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Septal Perforation

Causes, clinical features, investigations to exclude systemic disease, and the spectrum of management from conservative measures to surgical repair.

What is a Septal Perforation?

A septal perforation is a full-thickness defect in the nasal septum — a hole through both the mucoperichondrium (the vascular membrane lining the cartilage) and the underlying cartilage (or bone in the posterior septum). Because septal cartilage is avascular and depends entirely on the overlying mucoperichondrium for its blood supply and nutrition, any process that disrupts this lining on both sides of the septum simultaneously will result in ischaemia and eventual perforation.

Endoscopic view of a septal perforation
Endoscopic view of a septal perforation. The edges of the perforation are visible with the opposite side of the nasal cavity seen through it.

Clinical Features

Symptoms

  • Nasal whistling: A characteristic high-pitched whistling sound during nasal breathing, caused by turbulent airflow through the perforation. Typically heard on quiet breathing and often a source of social embarrassment for the patient.
  • Nasal crusting and discharge: Disrupted airflow leads to drying of the mucosa around the perforation edges, producing crusts that can be uncomfortable and malodorous.
  • Epistaxis (nosebleed): The crusted edges of the perforation are fragile and bleed easily, particularly when crusts are disturbed.
  • Nasal obstruction: Paradoxically, despite having a hole in the septum, patients often experience nasal obstruction due to disrupted nasal airflow dynamics and crusting.
  • Infection and pain: Superimposed bacterial infection of crusts can cause pain and offensive odour.
  • Saddle nose deformity: Large perforations, or those extending to include structural cartilage, can result in loss of nasal dorsal support, causing the characteristic saddle-shaped depression of the nasal bridge — this requires surgical reconstruction.

Relevant History to Elicit

Medical History

  • History of nasal trauma or previous nasal surgery (including septoplasty or cautery for epistaxis)
  • Nose picking (digital trauma is one of the most common causes)
  • Recurrent sinusitis, bronchitis, or otitis media — may suggest granulomatosis with polyangiitis (GPA, formerly Wegener's granulomatosis)
  • Known kidney disease — lupus nephritis and GPA both affect the kidneys
  • Malignancy
  • Known infectious diseases (tuberculosis, syphilis)

Social History

  • Smoking: Promotes microvascular disease and impairs mucosal healing
  • Alcohol use: Falls and nasal trauma that the patient may not recall; also associated with nutritional deficiencies
  • Recreational drug use: Intranasal cocaine causes potent vasoconstriction of the septal mucosa, leading to ischaemia and perforation — the single most common preventable cause of septal perforation in young adults. Intranasal amphetamines and crushed tablets can have similar effects.
  • Prescribed nasal medications: Long-term use of topical vasoconstrictors (e.g. phenylephrine, oxymetazoline) or, rarely, topical corticosteroid sprays (particularly if applied directly onto the septum rather than laterally)
  • Occupational exposures: Chromic acid fumes (electroplating industry), alkaline dusts (lime, cement), hexavalent chromium, arsenic. Always ask about occupation.
  • Transnasal oxygen: Prolonged use of nasal cannulae has a drying effect on the nasal mucosa and may cause direct septal trauma.

Causes of Septal Perforation

Traumatic Causes

  • Previous nasal surgery (septoplasty, rhinoplasty) — particularly if bilateral mucoperichondrial tears occur at the same level during surgery
  • Septal cautery for epistaxis, especially bilateral cautery in the same session
  • Nose picking (the most common cause in the general population)
  • Septal haematoma following blunt trauma — if untreated or incompletely drained, the resulting avascular necrosis leads to perforation
  • Nasal foreign bodies (particularly in children — batteries cause rapid liquefactive necrosis)
  • Chronic use of nasal cannulae

Inflammatory Causes (Autoimmune)

  • Granulomatosis with polyangiitis (GPA, formerly Wegener's granulomatosis): A systemic granulomatous vasculitis affecting the upper and lower respiratory tract and kidneys. Nasal involvement is extremely common (present in up to 90% of cases). Investigations: cANCA (anti-proteinase 3 antibody) is the most specific serological marker.
  • Sarcoidosis: A systemic granulomatous disease. Nasal involvement includes crusting, polyposis, and septal perforation. Investigation: serum ACE (angiotensin-converting enzyme), chest X-ray (bilateral hilar lymphadenopathy).
  • Systemic lupus erythematosus (SLE): An antinuclear antibody-positive systemic vasculitis. Check ANA, anti-dsDNA.
  • Polyarteritis nodosa: A necrotising vasculitis affecting medium-sized vessels.
  • Relapsing polychondritis: A rare inflammatory disease that attacks cartilage throughout the body, including the nasal septum and ear cartilage. Classically causes a saddle nose deformity.

Infective Causes

  • Tuberculosis: Haematogenous spread to the nasal mucosa causes granulomatous destruction. More common in immunocompromised patients and in high-prevalence populations.
  • Syphilis (tertiary): The gummatous stage of syphilis causes destructive granulomata. Historically a leading cause; now rare in the UK but re-emerging. Serology: VDRL, TPHA.
  • Rhinoscleroma: Caused by Klebsiella rhinoscleromatis; rare in the UK.
  • Leishmaniasis: Mucocutaneous leishmaniasis can cause extensive nasal destruction. Consider in returning travellers.

Neoplastic Causes

  • Squamous cell carcinoma (SCC), adenoid cystic carcinoma (ACC), basal cell carcinoma (BCC) — can erode through the septum
  • T-cell lymphomas (particularly NK/T-cell lymphoma, historically called "lethal midline granuloma") — cause rapidly progressive midfacial destruction; a biopsy is essential in any aggressive destructive nasal lesion

Drug-Related and Chemical Causes

  • Intranasal cocaine — the most important drug-related cause
  • Intranasal amphetamines and other recreational inhalants
  • Long-term intranasal vasoconstrictor sprays (phenylephrine, oxymetazoline — rebound rhinitis and ischaemia)
  • Chromic acid fumes (electroplating, leather tanning)
  • Alkaline industrial dusts (lime, cement)
  • Hexavalent chromium and arsenic compounds

Investigations to Exclude Systemic Disease

A septal perforation should never be treated in isolation without considering its underlying cause. The following investigations help exclude or confirm systemic disease:

  • cANCA / pANCA: cANCA (anti-PR3) is highly specific for GPA; pANCA (anti-MPO) is associated with microscopic polyangiitis and eosinophilic GPA (formerly Churg-Strauss)
  • ANA and anti-dsDNA: For SLE and other connective tissue diseases
  • Serum ACE: Elevated in active sarcoidosis
  • Chest X-ray: Bilateral hilar lymphadenopathy (sarcoidosis); upper lobe consolidation, cavitation (TB); nodules (GPA)
  • Urinalysis and renal function: GPA and SLE cause renal involvement (haematuria, proteinuria, renal impairment)
  • Syphilis serology: VDRL, TPHA (Treponema pallidum haemagglutination assay)
  • Mantoux test / IGRA (Interferon-gamma release assay): For TB (the Mantoux test can be falsely negative in immunocompromised patients; IGRA is more specific)
  • Biopsy: Essential for any atypical, aggressive, or unexplained perforation — send for histology and culture. A nasal mucosal biopsy is performed from the edge of the perforation.
  • CT sinuses: To assess extent of bony destruction, particularly for malignancy or aggressive granulomatous disease

Management

Conservative Management

Many small, asymptomatic perforations require no intervention beyond treatment of the underlying cause and symptom control. Conservative measures include:

  • Saline douching: Regular nasal saline irrigation (e.g. NeilMed or similar) moistens the nasal mucosa and softens crusts, reducing epistaxis and discomfort. This is the single most important conservative treatment.
  • Soft paraffin (Vaseline) or naseptin cream: Applied gently to the edges of the perforation with a cotton bud to prevent drying and crusting. Avoid intranasal fingers as this causes further trauma.
  • Cessation of causative agent: Stop cocaine, vasoconstrictors, or remove from occupational exposure — the perforation may stabilise once the injury is removed, though it rarely heals spontaneously once established.
  • Treat underlying systemic disease: GPA responds to immunosuppression (rituximab or cyclophosphamide with steroids); sarcoidosis with systemic steroids; syphilis with penicillin; TB with standard RIPE therapy.

Prosthetic Obturator

A custom-made septal button (a soft silicone prosthetic device) can be placed by a rhinologist to occlude the perforation. It reduces whistling, crusting, and epistaxis without surgery. It is particularly useful in patients unfit for surgery, in those with active systemic disease, or as a temporary measure. The device requires regular cleaning and follow-up.

Surgical Repair

Surgical repair is offered to symptomatic patients with perforations that do not respond to conservative management. It requires bilateral mucoperichondrial flaps to provide vascular coverage of the perforation from both sides. Various techniques exist depending on the size and location of the perforation — small anterior perforations have the best outcomes. Perforations greater than 2 cm are significantly more difficult to repair. Surgery is performed in theatre under general anaesthesia. The underlying cause must be quiescent before surgery is attempted — active GPA or cocaine use are contraindications.

Frequently Asked Questions

What is the most common cause of septal perforation?

In the general population, nose picking (digital trauma) is the most common cause, particularly for small anterior perforations. In younger adults, intranasal cocaine use has become a leading cause. Iatrogenic causes (previous nasal surgery, bilateral cautery) are also common. In a specialist ENT clinic, the most important causes to exclude are systemic inflammatory diseases such as GPA, which require specific immunosuppressive treatment.

Why does cocaine cause a septal perforation?

Cocaine is a potent local anaesthetic and vasoconstrictor. Repeated intranasal application causes sustained vasoconstriction of the septal mucosa, leading to ischaemia of the mucoperichondrium and, subsequently, the underlying cartilage. Chronic use results in mucosal atrophy, ulceration, and eventually full-thickness perforation. The damage is typically anterior and often extends to cause collapse of the nasal dorsum. Levamisole (a veterinary anthelmintic often used to cut cocaine) has additional vasculitic properties and may worsen the damage. Cessation of cocaine use will halt progression but the perforation will not heal spontaneously.

What investigations would you arrange for a new referral with a septal perforation of unknown cause?

This is a common ST3 viva question. A systematic approach: (1) cANCA and pANCA — screen for GPA and other ANCA-associated vasculitides; (2) ANA — for lupus and connective tissue disease; (3) serum ACE and chest X-ray — for sarcoidosis; (4) syphilis serology (VDRL, TPHA); (5) IGRA or Mantoux test for TB; (6) FBC, U&E, urinalysis — renal involvement in GPA and SLE; (7) CT sinuses — assess bony extent of disease; (8) biopsy of the perforation edge — essential for any aggressive or unexplained perforation. A careful social history (cocaine use, occupation) is equally important and must not be omitted.

Can a septal perforation heal on its own?

Spontaneous healing of an established perforation is extremely rare. The edges of the perforation become epithelialised and the defect becomes permanent. If the causative agent is removed early (e.g. stopping cocaine before perforation is complete, or before a haematoma progresses to necrosis), healing may occur. Once a perforation is established, it requires either conservative management, a prosthetic button, or surgical repair.

How does GPA (Wegener's granulomatosis) cause septal perforation?

Granulomatosis with polyangiitis (GPA) causes granulomatous inflammation and necrotising vasculitis of small blood vessels. In the nose, this results in a destructive granulomatous process that destroys the mucosa and underlying cartilage of the nasal septum. The perforation in GPA is typically associated with severe crusting, epistaxis, and a distinctive offensive nasal odour. It is also associated with saddle nose deformity and subglottic stenosis. Serological diagnosis relies on cANCA (anti-PR3), which is positive in approximately 90% of systemic GPA. Treatment requires immunosuppression with rituximab (now preferred first-line in many centres) or cyclophosphamide plus systemic corticosteroids.

What are the options for a patient with a symptomatic septal perforation who declines surgery?

For patients who decline or are unfit for surgery, the main alternatives are: (1) conservative measures — regular saline douching (the most important), soft paraffin applied to the edges, and treatment of any underlying systemic cause; (2) a septal button (silicone obturator) — a custom-made device inserted to occlude the perforation, reducing whistling, crusting, and epistaxis. The button requires regular cleaning (weekly saline rinse) and follow-up. It can be removed if the patient wishes. Symptom control rather than anatomical correction is the realistic goal in these patients.

What size of perforation is generally amenable to surgical repair?

There is no absolute cut-off, but surgical success rates decrease substantially as perforation size increases. Small perforations (under 1 cm) have the best outcomes. Perforations between 1 and 2 cm are technically challenging but achievable. Perforations greater than 2 cm are very difficult to repair primarily and may require interposition grafts or staged procedures. The location also matters — anterior perforations are more accessible; posterior perforations are surgically very difficult. Any patient with an active systemic disease driving the perforation (GPA in relapse, ongoing cocaine use) must have the underlying condition controlled before surgery is attempted.

What is Cottle's area and what is its relevance to septal perforation?

Cottle's areas are five anatomical zones of the nasal septum used to describe the location of pathology, including perforations. Area 1 is the nasal vestibule, area 2 is the valve region, area 3 is the anterior bony and cartilaginous septum, area 4 is the posterior cartilaginous and anterior bony septum, and area 5 is the posterior bony septum. Most traumatic and cocaine-related perforations occur in areas 2 to 3 (the anterior septum), whereas GPA and syphilis tend to cause more posterior destruction. Documenting the Cottle area of the perforation is useful for surgical planning and monitoring disease progression.

References

  1. Karaman E, Hacizade Y, Isildak H, Kaytaz A. Management of septal perforation. J Craniofac Surg. 2009;20(2):360–363.
  2. Facer GW, Kern EB. Nonsyphilitic sclerosing nasal septal perforation. Otolaryngol Head Neck Surg. 1979;87(2):219–224.
  3. Diamantopoulos II, Jones NS. The investigation of nasal septal perforations and ulcers. J Laryngol Otol. 2001;115(7):541–544.
  4. Stone JH, Merkel PA, Spiera R, et al. Rituximab versus cyclophosphamide for ANCA-associated vasculitis. N Engl J Med. 2010;363(3):221–232.
  5. Dosen LK, Haye R. Silicone button in the treatment of nasal septal perforations: long-term results. J Laryngol Otol. 2008;122(12):1303–1306.
  6. Gubisch W. Twenty-five years experience with extracorporeal septoplasty. Facial Plast Surg. 2006;22(4):230–239.