Epistaksis

01Pathophysiology

The nasal cavity has a dual blood supply derived from branches of both the internal carotid artery (via the anterior and posterior ethmoidal arteries, which are branches of the ophthalmic artery) and the external carotid artery (via the sphenopalatine artery and the superior labial artery). These vessels converge on the anterior nasal septum in a region called Kiesselbach plexus (Little area), which is a highly vascularized anastomotic network located on the anteroinferior septum. Because the mucosa here is thin and exposed to airflow, trauma, and desiccation, this area is extremely vulnerable to bleeding.

Anterior epistaxis accounts for approximately 90% of all cases and originates from Kiesselbach plexus. The mechanism is straightforward: mucosal drying, crusting, or direct digital trauma disrupts the superficial vessels in this plexus. Because the bleeding source is anterior, it is usually visible on examination and amenable to direct pressure or cautery.

Posterior epistaxis accounts for the remaining 10% but carries higher morbidity. It originates from the sphenopalatine artery or its branches (collectively forming Woodruff plexus, located on the posterolateral nasal wall near the middle turbinate). These are larger-caliber vessels under higher pressure, which is why posterior bleeds are more difficult to control and more commonly associated with hypertension and atherosclerosis in older adults. The blood drains posteriorly into the nasopharynx, so the patient may present with swallowing blood, hematemesis, or even aspiration rather than visible anterior bleeding.

In patients with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome), the underlying defect is abnormal vascular wall formation with arteriovenous malformations and telangiectasias throughout the nasal mucosa. These fragile vessels bleed recurrently and are often refractory to standard cautery.

Coagulopathy-related epistaxis (warfarin use, liver disease, von Willebrand disease, thrombocytopenia) results not from a primary vascular injury but from the inability to form a stable clot once the mucosa is disrupted. These patients often present with prolonged or recurrent bleeding disproportionate to the inciting event.

02Classification and Clinical Manifestation

03Diagnostic Workup

The workup for epistaxis begins with clinical assessment and anterior rhinoscopy. In most cases, the diagnosis is clinical and no laboratory testing is needed. The examiner will ask the patient to blow the nose to clear clots, apply a topical vasoconstrictor (oxymetazoline), and then inspect the anterior septum with a nasal speculum and headlight. If an anterior source is identified, the workup is essentially complete.

When no anterior source is found and the patient has blood draining posteriorly, nasal endoscopy becomes the key diagnostic tool. This allows direct visualization of the posterior nasal cavity and nasopharynx to localize the bleeding vessel.

Laboratory studies are reserved for situations where the clinical picture suggests an underlying disorder. Order a CBC when the bleeding is significant enough to cause hemodynamic changes or when you suspect chronic blood loss. Order PT/INR and aPTT when the patient is on anticoagulants, has liver disease, or presents with signs of a systemic bleeding disorder (easy bruising, bleeding from other sites, family history).

For recurrent epistaxis in a young patient with a family history of nosebleeds and visible telangiectasias on the lips or oral mucosa, the diagnosis of HHT should be considered. The Curacao criteria (epistaxis, telangiectasias, visceral AVMs, and first-degree relative with HHT) help clinch this diagnosis clinically without invasive testing.

CT angiography or conventional angiography is reserved for refractory cases that fail conservative management and nasal packing. Angiography has the added advantage of allowing embolization in the same session.

04Management and Treatment

The first action for any patient with epistaxis is to assess hemodynamic stability. If the patient is tachycardic, hypotensive, or showing signs of significant blood loss, establish IV access and begin volume resuscitation before addressing the local bleed.

For the stable patient, the next best step is always direct pressure: instruct the patient to sit upright (reduces venous pressure in the head), lean forward (prevents blood swallowing), and pinch the soft cartilaginous portion of the nose continuously for 15 minutes without checking. This alone controls the majority of anterior bleeds.

If direct pressure fails, apply topical oxymetazoline (0.05%) or place cotton pledgets soaked in a 1:1 mixture of lidocaine and phenylephrine into the nasal cavity. This provides both vasoconstriction and local anesthesia, allowing better examination.

Once the bleeding point is visualized, silver nitrate cautery is the treatment for a clearly visible anterior source. The critical pearl here: never cauterize both sides of the septum in the same session because bilateral cautery compromises the perichondrial blood supply and can lead to septal perforation.

When cautery fails or the bleeding is too brisk to identify a source, the next step is anterior nasal packing. A Merocel (compressed polyvinyl alcohol) sponge is inserted along the floor of the nasal cavity and expanded with saline. Alternatively, ribbon gauze coated with petroleum jelly can be layered in. The packing stays in place for 24 to 72 hours. Whenever nasal packing is placed, prescribe prophylactic antibiotics (typically amoxicillin-clavulanate 875/125 mg twice daily) to prevent staphylococcal toxic shock syndrome and secondary sinusitis.

If anterior packing does not control the hemorrhage and blood continues to drain posteriorly, suspect a posterior source. Posterior nasal packing using a Foley catheter (inflate the balloon in the nasopharynx, then pull anteriorly to tamponade the posterior choana) is performed. Posterior packing mandates hospital admission, ideally to a monitored or ICU setting, because of the risk of nasovagal reflex (bradycardia, hypotension), hypoxia, and airway obstruction.

For patients who fail both anterior and posterior packing, the definitive options are endoscopic sphenopalatine artery ligation (surgical) or angiographic embolization (interventional radiology). Embolization is preferred in patients who are poor surgical candidates.

In the anticoagulated patient, reversing the coagulopathy is critical. For warfarin, administer vitamin K (10 mg IV for life-threatening bleeding) and 4-factor prothrombin complex concentrate (PCC) or fresh frozen plasma for immediate reversal. For heparin, use protamine sulfate. For direct oral anticoagulants (DOACs), idarucizumab reverses dabigatran, and andexanet alfa reverses rivaroxaban or apixaban.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students get epistaxis questions wrong is by failing to distinguish anterior from posterior bleeding and therefore choosing the wrong management step. The exam will describe an elderly hypertensive patient with blood draining down the throat and no visible anterior source. Students who select "silver nitrate cautery" or "anterior packing" as the answer are missing the fact that this is a posterior bleed requiring posterior packing and admission.

Another classic trap involves the anticoagulated patient. The vignette gives a patient on warfarin with an INR of 8.0 and active nasal bleeding. Students jump to "reverse the INR" without recognizing that the immediate next step is still local control (direct pressure, then packing) while simultaneously addressing the coagulopathy. The exam tests whether you understand that hemorrhage control and anticoagulant reversal happen in parallel, not sequentially.

Watch for the adolescent male with recurrent unilateral epistaxis. This is the classic presentation of juvenile nasopharyngeal angiofibroma. The critical teaching point: the next step is imaging (CT with contrast), not biopsy. Biopsy of this highly vascular tumor without prior embolization risks uncontrollable bleeding.

Also be aware of the bilateral cautery trap: if the vignette describes a patient who had silver nitrate applied to one side and now presents with a septal perforation, the question is testing your knowledge that cauterizing both sides of the septum simultaneously destroys the blood supply to the cartilage. This is a preventable iatrogenic complication.

Finally, whenever nasal packing is placed, the exam expects you to know that prophylactic antibiotics are indicated to prevent toxic shock syndrome. Forgetting this step is a commonly tested error. The core competency being assessed across epistaxis questions is the ability to localize the source (anterior vs. posterior), sequence interventions correctly (pressure, then vasoconstriction, then cautery, then packing, then surgical/interventional options), and address the underlying etiology simultaneously.