SOURCE: Dept. of Otolaryngology, UTMB; Grand Rounds
DATE: October 16, 1996
RESIDENT PHYSICIAN: Stephanie Cordes, M.D.
FACULTY PHYSICIAN: Francis B. Quinn, Jr., M.D.
SERIES EDITOR: Francis B. Quinn, Jr., M.D.
See also: Editor's Comments
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Suggested remedies included: Lupton in 1601 advocated the use of the patients own blood to write the words ‘consummatum est’ on his forehead and Moncrief in 1716 would fry the patients own blood and apply it as snuff. Hippocrates was one of the earliest physicians to appreciate that pressure on the alae nasi was an effective way of controlling nosebleeds. Ali Ibn Rabban Al-Tabiri (AD 850) wrote that the complaint of epistaxis was due to the swelling of a vein and its rupture, or perhaps a reduction in the force which confines the blood within. Giovanni Battista Morgagni observed the extremely turgid blood vessels located about a finger’s breadth from the bottom of the nostril. Carl Michel (1871), James Lawrence Little (1879), and Wilhelm Kiesselbach identified the plexus of veins situated on the anterior part of the cartilaginous septum as a source of epistaxis. Pilz (1868) tied the common carotid artery for the treatment of epistaxis. Alfred Seiffert (1928) first introduced the ligation of the internal maxillary artery via a transantral approach. Henry Goodyear (1937) was the first to tie the anterior ethmoid artery for epistaxis.
The 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 and anteriorly, as well as the posterior lateral nasal branch which supplies the turbinates and meati ( as well as the ethmoid and maxillary sinuses). The greater palatine artery can originate from the 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. The greater palatine artery also gives off the lesser palatine artery which travels through the lesser palatine canal to supply the soft palate and pharyngeal wall.
The internal artery has no contributing branches in the neck. It passes through the petrous portion of the temporal bone and turns sharply, running near the lateral surface of the sphenoid bone. It runs close to the cavernous sinus and pierces the dura lateral to the anterior clinoid process. This is where it 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. The posterior ethmoid artery branches off the ophthalmic artery shortly after it enters the orbit. It 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. The anterior ethmoid artery, which is the larger of the two, 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 the cribiform plate). It nourishes the anterior superior septum and lateral walls.
Several areas within the nose are associated with a high frequency of epistaxis. The first is located along the anterior caudal septum where the sphenopalatine, greater palatine, anterior ethmoid, and superior labial arteries anastomose. This is the area that is known as Kiesselbach’s plexus or Little’s area. It is estimated that approximately 80% to 90% of all epistaxis occurs in this area, especially in children and young adults. The site associated most frequently with posterior epistaxis is known as Woodruff’s plexus and is located where the sphenopalatine artery enters the nasal cavity through the sphenopalatine foramen at the posterior limit of the middle turbinate.
There can also be epistaxis with trauma to the sinuses, orbits, middle ear, and base of skull (if the trauma involves the anterior sphenoid sinus wall causing laceration of the posterior septal branch of the sphenopalatine artery). Other causes of epistaxis from trauma include habitual nose picking which causes anterior septal nose bleeds. Chronic irritation in this area causes crusting and excoriation with formation of friable granulation tissue that bleeds easily on further nose picking. Surgical procedures of the nose and sinuses such as rhinoplasty, septoplasty, 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. Barotrauma sustained from flying or scuba diving can cause hemorrhage within the paranasal sinus cavities with subsequent epistaxis. Anatomical or structural deformities are another local etiology of epistaxis. Septal spurs and deviations involving the cartilaginous or bony septum 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 just posterior to a septal deformity may be difficult to arrest thus requiring removal with septoplasty. Septal perforations secondary to various etiologies can cause epistaxis. Granulation and crusting occur on the margins of the perforations which bleed easily. Inflammatory conditions usually manifest as congestion and blood streaked mucus, but can also develop frank epistaxis. 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 the vessels are characteristic of inflamed tissue. Such conditions causing local inflammation include: upper respiratory infection, allergic rhinitis, sinusitis, nasal polyposis, environmental irritants, and toxic chemicals. Patients with recurrent epistaxis may have fibrinolytically active bacteria in the nasal cavity that produce streptokinase and staphylokinase. Nasal foreign bodies, usually lodged in children and mentally retarded individuals, should be suspected with unilateral foul discharge. Foreign bodies that cause bleeding usually have sharp edges, irritating chemical properties, and/or porosity. Bleeding occurs from the inflamed mucosa and granulation tissue around the foreign body. Intra-nasal parasites, including leeches, can lodge in the nose or nasopharynx and cause bleeding. Benign and malignant tumors in the nasal cavities, nasopharynx, and sinuses can present with epistaxis. They cause bleeding indirectly from erosion into normal sino- nasal structures or directly from tumors of high vascularity. Bleeding is usually unilateral and can be intermittent or constant.
Some tumors to consider include nasal hemangioma, hemangiopericytoma, papilloma, squamous cell carcinoma, adenoid cystic carcinoma, adenocarcinoma, and melanoma. Juvenile nasal angiofibroma should be considered when a male adolescent presents with nasal obstruction, epistaxis, and a nasal or nasopharyngeal mass. Aneurysms of the extradural or cavernous sinus portion of the internal carotid artery can cause life-threatening epistaxis. Often a history of cranial surgery or head trauma with sudden onset of unilateral blindness and cranial nerve deficits such as anosmia and involvement of cranial nerves II - VI. Due to the inaccessibility of this area, bleeding from this is usually treated with arterial embolization.
The second major category of disorders causing epistaxis is the systemic factors. These factors usually cause repetitive episodes of epistaxis because of their effect on the vessels either directly or indirectly. Hypertension and atherosclerotic changes are associated with epistaxis, especially posterior nosebleeds in the older patient. Posterior epistaxis was often referred to in the past as “cardiovascular epistaxis” due to its association with hypertension. 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. Although no scientific studies have shown any significant differences in the prevalence of nosebleeds between patients with or without hypertension, the treatment of epistaxis should include measurement of blood pressure and treatment if needed.
Any condition that impairs or decreases clotting factors and/or platelets can cause epistaxis that is difficult to control. Blood dyscrasias are usually seen in the alcoholic patient or in the patient with a debilitating systemic disease, immunodeficiency, or a lymphoproliferative disorder. Thrombocytopenia is defined as < 100,000 platelets/mm3 , but no spontaneous bleeding until < 40,000. There can be spontaneous mucus membrane bleeding at 10-20,000. The thrombocytopenia can be due to decreased production caused by cytotoxic agents, aplastic anemia, malignancies, etc. or an increased destruction caused by prosthetic heart valves, DIC, sickle cell crisis, TTP, ITP, drugs, hypersplenism, etc. Platelet dysfunction occurs when there is sufficient quantity of platelets but they do not function properly. The most common cause is the use of aspirin and other NSAIDs which impair platelets by inhibiting cyclo-oxygenase which is associated with thromboxane production from arachdonic acid. This biochemical pathway is important for platelet aggregation. Systemic disorders such as uremia and liver failure, as well as vitamin deficiencies also predispose to platelet dysfunction causing epistaxis. Clotting factor abnormalities should be suspected if there is a history of easy bruising, prolonged bleeding, and/or family history of the former. Primary coagulopathies include: Factor VIII deficiency ( Hemophilia A) , Factor IX deficiency ( Hemophilia B or Christmas disease), Factor XI, and von Willebrand’s disease. Deficiencies of fibrinogen, prothrombin, factors V, X, VII, and XII are extremely rare.
Secondary coagulopathies such as liver disease and vitamin deficiencies can cause bleeding due to diminished synthesis of clotting factors or exacerbate epistaxis. Drugs can affect the clotting mechanism such as coumadin which antagonizes the action of Vitamin K and heparin which inactivates thrombin via anti-thrombin III. Systemic illnesses such as DIC can consume clotting factors. Hereditary hemorrhagic telangiectasia also known as Osler-Weber-Rendu disease is the most common disease of vascular structure. It is autosomal dominant disease.
The pathologic condition is the lack of contractile elements in the vessel walls which makes it difficult to stop the epistaxis spontaneously. The telangiectasias are composed of dilated venules and capillaries or small AV malformations that can be found in the skin and mucosal surface of the aerodigestive and genitourinary tracts, although they can occur anywhere on the body. The telangiectasias bleed in response to minor trauma. The most common symptom is recurrent, spontaneous epistaxis that begins with puberty and worsens with age. These patients often require hundreds of blood transfusions. Tests of clotting factor and platelet function are usually normal. Treatment is difficult and usually unsuccessful. Alcohol abuse can predispose to epistaxis by decreased clotting factor synthesis, bone marrow suppression, platelet inhibition, and vitamin deficiencies. Systemic toxic substances such as heavy metals and infectious diseases such as typhoid fever, nasal diphtheria, whooping cough, scarlet fever, rheumatic fever, and leprosy. Cardiovascular conditions such as congestive 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.
The history provides valuable information about the etiology of epistaxis and may suggest the bleeding site. Specific inquiry should be made regarding the following: side of bleeding; nasal bleeding alone or nasal bleeding associated with spitting blood; duration of bleeding and estimated blood loss; history of head/neck trauma or surgery; symptoms of orthostasis or hypovolemia; previous epistaxis, site and treatment; past medical history, such as HTN, DM, liver disease, alcoholism, cardiopulmonary disease; drug use, especially aspirin, NSAIDs, and coumadin, and family history of epistaxis or bruising and bleeding. Initially during the physical examination, the adequacy of the airway and circulating blood volume should be assessed. A general physical exam should be performed with particular attention to the skin and mucus membranes for vascular lesions. Thorough exam of the nasal cavity should then be performed in order to locate the site of bleeding as well as possible septal deviations or mucosal and structural abnormalities within. During the exam particular attention should be paid to assure both physician and patient comfort.
There should be adequate lighting available and the instruments which will be needed should be placed into reach. The instruments needed include: nasal speculum, bayonet forceps, suction to remove clots, adequate vasoconstriction and topical anesthesia, and a rigid zero degree or thirty degree telescope. Laboratory studies which should be initially sent include: CBC, prothrombin time, partial thromboplastin time, liver function test (if indicated), and type and cross (as needed).
Once the active or inactive bleeding site is identified, then chemical or electrical cautery can be used to attempt to arrest the bleeding. Silver nitrate should be applied to the bleeding site for at least 30 seconds. The excess silver nitrate should be removed from the nose to prevent it from spreading and injuring healthy nasal mucosa. Beware of performing overly aggressive cautery on both sides of the nasal septum as cartilage exposure or septal perforations can occur. Since and actively bleeding vessel is almost impossible to cauterize using silver nitrate, electrocautery with suction bovie may be the next choice. It provides a greater depth of penetration, so it is more likely to cause exposure of cartilage and/or septal perforation. Since electrocautery is more painful than using silver nitrate, the patient may need injection with local anesthetic. The patient should apply antibiotic ointment to the cauterized area until it is healed. Even posterior bleeding sites can be treated with chemical or electrical cautery after visualization with a rigid or flexible endoscope. This has been found to lessen the distress and morbidity associated with nasal packing and the need for more extensive surgical procedures.
In one study (O'Leary-Stickney et. Al.), they proposed selection factors which strongly suggested the initial consideration of using the rigid endoscope and cautery in posterior nasal bleeding. These were: (1) blood dyscrasias contraindicating packing, (2) refractory bleeding with a pack in place, (3) patients in whom arterial ligation is being considered, (4) postoperative hemorrhage after nasal surgery, (5) nasal anomaly preventing adequate packing, and (6) refusal or absolute patient intolerance to packing. They found good efficacy, low complication rate, economic feasibility, and high patient acceptance. Other non-surgical methods for treatment of epistaxis include cryotherapy and nasal packing.
Cryotherapy is not frequently used, but can attempt to control severe posterior epistaxis by the use of cold water flowing through elastic catheters. It has a low complication rate when used. If the above measures fail, and the bleeding appears to originate from an anterior site but can not be identified, the an anterior pack can be placed. The nose needs to be adequately anesthetized before attempting to place an anterior pack. The packing material is ½” Vaseline gauze impregnated with an antimicrobial ointment. This is packed into the nose under direct visualization with bayonet forceps. The space between the floor of the nose and the 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 the inferior turbinate may be necessary to allow for adequate packing. Only closed loops of gauze are placed posteriorly to prevent strands from dangling down from the nasopharynx and gagging the patient. It is better to pack only the bleeding side of the nose to avoid septal ulceration and necrosis, as well as to allow the patient to breathe through one patent nostril.
Anterior packs are usually left in place for 2-7 days depending on the severity and location of the epistaxis. Prophylactic antibiotics with activity against nasal flora and staphylococcus aureus should be given because of the risk of sinusitis from blockage of the sinus ostia and toxic shock syndrome. There are a variety of nasal tampons, sponges, and inflatable devices on the market that may be used instead of the traditional ½” by 72” Vaseline gauze. Nasal tampon (Merocel sponge) can be placed in the nose and expands to tamponade the mucosa with the addition of water. Gel-foam sponges, Surgical or surgical oxycel, and/or Avitene ( microfibrillar collagen) can also be used to control anterior epistaxis. They generally dissolve within 2-3 weeks. When used with antibiotic ointment, they are extremely helpful in patients with blood dyscrasias, thrombocytopenia, or HHT because it avoids the need to unpack the nose thereby not causing further bleeding. 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. The above packs function not only by direct mucosal pressure, but also by creating mucosal inflammation and edema.
A 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. The standard posterior pack is 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. The patient needs to be given sedation and adequate anesthesia prior to placing the pack. A small red rubber catheter is pass through the bleeding nostril and brought out the mouth. The two long ties are then secured to the distal end of the catheter and pulled back through the nasal cavity as the catheter is withdrawn from the nose until the pack is secure in place over the involved choana. Traction on the ties is maintained while an anterior pack is placed. The 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 in 4-7 days. There are also commercially available inflatable balloon packs. A foley catheter (12-16 french) placed along the floor of the nose until visualized in the nasopharynx. The balloon is then inflated and the catheter is retracted anteriorly to wedge the balloon snugly onto the posterior choana. After the anterior pack is placed, the catheter is secured with a piece of tubing slid tightly against the anterior pack.
Epistaxis balloon tampons such as Epi-stat provide a double balloon system that serves as both an anterior pack and a posterior pack. Advantages of inflatable balloon packs include: easily inserted, less traumatic to the patient, and allows a partial nasal airway. Disadvantages include: less effective than a standard pack since the pressure applied to the nose is not equal and some balloons are inflated with water whereas some need to be inflated with air. All patients with posterior packs should be admitted to the hospital. The elderly and patients with cardiopulmonary PMHx or blood gas changes should be admitted to an intensive care unit for close monitoring. These patients need to be observed for changes brought about by the abnormalities in respiratory function: hypoventilation, hypoxemia, cardiac arrhythmias, and possible cardiac arrest. Broad-spectrum antibiotics to counteract possible middle ear and sinus infections as well as aspiration pneumonia and septicemia are needed. Oxygen supplementation by 40% oxygen via facemask to counteract decreased pO2 and increased pCO2 which occurs in patients with posterior nasal packs. Mild sedation and analgesia needs to be used judiciously so as to not cause significant respiratory depression. The patient should be kept on intravenous fluid therapy as well as monitored with pulse oximetry, electrocardiography, blood gases, and serial hematocrits.
The last non-surgical modality used to treat epistaxis is the greater palatine foramen block. Nasal hemorrhage involving the distribution of the sphenopalatine artery can be controlled by injection of the pterygopalatine fossa through the greater palatine foramen. A small gauge needle( 27 gauge) is inserted into the greater palatine foramen which is located just medial to the last molar, and 3 ml of 1% Lidocaine with 1:100,000 Epinephrine is injected. The needle should not be inserted more than 25 mm since the orbit can be reached at 35 mm. The injection will provide good nasal anesthesia and temporary control of epistaxis ( about 3 hours). The mechanism of action is volume compression of the vascular structures in the fossa.
Before deciding which arteries to ligate to treat the epistaxis, the site of bleeding must be determined. If the bleeding is in the superior nasal cavity then it is coming from either the anterior or posterior ethmoid arteries. Blood coming from the inferior or posterior nasal cavity is from the external carotid or the internal maxillary artery. In general, ligation as close as possible to the bleeding site is preferable due to failure to control collateral circulation with more proximal ligations. Nasal septoplasty and/or submucous resection may be needed to correct a deviated septum in order to place nasal packing. Elevation of mucosal flaps with submucous resection may decrease the frequency of epistaxis in some patients by promoting scarring.
Internal maxillary artery ligation normally results in a decrease in the pressure gradient within the bleeding vessel, allowing a clot to form. Recurrence rates for bleeding have ranged from 5% to 13%. Criteria for the ligation procedures have not been established since there are proponents of early versus late ligation. A Waters view is first obtained to identify the presence of a maxillary sinus for a transantral approach for ligation. Under general anesthesia, Caldwell-Luc procedure is used to gain access to the posterior wall of the maxillary sinus, which is removed to gain access to the third portion (pterygopalatine) of the maxillary artery, located in the pterygopalatine space. The operating microscope is then used to identify pulsations of the distal branches, which are clipped. It is necessary to place surgical clips on the internal maxillary artery just proximal to the origin of the descending palatine artery, on the descending palatine artery distally, and on the distal portion of the internal maxillary artery. One advantage to this procedure is the ligation of the distal vessels supplying the nasal mucosa, minimizing the development of collateral vessels. Disadvantages include the inability to use this approach in children, patients with hypoplastic maxillary sinuses, or those with comminuted facial fractures, as well as the potential complications of: pain in the maxillary teeth, damage to the sphenopalatine ganglion or Vidian nerve, damage to the infraorbital nerve, oro-antral fistula, and sinusitis.
An intraoral approach to the maxillary artery provides access to the first and second parts of the artery between the ramus of the mandible and the temporalis muscle. The posterior portion of the maxilla is exposed through a posterior gingivobuccal incision beginning at the second molar. Blunt dissection is then performed with the finger and the buccal fat is dissected or retracted. After the temporalis muscle is split and partially dissected, the internal maxillary artery is visualized at the base of the wound or brought out into the field by a nerve hook then clipped and divided. The advantages of this procedure include its feasibility in children, patients with hypoplastic maxillary sinuses, and comminuted fractures of the maxilla. Disadvantages include: the site of ligation is more proximal than the transantral approach with a greater chance of failure due to collateral circulation, frequently results in trismus that may take up to 3 months to resolve due to the manipulation of the temporalis muscle, and can result in damage to the infraorbital nerve.
Ligation of the ethmoidal arteries is considered in patients who re-bleed following ligation of the internal maxillary artery, in those with superior nasal cavity epistaxis, or in conjunction with internal maxillary artery ligation when the bleeding site is ill-defined. Surgical access is from a standard Lynch incision down to the fronto-ethmoid suture line at the superior aspect of the lacrimal bone. 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. Once identified, the arteries are ligated and divided.
External carotid ligation is performed through an incision made in the neck along the anterior border of the sternocleidomastoid muscle. After two branches of the external carotid artery are identified to avoid ligation of the internal carotid artery, the external carotid artery is ligated. When doing the ligation care must be taken to avoid injury to the vagus, the superior laryngeal nerve, the hypoglossal nerve, the sympathetic chain, or the mandibular branch of the facial nerve. This technique is simple and the anatomy is familiar to most otolaryngologists. The disadvantages of this procedure is that it is less effective than other ligations due to greater collateral blood flow.
Selective angiography can be used as a diagnostic tool or a therapeutic tool to control epistaxis. Embolization is most effective in patients with epistaxis refractory to arterial ligation, bleeding sites difficult to reach surgically, or epistaxis due to a generalized bleeding disorder. After the anatomy is defined and the bleeding site is identified, the bleeding site is embolized with polyvinyl alcohol, Gel-foam particles, or coiled springs. This procedure can embolize vessels close to the bleeding site therefore minimizing collaterals. It is effective only when the bleeding rate is > 0.5 ml/min. Success rate is about 90%, with a complication rate of 0.1%. Disadvantages are that only external carotid artery or branches can be embolized and severe complications such as hemiplegia, facial paralysis, and skin necrosis can occur.
Septodermoplasty is used most often in patients with HHT. After telangiectatic anterior nasal mucosa is removed from the anterior half of the septum, floor of the nose, and lateral wall a spilt thickness skin graft is placed. Cutaneous, myocutaneous, or microvascular free flaps can also be used in place of the skin graft. There has also been good experimental results from the use of autografts of cultured epithelial sheets derived from the patients buccal mucosa. Patients will get recurrence of epistaxis due to ingrowth of telangiectasia into the grafts or flaps, but the severity and frequency of bleeding is significantly reduced. The Neodymium-yttrium-garnet (Nd-YAG) laser or argon laser has been used to photocoagulate epistaxis lesions, especially in those with HHT. Retreatment is usually necessary, but the severity and frequency of bleeding is generally improved.
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After some forty-two years of practice and literally hundreds of nosebleed patients, one stands out most clearly in my memory- a young man who bled to death through the nose while I watched. He had suffered a closed head injury in a motorcycle accident some months previously, had recovered and been released from hospital. He returned with a complaint of recurrent severe nosebleed, and difficulty with vision. Physical examination demonstrated impairment of ocular motility, but no bleeding point could be found in his nose or nasopharynx. He continued to bleed despite anterior packing. Repeated postnasal packing would arrest the hemmorhage, but bleeding would recurr soon after the postnasal packing was removed. He required multiple transfusions over the course of his illness. Almost in desperation, my attending and I ligated his external carotid artery. That evening, at dinnertime, he suddenly bled to death through his nose and mouth, while his resident physician stood helplessly at his bedside.
Postmortem examination demonstrated a carotid-cavernous sinus aneurysm which had eroded into his sphenoid sinus, from which he had bled into his nose and nasopharynx. My chagrin at his death motivated me to make a study of fatal epistaxis, and I should like to pass on to you the wisdom I gained.
First of all, Dr. Cordes has correctly pointed out that acute hypovolemia can invoke a fatal outcome in patients whose severe coronary atherosclerosis puts them at risk. Years ago one of my own patients succumbed in just this manner.
Secondly, the patient who has just suffered a nasal fracture, as from a softball striking his face for example, and who presents with brief episodes of remarkably brisk epistaxis which seems to subside only to recurr while you watch, is very likely to have had his anterior ethmoid artery torn by an extension of the fracture line into the ethmoid labyrinth. This condition has been responsible for at least one reported epistaxis fatality, and deserves immediate intervention. The anterior ethmoid artery is exposed through a Lynch incision under local anesthesia, and one or two metallic clips are placed across it as it exits the orbit. This can be (and has been) done in less than ten minutes skin to skin, and is attended by minimal morbidity.
Finally, the patient with the carotid-cavernous aneurysm reminds us that a high-velocity head injury, followed by (in many cases delayed) epistaxis, who presents with neurologic deficits related to the orbit with, perhaps, loss of sensation over the first and second divisions of the trigeminal nerve, is a proper candidate for angiography and balloon occlusion of a carotid-cavernous aneurysm. An excellent review of this condition can be found in The June 1994 issue of the ENT Journal, by Brad Millman and Neil A. Giddings, of the Geisinger Medical Center, Danville, PA.