Epistaxis

• Anterior Epistaxis Mechanism (90% of cases): The anteroinferior nasal septum, supplied by the anterior ethmoidal artery and terminal branches of the sphenopalatine artery, contains a highly vascular area known as Little's area (Kiesselbach's plexus). This anastomotic zone where multiple arteries converge creates areas of turbulent flow and increased shear stress. Trauma (including iatrogenic trauma from digital manipulation, aggressive nose-blowing, or nasal instrumentation) disrupts the superficial mucosa and exposes small vessels to atmospheric pressure and airflow, which prevents normal hemostasis. The exposed vessel lumen experiences relative hypotension compared to surrounding tissue, impairing the Venturi effect-mediated hemostasis that normally occurs during vasoconstriction and platelet aggregation.

• Posterior Epistaxis Mechanism (10% of cases): Posterior bleeding originates from larger caliber vessels, primarily the sphenopalatine artery and its branches in the nasopharynx, or occasionally from the posterior ethmoidal artery. These vessels are located deep within the nasal cavity near the choanae and lateral nasopharyngeal wall. Posterior epistaxis typically results from either severe trauma, significant hypertension, or severe coagulopathy that overwhelms local hemostatic mechanisms. Blood flows posteriorly into the nasopharynx and oropharynx rather than anteriorly out the nares, making posterior bleeds more difficult to visualize and control.

• Hemostatic Mechanism Failure: Normal hemostasis in the nasal cavity depends on several factors: intact vascular endothelium with functional endothelial cells expressing tissue factor and von Willebrand factor; adequate platelet count (>50,000/μL for spontaneous hemostasis) and platelet function; adequate fibrinogen and clotting factors; and intact local vasoconstrictor response mediated by endogenous epinephrine and sympathetic innervation. When local mechanical trauma occurs, platelets adhere to exposed collagen via von Willebrand factor bridging (primary hemostasis), followed by thrombin generation through the tissue factor pathway (secondary hemostasis), resulting in fibrin deposition and clot formation. Disruption at any step—inadequate platelets, impaired platelet function, factor deficiencies, or anticoagulation—prevents effective clot formation.

• Mucosal Vulnerability Factors: The nasal mucosa loses water continuously through respiration, creating a thin epithelial layer vulnerable to disruption. Dry indoor air, particularly in winter or high-altitude environments, desiccates the mucosa and increases epithelial friability. Topical irritants (cocaine, methamphetamine) cause direct mucosal injury and vasculitis. Chronic inflammation from allergic rhinitis, chronic rhinosinusitis, or granulomatous diseases (granulomatosis with polyangiitis, sarcoidosis) weakens the vascular wall architecture and predisposes to bleeding. Vascular dysplasias (hereditary hemorrhagic telangiectasia, angiomas) represent structural weaknesses in vessel walls with abnormal endothelial development, lacking normal muscular layer support.

• Hemodynamic Contributions: Systemic hypertension increases transmural pressure across nasal vessels, predisposing to rupture of already weakened vessels or preventing normal hemostasis in the setting of minor trauma. Each systolic contraction creates pulsatile shear stress on vessel walls. However, hypertension alone rarely causes epistaxis de novo in normotensive vessels; it typically acts as a cofactor with other causes. Venous congestion from Valsalva maneuver, heavy exertion, or straining increases nasal venous pressure and congestion, facilitating bleeding when vessels are already compromised.

Local Causes (most common)

• Anterior Epistaxis Etiologies: Digital trauma and manipulation (nose-picking, overly aggressive nose-blowing) accounts for approximately 25-30% of epistaxis cases, particularly in children; the exposed nasal septum in Little's area is easily traumatized. Environmental factors including low humidity, high altitude, heated indoor air, and seasonal changes cause mucosal desiccation and increased friability. Nasal instrumentation from nasal cannulae, nasogastric tubes, nasal medications (topical corticosteroids paradoxically increase bleeding risk with chronic use due to mucosal atrophy), or recent nasal surgery disrupts the mucosa. Topical irritants including tobacco smoke, cocaine, methamphetamine, and occupational exposures (chromic acid in electroplaters) cause direct mucosal injury and inflammation. Chronic rhinosinusitis and allergic rhinitis create chronic inflammation and increased blood vessel prominence. Benign tumors including angiofibroma (typically in adolescent males, highly vascular), papillomas, and hemangiomas are friable and bleed easily. Deviated nasal septum causes abnormal airflow patterns and localized drying.

• Posterior Epistaxis Etiologies: Hypertension, particularly when systolic blood pressure exceeds 180 mmHg or diastolic exceeds 120 mmHg, predisposes to posterior bleeding, especially in elderly patients; however, the relationship is not strictly causal. Posterior wall malignancies including nasopharyngeal carcinoma (particularly squamous cell carcinoma in endemic regions) erode through vessels and present with epistaxis, often unilateral and recurrent. Sphenopalatine artery aneurysms (pseudoaneurysms) can develop after trauma or surgery and present with massive hemorrhage. Atherosclerotic disease with vessel wall weakening, while uncommon, can lead to rupture.

Systemic Causes

• Coagulation Disorders: Acquired thrombocytopenia (from marrow suppression, ITP, medication-induced, or DIC) with platelets <20,000-30,000/μL significantly increases bleeding risk; epistaxis may be the presenting sign of acute leukemia or immune thrombocytopenia (ITP). Inherited thrombocytopathies including von Willebrand disease (most common inherited bleeding disorder, affecting 0.6-2% of the population) and platelet dysfunction disorders impair primary hemostasis. Liver disease reduces synthesis of factors II, V, VII, IX, and X, creating a severe secondary hemostatic defect, particularly when INR >1.5. Factor deficiencies from specific factor defects or vitamin K deficiency reduce thrombin generation. Disseminated intravascular coagulation (DIC) from sepsis, trauma, malignancy, or obstetric complications consumes platelets and factors, causing simultaneous thrombosis and hemorrhage.

• Anticoagulation Therapy: Warfarin (INR >3), unfractionated heparin, low-molecular-weight heparin, and direct oral anticoagulants (DOACs) including dabigatran, rivaroxaban, apixaban, and edoxaban impair thrombin generation (warfarin and heparin) or thrombin activity (thrombin inhibitors) or factor Xa activity (Xa inhibitors). Epistaxis is reported in 3-7% of patients on warfarin and increases significantly with higher INR values. Antiplatelet agents including aspirin, clopidogrel, and other P2Y12 inhibitors increase bleeding time and decrease platelet aggregation, particularly problematic in patients with underlying platelet dysfunction.

• Hereditary Hemorrhagic Telangiectasia (HHT, Osler-Weber-Rendu syndrome): Autosomal dominant mutation in genes encoding endoglin (ENG) or activin receptor-like kinase 1 (ALK1) disrupts endothelial cell function and vascular development, resulting in multiple telangiectasias (dilated vessels lacking normal muscular layer and adventitia) throughout the nasal cavity and mucous membranes. Epistaxis is often the first clinical manifestation, beginning in childhood and worsening with age, eventually causing iron-deficiency anemia in many patients. Diagnosis requires three of four Curaçao criteria: spontaneous recurrent epistaxis, telangiectasias, visceral lesions (pulmonary, hepatic, cerebral arteriovenous malformations), or family history. Patients require screening for pulmonary arteriovenous malformations (PAVMs) given risk of paradoxical embolism and stroke.

• Chronic Kidney Disease: Uremia impairs platelet function through accumulation of uremic toxins, particularly guanidine compounds, reducing platelet adhesion and aggregation. Chronic anemia from erythropoietin deficiency also reduces oxygen-carrying capacity and increases bleeding.

• Infections: Granulomatosis with polyangiitis (GPA, formerly Wegener granulomatosis) causes necrotizing vasculitis of small and medium vessels with granuloma formation, frequently involving the nasal cavity and sinuses; epistaxis may be accompanied by crusting, ulceration, or septal perforation. Sarcoidosis causes chronic granulomatous inflammation. Mucormycosis in immunocompromised hosts causes rapidly progressive necrosis. Syphilis and tuberculosis cause chronic granulomatous disease with vessel erosion.

Medication-Related

• Topical Corticosteroids and Decongestants: Chronic intranasal corticosteroid use causes mucosal atrophy paradoxically increasing bleeding risk. Topical decongestants (oxymetazoline, phenylephrine) with chronic use cause rebound congestion and mucosal damage. Topical NSAIDs impair local hemostasis.

• Anterior Epistaxis Presentation: Bright red blood flows anteriorly out the nares (or into the oropharynx if patient reclines), typically without posterior nasopharyngeal blood. Patients often describe the bleeding as starting unilaterally from one nostril. The bleeding is usually self-limited, stopping within 10-15 minutes with conservative measures in >90% of cases. Patients may report recent nasal trauma (digital manipulation), environmental dryness, or upper respiratory infection preceding the bleed. Anterior bleeds are typically less profuse than posterior bleeds and rarely cause hemodynamic compromise unless recurrent and severe.

• Posterior Epistaxis Presentation: Blood flows posteriorly into the nasopharynx and oropharynx, with patients describing blood in the throat or posterior mouth rather than blood exiting the nose. Patients may expectorate blood or experience hemoptysis-like symptoms. Posterior bleeds are often more profuse and prolonged, frequently requiring hospitalization. Older patients, those with hypertension, or those on anticoagulation are at higher risk. The bleeding may be accompanied by a sense of fullness in the nose or nasopharynx. Unlike anterior bleeds, posterior epistaxis rarely self-terminates with conservative measures.

• Systemic Symptoms from Significant Bleeding: Large-volume epistaxis can cause acute blood loss anemia with symptoms of dyspnea, dizziness, syncope, or chest discomfort if bleeding is rapid. Aspiration of blood into the tracheobronchial tree causes coughing, gagging, or lower airway irritation. Hypovolemic shock with tachycardia, hypotension, and altered mental status occurs with very large volume bleeds (rare in isolated epistaxis unless multiple episodes or recurrent bleeding). Swallowing of blood causes nausea, vomiting, abdominal distension, and potentially occult gastrointestinal bleeding on subsequent stool (visible as melena if a large volume is swallowed).

• Physical Examination Findings: Visualization of bleeding source on anterior rhinoscopy or nasal endoscopy is the gold standard; anterior septal bleeding near Little's area is classic. Blood clots partially obstructing the nasal cavity may mask the actual bleeding source until clots are gently removed with suction or saline irrigation. Crusting and granulation tissue on the anterior septum, particularly following repeated bleeding episodes, may be visible. Telangiectasias appear as small red or purple spots on the nasal mucosa, septum, lips, or oral mucosa (suggesting HHT). Septal perforation or ulceration may be visible with chronic or severe epistaxis, particularly in granulomatous diseases. Nasal masses including tumors, polyps, or angiofibroma may be apparent. Vital signs in significant bleeds show tachycardia and potentially hypotension if blood loss is substantial.

• Clinical Variants: Recurrent epistaxis (multiple episodes in a short period, >4 episodes in 6 months) requires investigation for systemic causes, particularly coagulopathy, chronic hypertension, or underlying malignancy, and may warrant definitive hemostasis. Severe epistaxis causing hemodynamic instability (BP <90/60, HR >120) or requiring transfusion indicates need for aggressive resuscitation and definitive intervention. Unilateral epistaxis in an adult, particularly if recurrent, raises concern for posterior wall malignancy or aneurysm and warrants imaging. Epistaxis in the setting of anticoagulation requires careful risk-benefit analysis of continuing anticoagulation versus stopping it temporarily.

Clinical History and Risk Stratification

• Anterior vs. Posterior Localization: Anterior epistaxis typically presents with blood flowing from the nose, easy visualization on anterior rhinoscopy, and self-limited bleeding <30 minutes. Posterior epistaxis presents with blood in the throat, difficulty visualizing bleeding source on anterior rhinoscopy alone, and bleeding >30 minutes or recurrent episodes. History of straining, coughing, or exertion may accompany posterior bleeds. Patient age >50 and hypertension history increase posterior bleed likelihood.

• Physical Examination Protocol: Anterior rhinoscopy performed after gentle suctioning and topical vasoconstriction (epinephrine 1:10,000 or phenylephrine 0.125%) allows visualization of Little's area and anterior septal bleeding sites with >90% sensitivity for anterior epistaxis. Visualization of the bleeding vessel with a pulsatile jet confirms the diagnosis. If no anterior source is identified and bleeding history suggests posterior origin, or if blood continues despite anterior intervention, flexible nasopharyngoscopy is essential to visualize the nasopharynx and identify posterior sources, lateral wall bleeding, or masses. Nasopharyngoscopy should be performed after topical anesthesia (4% lidocaine) and vasoconstriction. Assessment for telangiectasias on lips, oral mucosa, and digits during physical exam provides clinical evidence for HHT diagnosis.

Laboratory Evaluation

• Complete Blood Count (CBC): Hemoglobin and hematocrit quantify blood loss magnitude; acute bleeding may not reflect significant anemia if performed immediately. Platelet count <20,000-30,000/μL indicates significant thrombocytopenia requiring investigation (marrow exam, flow cytometry, or imaging for ITP). MCV helps identify chronic iron-deficiency anemia from recurrent epistaxis, seen as microcytosis and hypochromia. Leukocytosis with left shift or blasts suggests leukemia; lymphocytosis suggests CLL.

• Coagulation Panel (PT/INR, aPTT, Fibrinogen): PT/INR assesses vitamin K-dependent factors (II, VII, IX, X) and warfarin effect; INR >4 in patients on warfarin significantly increases

Immediate stabilization

• Airway and hemodynamics first: sit the patient upright and leaning forward to limit swallowing/aspiration of blood; suction clots. Large-bore IV access, type and screen, and volume resuscitation if tachycardic or hypotensive. Brisk posterior bleeding in an obtunded or anticoagulated patient is an airway emergency.

First-line (AAO-HNS Clinical Practice Guideline: Nosebleed/Epistaxis)

• Direct compression: firm continuous pinching of the cartilaginous (soft) anterior nose — not the bony bridge — for at least 5–15 minutes without peeking. This tamponades Kiesselbach plexus, where most bleeds arise.
• Topical vasoconstrictor (alpha-agonist class; representative agent oxymetazoline spray) applied on a pledget before or during compression; alpha-1 mediated arteriolar constriction slows flow enough for platelet plug formation. Topical antifibrinolytics (tranexamic acid on a pledget) are an accepted adjunct.

If bleeding persists

• Nasal cautery: after topical anesthesia and clot removal, identify the vessel on anterior rhinoscopy and apply silver nitrate — to one side of the septum only, and never to opposing surfaces at the same visit.
• Packing: absorbable/resorbable packing is preferred in coagulopathic or anticoagulated patients; non-absorbable expandable tampons or anterior balloons are used otherwise. AAO-HNS does not support routine systemic antibiotics for packing.
• Posterior bleeding: place a posterior balloon/dual-balloon device, admit for cardiorespiratory monitoring, and obtain urgent otolaryngology consultation — these patients do not go home.

Definitive management

• Endoscopic sphenopalatine artery ligation (with anterior ethmoid ligation if a superior source) is the preferred surgical escalation; endovascular embolization of internal maxillary/sphenopalatine branches is an alternative in poor surgical candidates.

Avoid

• Blind nasal packing with suspected basilar skull/cribriform fracture (risk of intracranial placement).
• Reflexive anticoagulant reversal or discontinuation; reverse only for severe or refractory hemorrhage.
• Office biopsy of a vascular nasal mass (juvenile nasopharyngeal angiofibroma) — image first.

Complications of the bleeding itself

• Hypovolemic shock (emergency): high-output posterior bleeding or repeated anterior bleeds; signaled by tachycardia, narrowed pulse pressure, hypotension, and altered mentation. Hemoglobin may be falsely reassuring early before hemodilution.
• Aspiration and airway obstruction (emergency): blood tracking into the nasopharynx in a supine or sedated patient; signaled by coughing, gurgling, hypoxemia, or a new infiltrate.
• Iron-deficiency anemia: chronic recurrent bleeding (classically hereditary hemorrhagic telangiectasia); microcytosis, low ferritin, fatigue.
• Occult swallowed blood: nausea, coffee-ground emesis, or melena mimicking upper GI hemorrhage — a common distractor.

Complications of cautery and packing

• Septal perforation: bilateral or overly aggressive silver nitrate cautery destroys the blood supply to septal cartilage from both sides; signaled by a whistling sound, crusting, and a visible defect. Repeated cocaine use causes the same lesion by chronic vasoconstrictive ischemia.
• Septal hematoma/abscess: blood dissecting between mucoperichondrium and cartilage; signaled by a boggy, fluctuant bluish septal swelling. Requires prompt incision and drainage — untreated it causes avascular cartilage necrosis and saddle-nose deformity.
• Pressure necrosis, alar/columellar injury, and sinusitis or otitis media: packing occludes sinus ostia and the eustachian tube.
• Toxic shock syndrome (emergency): staphylococcal TSST-1 superantigen release from a colonized pack; signaled by fever, diffuse erythroderma, hypotension, and multiorgan dysfunction — remove the pack immediately.
• Posterior packing hypoxemia/bradycardia (emergency): hypoventilation and vagally mediated dysrhythmias, which is why posterior packs mandate inpatient monitoring; balloon dislodgement can obstruct the airway.

Complications of definitive therapy

• Embolization: facial pain, skin or mucosal necrosis, and — because of internal carotid/ophthalmic collaterals — stroke or vision loss; the anterior ethmoidal artery is not embolized for this reason.
• Sphenopalatine ligation: palatal or dental numbness, crusting, rebleeding.

• The single best next step in most stems: have the patient sit upright, lean forward, and pinch the soft cartilaginous nose continuously for several minutes ± oxymetazoline. Pinching the bony bridge, tilting the head back, or jumping straight to packing are the classic wrong answers.
• Anatomy that examiners love: anterior bleeds arise from Kiesselbach plexus in Little's area on the anteroinferior septum (~90%); posterior bleeds arise from the sphenopalatine artery and present as blood dripping down the throat with a normal anterior rhinoscopy.
• Posterior bleed = admission: after a posterior balloon/pack, the patient is monitored inpatient with ENT consultation for hypoxemia, dysrhythmia, and rebleeding — never discharged.
• Adolescent male + recurrent unilateral epistaxis + unilateral nasal obstruction = juvenile nasopharyngeal angiofibroma. Answer contrast-enhanced imaging (CT/MRI), not biopsy — biopsy can cause catastrophic hemorrhage.
• Recurrent epistaxis + mucocutaneous telangiectasias + family history = hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu); screen for pulmonary AVMs because of paradoxical embolism and brain abscess.
• Adult with unilateral epistaxis, nasal obstruction, serous otitis media, and a neck node = nasopharyngeal carcinoma (EBV, Southeast Asian ancestry) — the answer is nasopharyngoscopy with biopsy.
• Fever, diffuse erythroderma, and hypotension days after nasal packing = staphylococcal toxic shock syndrome; remove the pack.
• Common distractors: hypertension is a cofactor, not the primary target — control the bleeding rather than acutely dropping the blood pressure; do not cauterize both sides of the septum at one sitting (septal perforation); and do not reflexively reverse or stop anticoagulation for a controllable anterior bleed, per AAO-HNS guidance.
• Septal perforation in a young adult with recurrent epistaxis points to intranasal cocaine use; a boggy fluctuant septal swelling after trauma is a septal hematoma requiring drainage to prevent saddle-nose deformity.