Deviated Nasal Septum

Displacement of the nasal septum from the midline, present to some degree in 70 to 80 percent of adults. The clinical question is never whether the septum is deviated, but whether the deviation explains the patient's symptoms, since most deviations are asymptomatic and operating on an asymptomatic deviation produces a dissatisfied patient.

Anatomy

The septum comprises the quadrangular cartilage anteriorly, the perpendicular plate of the ethmoid posterosuperiorly, and the vomer posteroinferiorly, resting on the maxillary crest and the anterior nasal spine.

Mucoperichondrium and mucoperiosteum cover both sides, and the plane between these layers and the cartilage or bone is the surgical dissection plane.

The blood supply is from the anterior and posterior ethmoidal arteries, the sphenopalatine artery, the greater palatine artery and the superior labial artery, which anastomose at Little area on the anteroinferior septum.

Aetiology

• Developmental, from differential growth rates between the cartilaginous septum and the bony framework, and from asymmetric facial growth.
• Birth trauma from moulding forces during delivery, which produces deviation identifiable in a proportion of neonates.
• Trauma in childhood and adult life, which is the commonest identifiable cause. Cartilage that is fractured and displaced heals in the deviated position.
• Associated with cleft lip and palate, where the septum deviates toward the non cleft side.

Physiological considerations that determine symptoms

• Nasal resistance accounts for around half of total airway resistance, and the nasal valve area contributes the majority of nasal resistance. A deviation at the nasal valve produces far more obstruction than a much larger posterior deviation.
• The internal nasal valve, the angle between the caudal edge of the upper lateral cartilage and the septum, is normally 10 to 15 degrees and is the narrowest point in the airway. Caudal septal deviation narrows this angle critically.
• The nasal cycle produces alternating congestion over 2 to 6 hours. In a deviated septum this becomes symptomatic, since the patient becomes completely obstructed when the wider side is in its congested phase. This explains the classical complaint of alternating and unpredictable blockage.
• Compensatory hypertrophy of the inferior turbinate on the concave side, which develops over years and which must be addressed at surgery or the patient will remain obstructed on that side after septal correction.

Classification

Deviations may be described as anterior or posterior, cartilaginous or bony, C shaped, S shaped, with a spur, or as a caudal dislocation from the maxillary crest. The Mladina classification defines seven types, of which caudal vertical deviation and deviation at the valve area are the most symptomatic.

• Nasal obstruction, typically unilateral or asymmetric, and often described as alternating with the nasal cycle.
• Obstruction that worsens on lying on the more patent side.
• Mouth breathing, dry mouth and snoring.
• Recurrent sinusitis, where a deviation obstructs the osteomeatal complex.
• Epistaxis from the exposed anterior septum, where a spur or convexity causes mucosal drying and crusting.
• Facial pain from a septal spur in contact with the lateral nasal wall or middle turbinate, producing contact point headache mediated by substance P release. This diagnosis is overused, and the pain should abolish with topical anaesthesia applied to the contact point before attributing it to the septum.
• Reduced smell where the olfactory cleft is obstructed.
• External nasal deformity where there is a significant caudal or dorsal deviation.

Examination

• Anterior rhinoscopy and endoscopy before and after topical decongestion. Decongestion is essential, since it separates the fixed structural component from the reversible mucosal component. Obstruction that resolves completely with decongestion is mucosal and will not benefit from septoplasty.
• Assess the caudal septum by lifting the nasal tip, which is where the most functionally significant deviations sit and where they are missed on posterior rhinoscopy.
• Cottle manoeuvre: lateral traction on the cheek to open the internal valve. Improvement suggests valve compromise. The modified Cottle manoeuvre, supporting the lateral wall directly with an instrument, is more specific and distinguishes internal valve collapse from septal deviation.
• Assess for external deformity, deviation of the dorsum, tip asymmetry and alar collapse on inspiration.
• Assess the turbinates for compensatory hypertrophy and for their response to decongestion.
• Examine for polyps, adenoid hypertrophy in children, and other causes of obstruction.

• Clinical, with the essential step being to establish that the deviation corresponds to the side and pattern of the symptoms.
• Nasal endoscopy after decongestion in every patient being considered for surgery.
• Photographic documentation of external deformity where rhinoplasty may be required.
• Computed tomography of the sinuses where there is coexisting sinus disease, recurrent sinusitis, or where surgery to the sinuses is planned. It is not required for isolated septal deviation.
• Objective airflow measurement with acoustic rhinometry, peak nasal inspiratory flow or rhinomanometry, which correlate imperfectly with symptoms but are useful for research and in medicolegal or complex cases.
• Validated symptom scoring with the Nasal Obstruction Symptom Evaluation scale, scored from 0 to 100, where a score above 30 indicates at least moderate obstruction and where a change of 15 to 20 points is clinically meaningful. Using a validated score before and after surgery both improves selection and documents outcome.
• Assessment for obstructive sleep apnoea with sleep studies where the history suggests it, since septoplasty alone rarely cures apnoea.
• Allergy testing, since untreated allergic rhinitis is a frequent cause of persistent obstruction after technically successful septoplasty.

Differential and contributory causes of nasal obstruction that must be excluded

• Allergic and non allergic rhinitis, which must be treated medically first.
• Turbinate hypertrophy.
• Nasal valve collapse, internal or external, which septoplasty does not correct and which requires a spreader graft or alar batten graft.
• Nasal polyps and chronic rhinosinusitis.
• Adenoid hypertrophy in children.
• Sinonasal tumour, in unilateral progressive obstruction with bleeding.
• Choanal atresia or stenosis.
• Rhinitis medicamentosa.

Medical therapy first

• Treat the mucosal component before considering surgery: intranasal corticosteroid for at least 6 to 8 weeks, an antihistamine where allergy is present, saline irrigation, and allergen avoidance.
• Many patients referred for septoplasty are adequately treated medically, and those who are not have a clearer surgical indication once the mucosal contribution has been removed.
• Nasal dilator strips and internal dilators as a non surgical option, particularly useful diagnostically, since good response predicts benefit from valve surgery.

Indications for septoplasty

• Symptomatic nasal obstruction attributable to the deviation, persisting after adequate medical therapy.
• Recurrent epistaxis from a septal spur or exposed convexity.
• Recurrent or chronic rhinosinusitis where the deviation obstructs the osteomeatal complex.
• To provide surgical access for endoscopic sinus surgery, skull base surgery, or transsphenoidal pituitary surgery.
• Contact point headache, only where the pain abolishes with topical anaesthesia to the contact point.
• Contribution to obstructive sleep apnoea, as an adjunct to other treatment and to improve continuous positive airway pressure tolerance, rather than as a cure.

Technique

• Killian incision, placed 1 to 1.5 cm posterior to the caudal edge, gives good access to the mid and posterior septum but does not permit correction of caudal deviation.
• Hemitransfixion incision at the caudal edge, which is required for caudal septal deviation and for access to the anterior nasal spine and maxillary crest.
• Open septorhinoplasty approach for severe caudal deviation, dorsal deviation, or where external correction is also required.
• Elevate mucoperichondrial flaps in the correct subperichondrial plane, which is relatively bloodless and preserves flap integrity. Straying superficially causes bilateral opposing tears and perforation.
• Preserve at least a 1 to 1.5 cm L strut of dorsal and caudal cartilage. This is the single most important technical principle. Failure to preserve the strut causes saddle nose deformity and tip ptosis, which are difficult to correct and are the source of most litigation in this operation.
• Correct rather than resect where possible: scoring, morselisation, cartilage batten grafting, spreader grafts, and repositioning of a dislocated caudal septum onto the maxillary crest with suture fixation.
• Extracorporeal septoplasty, in which the septum is removed, straightened on the back table and reimplanted, for severe deviations not correctable in situ.
• Address the inferior turbinates at the same time where there is compensatory hypertrophy, using tissue sparing reduction. Do not perform total turbinectomy.
• Address the nasal valve with spreader grafts or alar batten grafts where valve collapse coexists, since septoplasty alone will not relieve it.
• Quilting sutures to close the dead space are preferred to nasal packing, reducing pain and avoiding the complications of packing. Where packing or splints are used, remove at 3 to 7 days.

Complications and their management

• Septal haematoma, which must be recognised and drained immediately. It presents with increasing obstruction, pain and a bulging septum within hours to days, and untreated it causes cartilage necrosis within 3 to 4 days, producing saddle nose deformity and septal perforation. Drainage with a small incision, evacuation, quilting sutures and antibiotic cover is mandatory.
• Septal perforation in 1 to 5 percent, usually from opposing mucosal tears. Small posterior perforations are often asymptomatic; anterior perforations cause whistling, crusting, bleeding and pain, and repair is technically demanding.
• Saddle nose deformity and supratip depression from inadequate dorsal strut preservation.
• Tip ptosis and loss of tip support from inadequate caudal strut preservation.
• Persistent obstruction in 10 to 25 percent, usually from untreated turbinate hypertrophy, unrecognised valve collapse, uncontrolled rhinitis, or an unrealistic expectation.
• Epistaxis, adhesions between the septum and lateral wall, and toxic shock syndrome with packing.
• Anosmia, cerebrospinal fluid leak from fracture of the perpendicular plate extending to the cribriform plate, and dental or palatal numbness from injury to branches of the nasopalatine nerve.
• Empty nose syndrome where turbinate resection has been excessive.

Special considerations

• Children: septoplasty is generally deferred until facial growth is complete, around 16 to 18 years, because of concerns about disturbing the septal growth centres and producing midface hypoplasia. It is performed earlier only for severe functional obstruction, obstructive sleep apnoea, or after significant trauma, and then as conservatively as possible.
• Trauma: correct an acutely fractured and deviated septum within 10 to 14 days as part of nasal fracture management, since delay allows fibrous healing in the deviated position.
• Always drain a septal haematoma immediately regardless of age.

Follow up

Review at 2 to 4 weeks with endoscopy to remove crusts and divide any early adhesions, and again at 3 months with a repeat symptom score. Persistent obstruction should trigger reassessment for other causes rather than an assumption of surgical failure.