Juvenile nasopharyngeal angiofibroma !

A rare, benign but very vascular tumour at the back of the nose in adolescent boys. It causes a blocked nose and heavy, repeated nosebleeds.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

A benign, highly vascular fibrous tumour that arises near the sphenopalatine foramen on the posterolateral wall of the nasal cavity and grows into the nasopharynx. Although it does not metastasise, it is locally aggressive and can erode bone and spread into the sinuses, the pterygopalatine and infratemporal fossae, the orbit and the skull base.

Who gets it

Rare: about 0.5% of head and neck tumours. It occurs almost only in males, mostly between about 10 and 25 years of age. Any adolescent boy with recurrent one-sided nosebleeds and nasal blockage should raise suspicion.

Causes

Exact cause unknown
Hormonal influence is suspected (androgen-sensitive tissue), explaining the male adolescent predominance
Possible origin from vascular remnants near the sphenopalatine foramen
Higher frequency reported in familial adenomatous polyposis

Risk factors

Male sex
Adolescence (puberty)
Family history of familial adenomatous polyposis

Pathophysiology

The tumour is made of fibrous stroma with many thin-walled vessels that lack a normal muscular layer, so they do not contract and bleed heavily. It is fed mainly by branches of the maxillary artery (from the external carotid), especially the sphenopalatine artery, and in large tumours also by internal carotid branches. As it grows it blocks the choana and the auditory tube, bows the posterior wall of the maxillary sinus forward, widens the pterygopalatine fossa and can reach the orbit, cavernous sinus and middle cranial fossa.

Classification

Staged by extent on imaging (Fisch, Radkowski or UPMC systems)
Confined to nasal cavity and nasopharynx without bone destruction
Spread into sinuses or pterygopalatine fossa with bone erosion
Extension to infratemporal fossa, orbit or skull base
Intracranial extension, cavernous sinus or optic chiasm involvement

Symptoms and signs

Progressive one-sided nasal obstruction
Recurrent, heavy, one-sided nosebleeds that are hard to stop
Nasal discharge and hyponasal voice
Ear fullness or hearing loss from blocked auditory tube (middle ear effusion)
Swelling of the cheek, proptosis or double vision in advanced cases
Headache

Diagnosis

Clinical: Typical history in an adolescent male. Nasal endoscopy shows a smooth, lobulated, reddish-purple mass in the posterior nasal cavity and nasopharynx.
Tests: Office biopsy is generally avoided because of the risk of life-threatening bleeding; the diagnosis is usually made on characteristic imaging and confirmed on the resected specimen. Blood count and cross-matching before surgery because of expected blood loss.
Imaging: Contrast CT shows an avidly enhancing mass centred on the sphenopalatine foramen, widening of the pterygopalatine fossa and anterior bowing of the posterior maxillary wall (Holman–Miller sign). MRI defines soft-tissue and intracranial extent. Angiography maps the feeding vessels and allows preoperative embolisation.

Differential diagnosis

Antrochoanal or nasal polyp
Nasopharyngeal carcinoma
Adenoid hypertrophy
Rhabdomyosarcoma or lymphoma in children and adolescents
Other causes of recurrent epistaxis (anterior septal bleeding, coagulopathy)
Inverted papilloma

Goal of treatment

Complete removal of the tumour with control of bleeding, preservation of surrounding structures and close follow-up for recurrence.

Treatment

Acute: Massive epistaxis: airway protection, nasal packing, intravenous fluids and transfusion as needed, and urgent ENT and interventional radiology involvement.
Procedure: Preoperative angiographic embolisation of the feeding branches of the maxillary artery, usually one to a few days before surgery, to reduce intraoperative blood loss.
Surgical: Surgical excision is the treatment of choice: endoscopic endonasal resection for most tumours, with open or combined approaches for extensive disease.
Medical: Radiotherapy is reserved for unresectable, intracranial or residual disease; hormonal (anti-androgen) therapy has been studied but is not standard.
Follow-up: Postoperative care: monitoring for bleeding, airway and haemoglobin, care of nasal packing; then serial endoscopy and MRI to detect recurrence, which is most frequent in the first years.

Complications

Life-threatening haemorrhage, spontaneous or during biopsy or surgery
Recurrence or residual tumour
Intracranial and orbital extension with visual loss
Middle ear effusion and conductive hearing loss
Long-term effects of radiotherapy on growth and the skull base in young patients

Prognosis

Survival is excellent with treatment. Recurrence is reported in a substantial minority, mostly with extensive or skull-base disease and incomplete resection; follow-up imaging is needed for years. Some tumours slowly regress after adolescence.

Test yourself

Think of the answer, then tap the question to see it.

What is the classic patient with juvenile nasopharyngeal angiofibroma?

An adolescent male with progressive unilateral nasal obstruction and recurrent, heavy unilateral epistaxis.

Which artery mainly supplies the tumour?

The maxillary artery (a branch of the external carotid), mainly through the sphenopalatine artery.

Why is office biopsy usually avoided?

The tumour is highly vascular and its vessels lack muscle in their walls, so biopsy can cause severe, life-threatening bleeding.

What is the Holman–Miller sign?

Anterior bowing of the posterior wall of the maxillary sinus on CT, caused by tumour in the pterygopalatine fossa.

What is done before surgical resection to reduce bleeding?

Angiography with embolisation of the feeding vessels.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Juvenile Nasopharyngeal Angiofibroma (JNA) (Cleveland Clinic Health Library, 2025); Juvenile nasopharyngeal angiofibroma (Journal of Oral and Maxillofacial Pathology, 2016).

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Representative model, for educational purposes only.

Nasal cavity highlighted on the Durgical 3D model