Epistaxis — Little's Area, Woodruff's Plexus, Causes, Stepwise Management and HHT

Epistaxis is bleeding from the nostril, nasal cavity or nasopharynx. It is one of the commonest ENT emergencies. The AAO-HNS 2020 guideline notes that at least 60% of people have a nosebleed at some point, but only about 6% of them seek medical attention, and admission for severe bleeding is needed in about 0.2%.

The working classification is by site: anterior epistaxis (far more common, usually visible on anterior rhinoscopy) and posterior epistaxis (less common, harder to see, more often needs hospital care). Nosebleeds peak in two age groups — children aged 2 to 10 years and adults aged 50 to 80 years (StatPearls).

The nasal cavity is supplied by branches of both the internal carotid (via the ophthalmic artery → ethmoidal arteries) and the external carotid (via the maxillary and facial arteries). StatPearls names five vessels whose terminal branches supply the nose; their watershed on the anterior septum forms Kiesselbach's plexus.

Woodruff's plexus lies in the posterior nasal cavity. StatPearls describes it as the rear, fine terminal branches of the sphenopalatine and posterior ethmoidal arteries, and it is the presumed source of most posterior nosebleeds.

Telling the two apart is the key step, because it decides whether simple pressure and cautery will work or whether the patient needs posterior packing, admission and possibly an interventional procedure.

Most nosebleeds are spontaneous rupture of a mucosal vessel, but the history should always look for local, systemic, environmental and drug causes. Raised blood pressure can prolong an episode, and anticoagulants and clotting disorders lengthen bleeding.

Systemic vasculitis can also present with nosebleeds: granulomatosis with polyangiitis causes nasal crusting, epistaxis, septal perforation and saddle nose. See vasculitis classification.

1. Primary survey — confirm the airway is patent and check for haemodynamic compromise. Moderate to severe bleeding needs two large-bore IV lines and crystalloid (StatPearls).
2. Triage — the guideline's first action statement: separate the patient who needs prompt management from the one who does not.
3. History — duration, side, frequency, trigger, treatment already tried; anticoagulants, aspirin, NSAIDs, nasal steroids, intranasal drug use; personal or family history of bleeding disorders.
4. Examination — patient seated, suction ready, headlight and nasal speculum; remove clots first, then perform anterior rhinoscopy to find the bleeding point.
5. Investigations — full blood count, group and cross-match and coagulation studies when needed, but they must not delay treatment. X-ray and CT have no role in managing an actively bleeding nose.

Treatment escalates one rung at a time, moving up only when the previous step fails.

1. Firm, sustained compression of the soft lower third of the nose (the cartilaginous part, not the bony bridge) — the guideline says for 5 minutes or longer; StatPearls advises at least 10 minutes. The patient stays seated.
2. Topical vasoconstrictor such as oxymetazoline (with topical anaesthetic), or thrombogenic foams and gels.
3. Chemical cautery with silver nitrate to a visible bleeding point after anaesthetising it. Cauterise only the active or suspected site, and only one side of the septum, to avoid septal perforation.
4. Anterior nasal packing when bleeding continues or no site is seen — absorbable material, balloons, nasal tampons or petrolatum gauze. Use resorbable packing in patients with a bleeding disorder or on anticoagulants or antiplatelets.
5. Posterior control — longer (7.5 cm) tampons, a posterior balloon or a Foley catheter, always with an anterior pack to close the space. Posterior packing needs admission and monitoring.
6. Refractory bleeding — intubate if the airway is threatened, then endovascular embolisation or surgical ligation of the sphenopalatine and ethmoidal arteries.

For bleeding that persists or recurs despite packing or cautery, the guideline asks the clinician to assess the patient for surgical arterial ligation or endovascular embolisation. Nasal endoscopy should be done or arranged for recurrent bleeding despite packing or cautery, and for recurrent one-sided bleeding.

HHT is an autosomal dominant vascular disorder caused mainly by pathogenic variants in ENG (endoglin), ACVRL1 or SMAD4, genes of the TGF-β receptor pathway. Upward of 95% of affected people have recurrent epistaxis, with an average onset around 12 years; about 90% start before 30 (GeneReviews).

Three or more criteria = definite HHT; two = possible or suspected. In children the criteria often miss the diagnosis because features appear with age. Iron-deficiency anaemia occurs in about half; pulmonary AVMs in 30–50% (more often with ENG variants).

Treatment of HHT epistaxis: humidification and topical moisturisers, ablation, oral tranexamic acid, systemic antiangiogenic therapy (IV bevacizumab) in an expert centre, and for refractory cases septodermoplasty or Young's nasal closure. Patients should avoid vigorous nose blowing, heavy lifting and straining.

• Commonest site: Little's area — about 90% of anterior bleeds.
• Posterior bleeds: Woodruff's plexus (sphenopalatine + posterior ethmoidal branches), blood in the throat or from both nostrils.
• First aid: pinch the soft lower third of the nose for at least 5 minutes (StatPearls: 10).
• Silver nitrate on one side of the septum only — bilateral cautery risks perforation.
• Packing in an anticoagulated patient: choose resorbable packs.
• Bradycardia after packing = nasal-cardiac reflex → remove the pack.
• Refractory bleeding: embolisation or ligation of the sphenopalatine and ethmoidal arteries.
• Recurrent bilateral nosebleeds plus telangiectases plus family history = HHT (autosomal dominant).