Initial Assessment

The amount of blood loss should be estimated (the physician should ask about whether the patient has lost enough to soak a handkerchief, a facecloth, or a towel; the last would indicate a significant loss), and over what period (a regular minor bleed can cause anemia). A clinical assessment of the patient’s cardiac status and circulating blood volume should include looking to see if the patient is pale, sweating, or cool, or has tachycardia; any of these findings would indicate significant hypovolemia. A reduction in blood pressure is often a late sign, particularly in young people, who can maintain blood pressure until the circulatory volume is critical.

Obtaining intravenous access, checking for and correcting any clotting abnormalities, and taking blood for “group and save” and/or crossmatching may be required. In our unit patients admitted via the emergency department can be “fast-tracked” to the otorhinolaryngologic emergency unit if stable (Box 45-1). This practice helps avoid unnecessary and counterproductive nasal packing in the emergency department as well as transfer of patients before they are fit enough to travel.

First aid measures include asking the patient to apply constant firm pressure over the lower (non-bony) part of the nose for 20 minutes and to lean forward with the mouth open over a bowl so that further blood loss can be estimated. Otherwise, blood dripping postnasally will be swallowed, and the next warning sign of a serious loss could be several hundred milliliters of blood being vomited up.

It is important to establish both the site and the cause (Box 45-2; Figs. 45-6 to 45-12) of bleeding. The philosophy of this approach can be summarized as follows:

Figure 45-6. Endoscopic view in Wegener’s granulomatosis.

Figure 45-7. Postoperative severe epistaxis that has not been stopped by packing. Endoscopic investigation has determined that bleeding is coming from the septal branch, which was cut by sphenoidotomy performed on the right side.

Figure 45-8. Pyogenic granuloma on the septum, right side nasal vestibule.

Figure 45-9. Endoscopic view of an angiofibroma occluding the right nasal cavity and choana.

Figure 45-10. Squamous cell carcinoma of the right nasal cavity originating from the septum and occluding the olfactory cleft and middle meatus.

Figure 45-11. Septal perforation causing epistaxis and crusting.

Figure 45-12. Total septal perforation causing epistaxis and crusting in a patient with cocaine abuse.

The clinician must remember that epistaxis is frequently idiopathic but can be a manifestation of a possible underlying pathology (see Fig. 45-12). Your patient should undergo further investigation according to the history.

Headlamp Examination Using Local Anesthesia—Initial Overview

The key to controlling most epistaxis is to find the site of the bleeding, and although chemical cautery with silver nitrate can be used, bipolar diathermy is more effective for stopping the bleeding. Protection from blood contamination is important. A plastic apron for both parties is helpful in order to avoid staining of clothes, and eye protection is advisable if there is active bleeding because some patients have a reflex to blow away any fluid dripping down the upper lip, which can create a bloody aerosol. Once the clots have been sucked out, the nasal airway should be inspected, initially with a headlamp and then, if the bleeding point cannot be located, with an endoscope.

Epistaxis in Children

Young children usually bleed from a vessel just inside the nose at the mucocutaneous junction on the septum, and the bleeding invariably stops spontaneously. In children with epistaxis in whom no prominent vessel can be seen, the regular local application of a cream can help,¹² but petroleum jelly (Vaseline) alone does not.¹³ A Cochrane Collaboration systematic analysis of the efficacy of topical treatments for idiopathic epistaxis in children concluded that the best treatment still must be defined.¹⁴ As many as 5% to 10% of children with recurrent nosebleeds may have undiagnosed von Willebrand’s disease.^15,16 Children who have leukemia or are undergoing chemotherapy often have epistaxis associated with thrombocytopenia. Older children, adolescents, and adults often bleed from Little’s area or a maxillary spur.

Epistaxis in Adults

The caudal end of the septum, where several branches of the external and internal carotid anastomose in Little’s area or Kiesselbach’s plexus, is the most common site of bleeding in adults.¹⁷ Less commonly bleeding, comes from further back on the septum, and a septal deviation may make it difficult to visualize (Fig. 45-13). Some patients with seasonal allergic rhinitis complain of more nosebleeds in the hay fever season, and topical nasal steroids aggravate the bleeding in approximately 4% of users. Many people believe that a nosebleed signifies a release of pressure and may herald a stroke, and it is important for the clinician to address these anxieties for the patient. Although many patients are found to be hypertensive during nosebleeds, few remain so on follow-up. The association between hypertension and epistaxis is disputed.¹⁸ Many clinicians report that hypertension is not related to nosebleed.^19–21 However, nosebleeds in patients with hypertension are more likely to lead to admission and to be associated with comorbidity.²²

Figure 45-13. Endoscopic view of the bleeding site on the septum in epistaxis, just opposite the left middle turbinate in the olfactory cleft.

Bleeding disorders can manifest de novo as nosebleeds, although this situation is rare. A range of drugs has been linked with epistaxis, warfarin being one of the most common.^3,23 Nearly a third of patients admitted with epistaxis who were taking warfarin had an international normalized ratio (INR) value above the upper limit of the therapeutic range.²⁴ The need to reverse anticoagulation is uncertain as long as the INR value is within the therapeutic range.²⁵ In over-anticoagulated patients, fresh frozen plasma, clotting factor extracts, and vitamin K help. Vitamin K takes more than 6 hours to work, however, and it can delay anticoagulation for 7 days after warfarin is started. If the INR value is greater than 4, the warfarin should be stopped, and fresh frozen plasma given.²³ Clotting factor extracts should be given with extreme caution because of the risk of thromboembolic complications. Tranexamic acid, an antifibrinolytic agent, has not been shown to help.²⁶ Other drugs associated with bleeding are aspirin, which interferes with platelet function for up to 7 days, clopidogrel, and nonsteroidal anti-inflammatory drugs.^27,28 In patients who do not have a history of a bleeding disorder or undergoing anticoagulant therapy, routine clotting studies do not add to the management.^22,24 There is a higher incidence of epistaxis in patients with a high alcohol intake, even when there is no laboratory evidence of a coagulation abnormality.^29,30

Topical Treatment

A randomized controlled trial of silver nitrate cautery with topical antiseptic nasal carrier cream versus topical alone showed both to be effective.³¹ A study of patients applying weekly triamcinolone 0.025% and daily petroleum jelly reported that 89% of patients had no further bleeding.³² Various hemostatic compounds have been used but without consistent evidence of their efficacy. Collagen-derived particles with bovine-derived thrombin have been found to be better than nasal packs.³³

Cautery

Most anterior epistaxis can be controlled with identification of the bleeding point and cautery using a headlamp. The vast majority of posterior bleeding sites can be identified by endoscopy without the use of general anesthesia.³⁴ The majority of posterior idiopathic bleeds are from the septum, usually from the septal branch of the sphenopalatine artery as it runs submucosally (Fig. 45-14), although some workers report bleeding from the lateral aspect of the middle or inferior meatus or the posterior end of the turbinates (Fig. 45-15).³⁵ When the site of bleeding cannot clearly be identified with a headlamp, the use of a rigid nasal endoscope by an experienced endoscopist is best. The key is to identify the site of the bleeding and gain control using silver nitrate cautery or bipolar suction diathermy. Studies have shown that the use of endoscopic bipolar diathermy treats most cases of epistaxis.^36,37 Preparing the nose with lignocaine and epinephrine or cocaine for its decongestant and anesthetic effects often helps. It is worth noting that cophenylcaine has a significant decongestant effect at 6 minutes and a maximum anesthetic effect after 9 minutes,³⁸ so time must be allowed for it to take effect. An injection of local anesthetic and epinephrine gives better analgesia if there is a sizable vessel that needs bipolar diathermy; otherwise the patient may feel a “smarting” sensation.

Figure 45-14. Endoscopic view of the bleeding site in severe epistaxis. The bleeding vessel was found on the septum just opposite the superior turbinate (asterisk) in the right olfactory cleft. Monopolar suction cautery was performed to stop the bleeding.

Figure 45-15. Endoscopic view of the bleeding site in severe epistaxis coming from a conchal branch of the sphenopalatine artery on the right side, just before monopolar suction cautery was performed.

After cautery the patient should be advised against blowing the nose for about 10 days to allow the area to heal. A greasy antiseptic barrier cream should be applied several times daily for 2 weeks to prevent the eschar from drying and coming off with a resulting rebleed. The ointment should not be placed directly on the area treated but is best placed inside the rim of the nostril with the tip of the finger, and “milked up” by massaging the nostril rims, and then sniffed up. This advice can also be given to patients with a crusted septal area from picking or excessive drying. Although most nosebleeds come from Little’s area, or from the mucocutaneous junction in young children, a small proportion come from higher on the septum or more posteriorly. Endoscopy is very helpful in defining the bleeding point. Packing of the nose before endoscopy can complicate detection of the exact site of bleeding, because packing often causes mucosal trauma and misleads the clinician.

Rarely, nasal tumors can manifest as epistaxis, so it is important to check for a nasal mass, especially beyond a septal deviation. If there is crusting on the septum, it is worth asking whether it has been a problem. Crusting can follow an abrasion, picking, or a vasculitis such as Wegener’s granulomatosis.³⁹ If it looks likely that the problem is being perpetuated by the patient’s picking or blowing any crust off, it is usually not helpful to confront the patient about this possibility. Instead, the clinician should casually mention that nose-picking is very common (“You see people doing it in cars or waiting for a train, and many people do it when nobody is watching”), and say that dried crusts are irritating, and then ask whether the patient has to remove the crusts; the patient may confess to doing so, and some progress can be made.

If the bleeding point is not identified, gently packing the nose with oxidized cellulose in fine sheets avoids mucosal damage and promotes coagulation to control bleeding.

The majority of posterior idiopathic bleeds are from the septum, usually from the septal branch of the sphenopalatine artery as it runs submucosally. The key is to identify the site of the bleeding and gain control using bipolar suction diathermy. A severe septal deviation can make it difficult to define the bleeding point.⁴⁰ Controlling the bleeding avoids the discomfort associated with nasal packing and also avoids hospital admission.⁴⁰ A U.K. cost-benefit analysis of 38 adult patients with epistaxis concluded that £6804 (≈$13,600) could be saved by avoiding admission in 28 patients.³⁶ Endoscopic cauterization achieves hemostasis in more than 80% of patients with posterior epistaxis at the first attempt and more than 90% after a second attempt.²⁹ The bleeding point can be cauterized with the help of nasal endoscopy; this procedure has a reported failure rate of 17% to 33%.^41,42 Complications associated with this procedure are uncommon, but there are isolated reports of palatal numbness from thermal damage to the greater palatine nerve, damage to the lacrimal duct, and possible damage to the optic nerve if cautery is used in a patient who already has undergone an ethmoidectomy.⁴³

Nasal Packing

If a bleeding point cannot be found, ideally the nose is packed with an absorbable hemostatic agent that produces minimal mucosal trauma. Various nonabsorbable packs have been used, but their insertion is uncomfortable, as is their presence once in position. The insertion of a pack can cause local mucosal trauma and complicate localization of the bleeding point.

If an anterior pack fails and there is no access to an experienced surgeon who can examine, localize, and cauterize the bleeding point, more packing to tamponade the bleeding point may be required. This procedure requires good local anesthesia and analgesia to enable adequate pressure to be applied with the packs in position. Various proprietary packs are available. The insertion of a nasal pack has conventionally meant that the patient has to be admitted, although one study discharged 46 of 62 patients whose nasal airways had been packed, with outpatient follow-up arranged for 48 hours later. However, 28% of those discharged had unplanned returns to the emergency department.⁴⁴ If anterior packing fails, a posterior balloon may have to be placed and inflated in the postnasal space. An anterior pack is then placed, and gentle traction used to pull the balloon forward against the anterior pack; this arrangement is held by placement of a clip over the catheter anteriorly as it emerges through the anterior pack.⁴⁵ It is vital that any clip used to secure the catheter does not rest on the skin of the nostril; a clip in this position could produce necrosis of the area in as little as 4 hours (Fig. 45-16). The morbidity and physical discomfort associated with nasal packing includes pain, hypoxia, alar necrosis, and toxemia, and is well described in the literature.^46–49 Unfortunately, nasal packing is used routinely in some units where expertise in nasal endoscopy is not available; for example, in only 7% of ear, nose, and throat emergency departments in the United Kingdom is suction diathermy available.⁸ Packing not only traumatizes the nasal lining but also can cause cardiorespiratory complications and local infection.⁴⁶

Figure 45-16. Necrosis of the columella after bilateral posterior nasal packing.

The role of prophylactic systemic antibiotics in patients who have nasal packs is not well established. There appears to be wide variation in current practice in England.⁵⁰ The main concern is to avoid toxic shock syndrome. We would prescribe antibiotics if the patient has any cardiac anomalies that would require antibiotic prophylaxis for surgery.

If the patient does not experience rebleeding within 12 to 24 hours, the packs should be removed. The nose should be inspected with a rigid endoscope, if this procedure has not already been performed prior to packing, to exclude any disease that may have been responsible for the bleeding.

Posterior epistaxis controlled by posterior nasal packing has a failure rate between 26% and 52% and a complication rate between 2% and 68.8%.^43,51 The complications noted in two studies were synechia, angina, periorbital cellulitis, sinusitis, toxic shock syndrome, hypoxia, and otitis media.^43,51 “Gone are the days when a patient had an uncomfortable posterior nasal pack inserted then spent several days on the ward only to bleed again on its removal.”⁵² Endoscopic sphenopalatine artery ligation (ESPAL; see later) has replaced the need for posterior nasal packs, other than in an emergency situation, to control profuse bleeding. The goal is to achieve a high success rate and a low morbidity. Especially elderly patients with multiple medical problems (arteriosclerosis, hypertension, diabetes, hepatic and renal disease) tolerate packing poorly, and complications occur frequently; therefore, in such patients, the clinician should consider an early surgical intervention rather than packing of the nose.⁴⁹

Maxillary Artery Ligation

Another technique to control posterior epistaxis is ligation of the internal maxillary artery in the pterygopalatine fossa.⁵³ It has a reported success rate of approximately 90%.⁵⁴ Treatment failures are due to the difficulty in finding the artery and its branches. The technique is also associated with a complication rate of 28%.⁵⁴ Because this procedure is done through a Caldwell-Luc approach, complications include sinusitis, facial pain, oroantral fistula, and facial and dental paresthesia; also, dissection in pterygopalatine fossa can result in blindness, ophthalmoplegia, and decreased lacrimation.⁴¹

Ligation of the External Carotid Artery

Ligation of the external carotid artery has been advocated, but the rich anastomoses of vessels in the nose means that this procedure is not very effective.⁵⁵ Ligation of the external carotid artery prevents embolization that may be desirable because of bleeding that is in the distribution of that vessel but not in the vessels supplied by it, which are also supplied by cross-anastomoses from contralateral vessels. There are reports of cerebrovascular ischemia and infarction following external carotid ligation in elderly atherosclerotic patients, whose cerebral circulation has partially relied on anastomotic connections from the external to the internal carotid system.

The Role of Endoscopic Sphenopalatine Artery Ligation

If bleeding cannot be controlled after endoscopic examination and cautery and/or nasal packing, then examination with use of either a general anesthetic or a local anesthetic with sedation is indicated. Bipolar diathermy of any bleeding points or ESPAL is then the treatment of choice.⁹ Clipping or diathermy of the sphenopalatine artery is now the accepted treatment for management of persistent posterior epistaxis.^{40,43,56–60} The morbidity associated with ESPAL is low compared with that for ligation of the maxillary or external carotid artery and for embolization. Pooled case-series data have shown that epistaxis was controlled by this technique in 98% of patients.⁶¹ The endoscopic sinus surgeon should locate the sphenopalatine artery at the level of the crista ethmoidalis (Fig. 45-17).⁶² An incision is made over the posterior fontanelle, a submucosal flap is lifted, and the anterior branch is identified with its origin just posterior to the crista ethmoidalis. The anterior branch is then identified and then undergoes clipping or diathermy (Fig. 45-18). In the majority of cases the sphenopalatine foramen opens into the middle and superior meatus.⁶²

Figure 45-17. A, Endoscopic view of the right ethmoidal crest (asterisk) in a human skull. B, View of the right lateral wall of the nose injected with pink latex to show four branches of the sphenopalatine artery, three above and one below the crista ethmoidalis (asterisk).

Figure 45-18. A, Intraoperative endoscopic view of the dissection of the sphenopalatine artery just behind the ethmoidal crest (asterisk). Bipolar cautery is applied to the first branch just below the ethmoidal crest. B, Final view after cautery of all 4 branches, two below and two above the ethmoidal crest, suction within the right sphenoid sinus.

The sphenopalatine artery normally starts to branch lateral to the crista ethmoidalis, and these branches vary widely. It is important that the surgeon who undertakes ligation or cautery of the artery is aware that more than 97% of individuals have two or more branches medial to the crista ethmoidalis, 67% have three or more branches, and 35% have four or more branches.⁶³ The endoscopic sinus surgeon views the sphenopalatine artery at the level of the sphenopalatine foramen or a few millimeters medial to it. With a mucosal incision made in the posterior fontanelle area, anterior to the horizontal part of the base middle turbinate as it joins the lateral nasal wall, a submucosal flap is lifted, and the artery is identified posterior to the crista ethmoidalis and clipped. Some workers describe identifying the artery and clipping it without further dissection to verify whether there were any other branches.^56,59,60 The mistaken belief that the artery enters as a single trunk into the nose may have led to the failure of these procedures. One study specifically looked at the branching pattern of this artery from the endoscopic surgeon’s point of view.⁴¹ The researchers found two branches of the sphenopalatine artery near the sphenopalatine foramen. In their study, 16% of arteries branched within the foramen, allowing the two arteries to exit together; in 42%, the branches exited much more posteriorly; and in the remaining 42%, the septal branch exited through a separate foramen posterior to the sphenopalatine foramen.⁴¹ Simmen and colleagues⁶³ reported that in more than 97% of cadaver specimens examined there were 2 or more branches medial to the crista ethmoidalis, in 30% there were 3 branches, and in one specimen there were 10 branches. The variations in 77 specimens are shown in Figure 45-19.

Figure 45-19. Line diagrams to illustrate the possible numbers of branches of the sphenopalatine artery superior and inferior to the crista ethmoidalis in the sagittal plane medial to it.

(Redrawn from Simmen D, Raghavan U, Manestar M, et al. The anatomy of the sphenopalatine artery for the endoscopic sinus surgeon. Am J Rhinol. 2006;20:502-505.).

Various reports have claimed success rates for ESPAL between 92% and 100% in controlling epistaxis.^57,59,61 Failure to clip all the branches of the sphenopalatine artery may be the reason for continued epistaxis after the procedure. All divisions of the sphenopalatine artery take place in the pterygomaxillary fissure, and the branches enter the nasal fossa as separate blood vessels. The arrangement of these branches in relation to the sphenopalatine foramen varies widely. The largest and most anteriorly based branch is the posterior lateral nasal branch. This must be clipped and divided so that the flap can be lifted superiorly to locate the nasopalatine branch, which must be clipped and divided as well. Because there are such wide variations in the branching pattern of the sphenopalatine artery, careful dissection is required even after these two branches are clipped. A thorough search by careful dissection should be made all around the sphenopalatine foramen to find any other branches that can be clipped. Clipping or diathermy of the sphenopalatine artery has a failure rate between 0% and 8%⁶¹ and is not associated with any serious complications. The main complication, as previously mentioned, is failure to control epistaxis, which is usually due to the surgeon’s failure to clip all the branches of the sphenopalatine artery. The arrangements of these branches are unpredictable, as seen in our study, and can vary on the two sides in the same individual. In addition the branches of this artery can come out through separate foramina, and a surgeon who is not aware of this possibility can miss a few branches. Other complications are uncommon; they include nasal crusting, palatal numbness, acute rhinosinusitis, decreased lacrimation, and septal perforation.⁵⁹ A long-term study of ESPAL showed a 93% success rate.⁶⁴

We do not advocate packing and repacking for refractory epistaxis.

Embolization

Arterial embolization has been shown to be effective in the treatment of intractable epistaxis.^65,66 However, the procedure carries a risk of complications, which include cerebrovascular accident, hemiplegia, ophthalmoplegia, facial nerve palsy, seizures, and soft tissue necrosis.^67–70 The analysis of 31 cases of embolization of internal maxillary artery by Siniluoto and colleagues⁷¹ did not find any major and persistent complications. Because interventional neuroradiology is increasingly available, embolization has become an option when initial treatment fails. It is also important to state at this point that the arterial embolization technique is effective mainly for the external carotid artery supply and very dangerous for the internal carotid supply. Embolization for bleeding from the terminal branches of the ophthalmic artery is therefore not advocated because of the high risk of blindness due to reflux of the embolic materials.⁷²

We would advocate the use of this technique for patients with refractory epistaxis who are unfit for surgery or in whom surgery has failed to control the bleeding (Fig. 45-20). Persistent posterior epistaxis can be controlled by percutaneous embolization of bleeding arteries. The success rate for this procedure is between 71% and 95%, and the complication rate is 27%.^41,54,71

Figure 45-20. Bilateral superselective angiograms of the sphenopalatine arteries. A, The crossover anastomosis of the septal mucosa artery supply. B, Postembolization view.

Bleeding from the Anterior Ethmoidal Artery

An uncommon cause of severe epistaxis is associated with a nasoethmoid fracture when the bleeding originates from the anterior ethmoidal artery. Patients with anterior ethmoidal artery epistaxis form a distinct subgroup whose management differs in that they require surgery to the anterior ethmoidal artery, via either a traditional external approach or an endoscopic approach, because the bleeding rarely subsides with conservative measures (Fig. 45-21).⁷³

Figure 45-21. Intraoperative endoscopic view of bipolar suction cautery of the left anterior ethmoidal artery in epistaxis. Partial anterior ethmoidectomy and exposure of the vessel just below the skull base.

The anterior ethmoidal artery can also be damaged during sinus surgery. It is at risk as it passes through the roof of the ethmoid sinuses on its way from the orbit to the anterior cranial fossa.⁷⁴ Damage to the artery can lead to profuse epistaxis and intraorbital bleeding, and, at times, intracranial bleeding.⁷⁵ The development of a retro-orbital hemorrhage is an emergency because it can even lead to blindness. The bony canal in which the anterior ethmoidal artery crosses the skull base can be dehiscent, making it vulnerable to damage.⁷⁶ The rate of dehiscence of the anterior ethmoidal artery has been reported as 11% to 40%.⁷⁷

There are bony protrusions from the lateral end of the bony canal of the artery where it emerges from the orbit and medially where it goes through the lateral lamella. Some authorities have stated that the artery lies behind the frontal recess and can act as a landmark in the surgical approach to this area.^{74, 78}–⁸⁰ Stammberger⁷⁶ located the anterior ethmoid artery 1 to 2 mm behind the junction of the posterior wall of the frontal recess and the anterior ethmoid air cells.⁷⁶ Simmen and associates⁸¹ showed a mean distance from the posterior wall of the frontal recess to the artery of 11 mm (range 6-15 mm). In most cases the position of the artery is mirrored on the contralateral side. However, the position is very variable, so it is not safe to use the artery as a landmark for any endoscopic intervention, especially in locating the frontal recess. The anterior ethmoidal artery is always seen between the second and third lamellae, and the most common site to find it is in the suprabullar recess (85%). If pneumatization of the ethmoid sinus is marked, the artery is likely to be lying below the skull base and is more prone to surgical damage. Preoperative knowledge of the suprabullar recess and supraorbital cells through careful interpretation of computed tomography scans is helpful in avoiding damage to the anterior ethmoidal artery (Fig. 45-22).

Figure 45-22. A and B, Coronal CT scans of the paranasal sinuses. The preoperative checklist information will prove that in a well-pneumatized supraorbital recess (left side), the course of the anterior ethmoidal artery is below the skull base (asterisk), and if the supraorbital recess is poorly or not pneumatized (right side), the course of the ethmoidal artery will be within the skull base (plus sign).

(From Simmen D, Raghavan U, Briner HR, et al. The surgeon’s view of the anterior ethmoid artery. Clinical Otolaryngology. 2006;31:187-191.)

It should be emphasized that locating the anterior ethmoidal artery is usually unnecessary, and indeed undesirable, during most procedures because doing so will increase the risk of damaging it.

Hot Water Irrigation for Epistaxis

Hot water irrigation as a noninvasive treatment for posterior epistaxis has received some renewed attention.⁸² Obstetricians used hot water to irrigate a postpartum bleeding wound in the 19th century, and Guice⁸³ introduced this procedure for staunching blood in cases of epistaxis in 1879. Studies by Stangerup and colleagues⁸⁴ involving experiments with rabbits showed that irrigating the nose at 40° to 46°C does not lead to any histologic changes of the mucosa. Temperatures higher than 46°C result in vasodilatation and, in particular, edema of the mucosa. Only temperatures above 52°C trigger necrosis. It can be assumed that the temperature-induced mucosal edema leads to local compression of the bleeding vessel and at the same time may propagate the cascade for hemostasis.⁸⁴

After an examination with nasal endoscopy, topical anesthesia of the relevant nasal cavity is administered using 4% tetracaine. Then Stangerup’s modified bladder catheter is inserted in the affected nasal cavity. The balloon is inflated in the epipharynx and the catheter gently pulled back until the choana is blocked off. The affected nasal cavity is continuously irrigated with tap water at a temperature of 50°C. The treatment lasts approximately 3 minutes, with the patient sitting upright so that the irrigation water can flow forward from the nose into a basin. After the irrigation with 500 mL of hot water, the catheter can be removed. In a prospective study involving 84 patients, Schlegel and colleagues⁸² showed a success rate of 82% for hot water irrigation without any complications. This technique avoids painful packing, hospitalization, and immediate surgery but also allows the patient to breath normally through the open nasal cavity after the treatment.^82–84

Management of Epistaxis in Patients with Hereditary Hemorrhagic Telangiectasia

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant multisystemic disorder characterized by telangiectasia that affects cutaneous and mucosal surfaces as well as arteriovenous malformations in the pulmonary, cerebral, and hepatic circulations (Fig. 45-23). The most common symptom in patients with HHT is epistaxis, which affects more than 90% of individuals. The severity of attacks is variable; these episodes of epistaxis can be functionally and socially debilitating for the patient and may require frequent hospital admission; and for some patients, the bleeding is intractable.⁸⁵ Many methods of treatment for epistaxis due to HHT have been described in the literature, including medical strategies, such as the use of hormonal manipulation and the use of antifibrinolytic agents, as well as surgical options, including laser coagulation (see Fig. 45-23),⁸⁶ septodermoplasty,⁸⁷ and nasal closure.⁸⁸ No one method has proved itself entirely successful or without significant side effects, however.

Figure 45-23. Hereditary hemorrhagic telangiectasia with arteriovenous malformations, on an endoscopic view of the right nasal cavity.

A prospective study by Hitchings and coworkers⁸⁵ investigated the effect of various surgical options on quality of life scores in patients with HHT and epistaxis. The researchers concluded that nasal closure should be offered to patients with moderate to severe epistaxis that has proved unresponsive to other treatment options, either bipolar (see Fig. 45-23) or laser coagulation treatment (see Fig. 45-24), or septodermoplasty; 88% (7/8) of the patients in their series who were treated with nasal closure reported a complete cessation of nosebleeds. Closure of the nasal cavity—Young’s procedure—is based on the principle that the absence of desiccating airflow through the nasal cavity prevents the breakdown of mucosa overlying the fragile telangiectasias. An alternative to nasal closure is the use of nasal obturators.⁸⁹

Figure 45-24. Endoscopic view of the left lateral nasal wall with an arteriovenous malformation in a patient with hereditary hemorrhagic telangiectasia during bipolar suction coagulation.