Many patients with severe epistaxis benefit from endoscopic intervention for control of bleeding. Critical maneuvers to improve endoscopic visualization during surgery include head-of-bed elevation, application of topical vasoconstrictors, and local injection of vasonstrictors. Controlled, hypotensive anesthesia may also decrease intraoperative blood loss and improve visualization during surgery. Intractable posterior epistaxis can be controlled with high rates of success with endoscopic sphenopalatine artery ligation. Although less common, intractable anterior epistaxis may be controlled by anterior ethmoid artery ligation once this artery is identified as the primary source. Less common sources of severe epistaxis are also discussed in this article.
Key learning points
At the end of this article, the reader will:
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Be familiar with passive methods of bleeding management to optimize endoscopic visualization.
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Understand the anatomy of the anterior ethmoid artery and surgical approaches to ligate this artery.
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Understand the anatomy of the sphenopalatine artery (SPA) and the surgical steps in endoscopic SPA ligation.
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Know the results of SPA ligation for control of primary epistaxis.
Introduction
The true incidence of spontaneous epistaxis is unknown, but it is estimated that 60% of individuals experience epistaxis in their lifetime. Of these, 6% seek medical treatment. No standard definition of severe epistaxis exists, but a reasonable definition is any epistaxis that requires surgical intervention, extensive nasal packing, or blood products. In one study, 45% of patients hospitalized for epistaxis had systemic conditions that can contribute to severe epistaxis. Although high-dose aspirin increases bleeding risk and leads to higher chance of rebleeding after intervention for epistaxis, low-dose aspirin (81 mg daily) increases epistaxis risk only slightly (19.1 vs 16.7% in one study). Hypertension as a primary cause of severe epistaxis is controversial. If possible, systemic conditions should be addressed along with surgical intervention in severe cases of epistaxis.
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Alcohol
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Connective tissue disease
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Medications: aspirin, nonsteroidal anti-inflammatory drugs, clopidogrel, warfarin, other antiplatelet or anticoagulant therapy
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Renal disease
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Liver failure
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Hematologic malignancies
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Vitamin C deficiency
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Vitamin K deficiency
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Idiopathic thrombocytopenic purpura
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Disseminated intravascular coagulation
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Genetic bleeding tendency (eg, von Willebrand disease, hemophilia, Bernard-Soulier syndrome)
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Hereditary hemorrhagic telangiectasia
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Alternative medicinals (garlic, ginkgo, ginseng)
Introduction
The true incidence of spontaneous epistaxis is unknown, but it is estimated that 60% of individuals experience epistaxis in their lifetime. Of these, 6% seek medical treatment. No standard definition of severe epistaxis exists, but a reasonable definition is any epistaxis that requires surgical intervention, extensive nasal packing, or blood products. In one study, 45% of patients hospitalized for epistaxis had systemic conditions that can contribute to severe epistaxis. Although high-dose aspirin increases bleeding risk and leads to higher chance of rebleeding after intervention for epistaxis, low-dose aspirin (81 mg daily) increases epistaxis risk only slightly (19.1 vs 16.7% in one study). Hypertension as a primary cause of severe epistaxis is controversial. If possible, systemic conditions should be addressed along with surgical intervention in severe cases of epistaxis.
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Alcohol
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Connective tissue disease
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Medications: aspirin, nonsteroidal anti-inflammatory drugs, clopidogrel, warfarin, other antiplatelet or anticoagulant therapy
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Renal disease
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Liver failure
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Hematologic malignancies
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Vitamin C deficiency
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Vitamin K deficiency
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Idiopathic thrombocytopenic purpura
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Disseminated intravascular coagulation
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Genetic bleeding tendency (eg, von Willebrand disease, hemophilia, Bernard-Soulier syndrome)
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Hereditary hemorrhagic telangiectasia
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Alternative medicinals (garlic, ginkgo, ginseng)
Patient optimization
Many patients with severe epistaxis benefit from endoscopic intervention for control of bleeding. However, active bleeding worsens endoscopic visualization. A few initial maneuvers help the surgeon decrease the blood loss encountered at surgery to more accurately visualize, locate, and control the hemorrhage.
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Head of bed elevation as part of endoscopic surgical setup
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Topical epinephrine and other decongestants
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Intranasal injections
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Greater palatine injection
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Warm saline irrigation
Anesthetic strategies
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Blood pressure control to decrease bleeding
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Consider use of clonidine as a premedication
Elevation of the head of bed increases venous return and thus decreases overall bleeding in the surgical field. The optimal angle of head elevation is 15° to 20°. One study compared blood loss of sinus surgery performed at 5°, 10°, and 20° of head elevation. Blood loss was 231 mL, 230 mL, and 135 mL, respectively.
Topical decongestants include epinephrine, cocaine, oxymetazoline, phenylephrine, and Moffett solution (2 mL of 10% cocaine, 1 mL of 1:1000 epinephrine, and 2 mL of sodium bicarbonate). No randomized trials exist comparing one decongestant with another in endoscopic sinus surgery. One study showed no difference in blood loss between surgery performed using 1:100,000 and 1:200,000 epinephrine. The 1:1000 epinephrine causes particularly robust vasoconstriction and has been proven to be safe assuming the use of proper safeguards to prevent inadvertent injection. Regardless of surgeon preference, topical decongestants are all effective in producing vasoconstriction and improving surgical visualization.
Selective injection of local anesthetic/decongestant in areas of bleeding is effective in managing epistaxis. Injections can decrease local hydrostatic pressure and also produce vasoconstriction. Greater palatine injection effectively decreases posterior nasal blood supply. It can be performed before endoscopic evaluation of epistaxis by bending a 25-gauge needle 45°, 25 mm from the needle tip. The needle is inserted transorally into the greater palatine canal and the pterygopalatine fossa infiltrated with 1:100,000 epinephrine.
Warm saline irrigation at 49°C has been shown to decrease the rate of bleeding, but endoscopic visualization improves only in longer surgical cases. However, warm saline irrigation can be used to help identify the primary source of bleeding, which can then be treated effectively.
Controlled, hypotensive anesthesia can decrease intraoperative blood loss and improve visualization during surgery. One benefit may be decreased heart rate in addition to decreased blood pressure. Regardless of theoretic advantages, trials regarding the true efficacy of total intravenous anesthesia have not been entirely conclusive or convincing. This anesthetic technique remains controversial but can certainly be added to the surgeon and anesthesiologist armamentarium.
A more recent development in efforts to decrease blood loss during endoscopic sinus surgery is the use of clonidine as a premedication. Clonidine activates α 2 receptors within the central nervous system to decrease peripheral sympathetic tone. There is also α 1 agonist activity to a lesser extent, resulting in some peripheral vasoconstriction within the mucosal bed. More studies are required to demonstrate the benefit of this medication in endoscopic sinus surgery.
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Major vascular targets and techniques to control epistaxis
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Sphenopalatine artery (SPA)
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Anterior ethmoid artery (AEA)
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Posterior ethmoid artery (PEA)
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Vidian and pharyngeal artery
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Carotid artery
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Venous bleeding
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Sphenopalatine foramen (SPF) most commonly in the transition zone between middle and superior meatus
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Accessory foramen in 10%
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SPA may exit in multiple branches through the foramen in 35% to 40%
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SPA is generally identified emerging from posterior to the endoscopic landmark, crista ethmoidalis of the palatine bone
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Surgical clipping or diathermy or both?
Anatomy
The SPA is a branch of the internal maxillary artery and is the major blood supply of the posterior nasal cavity. Epistaxis from this arterial source is generally more severe than anterior epistaxis. The artery enters the nasal cavity from the pterygopalatine fossa via the SPF. Knowledge of the anatomic variations of the SPA and SPF improves surgical results. This article focuses on anatomy pertinent to endoscopic SPA ligation. Transantral ligation of internal maxillary artery branches is of historical interest and is not discussed.
The SPF is located most frequently (87%) at the transitional zone between the superior and middle meatus. It is less frequently found in the superior meatus. The crista ethmoidalis is a bony crest of the palatine bone that points to the SPF. The SPF lies behind this crest and may rest above or straddle this bony crest. A single foramen is usually encountered, but an accessory foramen exists in 10% of patients. Terminal branches of the SPA include the posterior septal artery and the posterior lateral nasal artery branches. The SPA exits the SPF as a single branch in 60% to 75%, as two branches in 20% to 30%, and three or more branches in less than 10%.
Surgical approach for endoscopic sphenopalatine artery ligation
The entry zone of the SPA within the nasal cavity is located approximately at the tail of the middle turbinate. The mucosa just anterior to the middle turbinate tail is infiltrated with local anesthetic (usually 1% lidocaine with 1:100,000 epinephrine). Next, the posterior fontanelle of the maxillary sinus and the perpendicular plate of the palatine bone are palpated. A standard maxillary antrostomy is optional for this procedure, but is often valuable in defining the area of mucosal incision at the palatine bone behind the antrostomy and back wall of the maxillary sinus. A vertical mucosal incision at the orbital process of the palatine bone is made, and submucosal dissection proceeds posteriorly to identify the crista ethmoidalis. The crista can be removed with Kerrison rongeurs but this is not always necessary. SPA branches are identified by wide exposure of soft tissue behind the crista ethmoidalis ( Fig. 1 ). A ball-probed seeker is helpful in this dissection because it can help define arterial branches with minimal trauma. Awareness of the considerable variation in the number of arterial branches and thorough dissection via wide exposure are critical. Arterial occlusion can be performed by Ligaclips or bipolar electrocoagulation on all isolated arterial branches. The mucosa previously elevated for this dissection is returned to original position.
