Acute Otitis Media

The overall incidence of intratemporal complications of AOM has decreased and the need for operative treatment is declining during the antibiotic era. Newer attempts of withholding antibiotics for 24 to 48 hours have not increased the incidence of acute mastoiditis, estimated at 1.2 to 4.2 cases per 100,000 per year. Most episodes of AOM occur in children; therefore, the prevalence of AOM with subsequent facial palsy is more frequent in children than in adults. Fischer et al published one of the largest series of 61 patients with facial nerve paralysis associated with acute suppurative otitis media.2 Most publications report on 10 to 20 patients within 5 to 10 years observation time. Patients with incomplete palsy (facial nerve paresis) may not be referred to larger centers as their outcome is excellent and surgery rarely indicated. Acute facial palsy may be the first symptom of AOM or may accompany acute mastoiditis as a complication of bacterial otitis media.3 The same organisms causing AOM alone have been associated with AOM with facial palsy, although factors such as virulence of the organism, host resistance, or a higher incidence of spontaneous fallopian canal dehiscences have been postulated. Pressure-induced lesions, venous congestion with subsequent swelling of the nerve, and toxic irritations have been implicated in the pathophysiology. Computed tomography (CT) scans are highly recommended to verify the severity of the AOM (subperiosteal abscess, coalescent mastoiditis, sigmoid sinus thrombosis) and to evaluate the course of the fallopian canal (search for dehiscences), as well as to exclude other pathology (e.g., indirect signs of an underlying cholesteatoma). In acute suppurative otitis media with purulent discharge, it is difficult to exclude an underlying cholesteatoma otoscopically at the first visit.

Surgical decompression has been previously recommended but randomized clinical trials do not exist and the overall excellent prognosis has questioned the beneficial role of surgery. Antibiotic treatment should always be initiated. Steroids may be added, but evidence for their effectiveness is lacking.4 The author favors myringotomy (for bacterial cultures) with ventilations tubes (to allow drainage through the middle ear). Mastoidecomy is indicated in cases of acute mastoiditis and/or subperiosteal abscess formation. However, the author does not advocate facial nerve exploration and decompression. A review of the literature does not support facial nerve decompression in AOM with facial palsy. Exploration of the facial nerve from the stylomastoid foramen to the geniculate ganglion in case of acute suppurative infection (e.g., bleeding granulation tissue, fibrinous adhesions in the middle ear) is technically demanding and superfluous.

Patients with incomplete palsy do have a very favorable prognosis with full recovery within a short time period of a few days to 3 weeks. Patients with complete paralysis during AOM also have a good prognosis, though with a prolonged time to maximum improvement of a few weeks to months.5 Most studies confirm complete recovery of facial nerve function in all cases.6 Few reports reveal incomplete recovery of House-Brackmann (HB) II in 3–15% or HB III in 3%2,7; however, unsatisfactory outcomes (HB IV-VI) have not been reported. Adults rarely present with AOM and therefore present a low risk of developing facial palsy during a course of AOM. Studies with adults are rare and confirm the excellent prognosis.8

Necrotizing External Otitis

Necrotizing external otitis may also be called malignant external otitis because it is a devastating and potentially lethal disease. Elderly and diabetic male patients seem to be at higher risk. Pseudomonas aeruginosa as the main infectious agent may spread through the fissures of Santorini and the tympanomastoid suture to induce a severe skull base osteomyelitis with further involvement of the infratemporal fossa and the jugular foramen. Patients often complain of pain in the early morning hours, awakening at night. Initially, the otoscopic finding is rather unspectacular with resistant granulation tissue at the bony-cartilaginous junction of the external ear canal. The close proximity of the mastoid segment of the facial nerve to the origin of the infection and the vicinity of the stylomastoid foramen to the extension of the infection toward the jugular bulb predisposes the facial nerve to become involved. Facial nerve and lower cranial nerve palsies can be the first alarming symptom and guide the physician to order CT and magnetic resonance imaging (MRI) scans, revealing evidence for osteomyelitis and spread of the infection along the skull base. On CT scans, limited opacification of mastoid air cells along with a thickening of the external ear canal skin may be the first faint signs of this devastating infection ( Fig. 13.1 ). MRI, however, reveals the true extent of the infection along the skull base into the soft tissues of the infratemporal fossa and toward the neural elements of the jugular foramen ( Fig. 13.2 ).

Involvement of the facial nerve is a poor prognostic sign.9 Further progression with involvement of the lower cranial nerves (IX-XII) or extension toward the petrous apex (VI palsy) precede a lethal outcome. The treatment of suspected or confirmed (radiologically or via biopsy) necrotizing external otitis has evolved from primarily surgical to a prolonged medical treatment using a combination of intravenous antibiotics against P. aeruginosa over 2 to 4 months. Ciprofloxacin as a single agent readily induces resistant strains and may worsen the outcome. Bacterial cultures from the external ear canal or the mastoid are suggested but may be negative due to previous antibiotic treatment. Controversies still exist regarding surgical debridement and facial nerve decompression.10 Reviewing the literature, the main treatment remains medical with intravenous antibiotic therapy. Mastoidectomy with surgical drainage of coalescent otomastoiditis seems appropriate in cases of disease progression (e.g., sigmoid sinus thrombosis, lower cranial nerve palsies, or facial nerve paralysis10 with radiographic signs of osteolysis). Facial nerve decompression with opening of the epineurium has not been widely performed and may not improve the outcome overall. It appears that full recovery of the infectious disease does not necessarily correlate with full recovery of facial function.10,11

Chronic Otitis Media

Facial palsy with chronic suppurative otitis media without cholesteatoma primarily affects adults or adolescents and rarely pediatric patients. An underlying cholesteatoma has to be excluded by otoscopy and imaging (CT and eventually non–echo-planar imaging diffusion MRI). Other differential diagnoses include tuberculosis, Wegener disease, or histiocytosis X. Dry perforations do not impair facial function; however, intermittent or chronic draining (suppurative) perforations may be complicated by acute or slowly progressive facial palsy. Facial palsy may not be the only symptom of a hostile environment. Vertigo, labyrinthitis, and sensorineural hearing loss with tinnitus are other symptoms of progressive middle ear infection. Imaging using CT scans is mandatory to evaluate the extent of the disease within the temporal bone and to check for dehiscences along the fallopian canal. Immediate broad spectrum intravenous antibiotics and steroids are routinely administered. Incomplete facial palsy (paresis) and early cessation of the drainage are in favor of a rapid recovery of normal facial function. Surgery to cure the underlying disease can then be postponed and electively planned. Progression to facial nerve paralysis requires surgical intervention at the earliest possible moment. Electrical testing prior to surgery (electroneuronography in acute or subacute paralysis, electromyography in long-standing facial paralysis) determines the extent of neural damage and has a prognostic implication. Total loss of electrical response may have a worse outcome. The type of surgical approach is dictated by the extent of the disease and the exposure required to follow the course of the facial nerve. In a well pneumatized temporal bone, a closed cavity setting with posterior tympanotomy and epitympanotomy/-ectomy can be sufficient; otherwise, an open mastoidoepitympanectomy allows complete exposure of the facial nerve from the geniculate ganglion to the stylomastoid foramen.12

The facial nerve should be explored throughout the middle ear and mastoid. In case of early surgery and acute facial paralysis, intraoperative facial nerve stimulation may enable the surgeon to verify the lesion site (often along the tympanic, dehiscent segment). Distal stimulation in these instances may still be possible (reaction audible at the monitor), whereas proximal stimulation does not reveal any reaction. The segment identified can then be exposed and decompressed distally and proximally. In most instances, intraoperative stimulation is no longer possible (due to the length and severity of facial nerve damage) and the facial nerve needs to be skeletonized from the stylomastoid foramen to the geniculate ganglion. If no lesion is identified, total facial nerve decompression does not seem to be necessary and may be an overtreatment.13 Early decompression and removal of the pathology within the middle ear does have a favorable prognosis, reaching normal or near-normal (HB II) function within a few months. In cases of long-standing facial paralysis or patients revealing no response on preoperative electric testing, the final outcome may be unsatisfactory.14

A postmortem study by Schuknecht revealed an osteolytic inflammatory lesion in an elderly diabetic patient with a large focus of osteitis invading the fallopian canal, compressing the nerve, and inflammatory cells had infiltrated the degenerated facial nerve.15 It therefore appears prudent to explore the facial nerve at surgery and to remove any lytic granulation tissue and osteitic bony debris. Fortunately, these types of lesions in patients with noncholesteatomatous chronic middle ear infections are becoming quite rare in Western countries.

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