Epistaxis and Nasal Disorders

Local (mucosal/vascular) causes — the majority

• Digital trauma and mucosal drying: nose-picking plus low-humidity winter air desiccates the thin anteroinferior septal mucosa overlying Kiesselbach's plexus, cracking it and exposing superficial vessels. The single most common cause in children.
• Chemical/pharmacologic mucosal injury: intranasal corticosteroid sprays aimed medially at the septum, decongestant overuse (rhinitis medicamentosa), and cocaine (vasoconstriction → ischemic ulceration → septal perforation).
• Foreign body: suspect in a toddler with unilateral foul-smelling, blood-tinged purulent discharge.
• Structural/neoplastic: septal deviation or perforation with turbulent airflow, prior septoplasty, and tumors. Juvenile nasopharyngeal angiofibroma in an adolescent male and nasopharyngeal carcinoma in an adult both present as recurrent unilateral bleeding with obstruction.

Systemic causes

• Antithrombotics: aspirin, P2Y12 inhibitors, warfarin, and DOACs — the risk factor examiners plant most often. The AAO-HNS Clinical Practice Guideline: Nosebleed (Epistaxis) directs clinicians to document anticoagulant/antiplatelet use at first contact.
• Intrinsic bleeding disorders: von Willebrand disease (most common inherited), hemophilia, immune thrombocytopenia, leukemia, and acquired defects from cirrhosis (factor deficiency) or uremia (platelet dysfunction).
• Vascular/inflammatory: hereditary hemorrhagic telangiectasia and granulomatosis with polyangiitis (crusting, saddle-nose, c-ANCA/PR3).

• Mucosal vessel injury and bleeding: Disruption of the nasal mucosa exposes submucosal blood vessels to atmospheric pressure, triggering hemorrhage. The Kiesselbach's plexus (Little's area) in the anteroinferior septum is the source of 90% of anterior bleeds due to superficial vasculature and exposure to airflow-induced drying.

• Impaired hemostasis and platelet dysfunction: Defects in coagulation cascade (vitamin K deficiency, warfarin therapy, hemophilia), platelet abnormalities (thrombocytopenia, aspirin use), or fibrinolytic disorders prevent normal clot formation and stabilization. The nasal mucosa's rich fibrinolytic activity further predisposes to bleeding.

• Vascular structural abnormalities: Hereditary hemorrhagic telangiectasia (HHT) involves abnormal direct arteriovenous connections without intervening capillary beds, causing recurrent severe epistaxis. Aneurysmal dilatation, atherosclerotic vessel weakening, and prior nasal surgery create sites of vessel fragility.

• Mucosal drying and irritation: Low humidity, topical decongestant overuse, and atrophic rhinitis damage protective mucus layer and cause direct mucosal inflammation and ulceration. Cocaine use combines vasoconstriction followed by rebound vasodilation and direct mucosal toxicity.

• Posterior nasal bleeding mechanisms: Sphenopalatine artery bleeding in the posterior nasopharynx results from systemic hypertension, posterior septal trauma, or coagulopathy. Blood drains posteriorly into the nasopharynx and oropharynx rather than externally, making aspiration risk greater.

• Anterior epistaxis with visible external bleeding: Blood drains from the nostrils; patient reports active dripping or wiping blood. This represents 90% of cases and typically originates from Kiesselbach's plexus; usually self-limited within 30 minutes.

• Posterior epistaxis with hemoptysis and gastrointestinal symptoms: Patient swallows blood (may report hematemesis or melena), experiences posterior nasopharyngeal sensation, and blood may not be visible externally. Often more severe and prolonged; associated with hypertension, anticoagulation, or severe trauma.

• Recurrent epistaxis in young patients: Multiple bleeds over weeks to months, often bilateral, suggests hereditary hemorrhagic telangiectasia. Patients may describe "red spots" on lips, oral mucosa, or fingers; family history positive in 80% of autosomal dominant HHT.

• Epistaxis with facial trauma or septal deformity: History of nasal surgery, septoplasty, or blunt trauma; may indicate iatrogenic or post-traumatic vessel injury. Septal hematoma is a surgical emergency.

• Associated systemic symptoms: Fever, upper respiratory congestion may precede epistaxis from inflammation. Unexplained recurrent bleeding warrants investigation for leukemia, platelet disorders, or occult malignancy.

• Clinical pearl: Patients often report unilateral bleeding but may actually have bilateral involvement; always examine both sides with adequate visualization.

• Direct visualization with anterior rhinoscopy or nasal endoscopy: Place patient in recumbent position (head forward, not back); use headlight, speculum, and suction to identify bleeding source. Document location (anterior septum vs. lateral wall vs. posterior), laterality, and presence of active bleeding or blood clots. Endoscopic examination superior for posterior bleeds and identifying underlying lesions.

• Clinical assessment of bleeding severity: Determine duration of current bleed, frequency of prior episodes, and amount of blood loss (minor vs. major—estimate as number of tissues used, episodes per day). Assess vital signs for hemodynamic instability; tachycardia and hypotension suggest significant hemorrhage.

• Coagulation studies when indicated: Order PT/INR, aPTT, platelet count, and fibrinogen if epistaxis is recurrent, severe, in patient on anticoagulation, or if family/personal history suggests coagulopathy. Consider bleeding time (now rarely used) and specific factor assays if abnormal screening results.

• Laboratory workup for underlying conditions: CBC to assess hemoglobin/hematocrit (baseline and post-transfusion); chemistry panel for renal function (hypertension). ESR/CRP if vasculitis suspected; consider granulomatosis with polyangiitis (GPA) in recurrent epistaxis with systemic symptoms.

• Imaging for refractory or posterior epistaxis: CT angiography or MRI to evaluate for mass, vascular malformation, or arteriovenous fistula if bleeding recurs after treatment or appears posterior. Angiography reserved for cases requiring endovascular intervention.

• Diagnostic considerations: Epistaxis from only one naris with recurrence in same location raises concern for malignancy (squamous cell carcinoma, adenocarcinoma, hemangioma)—obtain tissue diagnosis if lesion visualized. Unilateral bleeding in elderly smoker warrants biopsy; nasopharyngeal carcinoma may present as "epistaxis" with blood pooling posteriorly.

• First-line management (anterior epistaxis): Have patient sit upright (prevents blood aspiration), lean forward (not backward—backward position increases swallowing), and apply direct pressure by pinching the soft tissues (cartilaginous portion) of the nose for 10-15 minutes continuously. Concurrent use of topical vasoconstrictor (0.05% oxymetazoline or 1% phenylephrine) with 1% lidocaine ± epinephrine on pledgets placed in nasal cavity; this "vasoconstrictor soaked pledget" strategy is first-line. Application of ice packs to the bridge may provide additional hemostasis. Most anterior bleeds (80-90%) stop with conservative management.

• Topical hemostatic agents: If bleeding continues after initial pressure, apply topical thrombin (Thrombin-JMI), absorbable gelatin sponge (Gelfoam), or tranexamic acid (TXA—inhibits fibrinolysis). Chitosan-based dressings (HemCon) highly effective but expensive. These are biochemically active hemostats; leave in place 10-15 minutes, then remove gently. Caution: thrombin is protein-based; avoid in patients with thrombin allergy.

• Anterior nasal packing for refractory bleeds: If conservative measures and topical agents fail, place petroleum jelly-impregnated gauze packing (ribbon gauze, 0.5–1 inch width) layer-by-layer into the anterior cavity, starting laterally and working medially, ensuring each layer overlaps. Pack firmly but without excessive pressure (risk of alar necrosis). Alternative: nasal tampons (Rapid Rhino, Merocel) which expand with saline and conform to nasal cavity—faster and less traumatic than traditional ribbon gauze. Packing should remain for 48-72 hours; provide pain control and broad-spectrum antibiotics (amoxicillin-clavulanate or clindamycin) to prevent sinusitis and toxic shock syndrome. Patient requires follow-up in 48-72 hours for packing removal.

• Posterior packing for posterior epistaxis: Placement is technically difficult and associated with serious complications; considered if anterior packing fails OR if posterior source identified. Traditionally uses postnasal packing (4×4 gauze tied with string, placed behind soft palate via catheter), but Foley catheter technique (14-16 Fr catheter with balloon inflated with 10-15 mL saline in nasopharynx, then anterior packing added) is now preferred—faster, easier, and equally

Complications of the bleeding itself

• Hypovolemia and hemorrhagic shock (emergency): more typical of posterior sphenopalatine bleeding, where blood loss is occult because it drains into the nasopharynx. Tachycardia and narrowed pulse pressure precede hypotension; resuscitate and type/crossmatch before chasing the source.
• Aspiration and airway compromise (emergency): swallowed or aspirated blood in an obtunded, elderly, or intoxicated patient. Coughing, hypoxemia, or altered mental status during brisk posterior bleeding mandates airway protection.
• Iron-deficiency anemia: from chronic recurrent bleeds, classically in hereditary hemorrhagic telangiectasia.
• Nausea and hematemesis/melena: swallowed blood is a gastric irritant and a common distractor for upper GI bleeding.

Complications of treatment

• Toxic shock syndrome (emergency): Staphylococcus aureus TSST-1 superantigen proliferating on retained nasal packing. Fever, diffuse erythroderma, hypotension, and multiorgan involvement with later desquamation — remove the pack immediately, culture, and treat. This risk underlies the practice of antibiotic coverage and mandated 48–72 hour follow-up for pack removal.
• Pressure necrosis: over-tight packing causes alar rim or columellar skin necrosis; posterior balloons overinflated in the nasopharynx cause soft-palate necrosis or balloon migration with airway obstruction.
• Septal perforation: from cauterizing both sides of the septum at the same visit — the classic avoidable error, since bilateral cautery destroys the mucoperichondrial blood supply to avascular cartilage.
• Sinusitis and otitis media: packing obstructs the osteomeatal complex and eustachian tube drainage.
• Vasovagal/trigeminocardiac reflex bradycardia and hypoxemia during posterior packing.
• Untreated septal hematoma (emergency): cartilage necrosis → saddle-nose deformity or abscess; requires incision and drainage.
• Endovascular embolization: stroke, facial pain, and vision loss from non-target embolization of internal carotid collaterals.

• Kiesselbach's plexus anatomy is the most tested fact: an anastomosis in Little's area fed by the anterior ethmoidal (internal carotid → ophthalmic), the sphenopalatine and greater palatine (external carotid → maxillary), and the superior labial branch of the facial artery. Posterior bleeds arise from the sphenopalatine artery near Woodruff's plexus.
• Best next step in an actively bleeding, stable patient: sit upright, lean forward, and compress the soft cartilaginous nose — not the bony bridge — for a sustained 10–15 minutes. AAO-HNS nosebleed guidance puts firm compression with a topical vasoconstrictor ahead of any procedure.
• Adolescent male + recurrent unilateral epistaxis + nasal obstruction = juvenile nasopharyngeal angiofibroma. Diagnose with contrast CT/MRI; do not biopsy — this highly vascular testosterone-sensitive tumor can hemorrhage catastrophically. Preoperative embolization precedes resection.
• Packing plus fever, rash, and hypotension = toxic shock syndrome; remove the packing first.
• The one association to know: recurrent epistaxis + mucocutaneous telangiectasias + autosomal dominant family history = hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu), defined by the Curaçao criteria. International HHT guidelines advise screening for pulmonary and cerebral AVMs, since right-to-left shunting causes paradoxical embolic stroke and brain abscess.
• Never cauterize both sides of the septum at one sitting — septal perforation follows.
• Distractor to avoid: tilting the head backward. It does not stop bleeding and promotes swallowing and aspiration.
• Do not reflexively order coagulation studies in an otherwise healthy first-time anterior bleed; AAO-HNS reserves testing for known or suspected bleeding disorders, anticoagulant use, or severe/recurrent bleeding.
• Painless unilateral bleeding in an older smoker, or a child with unilateral foul discharge, points to neoplasm and foreign body respectively — not to Kiesselbach's plexus.