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Summary Table

Category	Details
Risk Factors	Dry climate, digital trauma (nose picking), hypertension, anticoagulant/antiplatelet use, coagulopathies (von Willebrand disease, hemophilia), hereditary hemorrhagic telangiectasia (HHT), nasal septal deviation, intranasal drug use, hepatic disease
Etiology	Anterior: rupture of vessels in Kiesselbach plexus (Little area). Posterior: rupture of sphenopalatine artery or its branches
Patient Presentation	Unilateral or bilateral nasal bleeding; anterior epistaxis presents with visible bleeding from the nostril, posterior epistaxis presents with blood draining into the oropharynx, hematemesis, or hemoptysis
Classic Physical Exam	Active bleeding from the anterior nasal septum on anterior rhinoscopy (anterior type); blood visible in the posterior pharynx without an identifiable anterior source (posterior type)
Key Diagnostic Results	Clinical diagnosis in most cases. CBC, PT/INR, aPTT if coagulopathy suspected. Nasal endoscopy for posterior bleeds. CT angiography or conventional angiography if refractory
Management	Direct pressure (pinch the soft part of the nose for 15 minutes), topical vasoconstrictors (oxymetazoline), chemical cautery (silver nitrate), anterior nasal packing, posterior nasal packing, arterial ligation or embolization for refractory cases
Keywords	"Bleeding from the nose after picking," "blood draining down the throat," "patient on warfarin with nosebleed," "Kiesselbach plexus," "Little area," "Woodruff plexus," "sphenopalatine artery"

1. Pathophysiology

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.

2. Classification and Clinical Manifestation

Type	Source	Typical Patient	Clinical Features	Severity
Anterior	Kiesselbach plexus (Little area) on the anteroinferior septum	Children, young adults, nose pickers, dry climate	Visible bleeding from one nostril, easily identified source on anterior rhinoscopy	Usually mild, self-limited
Posterior	Sphenopalatine artery / Woodruff plexus on the posterolateral wall	Older adults, hypertensives, patients on anticoagulants	Blood draining into the oropharynx, bilateral nasal bleeding, hematemesis, no visible anterior source	Often severe, may require ICU monitoring
Coagulopathy-associated	Either site, but bleeding is prolonged	Patients on warfarin/heparin, liver disease, von Willebrand disease, thrombocytopenia	Prolonged or recurrent bleeding, bruising elsewhere, family history of bleeding disorders	Variable, depends on underlying disorder
HHT-associated	Multiple telangiectasias across the nasal mucosa	Patients with family history, mucocutaneous telangiectasias, visceral AVMs	Recurrent epistaxis starting in childhood, worsening with age, telangiectasias on lips/tongue/fingers	Chronic, recurrent, often refractory

3. Diagnostic Workup

Test	Role	When to Order	Key Findings
Anterior rhinoscopy	Best initial step	All patients	Identifies bleeding site on anterior septum
Nasal endoscopy	Best test for posterior bleeds	When no anterior source is found	Identifies bleeding from sphenopalatine artery territory
CBC	Screening	Significant or recurrent bleeding	Anemia, thrombocytopenia
PT/INR, aPTT	Coagulation assessment	Suspected coagulopathy, anticoagulant use	Elevated INR (warfarin), prolonged aPTT (heparin, hemophilia, vWD)
Type and screen	Transfusion preparation	Severe hemorrhage	Blood group for crossmatch
CT angiography	Localization for refractory bleeding	Failed packing, recurrent posterior bleeds	Identifies the bleeding vessel for targeted intervention
Conventional angiography	Both diagnostic and therapeutic	Refractory posterior epistaxis, planned embolization	Localizes and embolizes the feeding vessel

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.

4. Management and Treatment

Step	Intervention	Details
1. Initial stabilization	ABCs, hemodynamic assessment	IV access, monitor vitals; if hemodynamically unstable, resuscitate with crystalloid/blood products
2. Direct pressure	Pinch the soft (cartilaginous) part of the nose	Continuous pressure for 15 minutes without releasing; patient sits upright, leans forward
3. Topical vasoconstriction	Oxymetazoline 0.05% spray or phenylephrine-soaked pledgets	Apply to the affected nostril to constrict mucosal vessels
4. Chemical cautery	Silver nitrate stick applied to the bleeding point	Only after the bleeding site is identified; apply for 5-10 seconds; do not cauterize both sides of the septum (risk of septal perforation)
5. Anterior nasal packing	Merocel sponge or ribbon gauze with petroleum jelly	Leave in place for 24-72 hours; prescribe prophylactic antibiotics (amoxicillin-clavulanate) to prevent toxic shock syndrome and sinusitis
6. Posterior nasal packing	Foley catheter balloon or posterior pack	For posterior bleeds not controlled by anterior packing; requires hospital admission and monitoring (risk of airway compromise, vagal response)
7. Arterial intervention	Endoscopic sphenopalatine artery ligation or angiographic embolization	For refractory posterior epistaxis that fails packing
8. Correct underlying cause	Reverse anticoagulation, treat coagulopathy	Warfarin: give vitamin K (IV for severe, oral for non-urgent) and fresh frozen plasma or 4-factor PCC for rapid reversal. Thrombocytopenia: platelet transfusion if count is critically low

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.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Nasal foreign body	Unilateral nasal bleeding in a child	Foul-smelling unilateral purulent discharge; foreign body visible on rhinoscopy; no Kiesselbach plexus bleeding point
Nasopharyngeal angiofibroma	Recurrent unilateral epistaxis in an adolescent male	Vascular mass visible on exam; CT shows enhancing mass in the posterior nasal cavity/nasopharynx; do not biopsy (risk of catastrophic hemorrhage)
Granulomatosis with polyangiitis (GPA)	Recurrent epistaxis with nasal crusting	Saddle-nose deformity, pulmonary and renal involvement, positive c-ANCA/anti-PR3, septal perforation on exam
Hereditary hemorrhagic telangiectasia	Recurrent epistaxis (may overlap as a cause)	Mucocutaneous telangiectasias (lips, tongue, fingertips), family history, visceral AVMs; Curacao criteria
Thrombocytopenia (ITP)	Epistaxis with prolonged bleeding	Petechiae and purpura elsewhere, isolated low platelet count, normal PT/aPTT
Von Willebrand disease	Mucosal bleeding including epistaxis	Family history of bleeding, prolonged bleeding time, prolonged aPTT, decreased vWF antigen and ristocetin cofactor activity
Nasal polyps	Nasal obstruction with occasional bleeding	Pale, translucent, grape-like masses on rhinoscopy; associated with asthma and aspirin sensitivity; bleeding is not the primary complaint
Squamous cell carcinoma of the nasal cavity	Unilateral epistaxis in an older adult	Unilateral obstruction, pain, cranial nerve deficits; destructive mass on CT; biopsy is diagnostic

6. Traps 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.

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