Epistaxis and catastrophic nasal bleeding

Operative Techniques in Otolaryngology (2014) 25, 194–200

Epistaxis and catastrophic nasal bleeding Mohammad H. Al-Bar, MD From the Department of Otolaryngology—Head and Neck Surgery, University of Miami Miller School of Medicine, Miami, Florida KEYWORDS Epistaxis; Sphenopalatine artery; Anterior and Posterior Ethmoidal arteries; Carotid artery; Cavernous sinus

Epistaxis is the most common otolaryngologic emergency. Its severity may range from mild to life threatening. Management of acute epistaxis varies depending on its severity, etiology, and site of bleeding. Endoscopic control of epistaxis is considered a highly effective and cost-effective treatment. It is important for the surgeon to weigh the potential benefits and risks. Ligation and cauterization of the sphenopalatine artery and anterior and posterior ethmoidal arteries is discussed. A plan of action and control of catastrophic bleeding from the internal carotid artery or cavernous sinus are also discussed. r 2014 Elsevier Inc. All rights reserved.

Introduction Epistaxis is the most common otolaryngologic emergency. Two-thirds of the population has a history of epistaxis during their life, with approximately 6% needing medical attention. Ranging from mild to life threatening, epistaxis is more frequent in children younger than 10 years and adults older than 40 years and occurs more often during cold winter months. It is most commonly idiopathic but causes including primary neoplasm, trauma, and iatrogenic events do occur. Comorbidities such as hypertension, and coagulopathies, as well as usage of anticoagulation medication and nasal septal abnormalities are major risk factors for epistaxis. The basic mechanism of epistaxis is unclear. Theories include superficial normal vessels, varices, telangiectasia, or aneurysms. Hypotension, which usually is a late sign, and tachycardia, are indication of significant blood loss, especially in young individuals.1-5 There are different approaches to classify epistaxis from a management standpoint. It can be classified as anterior or posterior epistaxis, based on the site of bleeding, but there are

Address reprint requests and correspondence: Mohammad H. Al-Bar, MD, Department of Otolaryngology—Head and Neck Surgery, University of Miami Miller School of Medicine, 1120 NW 14th St, CRB 5th Floor, Miami, FL 33136. E-mail address: [email protected]; [email protected] http://dx.doi.org/10.1016/j.otot.2014.02.010 1043-1810/r 2014 Elsevier Inc. All rights reserved.

no clear definitions of either. Most cases with intractable epistaxis would be classified as posterior owing to poor visualization, and hence the epistaxis that fails to stop with aggressive bilateral anterior packing may be termed posterior epistaxis. Another definition of posterior epistaxis is bleeding arising posterior to the maxillary sinus ostium.1,6 Epistaxis also can be classified based on the source of bleeding as venous or arterial and into high-flow or low-flow based on the rate of bleeding. Venous bleeding can involve low flow, such as mucosal oozing, or it can be high-flow bleeding from structures such as the cavernous sinus. Similarly, arterial bleeding can be low flow, as occurs from small perforating vessels, or high flow, as is the case with carotid artery injuries.7 Epistaxis is often controlled with first-line interventions such as chemical or thermal cautery, hemostatic agents, or nasal packing. Uncontrollable bleeding with these methods may need surgical intervention. Transnasal endoscopic sphenopalatine artery (SPA) ligation or cauterization provides excellent control.3,6,5 In 1965, Chandler and Serrins described the transantral approach to ligating the maxillary artery in the pterygopalatine fossa. In 1976, Prades described a microsurgical approach for ligating the SPA at its foramen, as a surgical landmark for Vidian nerve. In 1985, Stamm et al described the transnasal microscope approach to SPA ligation and showed a 94% success rate for controlling intractable posterior epistaxis with reduced patient morbidity. In 1992, Budrovich reported endonasal endoscopic approaches for

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Epistaxis and Catastrophic Nasal Bleeding

Figure 1 Kiesselbach plexus (Little area). The anastomotic triangle in the caudal septum is formed by thin-walled terminal branches of ethmoidal arteries, SPA, and the superior labial artery. (Adapted with permission from Casiano et al.15) (Color version of figure is available online.)

SPA ligation to treat epistaxis.6,8-12 Alternately, surgical ligation of the anterior or posterior ethmoid arteries may be indicated if this is the source of uncontrolled hemorrhage.

Anatomy Knowing the anatomy is of great importance. Both internal carotid artery (ICA) and external carotid artery (ECA) anastomose with each other to supply the nasal cavity. The ophthalmic branch of the ICA branches intraorbitally to give rise to the anterior ethmoid artery (AEA) and the posterior ethmoid artery (PEA). The internal maxillary artery (IMA) branch of the ECA gives rise to the SPA. The anastomotic triangle in the caudal septum known as Kiesselbach plexus (or also known as Little area) is formed by large thin-walled terminal branches of 3 major arteries (Figure 1). These arteries are the ethmoidal arteries (AEA and PEA), SPA, and the superior labial artery.7 This area is the most common site for epistaxis (90%-95%). Most cases of posterior epistaxis involve the SPA, which is the terminal branch of the IMA. On the contrary, bleeding due to AEA is uncommon. However, it usually occurs in patients with facial trauma, skull base fractures, or iatrogenic injury.1,3,6-13 The SPA enters the nasal cavity from the sphenopalatine foramen (SPF) in the posterior lateral wall and divides into a septal branch, which courses posteromedially along the inferior portion of the sphenoid rostrum, just inferior to the sphenoid sinus ostium, and a conchal branch, that supplies the lateral wall below the middle turbinates. The SPF is circular or oval in shape. It is usually found in the posterior part of the superior meatus at the transition between the

195 middle meatus and superior meatus, higher than the posterior attachment of the middle turbinate, and approximately 6.5 cm from the nasal spine. Therefore, during dissection, the lower limit should be the inferior edge of the posterior attachment of the middle turbinate.1,3,14,6,15 The ethmoid crest (crista ethmoidalis) is a small crest of the ascending process of the palatine bone that meets the posterior aspect of the middle turbinate.17 This bony “pointer” is an important surgical landmark as it usually points to the SPF (Figure 2). The SPF may consist of 1 common large opening (Class I in 20%), 2 separate openings with a smaller inferior opening and divided by a membranous or fibrotic bridge (Class II in 70%), or 2 separate openings, a large superior and small inferior opening, divided by a bony bridge (Class III in 10%). Other variations also may exist (Figure 3).1,3,14,6,4,15,16,5,17 The AEA and PEA are branches of the ophthalmic artery, running on the medial wall of the orbital beneath the lower border of the superior oblique muscle. Branches of ethmoidal arteries may occur within the ethmoid roof. They then enter the cranial cavity medially to the cribriform plate area. Both give meningeal branches to the dura as they enter intracranially (Figures 4 and 6). The AEA can be seen in the space between periorbita and lamina papyracea (LP), 2 cm posterior to the lacrimal crest, as it is penetrating the periorbita into its bony canal, coursing through the roof of the ethmoid sinus at the attachment of the ethmoid bulla lamella, or along the posterior aspect of the frontal recess. The AEA may also course within a mesentery (in 36%), a few millimeters below the level of the bony ethmoid roof. When located in a mesentery, it can be identified on computer tomography (CT) and tends to coexist with Keros type 2 or 3 cribriform plates (Figure 5).3,6,15,18

Figure 2 Ethmoid crest (crista ethmoidalis). A diagram showing the left nasal cavity with an opened maxillary sinus and sphenoid sinus. Ethmoid crest (crista ethmoidalis) is shown as it is an important surgical landmark pointing toward sphenopalatine foramen. (Adapted with permission from Casiano et al.15) (Color version of figure is available online.)

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Figure 3 Sphenopalatine foramen variations. Class I: 1 opening. Class II: 2 openings separated by soft tissue. Class III: 2 openings separated by bony bridge. (Adapted with permission from Casiano et al.15) (Color version of figure is available online.)

Management approach All comorbidity factors, such as uncontrolled hypertension, medications and coagulopathy, must be addressed. The priority is to control the active hemorrhage. In some cases, control may be achieved by simply applying pressure to the nose, while positioned upright and leaning forward for 20 minutes. Alternately, control may be obtained with appropriate nasal packing. The goal of both methods is to slow the blood loss rate by collapsing the bleeding vessels, and forming a clot, with eventual vessel obliteration, and also to prevent blood from exiting the posterior choanae, to protect the upper airway. Nasal packing of all types requires gram-positive antibiotic coverage for prophylaxis against toxic shock syndrome. Adding lidocaine with a vasoconstrictive agent facilitates nasal cavity decongestion and anesthetizes the nasal cavity. Anterior epistaxis is typically managed conservatively with external pressure, cautery, topical agents, packing, or a combination of these.1,2,6

Figure 5 Coronal CT scan shows the AEA running in a mesentery as indicated with the arrows.

Severe epistaxis is generally treated with ligation or cauterization of the main arteries supplying the nasal mucosa.2,3 A 3-step approach is advocated: (1) identification of the bleeding site, (2) stopping the bleeding, and (3) identification and treatment of the underlying cause.1 Approximately 5%-10% of epistaxis cases arise in an area where the SPA anastomoses with branches of the pharyngeal artery at a region called Woodruff area.2,13,5 External arterial ligation of the IMA or ECA or both is associated with a higher morbidity vs treatment of the distal vessels intranasally. In hereditary hemorrhagic telangiectasia, active bleeding may be exacerbated with nasal packing. However, during acute epistaxis, these patients may require packing, until more definitive measures can be undertaken. Treatments options are many, ranging from nasal packing to laser photocoagulation with the CO2, Potassium Titanyl Phosphate (KTP), Neodymium:Yttrium-Aluminum-Garnet (Nd:YAG), or argon laser, to embolization, avastin injection, septodermoplasty, and nasal closure (modified Young procedure). Recognizing the limitations of these options, telangiectasias are identified under general anesthesia and a microdebrider may also be used to systematically remove individual lesions (hereditary hemorrhagic telangiectasia ablation or stripping), followed by suction cautery with minimal power settings, to cauterize any oozing from normal mucosal edges surrounding the lesion.19

Transnasal endoscopic SPA ligation

Figure 4 Anterior (AEA) and posterior (PEA) ethmoidal arteries at the skull base. The AEA is located posterior to the frontal recess and above the suprabulla ethmoid cells. (Adapted with permission from Casiano et al.15) (Color version of figure is available online.)

The setup should be as for other endoscopic sinus surgical procedures, under general anesthesia. First, nasal packing material is removed, and the nasal cavity is cleaned and examined to locate the site of bleeding. Two pledgets soaked with a topical decongestant are used to decongest the mucosa for 3-5 minutes. A 25-gauge spinal needle is used to inject the SPF (tail of middle turbinate) region with 1% lidocaine and 1:100,000 epinephrine.3,6-13,8,20 Although

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there is no statistically significant difference in decreasing blood loss when injecting the greater palatine canal, in some studies, benefit has been shown.21,22 The canal can be identified through a transoral endoscopic examination looking for a mucosal depression over the hard palate, medial to the second molar, and palpated with the finger. A 25-gauge spinal needle is bent at a 451 angle and advanced not more than 25 mm.13,21,22 It is critical to “draw back” before injecting to avoid intravascular injection. The middle turbinate is then medialized or trimmed with a true-cut forceps. A maxillary antrostomy through the posterior fontanel may be performed to identify the posterior maxillary sinus wall and coronal plane of the SPA. However, it usually can be successfully performed with an isolated lateral nasal wall mucosal incision or debridement, over the orbital process of the palatine bone just anterior to the tail of the middle turbinate, with a knife, microdebrider, or metal tip of a monopolar suction cautery. A mucoperiosteal flap is then raised with a Cottle elevator posterosuperiorly until the ethmoid crest (pointer) and anterior border of the SPF are encountered. The elevation of the flap may continue posteriorly, to the face of the sphenoid, along the inferior and superior borders of the foramen. The pterygopalatine fossa can also be exposed by removing the vertical ridge (palatine bone anterior to the ethmoidal crest) of the antrostomy, and the adjacent thin posterior wall of the maxillary sinus with a Kerrison rongeur, through a middle meatal antrostomy, which can be extended into the inferior meatus (extended maxillary antrostomy), through the lateral nasal wall attachment of the inferior turbinate. The IMA and its branches, the sympathetic and parasympathetic nerve plexus, veins, and buccal fat can be seen within the pterygopalatine fossa. Superiorly, one can find the foramen rotundum (V2 branch of the trigeminal) superolateral to Vidian nerve.1,3,6,13,15,8,20,7 After exposing the main trunk of the SPA before the branching point, cauterization, clipping, or both may be used. Cauterization, rather than clipping, provides a higher or similar success rate.6,8,20 In cases of clipping, ideally, 2 should be placed, ensuring that the entire width of SPA is within the clip. Most patients can be discharged the same day the surgery is performed.1,3,13,8,7 Additional measures for controlling posterior epistaxis include finding the nasal septal artery coursing along the anteroinferior wall of the sphenoid sinus and rostrum, just above the choanal arch. Then the area between the superior turbinate and septum just above the choanal arch is generously cauterized to obliterate this branch as well.12

197 removal of surrounding bone and orbital lamina would be needed before ligation to expose the artery as it transitions from the orbit to the ethmoid cavity (transnasal-transorbital approach, Figures 6 and 7).23,24 Otherwise, the traditional technique is the external approach through Lynch incision with clipping of the artery as it passes between the periorbita and LP.1,3,6

Procedure A thorough study of a preoperative CT is necessary to identify the AEA, which is seen as a indentation or protrusion of the LP just posterior to the coronal plane of the frontal infundibulum on coronal CT view.6,23,24 Moreover, a CT is important to exclude other causes of epistaxis, such as neoplasm. The procedure is performed under general anesthesia. Ligation of the SPA may or may not be performed as discussed previously. A standard maxillary antrostomy is also suggested to identify the level of the orbital floor.6,23,24 A total ethmoidectomy is performed to expose the medial orbital wall and ethmoid roof.23 The bony canal of AEA is typically seen through the ethmoid roof traveling from the orbit to the cribriform plate in anteromedial direction.23,24 Ligation or cauterization of the AEA may be performed as it runs in its mesentery. However, most of the time, the superior LP is removed, and a subperiosteal plane is dissected with a Cottle elevator. The AEA is found at its entry point into its bony canal between the LP and periorbita. Care should be taken not to injure periorbita and skull base or to prematurely cut the artery too close to the periorbita, resulting in an orbital hematoma (Figures 6 and 7). PEA is similarly ligated at its entry point to its bony canal at the level of the posterior ethmoid air roof.23,24,7 Complications include cerebral spinal

Transnasal endoscopic AEA ligation AEA ligation is typically combined with SPA ligation.6 One barrier to reliable endoscopic ligation of the AEA is the variable anatomy of the artery itself; the vessel runs in a bony canal either within the skull base or a bony mesentery extending into the anterior ethmoid cavity.23,24 If it runs in a mesentery, ligation would be effective after total ethmoidectomy.6,18,25 If AEA runs within the bone of the skull base, frontal sinusotomy and total ethmoidectomy with

Figure 6 The bony canal of AEA and PEA is typically seen through the ethmoid roof traveling from the orbit to the cribriform plate in anteromedial direction. Ligation or cauterization of the AEA may be performed as it runs in its mesentery. (Adapted with permission from Casiano et al.15) (Color version of figure is available online.)

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Figure 7 Cauterization of AEA in a patient with left orbital hematoma. Total ethmoidectomy and frontal sinusotomy is performed. (A) The AEA is located through the ethmoid roof. (B) Lamina papyracea removed. (C) Cauterization of AEA performed. (D) The AEA is located crossing between the periorbita and the lamina as indicated with the arrow, cauterization or ligation performed. Care should be taken not to injure the periorbita or the skull base (*:AEA). (Color version of figure is available online.)

fluid leak, orbital injury, and failure to control epistaxis.6 A cerebrospinal fluid leak can occur, particularly with monopolar cautery, when there is direct cauterization of the artery in its bony canal as it courses through the ethmoid roof (anterior and posterior). This typically occurs when the tip of the metal monopolar cautery adheres to the skull base during the heating process, creating charcoal. On removal of the suction tip, the thin bony skull base (particularly medially) can fracture and a cerebrospinal fluid leak can occur.

ICA injury Rupture of ICA is the most feared and devastating complication and may result in death. Injury may also cause

spasm, thrombosis, embolism, formation of a pseudoaneurysm, or the formation of a caroticocavernous fistula with significant associated morbidity. Based on anatomical studies, the lateral sphenoid bony wall is dehiscent over the ICA in 4%-22% of cases and also may bulge into the sphenoid sinus in 71%, and may be located as close as 4 mm from the midline (Figure 8).26-30 Other risk factors for injury include revision surgery, radiotherapy, and acromegaly.26 The immediate concern and priority is to obtain good visualization to stop the bleeding. Head elevation, reverse trendelenburg position, and pressure application with neurosurgical cottonoids over the bleeding vessel should temporarily stop the bleeding, if the injury is simply a cut or puncture. More extensive pressure dressing may be necessary with larger injuries of the carotid artery. The anesthesiology

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Figure 8 Bulging ICA into sphenoid sinus. (Adapted with permission from Casiano et al.15)

199 happen, and bleeding can occur as late as 1 month following the surgery.7,26 Cavernous sinus bleeding may be controlled with several techniques, include packing, head elevation, warm-water irrigation, controlled hypotension, controlled hypocapnia, and bipolar electrocautery.7,31 A variety of hemostatic materials are currently available, which require direct contact with the bleeding tissues and work by promoting platelet aggregation and formation of a stable clot. Examples include powdered gelfoam with or without thrombin, SURGIFLO (Ethicon, Somerville, NJ), Avitene (Ethicon [Johnson and Johnson], Somerville, NJ), Floseal, (Baxter International, Inc, Deerfield, IL), and Syvek (Marine Polymer, Boston, MA). These materials are most effective for venous hemostasis and low-flow arterial bleeding.25 We recommend packing with Surgicel or small neurosurgical cottonoid filled with powder gelfoam. The cottonoid is introduced in the shape of a “taco” with the filling being the gelfoam powder. The open part of the “taco” is placed against the bleeding site, the cottonoid is compressed releasing the powdered gelfoam, while compression is maintained on the cottonoid for several minutes.

Conclusion team needs to maintain the blood pressure of the patient in a normotensive range and restore intravascular volume to maintain contralateral cerebral perfusion.7,26,31 In certain situations, adenosine has been used to induce transient asystole, and a brief period of hypotension, which aids in the visualization of the bleeding point. However, this has mainly been described in intracranial aneurysm surgery.32 This therapy may serve as a useful adjunct in the future for ICA injury. However, at this time, its use is not reported. Neurophysiological monitoring may provide early evidence of inadequate perfusion. Blood has a tremendous capacity for heat dispersion. Therefore, diffuse cauterization without identifying the small segment of the vessel with the laceration will not be effective. Ligation of the internal and external carotid arteries would not only waste time but also block the interventional radiologist access to the site of injury. Overpacking should be avoided, as it will not prevent bleeding intracranially. If the injury is just a small vascular branch off the carotid, the bleeding site may be identified and cauterized with a bipolar electrocautery as the pledget is moved aside. However, most carotid injuries will require transporting, while still under general anesthesia, to the angiography suite for further management by an interventional neuroradiologist. Options include stenting, coiling and embolization, or bypass surgery. Skull base surgery involving aggressive manipulation or drilling around the carotid artery, requires a multidisciplinary team and hospital resources able to care for this potential complication. An action plan, in the event of carotid bleeding, needs to be clearly understood by all team members, including the operating room personnel, before these surgical procedures. In addition, it is important to remember that not all ICA injuries manifest during the intraoperative period, as vasospasm may

Epistaxis is typically managed conservatively with external pressure, cautery, topical agents, packing, or a combination of these. Posterior epistaxis is generally more difficult to control. Endoscopic ligation of the SPA is now considered the most effective and cost-efficient definitive treatment for uncontrolled posterior epistaxis.3 In the case of high-flow bleeding, it is critical to define the specific portion of the artery to allow for the direct cauterization. With ethmoid artery bleeding, it is important for the surgeon to weigh the potential benefits of avoiding an external scar from the traditional external approach, with the potential for serious complications such as cerebral spinal fluid leak or orbital injury with endoscopic approach.6

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