|Year : 2020 | Volume
| Issue : 6 | Page : 688-691
A rare cause of bilateral facial nerve paralysis due to acute otitis media in a 52-year-old man
Santosh Kumar Swain, Alok Das, Sampada Munjal
Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University (Deemed to be), Bhubaneswar, Odisha, India
|Date of Submission||24-Jun-2019|
|Date of Decision||01-Oct-2019|
|Date of Acceptance||20-Dec-2019|
|Date of Web Publication||6-Nov-2020|
Santosh Kumar Swain
Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University (Deemed to be), Bhubaneswar, Odisha
Source of Support: None, Conflict of Interest: None
Facial nerve paralysis is a known complication of middle ear diseases such as chronic otitis media. However, it is rarely seen in acute otitis media (AOM). Bilateral facial nerve paralysis is an extremely rare incidence in AOM in an adult patient. As it is a rare clinical entity, the management of this condition is not very well outlined as per the standard guidelines. Aggressive and appropriate treatment in the earliest period helps patients to recover from facial nerve paralysis. Here, we present a case of bilateral facial nerve paralysis in a 52-year-old male with bilateral AOM. Facial nerve paralysis in both sides recovered to normal with appropriate treatment along with myringotomy.
Keywords: Acute otitis media, bilateral facial nerve paralysis, fallopian canal, myringotomy
|How to cite this article:|
Swain SK, Das A, Munjal S. A rare cause of bilateral facial nerve paralysis due to acute otitis media in a 52-year-old man. Med J DY Patil Vidyapeeth 2020;13:688-91
|How to cite this URL:|
Swain SK, Das A, Munjal S. A rare cause of bilateral facial nerve paralysis due to acute otitis media in a 52-year-old man. Med J DY Patil Vidyapeeth [serial online] 2020 [cited 2021 Jun 14];13:688-91. Available from: https://www.mjdrdypv.org/text.asp?2020/13/6/688/300127
| Introduction|| |
Facial nerve paralysis in patients suffering from acute otitis media (AOM) is usually due to intrafallopian inflammation which leads to ischemia with neuropraxia. This may be either due to bony dehiscence of the Fallopian canal More Details or vascular connections between the mastoid air cells and Fallopian canal. In preantibiotic era, the incidence of facial nerve paralysis in AOM was 0.5%–0.7% cases of middle ear inflammation. This complication has reduced to 0.005% in present-day clinical practice. Bilateral facial nerve paralysis in bilateral AOM is very rare and mostly found in children; however, it is extremely rare in an adult patient. Here, we report an extremely rare case of bilateral AOM causing bilateral facial nerve paralysis in a 52-year-old male.
| Case Report|| |
A 52-year-old male attended the Outpatient Department with complaints of otalgia and hearing loss for 10 days. He had also intermittent low-grade fever for 10 days. He was also presenting with a history of right-sided facial weakness for 3 days. On examination, the patient showed bilateral hyperemic tympanic membrane with moderate conductive hearing loss in pure tone audiometry. Tympanometry revealed bilateral B-type curve suggesting fluid in the middle ear. There was House–Brackmann Grade-IV facial nerve paralysis in the right side and Grade-IV in the left side [Figure 1]. Rigid nasal endoscopy, done to rule out any pathology in the nose and nasopharynx, was found to be normal. Examinations of the oral cavity and oropharynx were normal. The patient underwent computed tomography (CT) scan of both sides of the temporal bone to rule out mastoid pathology and any abnormality in the Fallopian canal. The CT scan of the temporal bone showed bilateral acute mastoiditis [Figure 2]. However, the Fallopian canal of both sides appeared to be normal. Then, the patient was started with broad-spectrum intravenous antibiotics (amoxicillin and clavulanate potassium) and adjuvant antihistaminics. Nasal decongestants such as xylometazoline and steam inhalation are also given. However, there was no improvement of facial palsy after 24 h of the treatment, so the patient underwent myringotomy and grommet (ventilation tube) insertion of both sides and fluid was aspirated. By the 5th day of hospitalization, the patient had a symptomatic improvement in hearing in both sides and decrease in hyperemia of the tympanic membrane on both sides. On day 6th of admission, facial nerve paralysis in both sides started improvement and comes to Grade II bilaterally by day 8th when he was discharged [Figure 3]. There was no surgical exploration such as mastoidectomy and or facial nerve decompression, as there was evidence of the improvement of facial nerve function with the above treatment. The patient was discharged with course of oral antibiotics, antihistaminics, and nasal decongestant drops. During follow-up 7 days after discharge, a pure tone audiogram showed normal hearing. Bilateral facial nerve functions returned to normal after 3 weeks.
| Discussion|| |
Bilateral facial nerve paralysis is rarely encountered in present-day clinical practice. When it is encountered, it is often difficult to diagnose due to the absence of facial asymmetry. In early period of AOM, facial nerve paralysis may be due to: retrograde infection inside the Fallopian canal or retrograde infection within the middle ear ascending through the chorda tympani to the facial nerve, reactivation of the latent infections of the virus due to middle ear suppuration, demyelination of the facial nerve due to the presence of bacterial toxins, and acute neuritis due to venous thrombosis causing inflammatory edema of the nerve. If middle ear infection continues, bone infection followed by resorption starts, leading to coalescence mastoiditis, then osteitis followed by bone erosion occurs, and facial nerve damage starts. However, this process takes 2–3 weeks for developing facial nerve paralysis after AOM. The pathophysiology for early facial nerve paralysis in AOM is still debated. Ischemia of the facial nerve due to the pressure effect through a dehiscence of the Fallopian canal may lead to facial nerve paralysis in AOM. Hence, draining of the middle ear can be a key treatment for facial nerve paralysis with AOM even though there are no signs of infections on the tympanic membrane. Demyelination of the facial nerve can occur secondary to the presence of ischemia and bacterial toxin. Taking into consideration of our case, demyelination of the facial nerve is less likely because of early recovery of the facial nerve paralysis after myringotomy. The absence of signs of active infection in the middle ear is not always responsible for facial nerve paralysis. Otitis media may be associated with ischemia of the facial nerve secondary to thrombosis of the microvessels to the nerve. The facial nerve can be damaged by compression over the nerve, vascular stasis, and thrombosis of the blood vessels supplying the facial nerve.
Diagnosis of facial nerve paralysis in AOM is usually done on the basis of the physical examination and imaging. Patients present with otalgia, fever, and headache. Otoscopic examination shows congested tympanic drum. The patient often shows radiographic evidence of facial canal dehiscence, but in few cases, it may not show dehiscence as microdehiscence which is not appreciated on thin-slice CT. Fluctuations of the middle ear pressure may compress directly the facial nerve or compress the vascular plexus present over the facial nerve sheath and can cause temporary ischemic neuropraxia. When AOM is complicated with facial nerve paralysis, treatment should include aggressive antimicrobial therapy for otitis media. Although myringotomy has an unknown outcome on curing the facial nerve paralysis, it still continues as the standard treatment care and remains part of the treatment until scientific studies refute its role in AOM with facial palsy. We had done myringotomy along with ventilation tube insertion for preventing early closure and help to assess the middle ear. Facial nerve paralysis in AOM is an otolaryngologic emergency. Urgent myringotomy with or without placement of grommet and culture of the middle ear fluid with aggressive IV antibiotic therapy are required for the treatment. The role of intravenous corticosteroids in this clinical condition is controversial but often routinely used in the management of facial nerve paralysis in AOM. If facial nerve paralysis does not improve within 1 week of conservative treatment, a temporal bone CT scan is advised. Electroneurography (ENoG) is an important tool to identify the prognosis and shows functional outcome of the facial nerve paralysis. It is usually done at 3–4 days after the onset of complete facial nerve paralysis to find the extent of the nerve injury. If ENoG is reduced( approximately 90% reduction of compound muscle action potential), a surgical decompression of the facial nerve is required. In majority cases of facial nerve paralysis in AOM, paralysis lasts for longer than 3 weeks.
As the prevalence of facial nerve palsy due to AOM is low, the treatment of choice is often difficult. The management of the facial nerve paralysis in AOM includes multidisciplinary team efforts. The first step in the management is medical treatment targeted for underlying etiology such as antibiotics or corticosteroids. Management with aggressive antimicrobial treatment and myringotomy will help to drain the pus from the middle ear cavity and release the pressure over facial nerve. Oral corticosteroids help to reduce the inflammatory process in the middle ear. If pharmacologic interventions have failed, surgical interventions may be indicated to restore the function and cosmesis. Many physicians recommend aggressive treatment with antibiotic and myringotomy with or without grommet insertion. In addition to this, steroid therapy is also advised for facial paralysis. In our case, myringotomy was done in both sides. In one study, mastoidectomy and facial nerve decompression was done where intraoperative bony dehiscence and edema of the tympanic segment of the facial nerve was seen, and this is similar to Tschiassny's theory described by Redaelli de Zinis et al. This theory says infectious involvement of the facial nerve occurs via bony dehiscence and neurovascular communication between the facial nerve and middle ear. Aggressive and appropriate treatment in earliest period helps patients to recover from facial nerve paralysis.
| Conclusion|| |
Bilateral AOM causing bilateral facial nerve paralysis is an extremely rare clinical entity in an adult patient. It has a tremendous impact on patient's social and family life. When an adult patient of AOM presents with facial nerve paralysis, detail history, clinical examination, and imaging are required. The treatment of this clinical entity included antibiotics, steroids, and myrigotomy with grommet insertion for drainage of fluid from the middle ear which is helpful for immediate facial nerve decompression.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]