titanyl-phosphate (KTP) or neodymium:yttrium-aluminum-garnet (Nd:YAG) lasers39,40 septodermoplasty, embolization, nasal closure, and/or estrogen-progesterone therapy. Topical estrogens combined with argon plasma coagulation in the management of epistaxis in HHT significantly prolong the hemorrhage-free interval.41 We find also a single case report of an intractable epistaxis secondary to HHT successfully controlled by the application of fibrin glue. Further studies are needed.42 In some very difficult cases, nasal obliteration (Young’s procedure)43 has been proposed, with more recently a variant through a nasal obturator.44 Systemic estrogen-progesterone at doses used for oral contraception may eliminate 38 B. Bertrand et al. bleeding in symptomatic HHT. Tamoxifen has been successfully used in two cases.45 6. Sequential management The therapeutic escalation has been discussed by Simmen and Heinz in a review of 335 hospitalized patients. Their conclusions can be summarized as follows: i) first, localization of bleeding and bipolar cautery have to be performed, ii) if they not succeed, Merocel® pack, iii) if rebleeding, there is the time for operating theater and general anaestesia for an endoscopic control and/or balloon and, iv) if failure again, embolization, ligation, endonasal obliteration can take place.46 6. Compared cost-effectiveness A retrospective review of Nationwide Inpatient Sample in the USA (1998-2000) was published recently by Goddard and Reiter.47 A total of 9778 admissions with admitting diagnosis “epistaxis” were identified. Among admissions involving 1 treatment, 454 (9.6%) received arterial ligation, 94 (2.0%) embolization, and 4188 (88.4%) nasal packing. There were no differences in length of stay, transfusions, complications, or deaths between groups. Mean total hospital charges were USD 6282 for the packing group, USD 12805 for the ligation group, and USD 17517 for the embolization group; differences between ligation and packing groups, and embolization and packing groups are statistically significant. They concluded that nasal packing is associated with lower hospital charges and similar complication rates as arterial ligation or embolization. And they conclude also that further studies are needed to quantify other outcome measures, such as recurrence rates and patient quality of life. In the treatment of recurrent posterior epistaxis ESAL was compared to conventional packing by Moshaver et al.48 The overall calculated cost of patients undergoing ESAL was CAD 5133 compared with CAD 12213 in the conservative group, resulting in an average saving of CAD 7080 per patient. There was overwhelming patient satisfaction with ESAL compared with nasal packings. At comparing endoscopic ligation to embolization Miller et al.49 demonstrated that the mean total charge was USD 14088 for embolization and USD 7561 for transnasal endoscopic sphenopalatine artery ligation (TESPAL). 7. Patient self cares Nose picking is a contributing factor in epistaxis. Adults can usually be instructed to be more careful. Children pick their nose at night and this is best controlled by placing a glove or sock over their hands so that they can not pick their nose any longer. Patients should avoid hot and spicy foods and drink plenty of fluids and strenuous activities, hot showers, and digital trauma. Nasal saline spray can be liberally used. Digital pressure and ice packs are to be used as needed for minor recurrences. Dry climates predispose to recurrent nose bleeds. Daily or twice daily application of vasolinated ointment provides substantial benefit. 8. Medications Pharmacotherapy plays only a supportive role in treating the patient with epistaxis. See Table 1 for details on use, doses, safety and level of proof. Let us cite: Adrenochromazone (Adrenoxyl‚)50-52 Etamsylate (Dycinone‚)53 Terlipressin (Glypressine‚) Vinayak et al found a statistically significant benefit compared to placebo with intravenous glypressin in acute epistaxis where no localized point was found and in place of a form of nasal packing.54 In an other study, although 50% of epistaxis with not clearly localized lesions did stop bleeding, there was no significant difference in effect with placebo.55 Tranexamic acid (Exacyl‚) Oral tranexamic acid is of no proven value as an adjunct in the treatment of epistaxis in patients requiring hospital admission concerning severe rebleeds. But the gel seemed to have a beneficial effect.56,57 9. Complications of treaments 1. Cautery Synechia, septal perforation 2. Anterior packing Synechia, rhinosinusitis, toxic shock syndrome, eustachian tube dysfunction 3. Posterior packing Synechia, rhinosinusitis, toxic shock syndrome, eustachian tube dysfunction, dysphagia, scarring of nasal ala and columella, hypoventilation, sudden death Guidelines to the management of epistaxis 4. Transantral internal maxillary artery ligation Anaestetic risks, rhinosinusitis, oroantral fistula, infraorbital numbness, dental injury 5. Transoral internal maxillary artery ligation Anaestetic risks, cheek numbness, trismus, tongue paresthesia 6. Anterior/posterior ethmoid artery ligation Anaestetic risks, rhinosinusitis, lacrimal duct injury, telecanthus 7. Embolization Facial pain, trismus, facial paralysis, skin necrosis, stroke, hematoma 10. Prognosis The prognosis is good but variable. With adequate supportive care and control of underlying medical problems, most patients may not experience any rebleeding. Others may have minor recurrences that resolve spontaneously or with minimal self-treatment. A small percentage of patients may require repacking or more aggressive treatments. Patient with Osler-WeberRendu disease tends to have multiple recurrences regardless of the treatment modality. Factors predicting rebleeding are age, prior hypertension, anticoagulant use, vital signs, type of posterior packing (gauze or balloon), prior severe posterior epistaxis and pack removal within 48 hours after admission.58 At a first sight rebleeding is not driven by whether the treatment was surgical or not. The rebleeding rate was 33% after embolization, 33% after endoscopic cautery and 20% 39 Table 2 Short guide to interrpret PT and PTT results PT PTT Long Normal Liver disease or vitamin K deficiency Long Lupus anticoagulant Acquired factor VIII inhibitor Long DIC, liver disease Normal Long Normal Acquired Disorder Congenital Disorder Normal Thrombocytopenia, qualitative platelet disorder after ligation in a study by Barlow et al.59 11. Patient education Use nasal saline spray Avoid hard nose blowing or sneezing Sneeze with the mouth open Do not use nasal digital manipulation Avoid hot and spicy foods Avoid taking hot showers Avoid aspirin and other NSAIDs, avoid local nasal sprays of corticosteroids for a while when possible Self treatment for minor epistaxis: firm digital pressure on the nasal pyramid for 5-10 minutes, use of an ice pack 12. Lab studies Lab tests to evaluate the patient’s condition and underlying medical problems may be ordered depending on the clinical picture at the time of presentation. If the bleeding is minor and not recurrent, then a lab evaluation may not be needed. If bleeding is recurrent or severe, studies to evaluate the fluid status, coagulation profiles, and relevant systemic diseases are needed. These may include a complete blood count (including platelet Factor VII deficiency Factor VIII (hemophilia A), IX (hemophilia B), or XI deficiency Fibrinogen, prothrombin, factor V or X deficiency Mild factor deficiency, mild von Willebrandt disease, factor XIII deficiency count), prothrombin time, activated partial thromboplastin time, and a chemistry panel (including liver function tests).Other more specialized studies, such as bleeding time and various assays for coagulation factors and platelet function, may be considered if warranted. These tests are to be performed in the absence of anticoagulant therapy but when bleeding suggests a coagulopathy. When results are out of range it could be suggested to address to a hematologist for further advices, investigations and treatments (See Table 2). a) Prothrombin time (PT) When increased, deficiencies of the “extrinsic” and “common” factors prothrombin, fibrinogen, V, VII, or X are suspected. b) Partial thromboplastin time (PTT) When increased, deficiencies of the “intrinsic” and “common” factors prothrombin, fibrinogen, V, VIII, IX, X, or XI are suspected. Deficiencies of the “contact” factors XII, Fletcher, or Fitzgerald fac- 40 B. Bertrand et al. tors also prolong the PTT but are not associated with bleedings. 13. Imaging studies CT scanning and/or MRI may be indicated to evaluate the surgical anatomy and to determine the presence and extent of rhinosinusitis, foreign bodies, benign tumours and neoplasms. Medico-legal pitfalls 1. Failure to recognize the severity of the bleeding, especially in patients with posterior epistaxis in whom most of the blood may be swallowed. 2. Failure to diagnose serious etiologies (e.g., neoplasm, aneurysm, systemic coagulopathies). 3. Failure to prescribe antibiotic therapy to prevent rhinosinusitis and possibly toxic shock syndrome in patients with nasal packing either anterior or posterior or both. References 1. Résultats de l’Observatoire français de l’épistaxis. Revue Officielle de la Société Française d’O.R.L. 2002;75: 62-67. 2. Juselius H. Epistaxis. A clinical study of 1,724 patients. J Laryngol Otol 1974;88:317-327. 3. Doyle DE. Anterior epistaxis: a new nasal tampon for fast, effective control. Laryngoscope. 1986;96:279-281. 4. McGarry GW, Gatehouse S, Vernham G. Idiopathic epistaxis, haemostasis and alcohol. Clin Otolaryngol. 1995;20:174-177. 5. Carlos CC, Oishi K, Cinco MT, et al. Comparison of clinical featurs and hematologic abnormalities between Dengue fever and Dengue hemorrhagic fever among children in the Philippines. Am J Trop Med Hyg. 2005; 73:435-440. 6. Sureau PH. Firsthand clinical observations of hemorrhagic manifesta- tions in Ebola hemorrhagic fever in Zaire. Rev Infect Dis. 1989;11 Suppl 4:S790-793. 7. Sandoval C, Dong S, Visintainer P, Ozkaynak MF, Jayabose S. Clinical and laboratory features of 178 children with recurrent epistaxis. J Pediatr Hematol Oncol. 2002;24:47-49. 8.Beran, M, B. Petruson. Occurrence of epistaxis in habitual nose- bleeders and analysis of some etiological factors. ORL J Otorhinolaryngol Relat Spec. 1986;48:297-303. 9. Lubianca Neto JF, Fuchs FD, Facco SR, et al. Is epistaxis evidence of endorgan damage in patients with hypertension? Laryngoscope. 1999;109: 1111-1115. 10. Herkner H, Laggner AN, Mullner M, et al., Hypertension in patients presenting with epistaxis. Ann Emerg Med. 2000;35:126-130. 11. Padgham N. Epistaxis: anatomical and clinical correlates. J Laryngol Otol. 1990;104:308-311. 12. Temmel AF Quint C, Toth J. Debate about blood pressure and epistaxis will continue. BMJ. 2001;322:1181. 13. Manfredini R, Portaluppi F, Salmi R, Martini A, Gallerani M. Circadian variation in onset of epistaxis: analysis of hospital admissions. BMJ. 2000;321:1112. 14. Vaghela HM. Using a swimmer’s nose clip in the treatment of epistaxis in the A&E department. Accid Emerg Nurs. 2005;29. [Epub ahead of print] 15. Murthy P, Nilssen EL, Rao S, McClymont LG. A randomized clinical trial of antiseptic nasal carrier cream and silver nitrate cautery in the treatment of recurrent anterior epistaxis. Clin Otolaryngol Allied Sci. 1999;24:228-231. 16. Lloyd S, Almeyda J, Di Cuffa R, Shah K. The effect of silver nitrate on nasal septal cartilage. Ear Nose Throat J. 2005;84:41-44. 17. O’Donnell M, Robertson G, McGarry GW. A new bipolar diathermy probe for the outpatient management of adult acute epistaxis. Clin Otolaryngol Allied Sci. 1999;24:537-541. 18. Thornton MA, Mahesh BN, Lang J. Posterior epistaxis: identification of common bleeding sites. Laryngoscope. 2005:115:588-590. 19. Mathiasen RA, Cruz RM. Prospective, randomized, controlled clinical trial of a novel matrix hemostatic 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. sealant in patients with acute anterior epistaxis. Laryngoscope. 2005;115: 899-902. Chandra RK, Conley DB, Kern RC. The effect of FloSeal on mucosal healing after endoscopic sinus surgery: a comparison with thrombinsoaked gelatin foam. Am J Rhinol. 2003;17:51-55. Makura ZG, Porter GC, Mac Cornick MS. Pediatric epistaxis: Alder Hey experience. J Laryngol Otol. 2002; 116:903-906. Derkay CS, Hirsch BE, Johnson JT, Wagner RL. Posterior nasal packing. Are intravenous antibiotics really necessary? Arch Otolaryngol Head neck Surg. 1989;115:439-441. Walshe P, Harkin C, Murphy S, Shah C, Curran A, McShane D. The use of fibrin glue in refractory coagulopathic epistaxis. Clin Otolaryngol Allied Sci. 2001;26:284-285. Strong EB, Bell DA, Johnson LP, Jacobs JM. Intractable epistaxis: transantral ligation vs. embolization: efficacy review and cost analysis. Otolaryngol Head Neck Surg. 1995; 113:674-678. Maceri DR, Makielski KH. Intraoral ligation of the maxillary artery for posterior epistaxis. Laryngoscope. 1984;94:737-741. Snyderman CH. Goldman SA, Carrau RL, Ferguson BJ, Grandis JR. Endoscopic sphenopalatine artery ligation is an effective method of treatment for posterior epistaxis. Am J Rhinol. 1999;13:137-140. O’Flynn PE, Shadaba A. Management of posterior epistaxis by endoscopic clipping of the sphenopalatine artery. Clin Otolaryngol Allied Sci. 2000;25: 374-347. Ram B, White PS, Saleh HA, Odutoye T, Cain A. Endoscopic endonasal ligation of the sphenopalatine artery. Rhinology. 2000;38:147-149. Wormanld PJ, Wee DT, van Hasselt CA. Endoscopic ligation of the sphenopalatine artery for refractory posterior epistaxis. Am J Rhinol. 2000;14:261-264. Scaramuzzi N, Walsh RM, Brennan P, Walsh M. Treatment of intractable epistaxis using arterial embolization. Clin Otolaryngol Allied Sci. 2001;26:307-309. Rockey JG, Anand R. A critical audit of the surgical management of Guidelines to the management of epistaxis 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. intractable epistaxis using sphenopalatine artery ligation/ diathermy. Rhinology. 2002;40:147-149. Woolford TJ, Jones NS. Endoscopic ligation of anterior ethmoidal artery in treatment of epistaxis. J Laryngol Otol. 2000;114:858-860. Elahi MM, Parnes LS, Fox AJ, Pelz DM, Lee DH. Therapeutic Embolization in the Treatment of Intractable Epistaxis. Arch Otolaryngol Head Neck Surg. 1995;121:65-69. Moreau S, De Rugy MG, Babin E, Courtheoux P, Valdazo A. Supraselective Embolization in Intractable Epistaxis: Review of 45 Cases. Laryngoscope. 1998;108:887-888. Tseng EY, Narducci CA, Willing SJ, Sillers MJ. Angiographic embolization for epistaxis: a review of 114 cases. Laryngoscope. 1998;108:615659. Romagnoli M, Marina R, Sordo L, Gaini RM. Indications for selective arterial embolization in the treatment of epistaxis. Acta Otorhinolayngol Ital. 2000;20:330-335. Oguni T, Korogi Y, Yasunaga T, et al. Superselective embolization for intractable idiopathic epistaxis. Br J Radiol. 2000;73:1148-1153. Lund VJ, Howard DJ. A treatment algorithm for the managemenbt of epistaxis in hereditary hemorrhagic telangiectasia. Am J Rhinol. 1999; 13:319-322. Mahoney EJ, Shapshay SM. Nd-YAG laser photocoagulation for epistaxis associated with hereditary hemorrhagic telangiectasia. Laryngoscope. 2005;115:373-375. Karapantzos I, Tsimpiris N, Goulis DG, Van Hoecke H, Van Cauwenberge P, Danielides V. Management of epistaxis in hereditary hemorrhagic telangiectasia by Nd:YAG laser and quality of life assessment using the HR-QoL questionnaire. Eur Arch Otorhinolaryngol. 2005;1. [Epub ahead of print] Bergler W, Sadick H, Gotte K, Riedel F, Hormann K. Topical estrogens combined with argon plasma coagulation in the management of epistaxis in HHT. Ann Otl Rhinol Laryngol. 2002;111:222-228. Farnan TB, Gallagher G, Scally CM. A novel treatment for patients with 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. hereditary haemorragic telengiectasia. J Laryngol Otol. 2002;116:849-850. Hitchings AE, Lennox PA, Lund VJ, Howard DJ. The effect of treatment for epistaxis secondary to hereditary hemorrhagic telangiectasia. Am J Rhinol. 2005;19:75-78. Woolford TJ, Loke D, Bateman ND. The use of a nasal obturator in hereditary haemorragic telangiectasia : an alternative to Young’s procedure. J Laryngol Otol. 2002;116:455-456. Jameson JJ, Cave DR. Hormonal and antihormonal therapy for epistaxis in hereditary hemorrhagic telangiectasia. Laryngoscope. 2004;114:705709. Simmen D, Heinz B. Epistaxis strategy-experiences with the last 360 hospitalizations. Laryngorhinootologie 1998;77:100-106. Goddard JC, Reiter ER. Inpatient management of epistaxis: outcomes and cost. Otolaryngol Head Neck Surg. 2005;132:707-712. Moshaver A, Harris JR, Liu R, Diamond C, Seikaly H. Early operative intervention versus conventional treatment in epistaxis: randomized prospective trial. J Otolaryngol. 2004; 33:185-188. Miller TR, Stevens ES, Orlandi RR. Economic analysis of the treatment of posterior epistaxis. Am J Rhinol. 2005;191:79-82. Peele JC. Control of hemorrhage from the nose and throat. Med Times. 1958;86:1228-1237. Peele JC. Further observations on the use of adrenosem salicylate in the control of hemorrhage from the nose and throat. N C Med J. 1956;17:98103. Peele JC. Adrenosem in the control of hemorrhage from the nose and throat; a preliminary report. AMA Arch Otolaryngol. 1955;61:450-464. Meunier A, Agostini J, Sultan A, Deligne. The antihemorrhagic qualities of dicynone. Its advantages in O. R. L. [in French]. Ann Otolaryngol Chir Cervicofac. 1966;83:446-451. Vinayak BC, Birchall MA, Donovan B, Stafford ND. A randomized double-blind trial of glypressin in the management of acute epistaxis. Rhinology. 1993;31:131-134. Bende M, Pipkorn U. Topical terli- 41 56. 57. 58. 59. pressin (Glypressin) gel reduces nasal mucosal blood flow but leaves ongoing nose-bleeding unaffected. Acta otolaryngol. 1990;110:124-127. White A, O’Reilly BF. Oral tranexamic acid in the manaement of epistaxis. Clin Otolaryngol. 1988;13:11-16. Tibbelin A, Aust R, Bende M, et al. Effect of tranexamic acid gel in the treatment of epistaxis. ORL J Otorhinolaryngol Relat Spec. 1995;57:207209. Viducich RA, Blanda MP, Gerson LW. Posterior epistaxis : clinical features and acute complications. Ann Emerg Med. 1995;25:592-596. Barlow DW, Deleyiannis WB, Pinczower EF. Effectiveness of surgical management of epistaxis at a tertiary care center. Laryngoscope. 1997;107:21-24. Further readings Anand VK. Practical Endoscopic Sinus Surgery. McGraw-Hill, Inc., New York; 1993. Bailey BJ. Head & Neck Surgery – Otolaryngology. Lippincott, Philadelphia; 2001. King HC. A Practical Guide to the Management of Nasal and Sinus Disorders. Thieme Medical Publishers Inc., New York; 1993. Marks SC. Nasal and Sinus Surgery. Saunders, Philadelphia; 2000. Navarro JAC. The Nasal Cavity and Paranasal Sinuses. Springer-Verlag, Berlin; 2001. Abelson TI: Epistaxis. In: Schaefer SD, ed. Rhinology and Sinus Disease. 1st ed. Mosby, New York; 1998:4350. Emanuel JM: Epistaxis. In: Cummings CW, ed. Otolaryngology-Head and Neck Surgery. 3rd ed. Mosby, St. Louis; 1998:852-865. McQueen CT, DiRuggiero DC, Campbell JP, Shockley WW. Orbital osteology: a study of the surgical landmarks. Laryngoscope. 1995;105:783-788. Prof. Bernard BERTRAND ENT and HNS Dept. Cliniques universitaires UCL de MontGodinne avenue Thérasse, 1, B-5530 Yvoir, Belgium. E-mail: [email protected] 42 B. Bertrand et al. CME questions 1. The sphenopalatine artery enters the nose through the sphenopalatine foramen which is situated : A - 10 mm dorsally to a theoretical line drawn between both the posterior attachments of the superior and middle turbinates B - 10 mm dorsally to a theoretical line drawn between both the posterior attachments of the inferior and middle turbinates C - 30 mm dorsally to a theoretical line drawn between both the posterior attachments of the inferior and middle turbinates D - 2 mm – 9 mm anterior to the optic canal E - on the lower third of the septal cartilage 2. Hereditary hemorrhagic telangiectasia is characterized by … except one A B C D E - autosomal dominant disease - formation of telangiectasia and arteriovenous malformation - high incidence of angiofibroma - a lack of elastic or muscular tissue in the vessel - multisystemic involvment 3. Endoscopic sphenopalatin artery ligation can be performed … except one A B C D - for posterior epistaxis - to ligate sphenopalatine artery - to ligate ethmoid anterior artery - after a mucosal incision on a line just posterior to the posterior attachments of the middle and lower turbinates E - under general anaestesia 4. Nasal packings require A B C D E - antihypertensive agents - thrombine - tranexamic acid - mupirocin - oral antibiotherapy 5. A 12 year old boy complaints of nasal obstruction and epistaxis. The demographics and symptoms are most typical of : A - Choanal polyp B - Cystic fibrosis C - Juvenile nasal angiofibroma D - Nasopharyngeal sarcoma E - Osler-Weber-Rendu disease 6. To determine which patients will have coagulopathy associated with epistaxis, the most complete and cost-effective method is : A - CBC, platelet count, and bleeding time B - platelet count C - bleeding time Guidelines to the management of epistaxis 43 D - history, prothrombin time and partial thromboplastin time E - careful history 7. Which one of the following arteries must not be embolized when treating epistaxis ? A B C D E - Anterior ethmoid artery - Sphenopalatine artery - Internal maxillary artery - Facial artery - Descending palatine artery 8. Which one of the followings signals the presence of a traumatic aneurysm ? A B C D E - Severe anterior epistaxis - Facial trauma - Fever and vomiting - Delayed epistaxis - Out of range results for PTT 9. In case of recurrent epistaxis PT normal and PTT long do not suggest one of the following coagulopathies A B C D E - Acquired factor VIII inhibitor - Factor VIII deficiency (hemophilia A) - Factor IX deficiency (hemophilia B) - Factor XI deficiency - Factor VII deficiency 10. Which one of these medical adjuntive therapies is granted of a Ia level of proof ? A B C D E - Adrenochromazone - Etamsylate - Terlipressin - Tranexamic acid - None of the above . Answers: 1B; 2C; 3C; 4E; 5C; 6D; 7A; 8D; 9E; 10E Cardiovasc Intervent Radiol (2014) 37:26–36 DOI 10.1007/s00270-013-0776-y REVIEW Radiological Diagnosis and Management of Epistaxis Antonı́n Krajina • Viktor Chrobok Received: 24 October 2012 / Accepted: 4 October 2013 / Published online: 15 November 2013 Ó The Author(s) 2013. This article is published with open access at Springerlink.com Abstract 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 A. Krajina (&) Department of Radiology, University Hospital Hradec Kralove and Medical Faculty of Charles University, 500 05 Hradec Kralove, Czech Republic e-mail: [email protected] V. Chrobok Department of Otorhinolaryngology and Head and Neck Surgery, University Hospital Hradec Kralove and Medical Faculty of Charles University, 500 05 Hradec Kralove, Czech Republic e-mail: [email protected] 123 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. Keywords Posterior epistaxis Selective percutaneous embolisation Endovascular intervention Introduction 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 A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis 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 [3] The most common factors associated with posterior epistaxis are hypertension [4, 5], acetylsalicylic acid or nonsteroidal anti-inflammatory drug use [6], previous episodes of epistaxis, alcohol use, and anticoagulant use. However, the majority of these cases are idiopathic [7]. 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 [8]. 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 B48 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 [10]. An endoscopic approach has been used for direct electrocauterisation of the active bleeding site and endoscopic ligation of the sphenopalatine and ethmoidal arteries [11]. 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. 27 Endovascular Therapy of Epistaxis Relevant Anatomy 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 [12–15]. The arterial branches involved in epistaxis include the following: the internal maxillary artery (IMA), the facial artery, and the ophthalmic artery (Fig. 1). The other branches of the ECA are rarely involved. The IMA is divided into three parts based on its relationship to the external pterygoid muscle [16, 17] (Table 1). The proximal portion is referred to as the ‘‘mandibular portion’’ and originates behind the neck of the mandible. The second, or pterygoid, portion is in contact with the external pterygoid muscle and varies in its location in relationship to this muscle. It is most commonly located superficial to the external pterygoid muscle, although in one third of cases, it is deep to this muscle. The middle meningeal artery arises in front of the inferior alveolar artery in the superficial variant and behind the inferior alveolar artery in the deep variant. The third, or pterygopalatine, portion is the terminal portion of the IMA, creating a loop within the pterygopalatine fossa. This vessel is the target for endovascular therapy in the treatment of posterior epistaxis (Table 2) (Fig. 2). The sphenopalatine artery, which is the branch of the third part of the IMA, leaves the pterygopalatine fossa by way of the sphenopalatine foramen [18] (Fig. 3). This artery is the major arterial supply to the nasal fossa and enters this fossa posteriorly to the superior meatus. Its lateral nasal branches supply the nasal turbinates, and the medial branches supply the nasal septum [19]. 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 123 28 A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis Fig. 1 Schematic arterial supply of the sinonasal cavity. The majority of the posterior epistaxis episodes arise from the septum. The arterial branches involved in epistaxis include the internal maxillary artery, the facial artery, and the ophthalmic artery (Courtesy of V. Machova) Table 1 Branches of the maxillary artery (modified according Allen et al. [16]) Table 2 Distribution of the third (pterygopalatine) portion of the maxillary artery (modified according Allen et al. [16]) I. First (mandibular) portion Direction a. Anterior tympanic b. Deep auricular c. Middle meningeala d. Accessory meningeala e. Inferior alveolar II. Second (pterygoid) portion a. Deep temporal Branch Route of exit Lateral Posterior superior alveolar Pterygomaxillary fissure Anterior Infraorbital Inferior orbital fissure Inferior Greater palatine Pterygopalatine canal Medial Sphenopalatine Sphenopalatine foramen Posterior Artery of foramen rotundum Foramen rotundum Artery of pterygoid canal Pterygoid canal Pharyngeal Palatinovaginal canal b. Pterygoid c. Masseteric d. Buccal III. Third (pterygopalatine) portion a. Posterior superior alveolar b. Infraorbital c. Greater (descending) palatineb d. Artery to foramen rotunduma e. Artery of pterygoid canal (vidian artery)a f. Pharyngeal g. Sphenopalatineb a Dangerous arteries for embolisation. The pterygoid artery and Vidian artery are considered to be two different branches by Lasjaunias et al. [20] b These arteries are targets for embolisation 123 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. The facial artery is in hemodynamic balance with the other branches of the ECA. The preferred arterial supply is established in accordance with local hemodynamic needs [20]. This situation means that the direction of blood flow through anastomoses among the facial, internal maxillary, and ophthalmic arteries depends on the force and rate of injection, proximal vasospasm, and pre-existing occlusion due to ligation or embolisation [15] (Fig. 4). A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis Fig. 2 A External carotid angiogram of a patient with HHT and multiple episodes of severe epistaxis. The target artery for embolisation is the sphenopalatine artery (double black arrows) and the terminal portion of the facial artery (double white arrows). A microcatheter for embolisation should be placed distal to the middle meningeal artery (small black arrowhead) and accessory meningeal artery (small white arrowhead). B Selective internal maxillary angiogram showing the position of a microcatheter (large white arrow). There are separate mucosal hypervascular areas caused by telangiectasias (small black arrows). C Selective facial angiogram that shows the supply to the nasal cavity 29 Fig. 3 A Angiographic anatomy of the distal internal maxillary artery. The descending palatine artery (black arrows) outlines the posterior wall and floor of the maxillary antrum. The infraorbital artery (double white arrows) enters the orbit through the infraorbital fissure. B Selective distal internal maxillary artery angiogram in a lateral view. C Completion angiogram after embolisation with microparticles (Courtesy of J. J. Vitek) 123 30 A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis 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. Underlying Coagulopathy 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 [22]. A proposed protocol for anticoagulants and epistaxis is as follows [1, 23]: 1. 2. 3. Fig. 4 A Internal carotid angiogram in a patient with recurrent epistaxis. There is a rich collateral supply to the nasal cavity from the ophthalmic artery (arrows). B The cause of such a collateral pathway is previous proximal embolisation of the internal maxillary artery using coils (arrow) (Courtesy of Dr. M. Vavrova) 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 [21]. Endovascular Therapy for Idiopathic Posterior Epistaxis Preprocedure Preparation 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 123 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. The first injection of 7–10 ml of iodinated contrast medium into the CCA is performed using the posterioanterior and lateral views. The angiogram should show any potential arterial pathology at the common carotid artery bifurcation, including atherosclerotic plaque or occlusion of the internal carotid artery (ICA) (Table 3). Because the A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis 31 Table 3 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 Fig. 5 External carotid angiogram showing the supply of the retina (arrows) 2. Perform flow-directed embolisation with PVA particles (250–500 lm) in nondiluted contrast agent using a 1-ml syringe the lateral view (Figs. 4B, 5). Most commonly, supply of the ophthalmic artery from the ECA branches occurs due to collateralisation observed in chronic ICA stenosis or occlusion. The terminal branches of the pterygopalatine segment are best seen in frontal views. 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 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-lm PVA particles if significant contribution to the nasal mucosa is angiographically visible majority of posterior epistaxis episodes treated by embolisation are idiopathic, angiographic findings in these cases may be normal. Specific angiographic signs are rare and may include the following: tumour blush, telangiectasia, traumatic pseudoaneurysm, and even contrast extravasation. Selective ICA angiography may show other sources of epistaxis, such as mycotic or traumatic aneurysm [12, 13]. 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]. A microcatheter that will allow the use of microparticles B500 lm in diameter is placed coaxially in the pterygopalatine segment of the IMA, and angiography is performed to determine if there are any large anastomoses involving the ICA or ophthalmic artery. The most useful projection to evaluate the ECA, IMA, and retinal blush is 123 32 A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis preserve the distal supply of the terminal alar artery, which supplies the skin of the nose. The PVA microparticles 200–500 lm 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 [26]. 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 [27–29]. 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 [30]. 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. Clinical Success The primary success rates of epistaxis embolization therapy range from 71 to 95 % in the literature (Table 4). The success rate is influenced by the embolisation protocol used. Embolisation of the bilateral distal IMAs and ipsilateral distal facial artery with 200-lm PVA microparticles 123 significantly decreases short-term failure rates and carries a very low risk for ischemic complications. The rate of early recurrence decreases with embolisation of more arteries [22]. Patients taking oral anticoagulants or antiplatelet medication are noted to have greater rate of early rebleeding than patients not taking these medications [22]. 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 [30]. 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 [11]. There are retrospective studies available comparing IMA ligation (with or without ethmoid artery ligation) [11] with PVA embolisation of the bilateral IMAs and ipsilateral facial artery [31] for the treatment of refractory epistaxis. The embolised arteries were not specified in one of those studies [11]. The success rates for IMA ligation and embolisation were 89 and 94 %, respectively [31]. The other study reported success rates of 73 and 79 %, respectively [11]. 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 [15]. 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. A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis 33 Table 4 Review of studies on posterior epistaxis treated with embolisation First author (reference) Yeara Vı́tek [30] 1991 30 62 34 Elden [32] 1994 97 53 Elahi [57] 1995 57 53.1 Tseng [7] 1998 112 Moreau [58] 1998 45 48.8 Leppanen [59] 1999 37 Oguni [60] Andersen [33] 2000 2005 Christensen [61] Sadri [34] No. of patients Mean age (year) Embolic material for ECA branches Immediate clinical success (%)b Severe complications (%)c GS 87 3.3 hemiparesis 108 PVA 88 2 stroke, skin slough 54 PVA 91 6 stroke PVA, GS 91 0.9 stroke 46 PVA 95 4 53 38 PVA, coils 89 0 37 22 57.3 59 40 30 GS PVA, spheres 95 87 0 5 nose necrosis 2005 70 59.1 70 PVA, GS, coils 87 1 stroke 2006 14 57 15 PVA 71 7 nose necrosis, palate necrosis Fukutsuji [62] 2008 22 56.8 23 GS, coils 77.3 0 Strach [35] 2011 48 58.7 53 PVA, coils 93.5 4 nose necrosis, hemiparesis Gottumukkala [56] 2013 84 63.8 85 PVA 89 1 55 No. of procedures 114 GS = gelatin sponge a The table includes studies with selective embolisation using microcatheters b The overall clinical success also depended on the proportions of patients with HHT c Definitions of severe stroke were variable Complications 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– 35]. Smaller particles (45–150 lm) carry a greater risk of collateral tissue ischemia, including ischemia of the vasa nervorum [36]. The most frequent causes of neurologic deficit and blindness [37] 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 [39]. Management of Angiographically Proven Causes of Epistaxis Traumatic Epistaxis The clinical presentation of traumatic epistaxis is lifethreatening haemorrhage at the time of trauma [40]. CT imaging is indicated in all cases of suspected arterial epistaxis. Angiogram may show focal active extravasation, pseudoaneurysm [41], 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 [42]. When trauma or infection [43] 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 [44]. Arterial injuries during craniofacial surgery are uncommon but have been well described [45–48]. 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 lifethreatening. 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 123 34 A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis 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 [38]. Since the introduction of embolisation of JNA by Roberson [49], 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 [13]. 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 [50]. 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 [51]. 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 longterm effect [32, 52]. Conclusion 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 [53–56]. 123 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 [22]. 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 Antonı́n Krajina and Viktor Chrobok have no conflicts of interest. Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. References 1. 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Ashwin PT, Mirza S, Ajithkumar N, Tsaloumas MD (2007) Iatrogenic central retinal artery occlusion during treatment for epistaxis. Br J Ophthalmol 91(1):122–123 38. Lasjaunias P (1980) Nasopharyngeal angiofibromas: hazards of embolisation. Radiology 136:119–123 39. Duncan IC, Spiro FI, van Staden D (2004) Acute ischemic sialadenitis following facial artery embolization. Cardiovasc Interv Radiol 27(3):300–302 40. Bynoe RP, Kerwin AJ, Parker HH III et al (2003) Maxillofacial injuries and life-threatening haemorrhage: treatment with transcatheter arterial embolisation. J Trauma 55:74–79 41. Kurata A, Kitahara T, Miyasaka Y, Ohwada T, Yada, Kan S (1993) Superselective embolisation for severe traumatic epistaxis caused by fracture of the skull base. Am J Neuroradiol 14:343–345 42. Komiyama M, Misao N, Masanori K, Tatsuhiro S, Arito K (1998) Endovascular treatment of intractable oronasal bleeding associated with severe craniofacial injury. J Trauma 44:330–334 43. Hurst RW, Judkins A, Boler W, Chu A, Loevner LA (2001) Mycotic aneurysm and cerebral infarction resulting from fungal sinusitis: imaging and pathologic correlation. Am J Neuroradiol 22(5):858–863 44. Chen D, Concus AP, Halbach VV, Cheung SW (1998) Epistaxis originating from traumatic pseudoaneurysm of the internal carotid artery. Diagn Endovasc Ther 108:326–331 45. Raymond J, Hardy J, Czepko R, Roy D (1997) Arterial injuries in transsphenoidal surgery for pituitary adenoma: the role of angiography and endovascular treatment. Am J Neuroradiol 18:655–665 46. Duncan IC, Fourie PA (2004) Acute severe epistaxis due to iatrogenic maxillary pseudoaneurysm: emergency control of haemorrhage by carotid compression and early recurrence after coil embolisation. Interv Neuroradiol 10:269–272 47. Schmerber S, Vasdev A, Chahine K, Tournaire R, Bing F (2008) Internal carotid false aneurysm after thermocoagulation of the Gasserian ganglion. Otol Neurotol 29:673–675 48. Schröck A, Jako M, Strach K et al (2012) Transarterial endovascular treatment in the management of life-threatening intraand postoperative haemorrhages after otorhinolaryngological surgery. Eur Arch Otorhinolaryngol 269:1677–1683 49. Roberson GH, Biller H, Sessions D et al (1972) Presurgical internal maxillary artery embolisation in juvenile angiofibroma. Laryngoscope 82:1524–1532 50. Shovlin CL, Guttmacher AE, Buscarini E et al (2000) Diagnostic criteria for hereditary hemorrhagic telangiectasia (Rendu–Osler– Weber syndrome). Am J Med Genet 91:66–67 51. Guttmacher AE, Marchuk DA, White RI Jr (1995) Hereditary hemorrhagic telangiectasia. N Engl J Med 333(14):918–924 52. Weaver EM, Chaloupka JC, Putman C et al (1999) Effect of internal maxillary arterial occlusion on nasal blood flow in swine. Laryngoscope 109:8–14 53. Viducich RA, Blanda MP, Gerson LW (1995) Posterior epistaxis: clinical features and acute complications. Ann Emerg Med 25(5):592–596 54. Godard JC, Reiter ER (2005) Inpatient management of epistaxis: outcomes and cost. Head Neck Surg 132:707–712 123 36 A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis 55. Nikolaou G, Holzman D, Soyka MB (2013) Discomfort and the cost in epistaxis treatment. Eur Arch Otorhinolaryngol 270:2239–2244 56. Brinjikji W, Kallmes DF, Cloft HJ (2013) Trend is epistaxis embolisation in the United States: a study of the Nationwide Inpatient Sample 2003–2010. J Vasc Interv Radiol 24:969–973 57. Elahi MM, Parnes LS, Fox AJ, Pelz DM, Lee DH (1995) Therapeutic embolisation in the treatment of intractable epistaxis. Arch Otolaryngol Head Neck Surg 121:65–69 58. Moreau S, De Rugy MG, Babin E, Courtheoux P, Valdazo A (1998) Superselective embolisation in intractable epistaxis: review of 45 cases. Laryngoscope 108:887–888 123 59. Leppänen M, Seppänen S, Laranne J, Kuoppala K (1999) Microcatheter embolisation of intractable idiopathic epistaxis. Cardiovasc Interv Radiol 22:499–503 60. Oguni T, Korogi Y, Yasunaga T et al (2000) Superselective embolisation for intractable idiopathic epistaxis. British J Radiol 73:1148–1153 61. Christensen NP, Smith DS, Barnwell SL, Wax MK (2005) Arterial embolisation in the management of posterior epistaxis. Otolaryngol Head Neck Surg 1333:748–753 62. Fukutsuji K, Nishiike S, Aihara T et al (2008) Superselective angiographic embolisation for intractable epistaxis. Acta Otolaryngol 128:556–560 Braz J Otorhinolaryngol. 2013;79(1):59-64. DOI: 10.5935/1808-8694.20130011 original article BJORL .org Surgical treatment of severe epistaxis: an eleven-year experience Paulo Saraceni Neto1, Leonardo Mendes Acatauassu Nunes2, Luis Carlos Gregório3, Rodrigo de Paula Santos4, Eduardo Macoto Kosugi5 Keywords: epistaxis; natural orifice endoscopic surgery; otorhinolaryngologic surgical procedures. Abstract E pistaxis is one of the most prevalent emergencies in ENT practice, and its surgical treatment is part of the routine at services for emergency care, especially in cases refractory to clinical procedures. Objective: To analyze the profile of patients and the results this service has had in the surgical treatment of epistaxis for the last 11 years. Method: Data from 98 patients submitted to surgery for epistaxis between 2000 and 2011 were analyzed retrospectively. Results: Most in the sample were males, and mean age was around 46 years. Hypertension was identified in 58% of patients, and most events occurred during fall and winter. The re-bleeding rate was 13.27%. Conclusion: This study concluded that the surgical treatment for epistaxis, when indicated, had good success rates and low incidence of complications. In our service, it remains as the gold-standard procedure for nosebleeds refractory to initial management measures. 1 ENT at UNIFESP-EPM (Fellow in Rhinology at UNIFESP-EPM). ENT at UNIFESP-EPM (Assistant Physician in the Rhinology Sector at UNIFESP-EPM). 3 PhD in Medicine from UNIFESP-EPM (Head of the Department of ENT & HNS at UNIFESP-EPM). 4 PhD in Sciences from UNIFESP-EPM (Head of the Rhinology Sector at UNIFESP-EPM). 5 PhD in Sciences from UNIFESP-EPM (Coordinator of the Rhinology Fellowship and Lead Preceptor in the ENT Medical Residency at UNIFESP-EPM). Division of Rhinology, Department of Otorhinolaryngology and Head and Neck Surgery UNIFESP. Send correspondence to: Eduardo Macoto Kosugi. Rua Prof. João de Oliveira Torres, nº 416. Jd. Anália Franco. São Paulo - SP. Brazil. CEP: 03337-010. Tel: (11) 2671-5883. E-mail: [email protected] Paper submitted to the BJORL-SGP (Publishing Management System - Brazilian Journal of Otorhinolaryngology) on August 18, 2012; and accepted on November 4, 2012. cod. 10394. 2 Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013 http://www.bjorl.org / e-mail: [email protected] 59 INTRODUCTION Epistaxis is one of the most frequent emergencies in ENT care. The prevalence rate of this potentially risky occurrence in the general population is of approximately 12%1. However, only 10% of the patients with epistaxis seek medical care, and the initial measures taken to treat these subjects usually suffice in handling nosebleeds. Among such measures are: keeping the airways patent, attaining hemodynamic stability, and packing the nose - an effective procedure in most cases, but unlike many think, a method that introduces considerable risk of morbidity2. Yet, approximately 1% of the patients require surgical intervention to manage epistaxis3,4. Several procedures to treat epistaxis refractory to clinical management have been described in the literature, such as irrigation with warm water, chemical and electrical cauterization of the nasal mucosa, arterial embolization, open and endoscopic artery ligation surgery5-7. The ligation of the distal arterial branches has been performed more recently to prevent direct and antegrade circulation of the carotid system that irrigates the nasal cavity and known to have plenty anastomoses. Consequence, the ligation of the maxillary or external carotid artery have been less used due to reduced efficacy and increased morbidity6,8. The vessels most frequently ligated to that end are the sphenopalatine and anterior ethmoidal arteries. The sphenopalatine artery ligation procedure was first described by Prades in 1970 through microsurgery. Only in 1992, with the development and refinement of nasal endoscopic surgery, did Budrovich & Saetti report the use of an endoscope to perform the procedure8. The anterior ethmoidal artery ligation technique is older. It was described in 1946 by Weddell, and was performed through external access via Lynch incision3. Potential consequences of the external access approach such as scars, edema, and facial ecchymosis led to the study and development of endoscopic techniques to approach this artery4. This study aimed to present data from the ENT Residency Program regarding the surgical management of severe epistaxis performed between June 2000 and June 2011. were no exclusion criteria. This study was approved by the institution’s Research Ethics Committee and given permit 87081. The patients seen for epistaxis at our service were submitted to the initial emergency protocol, which included airway and respiratory care, along with hemodynamic stabilization procedures. Then, they were offered specific care for epistaxis such as suction of clots and administration of topical vasoconstrictors to identify the sites of bleeding and elect the best course of therapy among the options of chemical cauterization with 70% trichloroacetic acid and anterior or anteroposterior nose packing. The patients submitted to surgery were the ones who still bled in spite of the nose packing, who bled soon after nose packing removal, and those submitted to anteroposterior nose packing without clinical contraindication for surgery. Surgery was carried out with the patients under general anesthesia by third-year medical residents supervised by medical doctors from the Rhinology Sector or attending physicians from the ENT emergency care unit. Ligation and/or cauterization of the sphenopalatine artery branches was carried out by transnasal endoscopy. Cauterization of the anterior ethmoidal artery was preferentially performed through the external approach (Lynch incision) with the aid of an endoscope, and occasionally by transnasal endoscopy. In our service we approach the sphenopalatine artery or the sphenopalatine and anterior ethmoidal arteries, depending on the site of bleeding. The following data were considered in the definition of the profile of our patients: age, gender, and present comorbidities. Bleeding-related characteristics were also considered, such as side, possible etiology, admission blood tests (hemoglobin, hematocrit, and platelet count), and need for blood transfusion. The following were considered in regards to surgery: date of the procedure, approached artery, number of approached branches of the sphenopalatine artery, time of surgery, complications, surgery effectiveness, and failure. The seasonality of cases of severe epistaxis was also analyzed. METHOD RESULTS This retrospective longitudinal study included the review of the medical charts of patients seen at the ENT emergency care unit for severe epistaxis and treated surgically between June 2000 and June 2011. Severe epistaxis was defined as a life-threatening episode of nasal bleeding, usually of posterior origin, requiring immediate anteroposterior nose packing to attain hemodynamic stability9,10. All patients treated endoscopically for severe epistaxis through sphenopalatine and/or anterior ethmoidal artery ligation were included. There The charts of 109 patients submitted to surgery for severe epistaxis between June 2000 and June 2011 were included. Seven charts were excluded for lack of information and another four subjects submitted to nose packing under general anesthesia were not included. The characteristics of the patients enrolled in the study are shown on Table 1. The characteristics related to bleeding can be seen on Table 2. Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013 http://www.bjorl.org / e-mail: [email protected] 60 Table 1. Characteristics of enrolled patients. Data Unit Age Years Gender Comorbidities Table 3. Blood transfusion characteristics. Value Data Unit Hemoglobin g/dL Mean 46.68 Mean 11.42 SD 15.28 SD 2.75 Minimum 13 Minimum 5.6 Median 48 Median 11.1 Female 28 (28.57) SD 8.2 SHT 57 (58.16) Minimum 12.2 Chronic alcohol abuse 10 (10.2) Median 33.05 DM 7 (7.14) Maximum 49.5 Chronic use of ASA 5 (5.1) Mean 241.779,41 120.787,32 Hematocrit % Platelet count N/mL Liver disease 4 (4.08) SD CKD 3 (3.06) Minimum 42.000 NHL 2 (2.04) Median 228.500 Arrhythmia 2 (2.04) Hypothyroidism 2 (2.04) Heart disease 1 (1.02) 1 (1.02) Maximum 972.000 Blood transfusion N (%) Yes 21 (21.43) No 77 (78.57) Transfusion patients PRBC units Mean 2.81 N: number; %: percentage; SD: standard deviation; SHT: systemic hypertension; DM: diabetes mellitus; ASA: acetylsalicylic acid; CKD: chronic kidney disease; NHL: non-Hodgkin’s lymphoma. Table 2. Features of epistaxis. N (%) Location Etiology N (%) N (%) 33.82 70 (71.43) Thrombocytosis Side 16.3 Mean 81 Male N (%) Unit Maximum Maximum N (%) Data Value SD 1.12 Minimum 2 Median 2 Maximum 6 N: number; %: percentage; SD: standard deviation; PRBC: packed red blood cells. Value Right 48 (48.98) Left 35 (35.71) Bilateral 15 (15.31) Data Anterior 14 (14.29) Approached arteries Table 4. Characteristics of initial surgical approach. Values N (%) Posterior 35 (35.71) Sphenopalatine 1 branch 93 (86.11) Not identified 49 (50) Sphenopalatine 2 branches 7 (6.47) Undefined 64 (65.31) Sphenopalatine 3 branches 1 (0.95) Hypertensive peak 19 (19.39) Anterior Ethmoidal 7 (6.47) Nose surgery FU 5 (5.1) Total 108 (100) Trauma 5 (5.1) Operated patients Coagulopathy 4 (4.08) Success 85 (86.73) Nasal tumor 2 (2.04) Failure 13 (13.27) Rendu-Osler-Weber 1 (1.02) Total 98 (100) N: number; %: percentage; FU: follow-up. N: number; %: percentage. Blood test and transfusion data can be verified on Table 3. The 98 patients enrolled in the study underwent surgery under general anesthesia, and had solely their sphenopalatine arteries or their sphenopalatine and anterior ethmoidal arteries approached, on one or both sides. Some patients had more than one artery approached. The data on the first procedure the patients underwent can be seen on Table 4. Epistaxis was successfully managed in 85 cases (86.73%). Six (46.15%) of the 13 patients with failed surgery bled within 24 hours of surgery. Table 5 shows what was done for the 13 patients whose first procedures failed. In the 13 patients with failed first surgery, only one branch of the sphenopalatine artery was found. More anterior ethmoidal artery ligations were indicated after the failure of the first procedure (eight of the nine re-operated Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013 http://www.bjorl.org / e-mail: [email protected] 61 Table 5. Conduct in failed surgery. Conduct N (%) Nose packing 4 (30.77) Sphenopalatine Revision 1 (7.69) Anterior ethmoidal + Sphenopalatine Revision 8 (61.54) Total 13 (100) N: number; %: percentage. patients) than as a first procedure (seven of 98 operated patients). Indication of anterior ethmoidal artery surgery was significantly higher in reoperations, as seen on Table 6. Graph 2. Distribution of surgical procedures per season. Table 6. Anterior ethmoidal artery. Time of surgery N (%) Initial approach 7 (46.67) Approach after failure 8 (53.33) Total 15 (100) Four complications (4.08%) were recorded. Two (2.04%) related to surgery (septum perforation and amaurosis), one (1.02%) to anesthesia (death by acute myocardial infarction during anesthesia recovery), and one (1.02%) to hospitalization (hospital-acquired pneumonia). N: number; %: percentage. DISCUSSION Hospitalization and surgery times are shown on Table 7. The ninety-eight surgical patients enrolled in this study represent a significant series when compared to other papers in the literature2,3,6,11,12. Patients with severe epistaxis are usually between the third and eighth decade of life, and the most numerous age group comprehends subjects in their seventies and eighties2,3,6,8. The mean age of the subjects in our study was lower (46 years), probably a reflection of the fact that endoscopic surgery was offered to all patients with anteroposterior nose packing, and not only to cases in which surgery failed. There is a slight predominance of males in studies on epistaxis1-3,5. In our study, males prevailed by a ratio of 2.5:1. The side of bleeding has been recently discussed, and a predilection for right epistaxis - albeit without statistical significance - was observed in a group of 326 patients11. Our study presented similar results, as 48.98% of the patients had right nasal fossa involvement (n = 48), 35.71% had left nosebleeds (n = 35), and 15,.31% had bilateral epistaxis (n = 15). In terms of the site of bleeding - anterior, posterior, or diffuse - the charts revealed that posterior bleeds were more frequent, with 35.71% (n = 35), against 14.29% (n = 14) of anterior nosebleeds. The remaining 50% did not have defined bleed sites or were described as ‘diffuse’. Most nosebleeds are known to occur in anterior sites associated with Kiesselbach’s plexus and account for approximately 85% of all cases1,11, but our study indicated a preponderant role of posterior bleeds in severe epistaxis. The etiology of severe epistaxis cannot be defined for all cases. There is confusion between predisposing and aggravating factors, and they do not necessarily establish a causal link to bleeding, which adds to the difficulty of comparing this study to others8,11. Clear nosebleed Table 7. Length of hospitalization and surgery. Duration Hospitalization (days) Surgery (minutes) Value Mean 3.38 SD 4.53 Minimum 1 Median 2 Maximum 41 Mode 2 Mean 113.48 SD 44.31 Minimum 20 Median 110 Maximum 250 SD: standard deviation. The distribution of procedures and months in which they were performed can be seen on Graphs 1 and 2. Graph 1. Distribution of surgical procedures per month. Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013 http://www.bjorl.org / e-mail: [email protected] 62 etiology is established for only 15% of the subjects, and idiopathic cases are more prevalent8. In our study, etiology was defined in 34.69% (n = 34) of the cases of epistaxis. The diagnoses included: hypertensive peaks (19.39%), bleeds following recent nose and paranasal sinus surgery (5.1%), trauma (5.1%), coagulopathy (4.08%), nasal tumors (2.04%), and hereditary hemorrhagic telangiectasia (1.02%). The treatment for severe epistaxis of known etiology must include, whenever possible, solutions for the cause of the problem; for example, the management of hypertensive peaks and reversal of coagulopathy13. Coagulopathy has been traditionally seen as a contraindication to surgery, but the ligation or cauterization of the branches of the sphenopalatine artery have provided for satisfactory results in these cases9. In epistaxis caused by nasal tumors, the role of arterial ligation alone is more limited. Treatment of such cases usually involves the resection of the tumor that originated the nosebleed, in addition to artery ligation13. Artery ligation is not the main option to treat hereditary hemorrhagic telangiectasia, and was used in one of our patients solely because of severe epistaxis, and not for the underlying condition. The most prevalent comorbidity found in the studied population was systemic hypertension, seen in 58.16% of the patients (n = 57), as similarly reported by other authors3,8. Despite the difficulties establishing a causal correlation between systemic hypertension and epistaxis and even more so severe epistaxis - it is important to stress that the prevalence rate seen in the studied population was considerably higher than the rates observed in the Brazilian population, which range around an estimated 20%14. Other aggravating factors and conditions related to nosebleeds include diabetes mellitus, chronic alcohol abuse accompanied or not by alcoholic liver disease, smoking, heart arrhythmias, tumors, use of antiplatelet drugs, anticoagulants, and illicit drugs such as cocaine. These factors have also been cited by other authors in varying degrees of relevance, although never at the same level of importance as systemic hypertension1,2,11. This study also assessed the hemodynamic impact of surgical cases of epistaxis. In some cases, this information was essential for surgical indication. It should be noted that the top platelet count seen in our study due to a case of thrombocytosis without clinical repercussions pulled up the mean value of this variable. The variation of blood test results observed in this study was similar to previous reports in the literature6,12. Low platelet count has been considered an isolated risk factor for early rebleed in patients submitted to epistaxis surgery1, but our study failed to reproduce such finding. The literature also indicates that 50% of the patients with epistaxis submitted to surgery require blood transfusion1,6,12, whereas in our study only 21.4% of the patients (n = 21) needed transfusion. A mean 2.8 units of packed red blood cells were administered to patients requiring transfusion. The number of arterial branches in the sphenopalatine foramen has also been a topic of controversy. A study done on cadavers submitted to nasal endoscopy showed that 67.21% of the nasal fossae had one arterial trunk leaving the sphenopalatine foramen, 21.31% had two branches, and 11.47% had three15. In our study, one branch in the sphenopalatine foramen was seen in 86.11% of the nasal fossae. The difference against the literature may be explained by the greater difficulty dissecting the sphenopalatine foramen during surgery in live patients than in fresh cadavers. Success rates were quite good, and rebleeds were seen in 13.27% (n = 13) of the patients. Most patients in this situation (n = 8) were reoperated and had the hemostasis of the sphenopalatine artery territory revised and the anterior ethmoidal artery (AEA) ligated. All rebleeds had one branch of the sphenopalatine artery identified. A study by Holzmann showed similar results, as higher rebleed rates were seen in cases in which only the lateral branches of the sphenopalatine artery were occluded2. This data supports the need to thoroughly explore the sphenopalatine foramen, in an active search for all branches arising from it. Holzmann also reported increased success rates when dissection and occlusion of the septal branches of this vessel were performed. Rebleeds occurring in those cases can be accounted for by the antegrade flow that occurs mainly in the septal territory, an area with many anastomoses between different arterial systems2. AEA ligation to manage epistaxis is still controversial. Although many authors believe that this vessel should be approached in the first procedure along with the sphenopalatine artery and its branches, most papers show this technique being used to manage rebleed cases2,16. The improvement of the techniques used to endoscopically approach the AEA may facilitate the indication of AEA ligation as the procedure of choice. The approach in use today includes external access using the Lynch incision which, aside from a scar, may leave other complications such as facial edema and epiphora - possibly the reasons why surgeons are no longer opting to indicate this procedure initially4. Time of hospitalization in the revision cases shows that, in addition to being effective, surgery does not lead to prolonged hospital stays. The mean hospital stay length was three days, as also reported in the literature8,16. The mean time of hospitalization was overestimated in our study, as one patient with complications had to stay in for 41 days. The mode, however, was two days of hospitalization. Surgery mean length was one hour and 53 minutes. The influence of weather conditions in the incidence of epistaxis has been analyzed by a number of authors17,18. However, controversy and contradicting results still abound. In our sample, more cases were seen in the fall and winter months. However, one cannot state that Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013 http://www.bjorl.org / e-mail: [email protected] 63 such finding is truly related to the weather. An inventory of meteorological data for each year of the study would have to be analyzed along with the variations in temperature and humidity before statements of this sort could be made. The observed complication rate of 4.08% shows how safe the employed procedures were, mainly if one takes into account that only half of these complications were related to surgery. The main of them, a case of amaurosis, may be explained by the lack of experience of the surgeon while performing electrocoagulation in an area too close to the nerve bundles of the orbit. 5.Novoa E, Schlegel-Wagner C. Hot water irrigation as treatment for intractable posterior epistaxes in an out-patient setting. J Laryngol Otol. 2012;126(1):58-60. 6. Santos RP, Leonhardt FD, Ferri RG, Gregório LC. Ligadura endoscópica endonasal da artéria esfenopalatina para epistaxe severa. Rev Bras Otorrinolaringol. 2002;68(4):511-4. 7.Kamani T, Shaw S, Ali A, Manjaly G, Jeffree M. Sphenopalatine-sphenopalatine anastomosis: A unique case of intractable epistaxis, safely treated with microcatheter embolization: a case report. J Med Case Rep. 2007;1:125. 8.Page C, Biet A, Liabeuf S, Strunski V, Fournier A. Serious spontaneous epistaxis and hypertension in hospitalized patients. Eur Arch Otorhinolaryngol. 2011;268(12):1749-53. 9. Shah AG, Stachler RJ, Krouse JH. Endoscopic ligation of the sphenopalatine artery as a primary management of severe posterior epistaxes in patients with coagulopathy. Ear Nose Throat J. 2005;84(5):296-7,306. 10.Barlow DW, Deleyiannis WB, Pinczower EF. Effectiveness of surgical management of epistaxis at a tertiary care center. Laryngoscope. 1997;107(1):21-4. 11.Reiss M, Reiss G. Epistaxis: some aspects of laterality in 326 patients. Eur Arch Otorhinolaryngol. 2012;269(3):905-9. 12.Rabelo FA, Prado VB, Valera FC, Demarco RC, Tamashiro E, Lima WT. Surgical treatment of nasal packing refractory epistaxis. Bras J Otorhinolaryngol. 2009;75(3):335-9. 13.Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North Am. 2008;41(3):525-36. 14.Passos VMA, Assis TD, Barreto SM. Hipertensão arterial no Brasil: estimativa de prevalência a partir de estudos de base populacional. Epidemiol Serv Saúde. 2006;(15):35-45. 15.Pádua FG, Voegels RL. Severe posterior epistaxis - endoscopic surgical anatomy. Laryngoscope. 2008;118(1):156-61. 16.Rockey JG, Anand R. A critical audit of the surgical management of intractable epistaxis using sphenopalatine artery ligation/diathermy. Rhinology. 2002;40(3):147-9. 17.Rezende GL, Granjeiro RC, Furtado PL, Pinheiro GB, Nakanishi M. Is dry climate related with hospitals admissions for epistaxis? Int Arch Otorhinolaryngol. 2009;13(2):172-7. 18.Danielides V, Kontogiannis N, Bartzokas A, Lolis CJ, Skevas A. The influence of meteorological factors on the frequency of epistaxis. Clin Otolaryngol Allied Sci. 2002;27(2):84-8. CONCLUSION This study presented the 11 years of experience of our service in surgically managing severe epistaxis with a success rate of 86.73%. In our series, careful identification of all arterial branches in the sphenopalatine foramen and early anterior ethmoidal artery ligation were identified as contributing factors to higher success rates. REFERENCES 1.Nouraei SA, Maani T, Hajioff D, Saleh HA, Mackay IS. Outcome of endoscopic sphenopalatine artery occlusion for intractable epistaxis: a 10-year experience. Laryngoscope. 2007;117(8):1452-6. 2. Holzmann D, Kaufmann T, Pedrini P, Valavanis A. 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