Epistaxis

Mark J. Shikowitz

Albert Einstein School of Medicine and Department of Otolaryngology and Communicative Disorders, Long Island Jewish Medical Center, New Hyde Park, New York, U.S.A.

■ Vascular Anatomy 442

■ Physiology of the Nose and the Nasal Lining 443

■ Etiology of Epistaxis 444

■ Local Factors 445

■ Systemic Factors 446

■ Epistaxis Management 447

■ Control of Epistaxis in the Outpatient Setting 447

■ Nasal Packing 448

■ Maxillary Artery Ligation 452

■ Endoscopic Management of Epistaxis 452

■ Endoscopic Ligation of the Sphenopalatine Artery 453

■ Septal Dermatoplasty 453

■ Ethmoid Artery Ligation 454

■ Selective Embolization 454

■ Juvenile Angiofibromas 456

■ References 457

VASCULAR ANATOMY

A clear understanding and knowledge of nasovascular anatomy is essential for expediency and safety in controlling nasal hemorrhage. Regardless of the type of technology, new or old, utilized to control nasal hemorrhage, it is the clear understanding of the various potential sources of the blood supply that is important. Whether control of the problem is via more traditional anterior or posterior packing of the nose, open surgical approach, or endoscopic approach followed by selective angiography and embolization, one premise still holds true: the offending source of blood supply to the region must clearly be defined and controlled to prevent potential unwarranted side effects and complications.

The internal and the external carotid artery systems are the primary vascular supply to the nose. The external carotid artery serves as the major contributor. The internal carotid artery supplies blood to the anterior and posterior ethmoid arteries. The larger anterior and smaller posterior ethmoid arteries branch off the ophthalmic artery within the orbit itself. Both of these vessels pass through the periorbital fascia through the shared wall of the medial orbit and lateral fovea ethmoidalis bone along the frontoethmoidal suture line. The frontoethmoidal suture line is approximately at the level of the cribriform plate. The posterior ethmoid artery enters its foramen within 4 to 7 mm of the optic nerve greater than 80% of the time. The anterior ethmoidal artery enters its foramen 14 to 22 mm posterior to the maxillolacrimal suture greater than 80% of the time (1). It has been noted that the anterior ethmoid artery may be absent 7% to 14% of the time (2,3). It has also been demonstrated that the posterior ethmoid artery may be absent 31% of the time (3). The anterior and the posterior ethmoid arteries pass through the ethmoid air cells and give rise to the medial and lateral branches. Of these, the medial branches of the ethmoid arteries supply the superior septum in the Little's area. The lateral branches of the ethmoid arteries supply the superior and the middle turbinates (Fig. 1).

The external carotid artery supplies blood to the nose through two different branches. The primary branch is the maxillary artery; the secondary supply is via the facial artery. The maxillary artery is the terminal branch of the external carotid artery. The facial artery supplies the superior labial artery, which then gives rise to the nasal arterial branches medial to the septum and lateral to the nasal ala. The maxillary artery then passes into the infratemporal fossa, either lateral to the superior and inferior heads of the lateral pterygoid muscle or between the superior and inferior heads. From here, the artery enters the pterygopalatine fossa through the pterygomaxillary fissure. The maxillary artery passes through the pterygopalatine fossa within the fat pad. The maxillary artery and its branches are usually anteroinferior to the maxillary and vidian nerves.

This is an important anatomical point to remember when undertaking a maxillary artery ligation for control of epistaxis. Although the maxillary artery gives rise to several branches, four primary vessels are relevant in the control of epistaxis. These include the descending greater palatine artery, the pharyngeal artery, the posterior nasal artery, and the sphenopalatine artery. The descending palatine artery may give rise to two or three branches. The largest is the greater palatine artery of the greater palatine canal. The lesser palatine artery passes through the lesser palatine canal and foramen, and supplies blood to the soft palate. The greater palatine artery has a varied course to the nose by first passing inferiorly through the greater palatine canal and foramen and then traveling within the lateral hard palatal mucosa. These bilateral paired arteries meet in the anterior portion of the nose in the midline and pass superiorly through the single midline incisor foramen. The greater palatine artery also supplies blood to the septum and floor of the nose. The maxillary artery bifurcates into the sphenopalatine and posterior nasal arteries at or distal to the sphenopalatine foramen. The sphenopalatine artery supplies the septal mucosa in the

Anterior ethmoidal a.

Anterior ethmoidal a.

FIGURE 1 A sagittal view demonstrating the arterial branches of the internal carotid artery. The nasal septum is supplied via branches from the facial artery and maxillary artery. "Little's area" is comprised of anastomosis from the sphenopalatine, anterior ethmoid, greater palatine, and nasal branches of the facial artery.

FIGURE 1 A sagittal view demonstrating the arterial branches of the internal carotid artery. The nasal septum is supplied via branches from the facial artery and maxillary artery. "Little's area" is comprised of anastomosis from the sphenopalatine, anterior ethmoid, greater palatine, and nasal branches of the facial artery.

region of the anterior inferior septum anastomosis with the greater palatine artery, the anterior ethmoidal artery, and the nasal branches of the facial artery forming Kiesselbach's plexus or Little's area (1,4). It is this complex meeting or net of vessels in the anterior portion of the septum that make this region play such a prominent role in epistaxis. The posterior nasal artery supplies the turbinates and the lateral nasal wall. Superiorly, it often anastomoses with the ethmoid arteries (5). Inferiorly, it anastomoses with the pharyngeal arterial branch of the maxillary artery, forming Woodruff's naso-nasopharyngeal plexus (6).

It can be seen that the nose and its surrounding structures have an extremely complex and often variable blood supply. It is for this reason that treatment of epistaxis is often a complicated process requiring both skill and superior knowledge of the anatomical vascular supply. With the development of newer and less invasive techniques such as nasal endoscopy, the exact location becomes even more important for selective control of bleeding. The use of angiographic techniques, both for identifying the offending vessel and for therapeutic control with embolization, is another means of utilizing and understanding anatomy to our and the patient' s benefit.

PHYSIOLOGY OF THE NOSE AND THE NASAL LINING

The functional design of the internal nose provides a streamlined passage for a laminar airflow and exchange. This laminar airflow may be considered similar to air passing over an airfoil or airplane wing. Any disruption of this airflow creates turbulence and will alter its physiology. The lining of the nose is comprised of pseudostratified ciliated columnar epithelium.

As air passes over this layer, particulate matter is filtered and the air is humidified. In addition to this, the nose has the capability of temperature control, from warming air from the subzero temperatures of the North and South Poles to cooling air from the high temperatures of the earth's deserts, to help the lungs function properly. In effect, it acts as the body's radiator to help in this process. The many convolutions within the nasal cavity itself increase its surface area, much as the fins do on a car's radiator. All of these factors help the nose to work more effectively. The lining of the nose along the inferior and middle turbinates contains a highly vascular lamina propria. The arterioles in the turbinates pass within the conchal bone and are surrounded by a venous plexus. Arterial dilatation will effectively block the venous outflow and result in mucosal congestion. This submucosal plexus of veins, also known as the cavernous nasal plexus, is similar to erectile tissue found in other parts of the body and provides for rapid engorgement under parasympathetic control. Stimulation of this parasympathetic process can occur from a variety of sources, including thermal, psychogenic, mechanical, sexual, or chemical (7). A crucial physiological point is that the nasoseptal cartilage does not have its own intrinsic blood supply and must depend on the vessels within the mucoperichondrial layer that covers it. A significant disruption of the mucoperichondrium may cause a loss of cartilage, resulting in either perforation of the nasal septum, or, when significant enough, nasal collapse. This point must always be taken into consideration when treating epistaxis. The nasal lining contains multiple mucous and serous glands, especially along the turbinates, which are responsible for maintaining the secretions and protective blanket for the mucosa. Any loss of these secretions may result in the loss of cilia or ciliary activity and prevent the normal passage of secretions and debris through the nose.

ETIOLOGY OF EPISTAXIS

The etiology of epistaxis may be divided into two major categories, local and systemic. The most common local factors seen by the otolaryngologist include trauma related to digital manipulation or sports injury. Relatively cold temperatures with low humidity will also result in increased epistaxis. This is common in the cooler northern climates during the winter, due to the relatively low humidity of the ambient air, complicated by the use of central heating systems without humidification. The chronic use of nasal decongestant sprays will also alter the nasal lining, in addition to chronically decreasing the blood supply to the nasal septum. In cases of prolonged use of nasal decongestants, septal perforation has been seen to occur. This will alter the change of nasal airflow from its usual laminar state to one of turbulence, thus increasing the drying and crusting of the remaining nasal mucosa, especially at the edges of the perforation. Anatomic deformities including deviated nasal septum may also alter the state of the nasal lining (8,9).

In children, foreign bodies may play a role. Intranasal tumors, both malignant and benign, can be heralded by recurrent and often significant epistaxis. The use of nasal prongs and oxygen in the hospital or home setting is another frequently seen cause. With the recognition of obstructive sleep apnea as a significant medical condition and the use of continuous positive airway pressure (CPAP) with its continuous flow of positive pressure through the nasal passages, there has been a rise in the number of patients with recurrent epistaxis (9). Any medication inhaled nasally, which can alter the pseudostratified columnar epithelium or effectiveness of the ciliary blanket, can cause epistaxis (8).

Systemic factors contributing to epistaxis include vascular disorders, blood dyscrasias, alcohol consumption, hypertension, various infectious diseases, vitamin deficiencies, inflammatory diseases, and granulomatous diseases.

Local Factors

By far, one of the most common causes of epistaxis, especially in children and participants in sporting activities, is trauma. It is for this reason that epistaxis occurs along the anterior nasal region in 90% to 95% of cases. It is often seen in children who suck their thumbs and in adolescents and adults as a result of chronic digital manipulation of the nose. Individuals who participate in sports with a high rate of contact with the nasal and facial structures also run the risk of recurrent epistaxis and complications related to its treatment (1). Basketball players, boxers, soccer players, and other athletes who do not wear headgear or facial protection have an increased incidence of recurrent problems: along with the risk of epistaxis, a septal hematoma secondary to repeat trauma can accelerate the risk of complications if not treated appropriately. Continuous trauma to the nasal structures may result in devitalization of the mucoperichondrium, with loss of the vascular supply to the cartilage and/or exposure of the cartilage with subsequent perforation. Septal perforations result in loss of laminar airflow, increase in turbulence, and increase in the drying, scab formation, and continued bleeding (10). Trauma to the nasal skeleton and surrounding facial structures may result in a simple nasal fracture or severe and often life-threatening midface and base-of-skull fractures. Motor vehicle accidents, especially in the days before the common use of seat belts and air bags, often resulted in exsanguinating arterial hemorrhage.

Trauma to structures adjacent to the nose, such as the orbit, sinuses, or middle ear, may result in nasal hemorrhage, without being primary nasal epistaxis. Recurrent and often massive epistaxis in a young adolescent male, with or without nasal obstruction, may be the initial symptoms of juvenile angiofibroma (JA) (11-13).

Massive epistaxis in a patient who presents with the classic triad of prior monocular blindness, ipsilateral orbital fractures, and delayed epistaxis with a recent history of head and neck trauma, should always make one suspicious of a post-traumatic pseudoaneurysm of the internal carotid artery. Delayed epistaxis is often seen following cosmetic and post-traumatic maxillofacial reconstructive surgery. Local irritation and inflammation of the nasal and sinus lining due to upper respiratory tract infections, sinusitis, allergic rhinitis, or environmental irritants such as tobacco, smoke, or chemical exposure, may alter the normal protective mucosal blanket, allowing drying, crusting, exposure, and hemorrhage. With the increasing use of nasal steroid sprays for the control of allergic rhinitis, there has been an increase in epistaxis secondary to their drying effects on the mucosa. Several companies have placed their steroids in an aqueous carrying agent, in an attempt to decrease some of these drying side effects. Persistent unilateral rhinorrhea, foul-smelling nasal discharge, and recurrent bleeding are cause for strong suspicion of foreign body or a tumor in the nose. It is often surprising upon questioning that a child remembers sticking something up his or her nose but was afraid to tell the parents. The foreign body often induces an intense inflammatory response, with the formation of granulation tissue. This granulation tissue often makes it difficult at first to differentiate the foreign body from some other possible source, such as a nasal tumor. Careful removal of the offending foreign body will often result in resolution of all of the nasal symptoms (1).

Any form of intranasal surgery including septoplasty, traditional sinus surgery, or endoscopic sinus surgery, can cause epistaxis as a postoperative complication. Epistaxis following surgery can be immediate or can occur up to several weeks after the surgical procedure.

Systemic Factors

The control of bleeding after blood-vessel injury involves a complex interaction among three systems: the blood vessel wall, the platelets, and the plasma coagulation protein. The three phases of hemostasis consist of (i) formation of a hemostatic plug, (ii) formation of fibrin, and (iii) stability of fibrin and fibrolytic activity (14,15). The interaction of these systems results in normal hemostasis, but if any portion is deficient, bleeding can occur.

The patient with hemostasis disorders may be identified early in life. A history of bruising without significant trauma, prolonged bleeding after dental work or minor cuts, and unusually heavy menorrhea, all are indicators. The most common hereditary bleeding disorder associated with epistaxis is Von Willebrand's disease (VWD). This disease is an autosomal-dominant inherited disorder that presents clinically with mucocutaneous hemorrhage, excessive bleeding after surgery or trauma, and epistaxis. Approximately 60% of patients with VWD complain of recurrent epistaxis. During the course of normal hemostasis, the subendothelium is exposed during injury to the vessel wall, causing platelet aggregation. This is induced by Von Willebrand factor (VWF). When this factor is deficient, there is an increased bleeding time. Unless the bleeding time is specifically performed as a part of the preoperative evaluation, the problem may be missed. The diagnosis is most commonly made with quantitative immunoelectrophoresis or enzyme-linked immunoassay.

Presurgical prophylaxis in patients with Von Willebrand' s is with desmopressin. Desmopressin increases VWF and factor VIII level. This non-blood-product therapy has been recommended over cryoprecipitate.

Functional defects often associated with epistaxis include hemophilia A. This is the most common hemophilia and is secondary to a functional defect of the procoagulant portion of factor VIII. Factor VIII is a complex of two molecules: VWF and procoagulant factor VIII. Hemophilia B is less common, and is secondary to factor IX deficiency. This is also known as Christmas disease. Both hemophilia A and B are sex linked, male inherited, and detected by a prolonged partial thromboplastin time. The difficulty with epistaxis may be variable and can be associated with the severity of the disease (1).

Factor XIII deficiency is a rare autosomal-recessive disorder in which only a homozygote shows the bleeding tendency. Factor XIII, also known as "fibrin-stabilizing factor," is essential in fibrin stabilization and in protection from proteolytic degradation. This may result in delayed bleeding after trauma or surgery as well as impaired wound healing (14). There may be an increase in mortality due to uncontrolled bleeding and intracranial hemorrhage. Acquired factor XIII deficiency can result from inflammatory bowel diseases and acute leukemia (15). Replacement therapy with fresh frozen plasma or factor XIII concentrates has been utilized to control postoperative hemorrhage (14,16,17).

Hereditary hemorrhagic telangiectasia, also known as Osler-Weber-Rendu disease, was first described by Babington in 1865. It is an autosomal-dominant inherited disorder characterized by a strong family history, multiple telangiectasias, arteriovenous malformations that may rupture and bleed, and epistaxis. Symptoms vary according to the location of the lesion; skin, nasal mucosa, gastrointestinal tract mucosa, and pulmonary, cerebral, and hepatic circulation are commonly affected (1,18,19).

Pathological examination reveals thin-walled vessels without smooth muscles and increased angiogenesis resulting in vascular proliferation (arteriovenous fistula and mucosal fragility). Even minor trauma such as nose blowing can cause epistaxis. Epistaxis is the presenting symptom in 90% of patients. Of the patients, 62% become symptomatic by age 16, and almost all patients by 40 years of age. Conservative methods of hemostasis without the use of cautery and cartilage sparing have been recommended as the initial means of treatment. More detailed and advanced forms of treatment will be discussed later in this chapter (20,21).

EPISTAXIS MANAGEMENT

Epistaxis is a common disorder treated by emergency department (ED) staff and otolaryngologists worldwide (22,23). It is the most common emergency in otorhinolar-yngology (24). The annual incidence of epistaxis is 11% (23), with 15 patients per 10,000 requiring physician care and 1.6 per 10,000 requiring hospital admission (22,25-27). Epistaxis is rarely life threatening; however, the complications and outcome of uncontrolled nasal bleeding can be serious and may include significant blood loss, myocardial infarction, stroke, and airway compromise (22). Uncontrolled or unrecognized epistaxis is more common from a posterior bleeding point. Fortunately, most cases of epistaxis originate in the anterior portion of the nasal septum in Kiesselbach's plexus (22,28).

Exsanguinating epistaxis is an uncommon condition but may be life threatening. This condition is more commonly seen in trauma patients with injury to the midface, resulting in maxillary artery laceration. These patients require immediate triage, evaluation, and control of the airway.

Control of the bleeding is essential, along with replacement of fluid loss to prevent hypovolemia and shock. Hypovolemia may be recognized by the effects of inadequate tissue perfusion, cool clammy skin, decreased urinary output, central nervous system symptoms, anxiety, depression, tachypnea, tachycardia, and weak pulses (1). The study reported by Beer et al. (28) on blood loss estimation in epistaxis found that once the measured volume was above 100 mL, visual estimation became grossly inaccurate, and staff tended to grossly underestimate larger blood volume loss. In many severely injured patients, the midfacial skeleton is unstable, making it difficult to adequately place packing and control epistaxis. These patients may require anterior and posterior nasal packs and additional nasopharyngeal packs, once the airway is controlled by intubation or tracheotomy. If packing fails to control the hemorrhage, then external carotid artery ligation and/or ethmoid artery ligation may be performed under local anesthesia (1,24,2931). If the patient can be stabilized, angiography with embolization may be the treatment of choice prior to carotid artery ligation. Patients with a prior history of sphenoid sinus surgery and recurrent epistaxis may have developed a carotid cavernous sinus fistula. Recurrent epistaxis in patients who have suffered head trauma may have also developed a pseudoaneurysm of the intracavernous internal carotid artery. This can occur weeks to years after the trauma and may be associated with monocular blindness and orbital fracture (32). Angiography with embolization has become the primary mode of diagnosis and treatment in these cases. The physician performing this procedure must have a high index of suspicion based on a good medical history and intimate knowledge of the anatomy and surrounding vascular structures.

Control of Epistaxis in the Outpatient Setting

Unlike the massive life-threatening epistaxis seen following trauma or surgical procedures, most patients seeking help for epistaxis in the ED or physician' s office are hemo-dynamically stable and able to respond to questions. After initial resuscitation, a careful medical history is vital. The relevant points to be covered should include frequency and duration of the epistaxis; length of time of each occurrence; recent traumas and surgeries; history of finger manipulation; conditions of the living environment, e.g., dry heat, air conditioning, or low moisture content; coronary or vascular disease; hypertension; connective-tissue disorder; coagulopathies; and hematologic disorders. Medications are import, particularly anticoagulants such as warfarin, aspirin, Plavix, Coumadin, and the like.

Identification of the bleeding point is essential in controlling the epistaxis with localized therapy. The majority of patients will present with anterior or posterior epistaxis. Anterior epistaxis most commonly arises in Little's area and is often venous in origin. Posterior epistaxis most commonly arises in the posterior septum, followed by the lateral nasal wall and Woodruff's naso-nasopharyngeal plexus. This is often arterial in nature (1,26,33). Identifying a specific bleeding point will often take a great deal of time, patience, understanding, and skill. Studies have shown that ED training is often deficient in this respect, and increased levels of training are required in order for the ED to be an effective first line (24). Where possible, the patient should be in a sitting position and as comfortable as possible. Proper equipment should include protective clothing and eye protection, appropriate head light or head mirror, nasal speculum, Bayonet forceps, Frazier and Yankauer suction, and a selection of topical vasoconstrictive and anesthetic agents. Commonly available vasoconstrictive agents for topical use include oxymetazoline hydrochloride 0.05%, phenylephrine hydrochloride 0.25%, and cocaine solution 4% or 10%. For anesthesia, topical lidocaine hydrochloride 4% is useful, as is cocaine in either concentration. These agents may be applied by spray or dropper, or on pledgets. Proper preparation of the nasal lining may be even more important in posterior epistaxis.

The increasingly widespread availability of rigid or flexible fiberoptic nasophar-yngoscopes in both EDs and otolaryngologist offices has dramatically improved visualization. After application of one of the vasoconstrictive agents and anesthetic agents, the nose can be more easily examined. Although these agents often may stop the bleeding before identification is made, every effort should be made to identify the offending vessel, since epistaxis may reoccur once their effect has worn off.

Other methods of controlling or decreasing epistaxis include local submucosal injection of 1% lidocaine plus 1:100,000 parts epinephrine.

An injection of local anesthetic with epinephrine into the pterygopalatine canal may be helpful in controlling a posterior nasal bleed. This may be effective by itself, or it may slow the bleeding substantially, allowing cauterization or packing under a more controlled situation. The ability to identify the greater palatine foramen is essential to this technique. It is located in the hard palate just anterior to the soft palate junction. It may be palpated as a slight depression in the mucosa just medial to the last molar tooth and in front of the hamulus process. Practicing palpating this point during routine surgical procedures, such as tonsillectomy, may be beneficial when an emergency with active bleeding arises.

Approximately 3 mL of local anesthesia 1% lidocaine (Xylocaine) with 1:100,000 epinephrine (adrenaline) should be injected into the pterygopalatine canal and then into the pterygopalatine fossa to block the sphenopalatine branch of the internal maxillary artery. A slight bend in the needle may help with accurate placement. The needle should only be advanced to 28 mm; at a depth of 40 mm, the needle may enter the orbit. As always, aspiration before injection is important (20).

Nasal Packing

Over the years, nasal packing techniques and materials have continued to evolve; however, the basic principle is not new. Nasal packing for epistaxis was first documented by Hippocrates in the fifth century BC (27). The nose is a complex and convoluted passageway. All packing works by one essential principle: maintaining pressure on the walls of damaged blood vessels and allowing an organized clot to form. The placement of nasal packing is uncomfortable and often traumatic for the patient. The use of topical vasoconstrictive agents and local anesthesia may help but not eliminate the discomfort. The removal of packing may also be uncomfortable and result in recurrent bleeding (22). Packing may remain in place for three to five days, resulting in additional complications.

Anterior Nasal Packing. Traditional anterior nasal packing consists of careful placement of Vaseline gauze (0.5 x 72 inch) coated with an antibiotic ointment in a layered fashion (Fig. 2). The use of local anesthesia not only decreases the pain, allowing the physician or ED staff better control, but may also reduce the risk of a vasovagal response by blocking the nasal-vagal reflex (11). This technique requires certain equipment and training for proper placement. The very end of the gauze should not be placed posterior in the nose, but the pack should be grasped several centimeters beyond the end, leaving the end near the anterior choana or nostril. This will help prevent aspiration or displacement of the pack. Care must be taken to place each ensuing section back toward the posterior choana, to be fully effective. Molding the finished pack with slight digital pressure will help to fill the convolutions of the nasal cavity. The technique is demonstrated in Figure 2. Removal of this gauze can often roughen the already friable mucosa, resulting in recurrent bleeding. If possible, a protective layer of Telfa or absorbable hemostatic material such as Surgicel or Oxycel (oxidized regenerated cellulose) may be placed over the bleeding site prior to traditional packing. This may help to prevent recurrent epistaxis upon removal. In significant bouts of epistaxis, this may not be feasible.

Because of the time involved, special training, and discomfort to the patient with traditional packing, new types of nasal packing material have been developed. One such innovation is compressed hydroxylated polyvinyl acetal (Merocel) or polyvinyl alcohol (PVA) (Expandacell® Rhino Rocket®). Rhino Rockets are hydrophilic and expand to many times their original size when wet. Often, newly developed packs are comprised of expandable preshaped balloons with a softer coating, e.g., Rapid Rhino Nasal Pack with Gel Knit (Shippert Medical Technologies, Englewood, New Jersey, U.S.A.) (Fig. 3). These new packs are more easily inserted by ED staff. Prospective studies examining these newer packs have shown that packing with coated expandable balloons may be easier to insert for some physicians. Both types of nasal packs, those with a coating and those without, were found to be equally effective in controlling epistaxis (1,22).

FIGURE 2 The proper technique is demonstrated for the placement of a traditional Vaseline gauze anterior nasal pack.

FIGURE 3 Various packing material and packs use to control epistaxis. (A) Merocel 2000 Laminated Nasal Dressing. 8 cm with drawstring (Medtronic XOMED, Jacksonville, FL, U.S.A.). (B) Ultracell Classic Nasal Pack (Ultracell Medical Technologies Inc., North Stonington, CT, U. S.A.). (C) 30 cc Foley Catheter. (D) 1/2" x 72" Vaseline Gauze Packing Strip. (The Kendall Co., Mansfield, MA, U.S.A.) (E) Rapid Rhino 7.5 cm Anterior-Posterior Nasal Pack (Applied Therapeutics Ltd., Glenfield Leicestershire, U.K.). (F) Surgicel Absorbable Hemostat (Oxidized Regenerated Cellulose) (Ethicon Inc., Somerville, NJ, U.S.A.).

FIGURE 3 Various packing material and packs use to control epistaxis. (A) Merocel 2000 Laminated Nasal Dressing. 8 cm with drawstring (Medtronic XOMED, Jacksonville, FL, U.S.A.). (B) Ultracell Classic Nasal Pack (Ultracell Medical Technologies Inc., North Stonington, CT, U. S.A.). (C) 30 cc Foley Catheter. (D) 1/2" x 72" Vaseline Gauze Packing Strip. (The Kendall Co., Mansfield, MA, U.S.A.) (E) Rapid Rhino 7.5 cm Anterior-Posterior Nasal Pack (Applied Therapeutics Ltd., Glenfield Leicestershire, U.K.). (F) Surgicel Absorbable Hemostat (Oxidized Regenerated Cellulose) (Ethicon Inc., Somerville, NJ, U.S.A.).

Even anterior nasal packing is not without risk. Toxic shock syndrome (TSS), diagnosed with the use of vaginal packing, can also occur with nasal packing. Staphylococcus aureus can colonize the nasal packages and produce TSS toxin I. The majority of TSS cases follow nasal or sinus surgery where the mucosal barrier is disrupted, but it also can occur after packing for epistaxis. Infection is accompanied by sudden onset of fever, vomiting, diarrhea, hypotension, rash, desquamation, and eventual shock. Early recognition and intervention is essential to prevent a potentially fatal outcome. Appropriate use of prophylactic oral antibiotics is recommended with nasal packing (1,34).

Special cases of anterior epistaxis that may require a less aggressive form of packing include those patients with chronic disorders that may lead to coagulopathies or mucosal vascular fragility. These disorders may include leukemia, collagen vascular diseases, septal perforations, or coagulopathies (35). Control of hemorrhage initially with Surgicel or Oxycel or Avitene® (microfibrillar cross-linked bovine tropocollagen) has been successful in many patients (36). This minimally invasive method has avoided further destruction of nasal mucosa and decreased rebleeding upon removal (1).

Posterior Nasal Packing. If a patient continues to bleed despite a well-placed deep anterior pack, a posterior nasal pack may be indicated. The placement of a posterior pack is not without potential complications and should be carefully evaluated. The traditional posterior pack is often constructed from cylindrical dental rolls (rolled gauze sponges, umbilical tape, and silk tie). Red rubber catheters are useful for pulling the umbilical tape or silk tie through the nose. Because of the cumbersome method of application, the patient must be well informed of the method, risks, and techniques utilized for placement. Intravenous access for fluid resuscitation and possible sedation is advised. If this is not feasible, then placement in the operating room under anesthesia may be considered. One technique is as follows:

Rolling a surgical sponge tightly or placing three long cylindrical dental rolls together may form the posterior nasopharyngeal pack. These may be tied together tightly with two #1-0 silk sutures. The silk suture should be left long enough that it can be brought out through the nose. An alternative is to tie two umbilical tapes to the nasopharyngeal roll once it is formed. Two red rubber catheters are passed to the already decongested nasal cavities, into the oral cavity, and withdrawn through the mouth. The ends of the silk sutures or umbilical tapes are tied to the red rubber catheters. The red rubber catheters are pulled through the nose, taking the sutures or umbilical tapes with them, and eventually the posterior pack. This is simultaneously passed into the oral cavity and advanced behind the soft palate. Once the posterior pack is in place, a good anterior pack is now placed. Finally, the posterior pack is secured by tying the sutures or umbilical tapes over a second bolster in front of the columella (Fig. 4).

All patients with a posterior pack should be admitted to the hospital, to be monitored in an appropriate setting. Pulse oximetry is highly recommended, since these patients may have decreased oxygen saturation or hypoventilation. IV hydration, antibiotics, and judicial analgesia are important. If not well protected, columellar necrosis or alar necrosis

FIGURE 4 The steps utilized to place a traditional posterior nasal pack. (A) Red rubber catheters are passed through the nose until visible in the oropharynx. The catheters are then tied with silk sutures or umbilical tape. (B) The catheters are pulled out through the nose. The silk sutures or the umbilical tapes are secured to the posterior pack. The posterior pack is pulled and manually pushed into place. An anterior pack is then placed. (C) The silk sutures or umbilical tape is secured over dental rolls to maintain forward pressure and protect the columella. (D) Finished view of posterior pack.

FIGURE 4 The steps utilized to place a traditional posterior nasal pack. (A) Red rubber catheters are passed through the nose until visible in the oropharynx. The catheters are then tied with silk sutures or umbilical tape. (B) The catheters are pulled out through the nose. The silk sutures or the umbilical tapes are secured to the posterior pack. The posterior pack is pulled and manually pushed into place. An anterior pack is then placed. (C) The silk sutures or umbilical tape is secured over dental rolls to maintain forward pressure and protect the columella. (D) Finished view of posterior pack.

may occur. This has been seen to develop several days after the pack is removed, secondary to vascular tissue compromise. The external nose should be checked routinely for any signs of vascular compromise. Posterior packs are routinely left in place for three to five days. The pressure may be slowly released and the pharynx observed for any signs of rebleeding. The patient who fails anterior and posterior packing may be a candidate for further intervention; this will be discussed later.

An alternative to the traditional posterior pack is the balloon pack. Initially, a 30 cc Foley catheter balloon was utilized. Passing the Foley catheter through the nose was easier, faster, and could be done in the ED without sedation or a trip to the operating room. Once the balloon was appropriately inflated, usually with saline, the catheter was held tightly in position with a clamp. It is imperative that the caudal structures of the nose be well padded with multiple surgical sponges. Even with this, necrosis was not uncommon. This concept was further improved with the development of specifically designed epistaxis balloon packs. Some are a combination of balloons with Merocel packing, with or without integrated breathing tubes. Like all other packs, these are placed blindly, and pressure on the specific bleeding site cannot be guaranteed.

Maxillary Artery Ligation

Transantral ligation of the maxillary artery has become a standard for the control of epistaxis. Hirsh reported this procedure in 1936 (36), and the names Caldwell and Luc have become synonymous with this approach (5,37,38). The Caldwell-Luc antrostomy can be performed under local anesthesia. The incision extends from the root of the canine tooth to the malar eminence over the first molar tooth. It should be located about 1 cm above the gingival margin to decrease bleeding and allow adequate tissue for suturing the incision closed. The upper lip flap is freed in the subperiosteal plane, being careful to preserve the infraorbital nerve. The antrum is entered with a fine osteotome or rotating cutting burr (37). The posterior maxillary sinus wall is identified and a laterally based U-shaped mucosal incision is made. The posterior maxillary wall is then removed. The remainder of the procedure is best performed under magnification with either surgical loops or operating microscope. The fat is carefully teased away, and the vessels, maxillary artery, and distal branches within the pterygopalatine fossa are clipped. Several studies have recommended that anterior ethmoid artery ligation be performed at the time of maxillary artery ligation (5,39); however, the overall benefit and long-term results are uncertain. Ligation of the sphenopalatine artery by a microsurgical approach was introduced in the 1970s (5,40-43). Selective sphenopalatine artery ligation where it exited the sphenopalatine foramen, using the transantral approach, was described by Simpson. The advantage of this technique was that it avoided the ptery-gomaxillary fossa. This was thought to avoid the complication from collateral circulation (44).

Endoscopic Management of Epistaxis

The nasal cavities have often been an area of uncertainty in the identification of bleeding sites. Limited visual access, even with a strong headlamp light, has often resulted in a less-than-satisfactory outcome. The advent of fiberoptic technology for illumination has made visualization of the deep recesses of the nose a reality. Surgical rigid endoscopes are available with various angles, making the visualization easier. They also allow cauterization of specific bleeding sites. Monopolar suction cautery has proven particularly well suited to this application (1). Bipolar cautery also has been utilized. Several reports have demonstrated lower complication rates, higher success rates, and shorter hospitalization times (41,42). Temporary palatal numbness is the major adverse effect of this procedure.

Endoscopic Ligation of the Sphenopalatine Artery

The transantral approach has been the gold standard for control of severe epistaxis, with a success rate of 80% to 95%. It has been considered to have a low complication rate; however, hypesthesia or neuralgia of the infraorbital nerve, scarring of the gingivolabial sulcus, painful sublabial incision, and oroantral fistula may occur. There is also the risk of collateral blood flow and continued or recurrent epistaxis. In order to prevent these complications, endoscopic ligation of the sphenopalatine artery via a transnasal approach has been described (43). If necessary, temporary control of bleeding is obtained with packing. This procedure can be performed under local anesthesia, but general anesthesia may be preferable. The anterior pack is removed, and the nose is decongested with oxymetazoline 0.05% solution on cottonoids or neurosurgical patties. The posterior pack may be led down to allow drainage of accumulated blood and reinflated if necessary to temporarily control bleeding. The nose is examined with a 30° 4 mm endoscope. Visibly bleeding vessels can be cauterized with a monopolar suction cautery or bipolar cautery. As in any surgery, adequate visualization is necessary; therefore, an endoscopic anterior ethmoidectomy or septoplasty may be indicated.

An uncinectomy is performed, followed by a large middle meatal antrostomy. Care should be taken not to injure the nasolacrimal duct. The antrostomy is enlarged in a posterior direction until level with the posterior wall of the maxillary sinus. A Cottle elevator is utilized to elevate the lateral nasal wall in a subperiosteal plane. This sphenopalatine foramen is located in the superomedial corner of the maxillary sinus. The surrounding bone is removed, with a Kerrison rongeur confirming the sphenopalatine artery. If the patient's nose permits entry of an endoscope with necessary instruments, the endoscope can be placed into the antrum with a trocar. The sphenopalatine artery may be coagulated or ligated with a hemoclip (43).

Some authors have reported that advantages of endoscopic ligation of the sphenopalatine artery have included decreased surgical time, decreased morbidity, and a shorter recovery (43). Other studies, however, have shown that inpatient treatment with nasal packing was associated with a lower overall hospital charge. It was thought that all three methods (packing, arterial ligation, and embolization) had similar complication rates (45). Further evaluation is necessary before a statement can be made for one method over the others.

Septal Dermatoplasty

The objective of dermatoplasty is to replace the fragile respiratory epithelium with a tougher epithelium such as skin. The procedure is most commonly described in the treatment of epistaxis in patients with Osler-Weber-Rendu disease. Saunders described the operation in 1960 (46). The best donor site is the anterior thigh wall above the knee. A split-thickness skin graft of about 0.014" is harvested with a dermatome. A ring curette is utilized to remove all of the mucosa from the anterior half of the nasal septum, floor, and lateral walls of the nose. Laterally, the mucosa of the inferior turbinate is also removed. A narrow strip of skin is resected from the mucocutaneous junction of the vestibule to act as a sewing edge to attach the graft with a #4-0 absorbable suture. The grafts are placed in the nose like a sleeve. Careful packing is very important. Packing should be coated with antibiotic ointment and left in place for five days. After several weeks, the interior of the nose can be cleaned daily with oil, soap, and water. Even after septal dermatoplasty, recurrent epistaxis can occur, but it is usually not as severe as it was preoperatively.

Ethmoid Artery Ligation

The anterior and posterior ethmoid arteries supply blood to the upper portion of the nose from the internal carotid artery system. Ligation of these arteries can decrease blood flow to decrease epistaxis. This is often performed conjointly with maxillary artery ligation. Knowledge of the anatomy of the region is extremely important to prevent complications. The anterior ethmoid artery foramen lies 14 to 22 mm posterior along the frontoethmoidal suture line. The posterior ethmoid artery is further back at a very variable location. Of significance is the location of the optic nerve, which lies 4 to 7 mm more posterior than the posterior ethmoidal artery.

The procedure to ligate these arteries has been extensively described. In brief, a Lynch incision is made in a curvilinear manner between the inner canthus and the middle of the nose. The area is first infiltrated with local anesthesia (1% lidocaine and 1:100,000 epinephrine) down to the level of the periosteum. The eye can be protected with a corneal shield or a #5-0 silk tarsorrhaphy stitch, after placement of ophthalmic antibiotic ointment. Dissection is carried down to the level of the periosteum. The periosteum is incised and elevated posteriorly down to the frontoethmoid suture line. Malleable retractors are very useful during this dissection. The artery can be ligated with bipolar cautery or vascular clips (Fig. 5). Ethmoid artery ligation is still an important surgical procedure, even with newer methods such as angiography and embolization. In specific cases, the artery may need to be ligated prior to angiography and embolization to prevent the embolization particles from entering the ophthalmic circulation.

Selective Embolization

Epistaxis is generally widespread, with 60% of the adult population having an episode during their life, while only 6% of patients require treatment (31,47). The conservative methods to control epistaxis have included pressure, vasoconstriction, and anterior and posterior packing. When these conservative methods have failed, surgical ligation has been undertaken. In 1974, Sokoloff et al. (48) described the embolization techniques to stop

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