----------------------------------------------------------------------------- TITLE: EPISTAXIS SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: January 5, 1994 RESIDENT PHYSICIAN: John Yoo, M.D. FACULTY: Francis B. Quinn, Jr., M.D. DATABASE ADMINISTRATOR: Melinda McCracken, M.S. ------------------------------------------------------------------------------ "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." I. Introduction A. Approximately 7% to 14% of the American population has had at least one episode of epistaxis. B. Only about 10% of these nosebleeds come to medical attention; of these, 5% to 10% require Otolaryngologic consultation to control bleeding. C. Most nosebleeds are usually minor, resolve spontaneously, and do not require medical attention. D. However, any episode of epistaxis should not be taken lightly for fatal consequences can and do occur: 1. Aspiration 2. Hypotension 3. Hypoxia with resultant myocardial infarction II. Vascular Anatomy For its role of humidifying and warming inspired air, the nasal mucosa has a rich blood supply derived from both the internal and external carotid systems, with extensive anastomoses between these blood vessels. A. External carotid 1. Main contributor to blood supply of nasal mucosa 2. Of its eight branches, the facial artery and maxillary artery are the main sources of blood to the nose. Facial artery(external maxillary artery) a. Gives rise to the superior labial artery, which enters the nose just lateral to the nasal spine; it sends two branches to the nose: i. Septal branch to the anterior nasal septum and floor ii.Alar branch to nasal ala Maxillary artery(internal maxillary artery) a. More important than facial artery b. Third part of internal maxillary artery enters the pterygopalatine fossa, giving off (among others) the sphenopalatine and greater palatine arteries. i. Sphenopalatine artery enters the nasal cavity through the sphenopalatine foramen located at the posterior limit of the middle turbinate. It gives off the posterior septal branch which courses over the nasal roof underneath the sphenoid bone to supply the septum inferiorly, as well as the posterior lateral nasal branch which supplies the turbinates and meati (as well as the ethmoid and maxillary sinuses). ii.Greater palatine artery can originate from internal maxillary, sphenopalatine, or descending palatine arteries. It descends through the pterygopalatine canal, to emerge from the greater palatine foramen as the greater palatine artery. It then courses anteriorly in close contact with the alveolar ridge where it makes an upward turn, passing through the incisive foramen to supply the anterior, inferior nasal septum. B. Internal Carotid 1. At the level of the anterior clinoid, the internal carotid artery gives off its first intracranial branch, the ophthalmic artery, which enters the superior orbital fissure and gives off (among others) the posterior and anterior ethmoid arteries. Posterior ethmoid artery a. Branches from the ophthalmic artery shortly after it enters the orbit. The posterior ethmoid passes medially to exit the orbit through the posterior ethmoid foramen, located 3 to 7 mm anterior to the optic nerve. It travels through the posterior ethmoid air cells, enters the anterior cranial fossa, and penetrates the cribiform plate to reach the nose. This artery supplies primarily the superior turbinate and a corresponding area of the septum. Anterior ethmoid artery (larger of the two) a. Branches from the ophthalmic artery anterior to the posterior ethmoid artery and exits the orbit through the anterior ethmoid foramen, located about 10 mm anterior to the posterior ethmoid foramen. It travels through the anterior ethmoid air cells, enters the anterior cranial fossa, and enters the nose through the open nasal slit(a space between the crista galli and cribiform plate). It nourishes the anterior third of the lateral and medial walls. C. Problem areas 1. Kiesselbach's plexus(a.k.a Little's area) is located in the area of the anterior caudal nasal septum where the sphenopalatine, greater palatine, anterior ethmoid, and superior labial arteries anastomose. It is estimated that approximately 80% to 90% of all epistaxis occurs in this area, especially in children and young adults. 2. Woodruff's plexus corresponds to the area where the sphenopalatine artery enters the nasal cavity through the sphenopalatine foramen at the posterior limit of the middle turbinate. Most of the posterior nosebleeds occurs here, especially in older adults and those with systemic illnesses. III. Epidemiology A. Anterior epistaxis more likely in children and young adults. B. Posterior epistaxis more likely in older adults, especially men in the fifth decade of life with hypertension and arteriosclerosis. C. Epistaxis more likely during winter months. This may be due to increased upper respiratory infections and dryer air caused by the use of overheated and underhumidified environments. D. Nosebleeds unusual in infants, but there is a steady rise in incidence with advancing age. IV. Physiology A. Nasal mucosa made up of respiratory epithelium. 1. Pseudo-stratified ciliated columnar epithelium 2. Basement membrane 3. Vascular channels 4. Mucoperiosteum\mucoperichondrium 5. Bone or cartilage B. Serous glands from middle and superior turbinates produce secretions which protect mucosa. C. If secretory function becomes compromised, mucosa becomes dry and crusty with loss of ciliary function. D. The mucosa cracks, allowing bacteria to penetrate injured mucosa, producing an inflammatory reaction with subsequent granulation tissue. E. The extremely friable granulation tissue bleeds easily with minimal trauma. F. The invading bacteria may also contribute to epistaxis by producing fibrinolytic enzymes such as staphylokinase and streptokinase. V. Etiology Causes of epistaxis can be divided into two broad categories: Local and Systemic. In 10% of cases, etiology of nosebleed is never determined. Local A. Trauma 1. Probably the most common cause of epistaxis. 2. Direct trauma to the nose without fracture can cause epistaxis by its shearing effect resulting in mucosal laceration, usually at the septum, lateral recesses of piriform aperture, junction of upper lateral cartilages with nasal bones, lateral turbinates, or at junction of quadrilateral cartilage with bony septum. 3. Direct trauma to the nose with fractures causes nosebleeds by mucosal laceration or arterial laceration due to the sharp, raw bone edges. Can have epistaxis with trauma to sinuses, orbits, middle ear, and base of skull (can cause epistaxis if involves the anterior sphenoid sinus wall because it lacerates the posterior septal branch of sphenopalatine artery as it crosses the nasal roof underneath the sphenoid bone to get to the septum). 4. Habitual nose picking, especially in children, causes anterior septal nosebleeds. Chronic irritation of this area causes crusting and excoriation with formation of friable granulation tissue that bleeds easily on further nose picking. 5. Surgical procedures of the nose and sinuses such as septoplasty, rhinoplasty, turbinate and sinus surgery, as well as orbital floor procedures can cause epistaxis usually from the mucosal incisions, but less frequently as a result of complications such as transection of vessels and septal perforations. 6. Barotrauma(flying or scuba diving) can cause hemorrhage within paranasal sinus cavities with subsequent epistaxis. B. Anatomic or structural deformities 1. Septal spurs and deviations involving the cartilaginous or bony septum, either congenital or acquired, can cause epistaxis by interrupting the normal airflow pattern inside the nasal cavity. Eddy currents are produced that dry the adjacent nasal mucosa and cause crusting with subsequent epistaxis. Bleeding at Little's area or just posterior to septal deformity. Can benefit from septoplasty or SMR. 2. Septal perforations due to various causes(septal surgery, nose picking, trauma, granulomatous disease, non-medical use of cocaine) also causes epistaxis. Granulation and crusting occur on the margins of the perforations which bleed easily. C. Inflammatory conditions 1. Usually manifests as congestion and blood-streaked mucus, but can develop frank epistaxis. 2. Various local inflammatory reactions can alter the normal mucosa, causing dryness and crusting, which allows introduction of bacteria and subsequent formation of granulation tissue. Increased vascularity and greater friability of of the vessels are characteristic of inflamed tissue. a. upper respiratory infection b. allergic rhinitis c. sinusitis d. nasal polyposis e. environmental irritants f. toxic chemicals (such as printer's ink, sulfuric acid, phosphorus, ammonia, gasoline) 3. Patients with recurrent epistaxis may have fibrinolytically active bacteria in the nasal cavity that produce streptokinase and staphylokinase. D. Foreign bodies 1. Usually lodged in children and mentally retarded individuals; should be suspected with unilateral foul discharge. 2. Foreign bodies that cause bleeding usually have (i)sharp edges, (ii)irritating chemical properties, and/or (iii)porosity. 3. Bleeding occurs from the inflamed mucosa and granulation tissue around the foreign body. 4. Intra-nasal parasites, including leeches, can lodge in the nose or nasopharynx and cause epistaxis. E. Tumors 1. Benign and malignant tumors in the nasal cavities, nasopharynx, and sinuses can present with epistaxis; causes bleeding indirectly from erosion into normal sino-nasal structures or directly from tumors of high vascularity(i.e. hemangioma). 2. Bleeding usually unilateral and can be intermittent or constant. 3. Some tumors to consider include nasal hemangioma, hemangiopericytoma, papilloma, squamous cell carcinoma, adenoid cystic carcinoma, adenocarcinoma, and melanoma. 4. Juvenile nasal angiofibroma should be considered when a male adolescent presents with nasal obstruction, epistaxis, and a nasal or nasopharyngeal mass. It can cause severe spontaneous epistaxis. F. Aneurysms 1. Aneurysms of the extradural or cavernous sinus portion of the internal carotid artery can cause life-threatening epistaxis. 2. Often a history of cranial surgery or head trauma with sudden onset unilateral blindness and cranial nerve deficits (anosmia and involvment of CN II-VI). 3. Due to the inaccessibility of this area, often treated with arterial embolization. Systemic A. Hypertension-Arteriosclerosis 1. Hypertension and atherosclerotic changes associated with epistaxis, especially posterior nosebleeds in the older patient. 2. Posterior epistaxis often referred to in the past as "cardiovascular epistaxis" due to its association with hypertension. 3. Accumulation of atheromatous material in the blood vessels and replacement of the muscular tunica media of the arteries by fibrous tissue decrease the hemostatic capabilities of the arteries. 4. Although no scientific studies have shown any significant differences in the prevalence of nosebleeds between patients with or without HTN, the treatment of epistaxis should include measurement of blood pressure and treatment if needed. B. Blood dyscrasias 1. Any condition that impairs or decreases clotting factors and/or platelets can cause epistaxis that is difficult to control. 2. Platelet abnormalities a. Thrombocytopenia defined as < 100,000 platelets/mm3, but no spontaneous bleeding until < 40,000. Can get spontaneous mucus membrane bleeding at 10-20,000. i. Decreased production: cytotoxic agents, aplastic anemia, malignancies, among others ii. Increased destruction: prosthetic heart valves, DIC, sickle cell crisis, TTP, ITP, drugs, hypersplenism, among others. b. Platelet dysfunction i. Quantitatively sufficient but platelets don't function properly. ii. The most common cause is the use of aspirin(permanent) and other NSAIDs(temporary) which impair platelets by inhibiting cyclo- oxygenase which is asso. with thromboxane production from arachidonic acid. This biochemical pathway is important for platelet aggregation. iii.Systemic disorders such as uremia and liver failure and vitamin deficiencies also predispose to platelet dysfunction causing epistaxis. 3. Clotting factor abnormalities a. Usually a history of easy bruising, prolonged bleeding, and/or family history of the former. b. Primary coagulopathies i. Factor VIII - Hemophilia A:the most common clotting factor defect(80% of the cases) ii. Factor IX - Hemophilia B or Christmas disease(13% of the cases) iii. Factor XI - (6% of the cases) iv. Von Willebrand's Disease - most common inherited bleeding disorder iv. Deficiencies of fibrinogen, prothrombin, factors V, X, VII, and XII extremely rare. c. Secondary coagulopathies i. Liver disease can cause bleeding due to diminished synthesis of clotting factors. ii. Vitamin deficiencies can exacerbate epistaxis (such as Vitamin K which is needed to activate factors II, VII, IX, and X). iii. Drugs can affect the clotting mechanism such as coumadin which antagonizes action of Vitamin K and heparin which inactivates thrombin via anti-thrombin III. iv. Systemic illnesses such as DIC can consume clotting factors. C. Hereditary hemorrhagic telangiectasia (HHT) 1. Also known as Osler-Weber-Rendu disease, it is the most common disease of vascular structure. 2. It is an autosomal dominant disease, and as such, affects both sexes. 3. Pathologic condition is lack of contractile elements in the vessel walls which makes it difficult to stop the epistaxis spontaneously. 4. The telangiectasias are composed of dilated venules and capillaries or small AV malformations that can be found in the skin or mucosal surface of the aerodigestive and genitourinary tracts, although they can occur anywhere on the body; these telangiectasias bleed in response to minor trauma. 5. Most common symptom is recurrent, spontaneous epistaxis that begins with puberty and worsens with age; patients often require hundreds of blood transfusions. 6. Tests of clotting factors and platelet function usually normal. 7. Treatment difficult and usually unsuccessful. D. Other 1. Alcohol abuse can predispose to epistaxis by decreased clotting factor synthesis, bone marrow suppression, platelet inhibition, and vitamin deficiencies. 2. Systemic toxic agents (i.e. heavy metals) 3. Infectious disease such as typhoid fever, nasal diphtheria, whooping cough, scarlet fever, rheumatic fever, leprosy. 4. Cardiovascular conditions such as congenital heart failure, mitral stenosis, and coarctation of the aorta can predispose to epistaxis because of increased systemic vascular resistance that is translated back to the nasal mucosa. 5. In 10% of the cases, no specific etiology or predisposing factor will be discovered. VI. Initial Management A. The degree, site, clinical state, and etiology of the nosebleed dictates the initial treatment. Initial treatment measures should focus on immediate control of hemorrhage and correction of hypovolemia(follow basic A-B-C's of resuscitation). B. Generally, Normal Saline or Lactated Ringer's sufficient for fluid management, but consider transfusion when volume loss is greater than 30%(1500 mL in adults) or if ongoing loss exceeds 100 ml/min: 1. Acute hemorrhage with hemodynamic instability 2. Pulse usually > 120/min 3. Respiratory rate 30-40/min 4. Blood pressure decreased C. Once patient is stable or if patient presents with mild epistaxis, important to get good history and physical examination. D. History 1. Past medical history(i.e., HTN, DM, liver disease, cardiopulmonary disease, alcoholism) 2. Duration and steps taken to stop bleeding 3. Estimated blood loss; symptoms of hypovolemia or orthostasis 4. Periodicity; previous epistaxis 5. Side of bleeding; nasal obstruction 6. Nasal bleeding alone or with spitting blood(suggests posterior epistaxis) 7. Recent head/neck trauma or surgery 8. Personal and family history of prolonged bleeding and easy bruisability 9. Medications(esp. ASA, Coumadin, and NSAID's) 10. Toxin exposure E. Physical Examination 1. Initially, evaluate adequacy of airway and circulating blood volume. 2. General physical exam with particular attention to skin and mucus membranes for vascular lesions. 3. Thorough exam of the nasal cavity should then be performed to seek the bleeding site as well as possible septal deviations or mucosal and structural abnormalities with: a. Patient and physician comfort b. Adequate lighting(head mirror or headlight) c. Nasal speculum d. Bayonet forceps e. Suction to remove clots(Frazer or Yankhauer) f. Adequate vasoconstriction and topical anesthesia (such as 4% cocaine solution on cotton pledgets) g. Rigid 0o or 30o telescope helpful F. Laboratory Studies 1. CBC 2. Prothrombin time (extrinsic) 3. Partial Thromboplastin time (intrinsic) 4. Liver function tests (as indicated) 5. Type and cross (as indicated) VII. Non-Surgical Modalities A. Most nosebleeds are minor and will cease spontaneously or following simple measures: 1. Have patient sit quietly, lean forward to avoid passage of blood posteriorly into the nasopharynx, and apply direct two-finger pressure over the anterior nose. 2. Topical decongestants such as AFRINTM and ice packs to midface may also control bleeding. 3. Adjunctive treatment includes: a. Humidity in the home and workplace b. Nasal saline sprays c. Avoid straining d. Sneezing with mouth open e. Avoid nose-picking and nose-blowing f. Discontinuing medications(such as aspirin and anticoagulants) B. Cautery 1. Once the active or inactive bleeding site is identified, can attempt to arrest nosebleed by chemical or electrical cautery. Patient should apply antibiotic ointment to cauterized area until healed. 2. Chemical cautery A. tracholoracetic acid should be applied to the bleeding site for at least 30 seconds b. Beware of performing overly aggressive cautery on both sides of septum as cartilage exposure or septal perforation can occur. 3. Electrical cautery a. Since an actively bleeding vessel is virtually impossible to cauterize with AgNO3, electrocautery with suction Bovie may be the next choice. b. It provides greater depth of penetration, but is also more likely to cause exposure of cartilage and/or septal perforation. c. Since electrocautery is more painful than AgNO3, may need injection with local anesthetic. d. Even posterior bleeding sites can be treated with chemical or electrical cautery after visualization with rigid or flexible endoscopes. C. Cryotherapy 1. Not frequently used, but can attempt control of severe posterior epistaxis by use of cold water flowing through elastic catheters. 2. Low complication rate. D. Anterior Packing 1. If the above measures fail, and the bleeding appears to originate from an anterior site but cannot be identified, need anterior packing. 2. Nose has to be adequately anesthetized prior to packing. 3. 1/2" Vaseline gauze impregnated with antimicrobial ointment is packed into the nose under direct visualization with bayonet forceps. 4. Space between floor of the nose and inferior turbinate is packed first, followed by placement of horizontal layers in a pleated fashion continued superiorly until the pack fits moderately tight. Out-fracturing of inferior turbinate may be necessary to allow adequate packing. 5. Only closed loops of gauze are placed posteriorly to prevent strands from dangling down from the nasopharynx and gagging the patient. 6. Better to pack only the bleeding side to avoid septal ulceration and necrosis, as well as to allow the patient to breathe through one patent nostril. 7. Anterior packs left in place for 2-7 days (depending on author), depending on severity and location of epistaxis. 8. Prophylactic antibiotics should be given because of the risks of: a. sinusitis from blockage of the sinus ostia b. toxic shock syndrome from staph. aureus 9. There is a variety of nasal tampons, sponges, and inflatable devices on the market that may be used in lieu of the traditional 1/2" by 72" Vaseline gauze: a. Nasal tampon(eg, MerocelTM sponge) can be placed into the nose that expands to tamponade the mucosa with the addition of water. b. Gel-foamTM sponges, SurgicelTM or surgical oxycel(oxidized regenerated cellulose), and/or AviteneTM(microfibrillar collagen) can also be used to control anterior epistaxis. They generally dissolve in 2-3 weeks. When used with antibiotic ointment, they are extremely helpful in patients with blood dyscrasias, thrombocytopenia, or HHT: avoids bleeding associated with unpacking the nose. c. Porcine strips(salt-cured subdermal fatty tissue) also appear to be helpful in patients with profound thrombocytopenia by promoting coagulation through a phospholipase-like activity. 10. Pack not only works by direct mucosal pressure, but also by creating mucosal inflammation and edema. E. Posterior Packing 1. Posterior pack should be placed if a posterior nosebleed is refractory to endoscopically-directed cautery or if epistaxis continues despite a properly placed anterior pack. 2. Can use a standard posterior pack or inflatable balloon to apply pressure posteriorly. 3. Standard posterior pack a. Made up of finely rolled gauze or lamb's wool tied in the center with two long pieces and one short piece of umbilical tape or 0-silk ties. b. Patient given adequate anesthesia and sedation. c. Small red, rubber catheter passed through bleeding nostril and brought out the mouth. The two long ties are then secured to distal end of the catheter and pulled back through the nasal cavity as the catheter is withdrawn from the nose until the pack is secured in place over the involved choana. Traction on the ties maintained while an anterior pack is placed. Ties are then fastened over a dental roll in front of the nostril. The small suture previously tied to the pack is used to retrieve the pack at the time of removal. d. Pack removed in 4-7 days(depending on author). 4. Inflatable balloon packs a. Foley catheter: 12-16 foley catheter placed along floor of the nose until visualized in nasopharynx. Balloon is inflated, and the catheter is retracted anteriorly to wedge the balloon snugly onto the posterior choana. After an anterior pack is placed, catheter secured with a piece of tubing slid tightly against anterior pack. b. Commercially available epistaxis balloon tampons(such as Epi-statsTM) provide a double- balloon system that serves as both an anterior and posterior pack. c. Advantages of inflatable balloon packs: i. more easily inserted ii. less traumatic to the patient iii.allows a partial nasal airway d. Disadvantages include: i. less effective than standard pack since the pressure applied to the internal nose is not even ii.some balloons inflated with water, others with air: the two are not interchangeable 5. Post-packing management a. All patients with posterior packs should be admitted; the elderly, patients with cardiopumonary PMH or blood gas changes should be admitted to ICU. Observe for changes brought about by abnormalities in respiratory function: hypoventilation, hypoxemia, cardiac arrhythmias, and possible cardiac arrest. b. Broad-spectrum antibiotics to counteract possible middle ear and sinus infections as well as aspiration pneumonia and septicemia. c. Oxygen supplementation by 40% O2 via facemask to counteract decreased pO2 and increased pCO2 which accompany patients with posterior packs. d. Mild sedation(careful not to cause significant respiratory depression) and analgesia e. IV fluids f. Labs: electrocardiographic monitoring, pulse oximetry, blood gases, and serial H/H. F. Greater Palatine Foramen Block 1. Nasal hemorrhage involving the distribution of the sphenopalatine artery can be controlled by injection of the pterygopalatine fossa through the greater palatine foramen. 2. Small gauge needle(27 gauge) inserted into greater palatine foramen located just medial to the last molar, and 3 mL of 1% Lidocaine with 1:100,000 Epinephrine injected. Needle should be inserted no more than 25 mm since orbit can be reached at 35 mm. 3. Will provide good nasal anesthesia and temporary control of epistaxis(about 3 hours). 4. Mechanism of action is volume compression of the vascular structures. VIII. Surgical Modalities A. General principles 1. Surgery usually employed when epistaxis refractory to packing, but some advocate surgery for immediate control of severe epistaxis to avoid packing and longer hospitalizations, as well as to obtain better patient tolerance. a. Wang and Vogel(1981) found surgical interventions to have a lower failure rate(14.3% vs 26.2%), decreased complication rate(40% vs 68%), and hospital stay 2.2 days less than with packing in patients with posterior epistaxis. 2. Must determine site of bleeding before deciding which arteries to ligate: a. superior nasal cavity: anterior and/or posterior ethmoid arteries b. inferior or posterior nasal cavity: external carotid or internal maxillary artery 3. In general, ligation as close as possible to the bleeding site is preferable due to failure to control collateral circulation with more proximal ligations. B. Nasal septoplasty and or submucous resection 1. Correction of deviated septum by septoplasty and/or SMR may be necessary just to insert nasal packing. 2. Elevation of mucosal flaps with SMR may decrease frequency of epistaxis in some patients by promoting scarring. C. Trans-antral ligation of maxillary artery 1. Need Waters view to confirm presence of maxillary sinus. 2. Under general anesthesia, Caldwell-Luc procedure used to gain access to posterior wall of maxillary sinus, which is removed to gain access to the third (pterygopalatine) part of the maxillary artery, located in the pterygomaxillary space. 3. Operating microscope then used to identify pulsations of the distal branches (eg, sphenopalatine, descending palatine), which are clipped. 4. Advantage is ligation of distal vessels supplying nasal mucosa, minimizing development of collateral circulation. 5. Disadvantages include inability to use in children, patients with hypoplastic maxillary sinuses, or those with comminuted facial fractures, as well as the potential complications: a. Pain in the maxillary teeth b. Damage to sphenopalatine ganglion and Vidian nerve c. Damage to infra-orbital nerve d. Oro-antral fistula e. Sinusitis D. Intra-oral ligation of maxillary artery 1. Provides access to the first and second parts of the maxillary artery between ramus of the mandible and temporalis muscle. 2. Posterior portion of the maxilla is exposed through a posterior gingivobuccal incision beginning at the second molar; blunt dissection performed with finger and the buccal fat is dissected or retracted. 3. After temporalis muscle split and partially dissected, internal maxillary artery visualized at the base of the wound or brought into the field by a nerve hook is clipped and divided. 4. Advantages include feasibility in children, patients with hypoplastic maxillary sinuses, and comminuted facial fractures of the maxilla. 5. Disadvantages include: a. Site of ligation is more proximal than trans- antral approach with greater chance of failure due to collateral circulation. b. Frequently results in trismus that may take up to 3 months to resolve due to manipulation of temporal muscle. c. Can result in damage to infra-orbital nerve. E. Ligation of ethmoidal arteries 1. Consider in patients who re-bleed following ligation of IMA or in those with superior nasal cavity epistaxis or in conjunction with IMA ligation when bleeding site is ill-defined. 2. Surgical access from a standard Lynch incision down to fronto-ethmoidal suture line at the superior aspect of lacrimal bone. 3. The anterior ethmoid artery is located about 14-18 mm posteriorly to this. If the posterior ethmoid artery has to be ligated, it is located 10 mm posterior to the anterior ethmoid artery. Care must be taken in this area since the optic nerve is only 5 mm posterior to the posterior ethmoid artery. 4. Once identified, the arteries are ligated and divided. F. External carotid artery ligation 1. Incision made in the neck along the anterior border of the sternocleidomastoid muscle. 2. After 2 branches of the ECA indentified to avoid ligation of ICA, the ECA is ligated. (Beware of injuring vagus, superior laryngeal nerve, hypoglossal nerve, sympathetic chain, or mandibular branch of facial nerve. 3. Advantage: technique is simple and anatomy familiar to most otolaryngologists. 4. Disadvantage: less effective than other ligations due to greater collateral blood flow. G. Embolization 1. Selective angiography can be used as a diagnostic or therapeutic tool to control epistaxis. 2. Most effective in patients with epistaxis refractory to arterial ligation, bleeding sites difficult to reach surgically, epistaxis due to generalized bleeding disorder. 3. After anatomy defined and bleeding site identified, bleeding site embolized with polyvinyl alcohol, Gel- foamTM particles, or coiled springs. 4. Effective only when rate of blood loss > 0.5 mL/min. 5. Can embolize vessels close to the bleeding site minimizing collateral blood flow. 6. Success rate of about 90%, with a complication rate of 0.1%. 7. Possible complication is CVA caused by ICA embolization. H. Septodermoplasty 1. Most effective in patients with HHT. 2. After telangiectatic anterior nasal mucosa removed from anterior half of septum, floor of nose, and lateral wall, STSG is placed. 3. Can also use cutaneous, myocutaneous, or microvascular free flaps in place of the STSG. 4. Good experimental results from the use of autografts of cultured epithelial sheets derived from buccal epithelium. 5. Patients will get recurrence of epistaxis due to ingrowth of telangiectasia into the grafts or flaps, but the severity and frequency of bleeding significantly reduced. I. Lasers 1. Neodymium-yttrium-aluminum-garnet(Nd-YAG) laser or argon laser used to photocoagulate epistaxis lesions, especially those in HHT. 2. Retreatment usually necessary, but severity and frequency generally improved. --------------------------------------------------------------------------- BIBLIOGRAPHY 1. Bailey, Byron J., ed. Head and Neck Surgery-Otolaryngology. Philadelphia, PA.: J.B. Lippincott Co., 1993. 2. 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