Medical Clinics of North America
Volume 83 Number 1 January 1999
Copyright 1999 W. B. Saunders Company

 


OTOLARYGOLOGY FOR THE INTERNIST

 


EPISTAXIS

Luke K. S. Tan 1 2 MD, MMedSci, FRCS

Karen H. Calhoun 1 MD, FACS

1 Department of Otolaryngology, University of Texas Medical Branch (KHC, LKST), Galveston, Texas
2 Department of Otolaryngology, National University of Singapore, Singapore (LKST)

Address reprint requests to
Karen H. Calhoun, MD
Department of Otolaryngology
University of Texas Medical Branch
Galveston, TX 77555-0521

Patients presenting with epistaxis are anxious and fear bleeding to death. Although death from epistaxis is rare, it can occur, and significant morbidity is relatively common. [5] [34] Although most pediatric epistaxis is treated on an outpatient basis, older patients (>60 years old) more often require hospital admission. [25] [44] Initial management of epistaxis is directed at stopping the bleeding, and long-term treatment is directed at discovering and correcting the underlying cause. This article updates current management options.

 

ANATOMIC CONSIDERATIONS IN EPISTAXIS

The blood supply to the nose arises from the internal maxillary and facial arteries via the external carotid and the anterior and posterior ethmoid arteries via the internal carotid artery. The anteroinferior septum (Little's area) is supplied by a confluence of both systems (Kisselbach's plexus). Little's area is a common site of epistaxis because it is ideally placed to receive environmental irritation (cold, dry air, cigarette smoke) and is easily accessible to digital trauma. This area is easy to access and treat. Bleeding arising further within the nasal cavity can be difficult to reach. Surgical ligation of the contributing arteries can be challenging because of their deep location and complex anatomy.

PATHOPHYSIOLOGY

Much epistaxis ceases with pressure (digital or packing) over the bleeding point. An intact coagulation system with accumulation of platelets and clot formation is required. Abnormal platelet numbers or function or any abnormality in the coagulation cascade leads to failure of clot formation and persistent bleeding.

CAUSE

Epistaxis results from an interaction of factors, damaging the nasal epithelial (mucosal) lining and vessel walls. The major causative factors include environmental factors (humidity, temperature), local factors (trauma, anatomic abnormalities, inflammation, allergies, iatrogenic, tumors), systemic factors (hypertension, platelet and coagulation abnormalities, renal failure, alcohol abuse), and medications affecting clotting (anticoagulants, nonsteroidal anti-inflammatory drugs [NSAIDs]).

Environmental Factors

Cold, dry air increases cases of epistaxis. In countries with seasonal climates, hospital admissions for epistaxis increase during the winter months. [24] [44] [61] Patients were admitted at a rate of 0.829 patients per day for temperatures less than 5C compared with 0.645 patients per day for temperatures between 5.1C and 10C. [61] Most had some form of dry air heating, without humidification, in their homes.

 

Nasal ciliary activity decreases as temperature drops. Normal ciliary activity (at 32C to 40C) occurs at about 15 Hz frequency, dropping to less than 5 Hz below 20C. [16] Although extremely dry air is known to promote epistaxis, the exact humidification as a preventive measure remains undefined. Temperatures of above 52C have been associated with cellular damage. [56]

Local Factors

Trauma

Nose picking and accidental injury are the commonest traumatic causes of epistaxis. Except with severe facial trauma, such as motor vehicle accidents, this epistaxis is usually from an anterior nasal source and easily treated. [18]

 

Nasal Septal Deviation

 

Nasal septal deviation is common, but its role in epistaxis is not certain. In one study, 16% of patients with severe refractory epistaxis had marked septal deviation. [23] In another study of patients with recurrent epistaxis, 81% had septal deviation versus 31% in the control group. [46] The epistaxis group also had a higher incidence of radiologically demonstrated septal deviation compared with the control group (62% versus 37% [P<.02]). The bleeding tended to occur from the side to which the septum was deviated. Exactly how a septal deviation could cause bleeding is not clearly established. Because septal deviations do cause nasal obstruction turbulent air flow, this may cause abnormal mucosal drying, making the mucosa more susceptible to bleeding.

 

Iatrogenic

 

Septal, turbinate, nasal, sinus, or orbital surgery can be followed by epistaxis. Blood-stained nasal discharge is common in the initial week or two after surgery. Severe epistaxis can occur, especially after partial turbinate resection (0.9% to 8.9%). [14] Management of such patients is aimed at controlling the bleeding and contacting the surgeon to provide appropriate follow-up.

 

Inflammation (Infection and Allergy)

 

Epistaxis can result from nasal lining inflammation, with acute respiratory infections, chronic sinusitis, or allergic rhinosinusitis. In children and the mentally disabled, intranasal foreign bodies cause unilateral foul-smelling discharge that can be accompanied by epistaxis. Children with both nasal allergy symptoms and positive skin tests have more frequent epistaxis (20.2%) than those with symptoms alone (9.9%), positive skin test alone (3.4%), or neither symptoms nor positive skin test (2.1%). This study suggests that allergic rhinitis predisposes to epistaxis, either by mucosal irritation or possibly by the atopic state contributing to a hemostasis disorder. [43]

 

Tumors

 

Epistaxis can be the only symptom in patients with a nasal tumor. In adolescents, the most serious cause of recurrent epistaxis is the intranasal tumor, juvenile angiofibroma. Other neoplastic causes of pediatric epistaxis include papillomas, polyps, and meningoceles or encephaloceles (infants). [8] In adults, almost any benign or malignant intranasal tumor can present with epistaxis. Intranasal lesions can sometimes be seen by looking in the nose with the otoscopic ear piece. Biopsy of intranasal lesions is approached with caution because biopsy of highly vascular lesions, such as a juvenile angiofibroma, can cause significant blood loss and morbidity.

 

Chemicals

 

Many airborne irritants and toxic chemicals (sulfuric acid, ammonia, gasoline, chromates, glutaraldehyde) [65] irritate or harm the nasal mucosa, resulting in epistaxis. Cigarette smoke, primary or secondary, is another common irritant.

Systemic Factors

Hypertension

 

Although hypertension is often cited as a cause of epistaxis, several large studies have shown no higher rate of underlying hypertension among epistaxis patients than in patients without epistaxis. [41] [67] Hypertension patients taking diuretic or methyldopa medications may have more epistaxis than those taking beta-blockers (60%). [9] Hypertension at the time of epistaxis treatment may be anxiety related, returning to normal on control of the epistaxis and reassurance. [23] Epistaxis patients with hypertension must be followed after control of the bleeding, to ensure that blood pressure returns to normal on control of epistaxis because some are found to have underlying hypertension requiring ongoing treatment.

 

Renal Disease

 

Persistent epistaxis may be encountered in chronic renal failure patients undergoing hemodialysis, but the true incidence remains unknown. [64] Contributing causative factors may include elevated prostacyclin levels (platelet antiaggregatory activity) [40] and prolonged use of low-molecular-weight heparin. [54] An 8% incidence of septal perforations has been noted in renal failure patients. Localized irritation caused by turbulent air flow around the perforation could also contribute to epistaxis in these patients. [1]

 

Alcohol

 

Heavy alcohol consumption increases the risk of epistaxis. The same platelet reactivity inhibition that provides a protective effect for the coronary arteries may also increase bleeding time, making epistaxis more difficult to control. [37] [50] Bleeding risk, however, was not linearly related to alcohol consumption, with those consuming 1 to 10 alcoholic drinks per week most affected and those drinking more than 10 drinks per week less affected. Rebound of platelet activity may explain this finding, but the mechanics have yet to be elucidated. The use of NSAIDs did not confer an additional risk of increased bleeding time. [50]

 

Coagulation and Vascular Abnormalities

 

Patients with hereditary conditions, such as hemophilia, von Willebrand's disease, and thrombocytopenia, frequently experience epistaxis. Thrombocytopenia can also occur with hematologic malignancy, chemotherapy, or viral infections, such as dengue hemorrhagic fever [21] and human immunodeficiency virus (HIV), [15] or can be idiopathic.

 

Hereditary hemorrhagic telangiectasia patients are particularly prone to epistaxis problems. [17] The abnormal vessel walls and focal endothelial degeneration contribute to refractory epistaxis, which can be challenging to manage. Treatment is aimed at decreasing the frequency of bleeds and need for transfusion because permanent cure is not possible.

Medications

Numerous medications interfere with normal clotting. NSAIDs (including aspirin) are probably the most common, with up to 75% of epistaxis patients using one of these medications. [36] One study found that 42% of epistaxis patients were taking warfarin, dipyridamole, or NSAIDs versus 3% of the nonepistaxis control group. [66] These medications interfere with the cyclooxygenase pathway in arachidonic acid metabolism, inhibiting platelet aggregation. [33] One author suggested that a history of epistaxis may be a relative contraindication to the use of NSAIDs. [66] In addition, because 74% of aspirin use is self-administered, the public needs to be made aware of the relationship between aspirin and nosebleeds as potential side effects. [2]

 

Other medications associated with epistaxis include thioridazine, topical hyperosmolar sodium chloride, and dipyridamole (Persantine). Epistaxis resolving when the drug is stopped has occurred with thioridazine. The nasal mucosal drying from the anticholinergic effects of this low-potency phenothiazine, coupled with home heating in the dry winter season in hypertensive patients was thought to be the underlying cause of epistaxis. [22] Dipyridamole inhibits adenosine diphosphate and collagen-induced platelet aggregration, enhancing disaggregation and prolonging bleeding time. [42] Epistaxis has also occurred in a patient using hyperosmolar sodium chloride (2%) eye drops. [29] The patient developed dry nasal mucosa, presumably from osmosis, when the eye drops arrived in the nasal cavity via the nasolacrimal duct. The problem resolved when sodium chloride ointment was substituted for the drops. Use of steroid nasal sprays can also be complicated by epistaxis, which is usually mild and stops after cessation of use of spray. [24]

MANAGEMENT

There are three levels of epistaxis management: (1) first-aid measures, (2) acute management, and (3) interventions.

First-Aid Measures

In one series of patients taking systemic anticoagulants, 25% had experienced epistaxis in the previous year. Less than half of the patients [31] could think of a single first-aid measure to stop nosebleeds. Clearly, additional education in this at-risk population could reduce both morbidity and patient anxiety.

First-aid measures include the following:

  1. Digital compression. Although so simple as to seem reflexic, fewer than 50% of emergency department personnel could describe the correct site to apply digital pressure in a nosebleed (Fig. 1) . [38] A swimmer's clip has also been used for epistaxis. [62]
  2. Cotton or tissue plug in the nose. Patients often arrive in the office with a piece of tissue pushed into the nostril that has been bleeding.
  3. Bending forward at the waist. This position allows gravity to keep blood flowing out the nostrils, rather than posteriorly down the throat. [9]
  4. Spitting out any blood that trickles down the back of the throat. The patient is prevented from swallowing large amounts of blood.
  5. Cold compress on nasal bridge. This practice has a vasoconstrictive effect. [35]

Acute Management

Hypotension associated with epistaxis can precipitate acute myocardial events or aspiration, sometimes leading to death. The patient with an actively bleeding nose is apprehensive and often has reactive hypertension, accentuating the bleeding. The basics of airway, breathing, and circulation remain key principles. Securing the airway via endotracheal intubation or trachesotomy in the severely injured unconscious patient allows suctioning and packing of the nose and, if necessary, the oral cavity and pharynx. Oxygen ensures good systemic oxygenation, especially important in patients with underlying cardiopulmonary disease. Intravenous access is established in all patients presenting with active epistaxis because significant bleeding has usually occurred before the patient seeks medical attention. When inserting the intravenous line, it is usually convenient to obtain blood for complete blood count and, if clinically indicated, type and screen, coagulation profile, and electrolytes (in anticipation of surgical intervention).

 

An assessment of the amount of blood lost is made from the history, including the onset of the bleeding, precipitating factors, duration and quantity (i.e., number of soaked towels), past history of epistaxis and treatment, and history of blood dyscrasias. In adults, a history of medication (including NSAIDs, anticoagulants), hypertension, ischemic heart disease, diabetes mellitus, and alcohol abuse may influence management. In children, a history of epistaxis with unilateral nasal discharge alerts the physician to the possibility of an intranasal foreign body. Consent for blood transfusion is recommended. The vital statistics (blood pressure and pulse) of the patient should be charted.

 

The patient is supplied with folded gauze 4 4 pads to soak up blood trickling from the nose. A chart is started to keep track of the number of pads required, as further assessment of the amount of blood lost.

 

Local Compression

 

Thumb and index finger nasal compression pressure is used as the first measure by the physician while other treatments are being instituted. Local finger compression should be employed for at least 5 minutes to allow formation of a hemostatic plug over the bleeding vessel.

 

Cauterization

 

Most epistaxis originates in the anterior nasal cavity, often in Little's area. Effective local vasoconstrictive measures include pseudoephrine (Afrin), phenylephrine (Neo-Synephrine), or epinephrine (1:10,000) applied to the area on cotton pledget.

 

The area of bleeding can be cauterized. Silver nitrate is the most convenient cauterization agent, available in ready-made sticks. Local anesthesia with 4% lidocaine solution (applied by cotton pledget for 5 minutes) can reduce the stinging of cautery. Accurate identification of the bleeding points and a good light for intranasal examination are the keys to successful cauterization. The temptation to cauterize a large area of the septum to cover all bleeding points should be resisted. The authors routinely use a cotton-tipped applicator to mop up residual silver nitrate after application, to prevent local damage to the underlying perichondrium. Postcautery, antibiotic cream or ointment is applied to the cauterized area twice a day for 5 days to prevent crusting and infection. Both sides of the septum should not be cauterized at the same time because of the risk of septal perforation. Repeated cauterization in the same area can also lead to septal perforations.

 

Other Measures

 

Other local measures include

  1. Electrocautery.
  2. Other chemical cautery (trichloroacetic acid).
  3. Light packing with petroleum jelly (Vaseline) gauze.
  4. Direct endoscopic electrocautery (detailed later).
  5. Hemostatic chemical agents (thrombin-soaked absorbable gelatin powder [Gelfoam], oxidized cellulose [Surgicel], microfibrillar collagen [Avitene], porcine fat, oxymetazoline, or calcium alginate fiber [Kaltostat]).
  6. Oxymetazoline hydrochloride (an imidazole derivative) is a topical vasoconstrictor commonly used as a nasal decongestant. [28] Of 60 patients coming to an emergency department with epistaxis, there was a 65% success rate with oxymetazoline alone. A further 18% of patients required silver nitrate cautery, and the remaining 17% required nasal packing.
  7. Cryotherapy. This procedure for applying cold temperatures within the nose to control epistaxis reportedly has less morbidity than other local methods. [20] It requires a machine capable of delivering the necessary temperature to freeze the target tissues.
  8. Hot-water irrigation. Success in treatment of epistaxis has been reported, although patient compliance is variable. [56]
  9. Desmopressin (1-desamino-8- D-arginine vasopressin) spray. Desmopressin spray has been effective in decreasing the duration of epistaxis [32] and Ehlers-Danlos syndrome. [57]
  10. Laser therapy, diathermy, septodermoplasty, and other surgery. Surgery has been advocated for hereditary hemorrhagic telangiectasia with variable success. [10] [49] [63]

 

Anterior Nasal Packing

 

Packing is needed when local measures are unsuccessful in controlling epistaxis. Nasal packing is an uncomfortable procedure and can have life-threatening complications, anterior packing less so than combined anterior-posterior packing. Classic anterior packing is performed with Vaseline-impregnated narrow gauze, placed in the nose until sufficient pressure exists to tamponade the bleeding. Although the tidy textbook diagrams of layered packing are somewhat misleading, the general goal is to place the packing from the back and bottom of the nose forward. A training model for nasal packing has been reported to improve confidence and competence in the procedure. [59]

 

Other options for anterior nasal packing include synthetic sponge packs (tampons) such as Merocel that expand when moistened or balloon packing. Merocel packs are easy and quick to insert and can be used for bilateral epistaxis as well. The success rate of such packing exceeds 90%, even when performed by inexperienced physicians. [48] Both nasal tampons and gauze packing are efficacious and well tolerated. [7]

 

After anterior packing, the oropharynx is inspected. If blood is still visible trickling from the nasopharynx, either the anterior pack is suboptimally placed, or there is a posterior nasal bleeding source. The nasal cavity measures about 7 cm from columella to nasopharynx, so the most common error in anterior nasal packing is failure to pack adequately the posterior aspects of the anterior nasal cavity.

 

Adequate lighting and long forceps (bayonet or Tilley's nasal packing forceps) are necessary for placement of an effective anterior gauze pack. Gauze coated with BIPP (bismuth iodoform paraffin paste) can be left in the nasal cavity for up to a week with low risk of infection. Vaseline gauze packing is usually removed by 72 hours. Antibiotic prophylaxis is usually administered.

 

Elderly or frail patients with anterior nasal packing and most patients with posterior nasal packing should be hospitalized for oxygen supplementation, intravenous hydration, bed rest, and mild sedation. Because bilateral nasal packing obstructs the nose and prevents nasal breathing, it often causes hypo-oxygenation. Anterior-posterior nasal packing with sedation is accompanied by decreased arterial oxygen tension and altered pulmonary mechanics. [5] Oxygen is usually administered via face mask with anterior and posterior packing (unless the carbon dioxide is elevated). Sedation is carefully titrated, keeping in mind the patient's cardiopulmonary status.

 

Other materials used for nasal packing include Kaltostat, Ativene, and porcine fat (salt pork). A randomized trial comparing Kaltostat and bismuth tribromophenate (Xeroform) showed similar efficacy and patient acceptance. [39] Ativene successfully controlled 77% of idiopathic anterior epistaxis and can be useful in hereditary telangiectasia epistaxis. [60] Salt pork has been used for nasal packing in patients with thrombocytopenia, commonly secondary to renal failure or medications. Homogenates of salt pork contain an aqueous factor that serves as a platelet substitute, inducing platelet aggregation and enhancing adenosine diphosphate and collagen-induced aggregation. The pork fat is less irritating to the mucosa on removal than gauze packs. [4] This material is not used in patients who avoid pork for religious reasons.

 

Posterior Nasal Packing

 

Only about 5% of epistaxis originates from a posterior nasal source. [64] The posterior nasal space is cylinder shaped, opening anteriorly into the nasal cavity and posteriorly into the nasopharynx. Packing in this space tends to fall back and down, into the oropharynx. To pack the posterior nasal cavity, a conforming pack is first placed in the nasopharynx, secured anteriorly near the nostrils. Gauze or other anterior packing can then be firmly placed against this resistance.

 

Classically a posterior pack is made of rolled gauze secured with umbilical tape, although balloon packs are sometimes used (Foley catheter, Brighton Balloon, Simpson Balloon). Posterior pack insertion begins with passing a rubber catheter through each nostril, into the oropharynx. They are grasped here and brought out anteriorly through the mouth. Long ties attached to each side of the gauze pack are attached to the catheters, and the catheters are gently withdrawn through the nose, leaving a gauze pack held in the physician's hand, with the attached long ties entering the mouth and exiting both nostrils. With gentle traction on the nostril ends, the pack is pulled and pushed into the oropharynx, then tucked up into the nasopharynx. The mouth ends of the ties are left long, to be grasped later and used in pack removal. The nostril ends are secured anteriorly, usually around the columella. Care is taken to pad and protect the columella from excessive pressure that could cause ischemic necrosis. This unpleasant procedure can be performed under mild sedation, but use of general anesthesia when possible is a kindness to the patient. Posterior packs are usually left in place for 48 to 72 hours because earlier removal is associated with an increased risk of rebleeding.

 

An alternative to posterior packing with gauze is balloon catheters inserted in the nasopharynx via the nostrils and inflated with sterile water. The balloons are secured anteriorly using a clamp (e.g., umbilical cord clamp). Either Foley catheters or balloons designed specifically for the nasopharynx can be used. The balloons have a tendency to deflate with time, and volume can drop by 30% or more in 72 hours. [45] The authors usually deflate the balloons at 48 hours and remove both anterior and posterior packings at 72 hours.

 

Complications of Nasal Packing

 

Nasal packing can be complicated by death. [5] Aspiration of blood, cardiopulmonary failure secondary to hypoxia, and toxic shock syndrome have led to mortality in patients with epistaxis. Complications in nasal packing include

  1. Nasal trauma from the packing.
  2. Nasal-vagal response (bradycardia, hypotension, apnea).
  3. Dislodged packing.
  4. Aspiration.
  5. Persistent bleeding.
  6. Infection, toxic shock syndrome.
  7. Hypoxia resulting from nasal obstruction--may result in myocardial infarction, disorientation.

Most complications can be avoided if anticipated. Firm and gentle packing avoids excessive nasal mucosal trauma. Sedation is kept to the minimum necessary to decrease aspiration risk and respiratory suppression. Oxygen should be given when there are no contraindications. All patients receive prophylactic antibiotics.

 

Toxic shock syndrome occurring with nasal packing can cause significant morbidity and mortality. More than one third of patients undergoing nasal packing are Staphylococcus aureus carriers. Comparison of NuGauze packs to Merocel packs removed from patients' noses revealed NuGauze grew out substantially more S. aureus. [3] This may occur because Merocel is a single homogeneous structure, whereas NuGauze packing has interstices and folds of varying sizes that more readily pool secretions. Toxic shock syndrome begins with fever, vomiting, diarrhea, hypotension, and body rash secondary to the production of TSST-1, the primary toxin causing toxic shock syndrome. S. aureus is often sensitive to bacitracin, so use of this intranasally can help prevent toxic shock syndrome. Oxytetracycline and polymyxin B can also decrease the number of bacterial strains cultured from packing used for nasal packs. [19]

Interventions

Surgery

Endoscopic Cauterization.

Endoscopes have revolutionized sinonasal surgery over the past two decades. In the management of epistaxis, use of the endoscope can permit identification of posterior bleeding sites, which can then be directly cauterized, avoiding packing. [12] [51] It is especially useful in patients who continue to bleed through well-placed nasal packs.

 

For these patients, the packings are usually removed when the patient is under general anesthesia. The nasal cavity is cleansed and endoscopically examined. Common bleeding sites include the region of distribution of the sphenopalatine artery, posterior end of inferior turbinate, posterior-inferior septum, and anterior sphenoid face. The suction electrocautery is useful. In the rare cases in which no bleeding sites are located, Merocel packs are placed for 48 hours.

 

The authors have been using endoscopic examination in the outpatient setting with selected patients. Using good topical anesthesia and mild sedation and a suction/electrocautery unit, some more posteriorly placed bleeding points can be identified and cauterized with minimal patient discomfort. Many of these patients would traditionally have required nasal packing and hospitalization, so avoidance of this is popular with both patients and managed care companies.

Arterial Ligation.

Arterial ligation decreases arterial blood flow to the bleeding area. Commonly ligated supplying branches include the internal maxillary artery (terminating as the sphenopalatine artery) and the anterior ethmoidal artery. Ligation of the external carotid artery is also possible, although uncommonly needed.

 

Posterior epistaxis is usually supplied by the terminal branches of the internal maxillary artery. The third part of the internal maxillary artery courses behind the maxillary antrum to the sphenopalatine foramen at the superomedial sinus. As the internal maxillary artery exits the sphenopalative foramen, it divides into medial (to the sphenoid/septum) and lateral (lateral nasal wall) divisions. The transantral (via the maxillary antrum) approach allows ligation just before the terminal branching. Traditionally the transantral approach involved the removal of anterior wall of the maxillary sinus (Caldwell Luc) for surgical access. [6] The microscope is used for dissection behind the posterior wall of the antrum. The endoscope has provided an alternative approach with less morbidity, although it is technically more difficult.

 

Ethmoidal arterial ligation is performed when bleeding arises in the superior nose (above the middle turbinate). Ethmoidal artery ligation uses a curved incision around the medial canthus. The globe is retracted away from the lamina papyracea, and the anterior ethmoidal artery is encountered about 24 mm from the anterior lacrimal crest. The vessels are clipped and ligated under direct vision. Patients with intractable epistaxis without an identifiable bleeding point may benefit from ligation of both the anterior ethmoidal artery and the internal maxillary artery.

Embolization.

An alternative to surgical ligation is embolization of external carotid artery branches. [11] [26] [58] This procedure is particularly useful in patients at high risk for a general anesthetic or with unfavorable anatomy (small maxillary antra). [47] Embolization is successful in up to 96% of cases, although vascular anatomic variations limit application in some cases. One benefit of embolization over arterial ligation is that more selective blockade of smaller branches is possible.

 

Complications of embolization include up to 6% of neurologic sequelae. The risk of particulate material embolization to the internal carotid systems has been minimized by the current use of microcoils. [13]

 

Blood Transfusion

 

With the risk of disease transmission through blood products increasing, epistaxis is treated to minimize the need for transfusion. Nasal packing has been the first-line treatment of patients whose bleeding cannot be managed on an outpatient basis. Packing provides a tamponade and encourages thrombosis of vessels. There have been signs of this shifting toward early and prophylactic intervention. [52] One study compared the cost of hospitalization with nasal packing to hospitalization with surgical intervention and reported a higher cost and complication rate with surgical intervention. These patients, however, received surgical intervention only after failing nasal packing. There was a 27% transfusion rate (3 units per patient) with nasal packing compared with 41% (5.8 units per patient) with nasal packing failure and subsequent surgery. Another study also noted a greater transfusion requirement with surgical intervention than without (0.91 units versus 2.93 units, P<.01). [53] These authors suggest that patients requiring more than 3 units of blood should be considered for surgical intervention. The cost and risk of surgical intervention must be weighed against the risks of transfusion and compromised cardiovascular status if rebleeding occurs.

 

Dealing with a patient with active severe epistaxis can be bloody. The authors recommend universal precautions for all health care personnel involved in the care of these patients, including face mask with shields, gowns, hair coverage, and double-gloving.

SUMMARY

Epistaxis is a common clinical problem. The widespread availability of endoscopic equipment is shifting management philosophy toward targeting the bleeding point. This shift may have a significant impact on decreasing length of stay and blood transfusion rates. Advances in interventional radiology have also reduced the risk of embolization. Patient education, especially teaching first-aid measures to patients at high risk for nosebleeds, also encourages more effective use of health care resources.

 

ACKNOWLEDGMENTS

The authors thank Carol Chan for her assistance with the illustrations.

 

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