Nasal Septal Perforation

A full thickness defect of the septal cartilage or bone with loss of mucoperichondrium on both sides, creating a communication between the two nasal cavities.

Why perforations cause symptoms

Normal nasal airflow is laminar and follows a smooth path from the vestibule over the inferior turbinate to the choana. A perforation, particularly an anterior one, disrupts laminar flow and produces turbulence and crossflow between the cavities. Turbulent airflow dries the mucosa at the perforation edge, causing crusting, ulceration, bleeding and further enlargement. This is why anterior perforations are symptomatic and posterior perforations, sitting behind the region of maximal airflow, are often silent.

Causes

Iatrogenic and traumatic:

Septoplasty and submucous resection, the commonest single cause.
Nasal packing, cautery performed bilaterally at the same site, and cryotherapy.
Nasogastric and nasotracheal tubes.
Digital trauma, that is nose picking, which is a genuine and frequent cause.
Untreated septal haematoma and abscess.
Nasal piercing.

Inflammatory and granulomatous:

Granulomatosis with polyangiitis, which is the most important cause to exclude and which presents with crusting, granulation, a saddle nose, and systemic disease.
Sarcoidosis, with a strawberry mucosa appearance.
Eosinophilic granulomatosis with polyangiitis.
Systemic lupus erythematosus and other connective tissue disease.

Infective:

Tuberculosis, syphilis, which classically destroys bone and produces a saddle deformity, leprosy, rhinoscleroma, mucormycosis and other invasive fungal disease.

Drug related:

Intranasal cocaine, which causes vasoconstriction, ischaemia and direct toxicity, and produces large destructive perforations extending to the hard palate in severe cases.
Intranasal corticosteroid sprays directed at the septum, particularly with poor technique, which is a preventable cause.
Topical decongestant abuse.
Bevacizumab and other antiangiogenic agents.

Occupational and environmental:

Chromic acid, nickel, arsenic, cement dust, and other industrial exposures.

Neoplastic:

Squamous cell carcinoma, adenocarcinoma, natural killer T cell lymphoma of nasal type, and other malignancy. Any perforation with an atypical appearance, mass, bleeding or pain requires biopsy.

Symptom severity relates to position and size rather than to size alone. Anterior perforations are symptomatic; posterior perforations are usually not.

Crusting, which is the most consistent symptom, formed at the perforation edges where turbulent airflow dries the mucosa.
Recurrent epistaxis from the crusted, ulcerated edges.
Whistling on inspiration, which occurs with small anterior perforations, typically under 1 cm, and is a common presenting complaint. Larger perforations do not whistle.
Nasal obstruction, paradoxically, from turbulent airflow and from crusts.
Nasal dryness, discomfort and pain.
Foul smell and, in large perforations, malodour noticed by others.
Saddle nose deformity where dorsal support is lost, indicating a large perforation involving the dorsal strut or an underlying destructive process.

Examination

Anterior rhinoscopy and endoscopy with careful documentation of the perforation site, size in millimetres in both dimensions, the distance from the caudal edge and from the dorsum, the width of the remaining superior and inferior cartilage rims, and the state of the surrounding mucosa.
These measurements determine repairability. A perforation with an intact rim of at least 1 cm superiorly and inferiorly, and located anteriorly with adequate mucosa available, is more likely to be repairable.
Assess the mucosa for granulation, crusting, ulceration, atrophy and neovascularisation, which suggest an underlying inflammatory or infective cause rather than simple trauma.
Examine the external nose for saddle deformity, tip ptosis and columellar retraction.
Examine the palate, since cocaine induced disease and lymphoma extend to it.
Look for systemic features: rash, joint disease, ocular inflammation, haemoptysis, mononeuritis.

Establishing the cause matters more than describing the defect, because repairing a perforation in active vasculitis or ongoing cocaine use will fail.

Detailed history: previous nasal surgery, packing, cautery, trauma, occupational exposure, nasal spray use and technique, digital trauma, and drug use. Ask directly and non judgementally about cocaine, since it will not be volunteered and it is a frequent cause in younger patients with large perforations.
Nasal endoscopy with photographic documentation.
Biopsy of the perforation edge in every case where the cause is not clearly iatrogenic or traumatic, sent for histology, mycobacterial culture and fungal culture. Take the biopsy from the edge, not the centre, and take adequate tissue, since the yield in vasculitis is low and repeat biopsy is often needed.
Antineutrophil cytoplasmic antibody testing with proteinase 3 and myeloperoxidase specificity, urinalysis for haematuria and casts, renal function, and chest imaging where granulomatosis with polyangiitis is suspected. Proteinase 3 antineutrophil cytoplasmic antibody is positive in the majority of generalised disease but in a lower proportion of limited disease confined to the nose, so a negative result does not exclude it.
Erythrocyte sedimentation rate, C reactive protein, full blood count with eosinophil count.
Serum angiotensin converting enzyme and chest imaging for sarcoidosis.
Syphilis serology, tuberculosis testing including interferon gamma release assay, and HIV testing.
Antinuclear antibody and extractable nuclear antigens.
Urine toxicology for cocaine where use is suspected and denied, with the patient's consent.
Computed tomography of the sinuses where there is bone destruction, sinus involvement or suspected malignancy, and magnetic resonance imaging where a mass is present.

Treat the cause first, then manage symptoms medically, and reserve surgery for symptomatic patients with an inactive underlying condition.

Treat the underlying cause

Granulomatosis with polyangiitis: induction with corticosteroid plus rituximab or cyclophosphamide, then maintenance, under rheumatology supervision. Surgical repair must be deferred until sustained remission, generally at least 12 months, since operating on active disease fails and can accelerate destruction.
Sarcoidosis: corticosteroid and steroid sparing agents.
Infection: specific antimicrobial therapy.
Cocaine: complete cessation with substance misuse support, and documented abstinence for at least 12 months before any repair is considered. Repairing a perforation in a patient who continues to use will fail.
Stop septal directed nasal sprays and retrain technique, aiming laterally away from the septum.
Remove occupational exposure.
Malignancy: oncological management.

Medical management of symptoms, which is sufficient for many patients

Nasal saline irrigation with large volume isotonic solution two or three times daily, which is the single most effective measure for crusting.
Emollients applied to the perforation edges: petroleum jelly, glucose in glycerine 25 percent, sesame or almond oil, or a proprietary nasal gel, applied two or three times daily.
Humidification of the bedroom air.
Antibiotic ointment such as mupirocin 2 percent for secondary infection and for staphylococcal colonisation of the crusts.
Avoid digital trauma, which perpetuates enlargement.
Stop smoking.
Manage epistaxis conservatively. Avoid bilateral cautery at the same point, which caused the perforation in many patients and will enlarge it.

Septal button prosthesis

A silastic obturator with flanges on both sides, sized to the perforation, inserted under local or general anaesthesia.
Indicated for symptomatic perforations in patients unsuitable for or unwilling to undergo surgery, for very large perforations, for those with active underlying disease, and as a trial to predict the benefit of surgical closure.
Custom made buttons from a mould fit better and are tolerated longer than stock sizes.
It abolishes whistling and reduces crusting and bleeding in the majority.
Complications: irritation, crusting at the flange edges, extrusion, and enlargement of the perforation from pressure necrosis. Requires regular cleaning and periodic review.

Surgical repair

Indications: symptomatic perforation with crusting, bleeding or whistling that persists despite medical therapy, in a patient with an inactive underlying cause, who does not use cocaine, and who does not smoke.

Principles:

Three layer closure is the aim: mucosal flaps on both sides plus an interposition graft between them.
The interposition graft provides a scaffold for mucosal regrowth and prevents re perforation. Options are temporalis fascia, which is the most commonly used, mastoid periosteum, perichondrium, conchal cartilage, and acellular dermal matrix.
Closure of both mucosal layers is ideal, but closure of one side plus an interposition graft frequently succeeds, since the other side epithelialises over the graft.

Approaches:

Open septorhinoplasty approach with a columellar incision, which gives the best exposure for large perforations and allows simultaneous correction of external deformity. This is the preferred approach for perforations above 2 cm.
Endonasal or endoscopic approach for smaller perforations, with less morbidity but more restricted access.
Bilateral mucosal advancement and rotation flaps, releasing the mucosa along the nasal floor and at the junction with the lateral wall to allow tension free advancement.
Inferior turbinate flaps, pedicled anteriorly or posteriorly, which bring in well vascularised tissue for large defects.
Anterior ethmoidal artery based flaps and nasal floor flaps.
Nasoseptal flap based on the posterior septal branch of the sphenopalatine artery, for posterior defects.
Facial artery musculomucosal flap and free tissue transfer for very large or previously failed repairs.

Outcomes:

Complete closure rates of 80 to 95 percent for perforations under 2 cm with an experienced surgeon, falling substantially for larger perforations and for revision cases.
Even where complete closure fails, symptoms frequently improve if the perforation is reduced in size.
Perforations larger than 3 cm, those in active vasculitis, those in continuing cocaine users, and those in smokers have high failure rates, and a button may be a more honest recommendation.

Postoperative care

Silastic splints for 2 to 4 weeks to protect the repair and prevent adhesions.
Saline irrigation and emollients from the first week.
Avoid nose blowing, straining and nasal instrumentation for 4 to 6 weeks.
Endoscopic review at 2 weeks, 6 weeks and 3 months.
Absolute smoking cessation, since smoking is strongly associated with failure.

Follow up in unrepaired perforations

Review periodically to detect enlargement, dorsal collapse and any change in appearance suggesting an evolving underlying disease, and repeat biopsy where the perforation enlarges without explanation.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Persistent Postural Perceptual Dizziness

Also known as: PPPD

A chronic functional vestibular disorder characterised by persistent non vertiginous dizziness and unsteadiness lasting three months or longer, exacerbated by upright posture, active or passive motion, and exposure to complex or moving visual environments. It unifies and replaces the older concepts of phobic postural vertigo, space and motion discomfort, visual vertigo and chronic subjective dizziness.

Pathophysiology

Following an acute vestibular insult, the brain adopts a high risk postural control strategy with increased reliance on visual and somatosensory input and stiffened postural responses. In most people this reverts to normal as recovery proceeds. In persistent postural perceptual dizziness it becomes fixed. There is a shift toward visual dependence, a failure to reweight sensory inputs appropriately, and altered connectivity between vestibular cortical areas, visual cortex and anxiety related networks including the amygdala and insula, with reduced activity in vestibular cortex and increased visual cortical processing.

This is a genuine disorder of function, not a psychiatric diagnosis and not malingering. It should be explained to patients as a software problem rather than a hardware problem, since patients frequently arrive having been told there is nothing wrong.

Precipitants

Vestibular neuritis and labyrinthitis, in around 25 percent.
Benign paroxysmal positional vertigo, including after successful repositioning.
Vestibular migraine, in around 15 to 20 percent.
Panic attacks and generalised anxiety, in around 15 percent.
Concussion and whiplash.
Cardiac arrhythmia, syncope and orthostatic intolerance.
Adverse drug reactions.

Pre existing anxiety, neuroticism and a tendency to bodily vigilance increase the risk of the acute insult becoming chronic.

Diagnostic criteria require all of the following

Dizziness, unsteadiness or non spinning vertigo present on most days for 3 months or more, with symptoms lasting for prolonged periods that may wax and wane in severity.
Symptoms occur without specific provocation but are exacerbated by upright posture, active or passive motion regardless of direction, and exposure to moving or complex visual stimuli.
Precipitated by a condition causing vertigo, unsteadiness or balance disruption.
Causes significant distress or functional impairment.
Not better accounted for by another disease.

Typical description

Constant background dizziness, described as swaying, rocking, floating, or a sense of being on a boat, rather than spinning.
Worse on standing and walking, better when lying down or when moving with a clear task and purpose, which patients notice as being better when distracted.
Marked worsening in supermarkets, shopping centres, busy streets, crowds, on escalators, when scrolling on a phone, watching action films, and in environments with patterned floors or striped surfaces.
Symptoms fluctuate through the day, typically worse as the day progresses and worse under stress or fatigue.
Discrete attacks of true rotational vertigo do not occur, and their presence indicates a coexisting active condition.
Avoidance behaviours develop: avoiding shops, public transport, driving, exercise and social activity, producing deconditioning and reinforcing the disorder.
Anxiety and depression are common but are not required for the diagnosis. Where they coexist they perpetuate the symptoms.

Examination

Neurological and vestibular examination is normal or shows only residual findings of the precipitating condition that do not explain the current disability.
Patients frequently have a stiff, cautious, wide based gait with reduced arm swing, which improves markedly when they are distracted by a cognitive task. This distraction effect is a useful clinical sign.
Romberg may appear positive with excessive sway that reduces on distraction.

This is a positive clinical diagnosis based on the criteria, not a diagnosis of exclusion. Endless further investigation is itself harmful, reinforcing the patient's conviction that a serious undiagnosed disease is present.

Detailed history establishing the precipitant, the chronicity, and the three exacerbating factors, which are the diagnostic core.
Full neurological, oculomotor and vestibular bedside examination including head impulse, nystagmus assessment, test of skew, Dix Hallpike and supine roll tests.
Pure tone audiometry.
Vestibular function testing, which may show residual abnormality from the precipitating event. Abnormal test results do not exclude the diagnosis, and normal results do not confirm it.
Magnetic resonance imaging where there are red flags or where it has not already been done for the precipitating condition. Repeated imaging in the absence of new features is counterproductive.
Orthostatic blood pressure measurement and electrocardiogram to exclude orthostatic and cardiac causes.
Screen actively for coexisting and treatable conditions, since persistent postural perceptual dizziness frequently coexists with benign paroxysmal positional vertigo and vestibular migraine. Any untreated coexisting condition will prevent recovery.
Validated questionnaires such as the Dizziness Handicap Inventory and the Niigata PPPD Questionnaire for baseline severity and response monitoring.
Screen for anxiety and depression.

Differential diagnosis

Uncompensated unilateral vestibular loss, which improves with vestibular rehabilitation and shows head movement provoked rather than visual environment provoked symptoms.
Vestibular migraine, which produces discrete episodes with migraine features, and which frequently coexists.
Bilateral vestibulopathy, with oscillopsia, bilaterally positive head impulse and objective test abnormality.
Orthostatic hypotension and postural orthostatic tachycardia syndrome, distinguished by the relation to standing and by haemodynamic measurement.
Cerebellar disease and neurodegenerative disorders, with objective neurological signs.
Medication effects.
Anxiety and panic disorder, which may be primary rather than secondary.

Four components: explanation, vestibular rehabilitation, medication, and cognitive behavioural therapy. Combining them works better than any alone.

Explanation, which is the foundation and takes time

Give the diagnosis a name and explain the mechanism: after the original problem, the balance system stayed on high alert, relying too heavily on vision and stiffening posture, and this pattern became habitual.
State explicitly that the symptoms are real, that the condition is recognised and treatable, and that it is not imagined, not psychiatric in origin, and not a sign of undiagnosed serious disease.
Explain that further scans are not needed and that repeated testing perpetuates the problem.
Explain that avoidance behaviour worsens the condition and that gradual re exposure is the treatment.
Patients who accept the explanation do markedly better. Time spent here determines the success of everything that follows.

Vestibular rehabilitation, adapted for this condition

Habituation exercises with graded exposure to provoking movements and environments.
Optokinetic and visual desensitisation training, using moving visual stimuli of increasing complexity, which targets the visual dependence directly.
Balance retraining on progressively challenging surfaces to encourage reweighting toward somatosensory and vestibular input.
Postural retraining to reduce the stiffened high risk strategy, including work on relaxed natural gait with normal arm swing.
Progression must be gradual. Aggressive provocation causes symptom flare and drop out, in contrast to acute unilateral loss where vigorous provocation is beneficial.
Aerobic exercise to reverse deconditioning.
Programmes typically run for 3 to 6 months.

Pharmacological treatment

Selective serotonin reuptake inhibitors and serotonin noradrenaline reuptake inhibitors are effective, with response rates of around 60 to 70 percent, and this benefit occurs independently of whether the patient has depression or anxiety.
Sertraline 25 mg daily for 1 week then 50 mg daily, titrated to 100 to 200 mg daily. Start at half the usual dose, since these patients are sensitive to initial adverse effects and early worsening of dizziness is the commonest reason for stopping.
Alternatives: escitalopram 5 mg daily increased to 10 to 20 mg; fluoxetine 10 mg increased to 20 to 40 mg; venlafaxine modified release 37.5 mg increased to 75 to 150 mg.
Warn about a transient increase in dizziness, nausea and anxiety in the first 1 to 2 weeks, which settles. Preparing the patient for this substantially improves adherence.
Continue for at least 12 months after a response before considering gradual withdrawal, since early discontinuation leads to relapse.
Monitor for hyponatraemia in the elderly, sexual dysfunction, and interactions.
Vestibular suppressants including prochlorperazine, cinnarizine and betahistine are ineffective and actively harmful in this condition, since they impair the sensory reweighting that constitutes recovery. Stopping them is an important therapeutic step. Many patients arrive on long term prochlorperazine and improve simply on withdrawal.
Benzodiazepines should be avoided for the same reason and because of dependence.

Cognitive behavioural therapy

Targets the catastrophic interpretation of symptoms, hypervigilance to bodily sensation, and avoidance behaviour.
Effective even in patients without a formal anxiety disorder.
Delivered individually, in groups or through structured digital programmes.
Combining cognitive behavioural therapy with vestibular rehabilitation and medication gives the best outcomes.

Treat coexisting conditions

Treat any active benign paroxysmal positional vertigo with repositioning.
Treat vestibular migraine with prophylaxis, which is frequently transformative in the overlap group.
Treat depression and anxiety in their own right.

Follow up and prognosis

Review at 6 to 8 weeks with a repeat severity questionnaire.
Most patients improve substantially with combined treatment, though a proportion have residual symptoms.
Longer duration before diagnosis predicts poorer outcome, which is the argument for recognising the condition early rather than after years of investigation.
Resist the temptation to reinvestigate on the basis of persistent symptoms alone. Reinvestigate only for genuinely new features.

Nasal Septal Perforation

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management