Malignant Otitis Externa

Also known as: Necrotising otitis externa

Invasive osteomyelitis of the temporal bone and skull base originating in the external auditory canal. The term malignant reflects the historically high mortality rather than neoplasia. Necrotising otitis externa is the more accurate designation.

Host factors

Elderly diabetics account for the large majority. Microangiopathy of canal skin, impaired neutrophil chemotaxis and phagocytosis, and a higher cerumen pH combine to permit invasion.
HIV infection, haematological malignancy, chemotherapy, transplantation and long term corticosteroids produce the disease at younger ages and often with normal glucose.
Frequently precipitated by aural irrigation or instrumentation in a diabetic patient.

Microbiology

Pseudomonas aeruginosa in more than 90 percent of bacterial cases, using elastase, alkaline protease and exotoxin A to invade cartilage and bone.
Staphylococcus aureus, Proteus, Klebsiella and Burkholderia in a minority.
Aspergillus fumigatus in the profoundly immunosuppressed, characteristically presenting with cranial neuropathy earlier and with less canal granulation.

Route of spread and the anatomy that explains the deficits

Infection passes through the fissures of Santorini and the bony cartilaginous junction into the retromandibular and parotid tissue, then along the skull base.

Stylomastoid foramen: facial nerve palsy, the earliest and commonest cranial deficit, occurring in roughly 20 to 30 percent.
Jugular foramen: glossopharyngeal, vagus and accessory involvement with dysphonia, dysphagia and shoulder weakness.
Hypoglossal canal: tongue deviation.
Petrous apex: trigeminal and abducens involvement.
Further spread produces sigmoid sinus thrombosis, meningitis, temporal lobe abscess and, rarely, carotid erosion.

Mortality was historically around 50 percent and is now approximately 10 to 20 percent with antipseudomonal therapy, rising substantially once multiple cranial neuropathies or intracranial extension appear.

Severe deep boring otalgia, characteristically nocturnal, disproportionate to canal findings and poorly responsive to standard analgesia.
Persistent purulent otorrhoea unresponsive to topical treatment.
Granulation tissue on the floor of the canal at the bony cartilaginous junction, the single most characteristic sign. Exposed bone may be visible.
Temporal headache, temporomandibular pain and trismus from pterygoid and joint involvement.
Fever is often absent and the white cell count is frequently normal. Their absence provides no reassurance.
Preauricular and parotid swelling and tenderness.
Cranial neuropathy, weight loss and malaise in advanced disease.

Red flags mandating immediate escalation

Any new facial weakness in a diabetic with a discharging ear.
Pain persisting beyond 2 to 3 weeks of correct topical therapy.
Multiple lower cranial nerve deficits, indicating jugular foramen disease.
Altered consciousness, meningism, seizure or focal neurology, indicating intracranial extension.

Diagnosis rests on the combination of a susceptible host, disproportionate pain, canal granulation and a markedly raised erythrocyte sedimentation rate, supported by imaging.

Laboratory

Erythrocyte sedimentation rate is characteristically above 60 mm per hour and often exceeds 100. It is the most useful marker for tracking response and for deciding when to stop therapy.
C reactive protein falls earlier and reflects short term response.
White cell count is commonly normal.
Capillary glucose, HbA1c, renal function, HIV testing.

Microbiology and histology

Deep tissue biopsy from granulation under the microscope, sent for bacterial, fungal and mycobacterial culture and for histopathology. Superficial swabs grow colonisers and are insufficient.
Histology is mandatory to exclude squamous cell carcinoma, which is the principal mimic and coexists occasionally.
Blood cultures when systemically unwell.

Imaging

High resolution computed tomography of the temporal bone shows soft tissue in the canal and skull base, erosion of the tympanic bone, and involvement of the mastoid, petrous apex and nasopharyngeal soft tissues. Approximately 30 to 50 percent bone demineralisation is required before erosion is visible, so an early normal scan does not exclude disease.
Magnetic resonance imaging is superior for marrow signal change, dural enhancement, cavernous and sigmoid sinus thrombosis, prevertebral and nasopharyngeal soft tissue extension, and intracranial complications. It is the study of choice for defining extent.
Technetium 99m methylene diphosphonate scintigraphy is highly sensitive early but remains positive for months after cure and cannot define an endpoint.
Gallium 67 citrate scintigraphy or labelled white cell imaging normalises with resolution and is used to guide cessation of antibiotics.

Differential diagnosis

Squamous cell carcinoma of the external canal: bleeding friable mass, tissue that recurs after debridement, similar imaging. Only biopsy separates them.
Nasopharyngeal carcinoma with skull base invasion: nasal symptoms, neck node, unilateral middle ear effusion. Requires nasoendoscopy and biopsy.
Metastatic disease, lymphoma, granulomatosis with polyangiitis, tuberculous osteomyelitis and Langerhans cell histiocytosis.
Refractory bacterial otitis externa without bone involvement: pain settles with toilet and drops, erythrocyte sedimentation rate normal, no granulation at the junction.

Treat as osteomyelitis, not as a severe canal infection. Admission, prolonged targeted antipseudomonal therapy and metabolic control determine outcome.

Immediate actions

Admit, obtain deep biopsy and culture before or at the start of therapy where feasible without delaying treatment in the septic patient.
Correct hyperglycaemia aggressively, usually with a basal bolus insulin regimen during the acute phase. Persistent poor control predicts relapse.
Complete cranial nerve examination and document baseline function.
Aural toilet by microsuction, repeated regularly, plus topical ciprofloxacin drops as an adjunct.
Adequate analgesia including opioids. Regular paracetamol 1 g every 6 hours with oxycodone or morphine titrated to effect, with caution in renal impairment and the elderly.

Antimicrobial therapy

Ciprofloxacin 400 mg intravenously every 8 to 12 hours, or 750 mg orally twice daily where absorption is reliable and the isolate susceptible. Oral bioavailability is high and oral therapy is appropriate for much of the course.
Ceftazidime 2 g intravenously every 8 hours as an alternative or in combination.
Piperacillin with tazobactam 4.5 g intravenously every 6 to 8 hours.
Meropenem 1 to 2 g intravenously every 8 hours, or cefepime 2 g every 8 hours, for resistant isolates.
Add an aminoglycoside such as gentamicin or amikacin only for documented resistant Pseudomonas, with levels, and recognise renal and cochleovestibular toxicity in an elderly diabetic population.
Adjust all doses for creatinine clearance.
Fungal disease: voriconazole 6 mg/kg intravenously twice daily for two doses then 4 mg/kg twice daily, converting to 200 mg orally twice daily, or liposomal amphotericin B 3 to 5 mg/kg daily. Treat for at least 3 months with imaging surveillance.

Duration and monitoring

Minimum 6 to 8 weeks. Extend to 3 months or longer with cranial neuropathy, extensive skull base involvement or fungal aetiology.
Weekly erythrocyte sedimentation rate and C reactive protein. Aim for symptom resolution, healing of granulation and normalisation or plateau of the erythrocyte sedimentation rate before stopping.
Repeat magnetic resonance imaging or gallium scintigraphy before cessation in extensive disease.
Quinolone cautions across a prolonged course: tendon rupture, aortic aneurysm and dissection, QT prolongation, dysglycaemia in diabetics on sulfonylureas, delirium in the elderly, and reduced absorption with calcium, iron, magnesium, zinc and antacids taken concurrently.

Role of surgery

Limited and adjunctive. Indications are biopsy, debridement of sequestrum and necrotic tissue, drainage of an abscess, and management of intracranial complications.
Radical temporal bone resection has no routine place and does not improve survival.
Facial nerve decompression does not reliably restore function and is not routinely performed. Facial palsy is treated by controlling the infection, with eye protection using ocular lubricant, taping at night and ophthalmology review.

Adjuncts

Hyperbaric oxygen is considered in refractory disease, relapse or extensive skull base involvement, though evidence remains limited. It does not substitute for antibiotics and debridement.

Complications to anticipate

Progressive cranial neuropathies, which often recover incompletely.
Sigmoid or cavernous sinus thrombosis, meningitis, subdural empyema and temporal lobe abscess, requiring urgent imaging, neurosurgical involvement, and antibiotic regimens with central nervous system penetration.
Temporomandibular joint involvement with trismus.
Relapse in 15 to 20 percent, typically within 6 to 12 months, usually reflecting inadequate duration or persistent hyperglycaemia.

Follow up

Review monthly for at least 12 months with examination of the canal, cranial nerve assessment and inflammatory markers. Any recurrence of deep otalgia in a previously treated patient represents relapse until proven otherwise. Enforce lifelong avoidance of aural irrigation and self instrumentation, and maintain glycaemic control as an infection control measure.

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

Peritonsillar Abscess

Also known as: Quinsy

A collection of pus in the potential space between the tonsillar capsule and the superior constrictor muscle. It is the commonest deep neck space infection, with an incidence of around 30 per 100000 in adults, peaking between 20 and 40 years.

Pathogenesis

Two mechanisms are recognised.

Progression from acute tonsillitis with spread of infection through the tonsillar capsule into the peritonsillar space, forming a cellulitis, that is peritonsillitis, which then suppurates.
Infection of the Weber glands, a group of 20 to 25 minor salivary glands in the supratonsillar space that drain through ducts into the tonsillar surface and clear debris from the crypts. Obstruction and infection of these glands produces an abscess in the supratonsillar position, which is why the great majority of abscesses are found superior and lateral to the tonsil. This mechanism explains why peritonsillar abscess occurs in patients who have had tonsillectomy and in those with no preceding tonsillitis.

Anatomy that determines drainage technique and its hazards

The abscess lies between the tonsillar capsule medially and the superior constrictor laterally, most often in the superior pole. Lateral to the superior constrictor lies the parapharyngeal space, which contains the carotid sheath. The internal carotid artery lies approximately 2 to 2.5 cm posterolateral and deep to the tonsil, and closer in children and in patients with a tortuous or medially displaced vessel. Needle aspiration and incision must therefore be directed in a strictly sagittal or slightly medial direction and must not be angled laterally, and depth must be controlled by using a needle guard or by exposing only 1 cm of the blade.

Microbiology

Polymicrobial, with a mixture of aerobes and anaerobes.

Streptococcus pyogenes, which is the most frequently isolated single aerobe.
Fusobacterium necrophorum, which is disproportionately common in adolescents and young adults and which carries the risk of Lemierre syndrome.
Streptococcus milleri group, Staphylococcus aureus, Haemophilus influenzae.
Anaerobes: Prevotella, Porphyromonas, Peptostreptococcus, Bacteroides.

Severe unilateral sore throat, which is markedly worse on one side and which typically follows several days of tonsillitis.
Odynophagia progressing to inability to swallow saliva, with drooling.
Trismus, from irritation and spasm of the medial pterygoid muscle, which is present in around two thirds and which is a key discriminating sign from simple tonsillitis.
Muffled hot potato voice, from soft palate swelling and reduced palatal movement.
Referred otalgia on the affected side.
Fever, rigors, malaise and dehydration.
Neck pain and torticollis, with the head tilted toward the affected side.
Foetor oris.

Examination

Marked unilateral swelling of the soft palate and the supratonsillar region, with the tonsil displaced medially and inferiorly.
Contralateral deviation of the uvula, which is the classical sign.
Erythema and fullness of the anterior pillar, often with a visible point of maximal bulge.
Trismus, which may make examination difficult and which is itself diagnostic information.
Ipsilateral cervical lymphadenopathy.
Assess hydration, airway patency and ability to handle secretions.

Red flags requiring escalation beyond simple drainage

Stridor, respiratory distress or inability to lie flat, indicating airway compromise.
Neck swelling, induration or crepitus, indicating extension into the parapharyngeal space or necrotising infection.
Torticollis with severe neck pain and neck stiffness, indicating parapharyngeal or retropharyngeal extension.
Rigors with unilateral neck tenderness along sternocleidomastoid and pulmonary symptoms, indicating Lemierre syndrome.
Failure to improve after adequate drainage and antibiotics, which requires imaging for a second collection or deep neck extension.
Bilateral swelling, which is uncommon and should raise the possibility of lymphoma or another diagnosis.
Immunocompromise or diabetes, which predisposes to rapid deep extension and necrotising infection.

Clinical in most cases. The combination of unilateral peritonsillar swelling, uvular deviation and trismus is sufficient to proceed to drainage.

Distinguish peritonsillar cellulitis from abscess. Cellulitis produces swelling without a drainable collection and responds to antibiotics alone; abscess requires drainage. Aspiration is the practical test.
Intraoral ultrasound with an endocavity probe, which distinguishes cellulitis from abscess with good accuracy and can guide aspiration, and which is particularly useful where trismus limits examination. Transcervical ultrasound is an alternative where intraoral access is impossible.
Contrast enhanced computed tomography of the neck, indicated where there is trismus preventing examination, suspected deep neck space extension, failure to respond to drainage, an immunocompromised patient, a child in whom examination is limited, or any airway concern. It defines the collection, identifies parapharyngeal and retropharyngeal extension, and shows vascular complications.
Full blood count, C reactive protein, urea and electrolytes, and blood cultures where systemically unwell.
Pus culture at drainage for aerobic and anaerobic organisms.
Monospot or Epstein Barr virus serology, since peritonsillar abscess can complicate infectious mononucleosis and the management differs, with a greater risk of airway obstruction and a strong reason to avoid amoxicillin.
Human immunodeficiency virus testing where clinically indicated.
Contrast computed tomography with venous phase and chest imaging where Lemierre syndrome is suspected.

Differential diagnosis

Peritonsillar cellulitis.
Severe acute tonsillitis, which is bilateral without uvular deviation or trismus.
Parapharyngeal and retropharyngeal abscess, which produce neck signs and are defined on imaging.
Infectious mononucleosis with marked tonsillar hypertrophy.
Dental infection with a masticator space abscess, which produces trismus with a normal oropharynx.
Tonsillar or oropharyngeal malignancy, particularly lymphoma, which may present with unilateral swelling. Persistent asymmetry after resolution requires biopsy.
Internal carotid artery aneurysm presenting as a pulsatile peritonsillar mass, which is rare but which is the reason to look and palpate before incising.

Drainage plus antibiotics plus analgesia plus rehydration. Antibiotics alone treat cellulitis but not an established abscess.

Drainage

Needle aspiration is the first line procedure. Topical anaesthesia with lidocaine spray followed by infiltration with lidocaine 1 or 2 percent with adrenaline. Use an 18 gauge needle on a 10 mL syringe, with the sheath of a needle guard or with the plastic needle cover trimmed to expose only 1 cm, preventing deep penetration.
Aspirate at the point of maximal bulge, usually superolateral to the upper pole, directing the needle in the sagittal plane, parallel to the sagittal axis and never laterally. If no pus is obtained, redirect slightly inferiorly and then at the middle pole, but do not go deeper or angle laterally.
Incision and drainage under local anaesthesia is an alternative and achieves more complete evacuation. Use a number 11 blade with all but 1 cm of the blade wrapped in tape, make a 1 cm incision at the point of maximal bulge, then spread with Tilley or artery forceps to break loculations.
Have suction ready and position the patient sitting upright leaning forward, so that pus is not aspirated.
Both techniques have similar success rates of around 90 percent. Aspiration is less painful and is repeatable; incision provides more sustained drainage.
Reaccumulation occurs in around 10 to 15 percent and requires repeat aspiration.

Indications for drainage under general anaesthesia

Children, and uncooperative adults.
Severe trismus preventing intraoral access.
Failed local anaesthetic drainage.
Airway compromise.
Suspected extension into the parapharyngeal space requiring external drainage.

Antibiotics

Intravenous therapy for patients requiring admission: co amoxiclav 1.2 g every 8 hours, or benzylpenicillin 1.2 g every 6 hours plus metronidazole 500 mg every 8 hours.
Clindamycin 600 mg every 6 hours intravenously in penicillin allergy, which covers streptococci and anaerobes well.
In children, co amoxiclav 30 mg/kg every 8 hours, or benzylpenicillin 25 mg/kg every 6 hours plus metronidazole 7.5 mg/kg every 8 hours.
Convert to oral therapy when swallowing improves and the patient is afebrile, usually within 24 to 48 hours, completing a total of 10 days with co amoxiclav 625 mg three times daily or clindamycin 300 to 450 mg four times daily.
Cover Fusobacterium adequately in adolescents and young adults, since Lemierre syndrome arises from inadequately treated peritonsillar infection.
Do not use amoxicillin alone where infectious mononucleosis has not been excluded.

Corticosteroid

A single dose of dexamethasone 10 mg intravenously in adults, or 0.6 mg/kg to a maximum of 10 mg in children, reduces pain, trismus and fever and shortens the time to symptom resolution. It is a reasonable adjunct in most cases.

Supportive care

Intravenous fluids with 0.9 percent sodium chloride, correcting the deficit, since these patients are usually significantly dehydrated.
Regular intravenous paracetamol 1 g every 6 hours plus a nonsteroidal anti inflammatory drug where tolerated, with opioid titration for severe pain.
Topical benzydamine.
Airway observation. Involve anaesthetics early where there is any airway concern.

Tonsillectomy

Interval tonsillectomy, performed 6 weeks or more after resolution, is indicated for a second episode of peritonsillar abscess, for a first episode in a patient with a significant history of recurrent tonsillitis, and for patients with airway obstruction from tonsillar hypertrophy.
After a single episode in a patient with no history of tonsillitis, the recurrence rate is only around 10 to 15 percent, and routine tonsillectomy is not justified.
Quinsy tonsillectomy, that is tonsillectomy during the acute episode, achieves drainage and definitive treatment in one procedure and avoids a second admission. It carries higher intraoperative bleeding and is more technically demanding but does not carry a materially higher complication rate in experienced hands. It is indicated where drainage cannot be achieved under local anaesthesia, where there is airway compromise, in children requiring general anaesthesia anyway, and where recurrent tonsillitis already justifies tonsillectomy.

Complications

Airway obstruction.
Aspiration of pus, particularly if drainage is performed with the patient supine.
Extension to the parapharyngeal, retropharyngeal and prevertebral spaces, and descending mediastinitis, which carries high mortality and which requires urgent contrast imaging of the neck and chest with surgical drainage.
Lemierre syndrome with internal jugular thrombophlebitis and septic pulmonary emboli, treated with prolonged intravenous antibiotics with anaerobic cover for 4 to 6 weeks, drainage of metastatic collections, and a case by case decision on anticoagulation.
Necrotising fasciitis of the neck, particularly in diabetic and immunocompromised patients, requiring urgent radical debridement.
Carotid artery erosion and pseudoaneurysm, presenting with sentinel bleeding, which requires immediate angiography.
Sepsis and streptococcal toxic shock syndrome.

Follow up

Review at 4 to 6 weeks to confirm resolution and to reassess tonsillar symmetry. Persistent unilateral tonsillar enlargement after an abscess has settled requires tonsillectomy with histology, since lymphoma and carcinoma present in this way and are sometimes discovered only after an apparent abscess fails to resolve completely.

Malignant Otitis Externa

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management