Vascular anatomy

It is important to understand the vascular anatomy to apply the appropriate treatment modalities. Blood supply to the nasal cavity originates from both the internal and external carotid systems and contains multiple anastomoses, the most prominent of which is Kiesselbach’s plexus in the anterior nasal septum.

The external carotid supplies the facial artery and internal maxillary artery (IMA). The superior labial artery derives from the facial artery and gives off branches near the columella that supply the anterior nasal septum. The IMA courses through the pterygopalatine fossa and divides into multiple branches, terminating in the sphenopalatine artery (SPA), which enters the nasal cavity through the sphenopalatine foramen on the lateral nasal wall. The SPA typically divides into two branches upon passing through the foramen, but may divide into three or more branches. It may also divide within the pterygopalatine fossa, before passing through the foramen. These anomalies are of great importance during ligation of the artery because the surgeon must search for multiple vessels to treat bleeding from the SPA effectively. The two most common branches of the SPA are the nasopalatine artery, which supplies the posterior nasal septum, and a posterior superior branch, contributing to the middle and inferior turbinates. The descending palatine artery is the other terminal branch of the IMA, separating from the SPA within the medial portion of the pterygopalatine fossa. It traverses inferiorly within the greater palatine canal, travels anteriorly along the palate, and supplies the anterior septum through the incisive foramen.

The internal carotid artery system supplies the nasal cavity through the anterior and posterior ethmoidal arteries. These are branches of the ophthalmic artery, which enters the orbit with the optic nerve. These arteries enter the nasal cavity through foramina in the medial orbital wall, within the frontoethmoidal suture. The anterior ethmoidal foramen is located 24 mm posterior to the lacrimal crest. The posterior ethmoidal foramen can be found 12 mm posterior to the anterior one, although the posterior ethmoidal artery can be absent in up to one third of individuals . The optic nerve is located 6 mm posterior to the posterior ethmoidal artery, when the artery is present. During open ligation of the ethmoidal arteries, these measurements serve as useful guides to prevent injury to the optic nerve. Once the ethmoidal arteries leave the orbit, they course medially along the roof of the ethmoid sinuses and supply the nasal septum. The anterior ethmoid artery crosses the roof of the ethmoid sinuses just posterior to the frontal sinus ostium. The artery’s position may be within the ethmoid roof or, occasionally, may lie more inferiorly, within a bony partition that acts like a mesentery. In this situation, it is more easily injured during endoscopic procedures ( Fig. 1 ) .

Anterior ethmoid arteries. The left artery ( arrowhead ) crosses the skull base in a bone partition, leaving an air space posterosuperiorly. If the presence of the artery within the partition is not recognized, it can be injured during endoscopic sinus surgery. The right anterior ethmoidal foramen is also seen ( asterisk ).

Causes of epistaxis

Epistaxis results from a multitude of causes, both local and systemic . Common local factors include digital trauma, nasal septal deviation, neoplasia, and chemical irritants, whereas coagulopathies, renal failure, alcoholism, and vascular abnormalities are common systemic factors. A personal or family history of frequent bleeding, heavy bleeding, or easy bruising suggests a systemic bleeding disorder. Although these conditions are rarely the cause of epistaxis, a thorough investigation is indicated in these patients to rule out systemic disease. Likewise, epistaxis is rarely caused by neoplasm, but persistent unilateral bleeding should prompt a nasal endoscopy and possibly radiologic imaging to rule out a tumor.

Local digital trauma to the nose is the most common cause of epistaxis, usually resulting in mild hemorrhage of the anterior nasal septum. Mucosal dryness can also predispose an individual to bleeding from this same area. Mucosal dryness can be due to turbulent airflow, caused by septal deviation or spurs, and low humidity. Epistaxis is more frequent during the winter months, presumably because of the lower humidity during that time. Intranasal corticosteroids can be a cause of mucosal bleeding. Patients should be counseled on proper application, directing the spray laterally to avoid direct application to the septum. Traumatic nasal bone fracture or septal fracture can result in significant acute epistaxis. Bleeding may recur or be delayed following maxillofacial trauma because of posttraumatic aneurysm of the septal vasculature. Rhinosinusitis may be a coexisting factor, particularly in children, and may lead to increased inflammation, nose blowing, or, potentially, digital trauma, resulting in epistaxis.

Systemic factors frequently contribute to severe uncontrollable epistaxis. Von Willebrand’s disease and hemophilia are inherited coagulopathies and must be considered with a history of significant bleeding from minor wounds or severe bruising. Thrombocytopenia with a platelet counts of less than 20,000/mm ³ can make controlling epistaxis challenging. Hematologic malignancies can produce a similar coagulopathy because of poor platelet production. Similarly, chemotherapy regimens can produce thrombocytopenia. Chronic alcohol intake, aspirin and other nonsteroidal anti-inflammatory medication usage, and renal failure affect platelet function, despite normal counts. The role of hypertension is debated and no clear independent association has been firmly established as a lone factor in epistaxis. However, hypertension may make controlling a bleed more difficult. Osler-Weber-Rendu disease (hereditary hemorrhagic telangiectasia) is an autosomal dominant disease that results in fragile telangiectasias and arteriovenous malformations that can also cause significant recurrent bleeding.

Anticoagulant medication use should be ascertained during evaluation. The use of coumadin, enoxaparin, and heparin all alter the coagulation cascade. Aspirin and other nonsteroidal anti-inflammatory drugs are commonly used medications that affect platelet function. It is also important to inquire about alternative medicines. Garlic, ginkgo, and ginseng (the “3 Gs”) are known to inhibit platelet function specifically by affecting aggregation. A coagulation panel should be checked on admission in anticoagulated patients, and reversal of the anticoagulant should be considered.

Any individual with recurrent bleeding and a lack of other systemic factors should be evaluated for neoplasia, especially when the bleeding is unilateral. Juvenile nasal angiofibroma is an uncommon tumor that selectively affects teenage boys. Other common nasal neoplasia include papillomas, hemangiomas, squamous cell carcinomas, esthesioneuroblastomas, melanomas, and adenocarcinomas. These lesions typically result in recurrent epistaxis which is associated with nasal obstruction. Patients with this history should undergo nasal endoscopy and radiologic imaging to rule out neoplasia.

Causes of epistaxis

Epistaxis results from a multitude of causes, both local and systemic . Common local factors include digital trauma, nasal septal deviation, neoplasia, and chemical irritants, whereas coagulopathies, renal failure, alcoholism, and vascular abnormalities are common systemic factors. A personal or family history of frequent bleeding, heavy bleeding, or easy bruising suggests a systemic bleeding disorder. Although these conditions are rarely the cause of epistaxis, a thorough investigation is indicated in these patients to rule out systemic disease. Likewise, epistaxis is rarely caused by neoplasm, but persistent unilateral bleeding should prompt a nasal endoscopy and possibly radiologic imaging to rule out a tumor.

Local digital trauma to the nose is the most common cause of epistaxis, usually resulting in mild hemorrhage of the anterior nasal septum. Mucosal dryness can also predispose an individual to bleeding from this same area. Mucosal dryness can be due to turbulent airflow, caused by septal deviation or spurs, and low humidity. Epistaxis is more frequent during the winter months, presumably because of the lower humidity during that time. Intranasal corticosteroids can be a cause of mucosal bleeding. Patients should be counseled on proper application, directing the spray laterally to avoid direct application to the septum. Traumatic nasal bone fracture or septal fracture can result in significant acute epistaxis. Bleeding may recur or be delayed following maxillofacial trauma because of posttraumatic aneurysm of the septal vasculature. Rhinosinusitis may be a coexisting factor, particularly in children, and may lead to increased inflammation, nose blowing, or, potentially, digital trauma, resulting in epistaxis.

Systemic factors frequently contribute to severe uncontrollable epistaxis. Von Willebrand’s disease and hemophilia are inherited coagulopathies and must be considered with a history of significant bleeding from minor wounds or severe bruising. Thrombocytopenia with a platelet counts of less than 20,000/mm ³ can make controlling epistaxis challenging. Hematologic malignancies can produce a similar coagulopathy because of poor platelet production. Similarly, chemotherapy regimens can produce thrombocytopenia. Chronic alcohol intake, aspirin and other nonsteroidal anti-inflammatory medication usage, and renal failure affect platelet function, despite normal counts. The role of hypertension is debated and no clear independent association has been firmly established as a lone factor in epistaxis. However, hypertension may make controlling a bleed more difficult. Osler-Weber-Rendu disease (hereditary hemorrhagic telangiectasia) is an autosomal dominant disease that results in fragile telangiectasias and arteriovenous malformations that can also cause significant recurrent bleeding.

Anticoagulant medication use should be ascertained during evaluation. The use of coumadin, enoxaparin, and heparin all alter the coagulation cascade. Aspirin and other nonsteroidal anti-inflammatory drugs are commonly used medications that affect platelet function. It is also important to inquire about alternative medicines. Garlic, ginkgo, and ginseng (the “3 Gs”) are known to inhibit platelet function specifically by affecting aggregation. A coagulation panel should be checked on admission in anticoagulated patients, and reversal of the anticoagulant should be considered.

Any individual with recurrent bleeding and a lack of other systemic factors should be evaluated for neoplasia, especially when the bleeding is unilateral. Juvenile nasal angiofibroma is an uncommon tumor that selectively affects teenage boys. Other common nasal neoplasia include papillomas, hemangiomas, squamous cell carcinomas, esthesioneuroblastomas, melanomas, and adenocarcinomas. These lesions typically result in recurrent epistaxis which is associated with nasal obstruction. Patients with this history should undergo nasal endoscopy and radiologic imaging to rule out neoplasia.

Evaluation

Once confirmation of hemodynamic stability and airway patency is complete, a directed history can quickly identify most of the factors contributing to a severe nosebleed. Laterality of the nosebleed, amount of blood loss, severity, and duration should be ascertained. The presence of nasal obstruction may indicate a neoplasm, especially with recurrent bleeding from the same side. If the nosebleed is traumatic in nature, one should consider other associated injuries. Attention must be given to other medical conditions, medications, alcohol use, and a history of severe nosebleeds or easy bruising. A family history of bleeding should also be investigated. Laboratory studies should be dictated by the history, physical examination, and severity of the bleeding and may include hematologic, coagulation, renal, and hepatic indices.

The examination seeks not only to rule out predisposing factors, such as telangiectasias or neoplasm but also to define precisely the source of bleeding. Epistaxis is typically classified as either anterior or posterior. These classifications do not have a defined dividing line between them; instead, the definition is an operational one. Anterior epistaxis has traditionally been defined as bleeding controlled through anterior rhinoscopy or anterior nasal packing, whereas posterior epistaxis is bleeding not easily visible anteriorly or that which is controlled only through posterior packing. Recent advances in endoscopy and endoscopic ligation/cauterization techniques blur the lines between these two divisions. It may be more appropriate to define anterior epistaxis as bleeding arising from the more anterior vessels (anterior ethmoid artery, superior labial artery branches) and posterior epistaxis as bleeding arising from the more posterior vessels (sphenopalatine and posterior ethmoidal arteries). Although these definitions have a significant “gray area” because of anastomotic networks, such a classification helps define which treatment methods will likely be necessary.

The examination begins with anterior rhinoscopy, which should identify the most common locations for anterior bleeds and can also be performed easily in most children. Significant hemorrhage will require suction, a light source, and a nasal speculum. If no anterior source is identified, a nasal endoscope can be used to visualize the remainder of the nasal cavity. Attention should be paid to mucosal lesions or submucous masses within the middle meatus and nasopharynx. Commonly, multiple small abrasions are encountered in the nasal cavity, which is typically the result of previous attempts at control of the bleeding by other care providers. Topical vasoconstriction with oxymetazoline or phenylephrine mixed with a topical anesthetic such as lidocaine or pontocaine will enhance the examination and slow some of the bleeding. Suction may also be necessary, in a cooperative patient, for visualization. Care must be taken when manipulating clots in the nasopharynx, because they may be dislodged into the hypopharynx, impacting the airway.

Another useful adjunct for anatomic diagnosis during significant posterior bleeding is a transpalatal injection of the SPA where it enters the nasal cavity . A 25-gauge needle is bent at 2.5 cm and inserted transorally into the greater palatine foramen to the bend. After withdrawing slightly to ensure the needle is not within a vessel, 1.5 mL of a 1:100,000 epinephrine solution is then injected slowly . This vasoconstrictive injection will slow bleeding from the SPA branches, effectively making the diagnosis of “posterior epistaxis.” Moreover, bleeding will usually slow substantially or even stop, typically allowing endoscopy to find the exact bleeding source. Quality endoscopy helps establish the bleeding location, which is essential in determining an appropriate treatment plan.