Nasal Septal Abscess

A collection of pus between the septal cartilage and mucoperichondrium, almost always arising from infection of an untreated or inadequately drained septal haematoma. It destroys cartilage faster than a haematoma alone and carries a real risk of intracranial spread.

Why it is more urgent than a haematoma

Bacterial proteolytic enzymes and inflammatory mediators liquefy cartilage within 24 to 48 hours, compared with the 3 to 7 days of avascular necrosis from a sterile haematoma. Loss of the quadrangular cartilage removes dorsal and tip support, producing saddle nose deformity, columellar retraction and tip ptosis.

Route of intracranial spread

The anterior facial vein and the angular vein are valveless and communicate with the superior and inferior ophthalmic veins, which drain to the cavernous sinus. Infection in the danger area of the face, extending from the upper lip and nose to the glabella, can therefore reach the cavernous sinus directly. Cavernous sinus thrombosis, meningitis, subdural empyema, frontal lobe abscess and orbital cellulitis are all recognised complications.

Aetiology

• Infected septal haematoma after trauma, which accounts for the great majority.
• Post septoplasty or post rhinoplasty haematoma.
• Extension from dental infection, particularly of the upper incisors.
• Furunculosis of the nasal vestibule, nasal picking and hair plucking.
• Spread from acute rhinosinusitis, particularly ethmoid disease.
• Immunosuppression, diabetes and haematological malignancy, in which spontaneous abscess without trauma can occur.

Microbiology

Staphylococcus aureus in the majority, including methicillin resistant strains. Streptococcus pneumoniae, Streptococcus pyogenes, Haemophilus influenzae, and anaerobes including Bacteroides and Peptostreptococcus in dental or sinus related disease. Consider unusual organisms in the immunocompromised, including fungi.

• Progressive bilateral nasal obstruction, typically days after nasal trauma, following an initial period of improvement.
• Severe nasal pain and pressure, disproportionate to the injury and worsening rather than settling.
• Fever, rigors, malaise and anorexia, which distinguish abscess from simple haematoma.
• Frontal headache.
• Swelling, erythema and tenderness of the nasal dorsum, tip and columella, with cellulitis extending onto the upper lip and cheek.
• Purulent nasal discharge, occasionally with spontaneous drainage.
• In infants, feeding difficulty and respiratory distress, since neonates are obligate nasal breathers.

Signs demanding emergency escalation

• Periorbital oedema, proptosis, chemosis, ophthalmoplegia or reduced visual acuity.
• Bilateral eye signs, which indicate cavernous sinus thrombosis.
• Meningism, photophobia, altered consciousness, seizure or focal neurology.
• Rapidly spreading facial cellulitis.
• Signs of sepsis: tachycardia, hypotension, tachypnoea, confusion.

Examination

• Bilateral, tense, erythematous, exquisitely tender fluctuant septal swelling obstructing both nasal cavities.
• Marked tenderness on gentle palpation with a cotton tipped applicator, which is far greater than with a haematoma.
• External nasal and facial inflammation.
• Full ophthalmological assessment including acuity, colour vision, pupils, eye movements and proptosis.
• Neurological examination including for neck stiffness.
• Assess the dentition.

Clinical. Drainage must not be delayed for investigations.

• Full blood count, C reactive protein, blood cultures, glucose and HbA1c.
• Pus culture at drainage for aerobic, anaerobic and fungal organisms, with specific request for methicillin resistant Staphylococcus aureus screening.
• Contrast enhanced computed tomography of the sinuses, orbits and brain where there is any orbital or neurological sign, facial cellulitis, or failure to improve within 48 hours. It defines the extent of the collection, orbital involvement, sinus disease and intracranial extension.
• Magnetic resonance imaging with contrast and venography where cavernous sinus thrombosis or intracranial extension is suspected, which is more sensitive than computed tomography for these.
• HIV testing and immune assessment where the abscess is spontaneous or recurrent.
• Histology of any tissue removed where the presentation is atypical, to exclude granulomatosis with polyangiitis, cocaine induced midline destructive lesion, lymphoma and other neoplasia. A septal destructive lesion without clear trauma must not be assumed to be simple abscess.

Differential diagnosis

• Septal haematoma without infection: no fever, less pain, no external cellulitis.
• Nasal vestibulitis and furuncle: localised to the vestibule, unilateral, no septal mass.
• Granulomatosis with polyangiitis: crusting, granulation, saddle nose, positive antineutrophil cytoplasmic antibody, systemic features.
• Cocaine induced midline destructive lesion.
• Sinonasal lymphoma, particularly extranodal natural killer T cell lymphoma of nasal type, which presents with midline destruction, necrosis and constitutional symptoms.
• Invasive fungal sinusitis in the immunocompromised, with black necrotic mucosa and anaesthesia.

Emergency surgical drainage with intravenous antibiotics. Admission is the default.

Immediate measures

• Admit, obtain intravenous access, blood cultures and baseline bloods.
• Analgesia: paracetamol 1 g every 6 hours plus a nonsteroidal anti inflammatory drug where not contraindicated, with opioid titration for severe pain.
• Fluid resuscitation if septic.
• Optimise glycaemic control.

Surgical drainage

• General anaesthesia is preferred, and is required in children.
• Incise over the most dependent part of the collection, ideally unilaterally to reduce perforation risk. Where bilateral incisions are needed, offset them so they do not oppose each other.
• Evacuate all pus, break down loculations, and irrigate copiously with saline.
• Debride frankly necrotic cartilage, but preserve every fragment of viable cartilage, since each contributes to later support.
• Send pus and tissue for culture and histology.
• Prevent reaccumulation with a corrugated or vessel loop drain left for 24 to 48 hours, or quilting sutures, or silastic splints. In an abscess a drain is preferred to complete closure, since further pus may accumulate.
• Repeat drainage is frequently required, and the patient should be reviewed daily.

Antibiotics

• Intravenous therapy from the outset: co amoxiclav 1.2 g every 8 hours in adults, or 30 mg/kg every 8 hours in children.
• Alternatively flucloxacillin 2 g every 6 hours plus metronidazole 500 mg every 8 hours.
• Ceftriaxone 2 g daily in adults or 50 mg/kg daily in children plus metronidazole where sinus or intracranial extension is a concern, given better central nervous system penetration.
• Add vancomycin with a target trough of 15 to 20 mg/L, or teicoplanin, where methicillin resistant Staphylococcus aureus is prevalent or suspected.
• Clindamycin 600 mg every 6 to 8 hours in penicillin allergy, which also covers anaerobes and reduces toxin production.
• Narrow to culture as soon as results are available.
• Convert to oral therapy when afebrile with clinical improvement, typically after 48 to 72 hours, completing a total of 10 to 14 days. Extend to 4 to 6 weeks with osteomyelitis or intracranial involvement.

Management of intracranial and orbital complications

• Immediate imaging with contrast enhanced computed tomography and magnetic resonance venography.
• High dose intravenous ceftriaxone 2 g every 12 hours plus metronidazole 500 mg every 8 hours plus vancomycin.
• Neurosurgical involvement for empyema and abscess, which require drainage.
• Ophthalmology involvement for orbital disease.
• Anticoagulation in cavernous sinus thrombosis is used in many centres to prevent propagation, and should be decided jointly with neurology and neurosurgery, weighing thrombus extension against haemorrhagic risk.
• Corticosteroids are used selectively for cranial neuropathy and orbital inflammation in cavernous sinus thrombosis, after antibiotics are established.

Follow up and reconstruction

• Daily review during admission with inspection of the septum for reaccumulation.
• Endoscopic review at 1 week, 1 month and 3 months.
• Expect septal perforation in a substantial proportion, and saddle nose deformity where cartilage loss is extensive.
• Counsel the patient and family at the outset that deformity is likely, since discovering it later without warning is a frequent source of complaint.
• Definitive reconstruction is delayed at least 6 to 12 months after complete resolution of infection. Dorsal augmentation with autologous costal cartilage or calvarial bone, with caudal septal reconstruction to restore tip support, is the usual approach. Alloplastic implants should be avoided in a previously infected field.
• In children, defer reconstruction until facial growth is complete, and follow up through adolescence, since growth centre disruption produces progressive midface hypoplasia that only becomes evident with growth.

Prevention

Immediate drainage of every septal haematoma with antibiotic cover, and clear safety netting after nasal trauma. Almost every septal abscess is a preventable consequence of a missed or inadequately treated haematoma.