|Year : 2012 | Volume
| Issue : 2 | Page : 92-94
Spectrum of facial paralysis in chronic suppurative otitis media
Shyam S Kumar, Alok Thakar
Department of ENT and Head and Neck Surgery, AIIMS, New Delhi, India
|Date of Web Publication||6-Sep-2012|
Department of Otorhinolaryngology and Head-Neck Surgery, All India Institute of Medical Sciences, Ansari Nagar, Room no 4057, Teaching Block, New Delhi
Source of Support: None, Conflict of Interest: None
Surgical management of facial paralysis associated with Chronic suppurative otitis media (CSOM) may vary depending on the duration and extent of paralysis and also the pathology affecting the nerve. Four illustrative cases are described. The literature is reviewed with regard to the management of the facial nerve in different situations.
Keywords: Chronic suppurative otitis media, Facial nerve decompression, Facial palsy
|How to cite this article:|
Kumar SS, Thakar A. Spectrum of facial paralysis in chronic suppurative otitis media. Indian J Otol 2012;18:92-4
| Introduction|| |
Chronic suppurative otitis media (CSOM) is one of the common causes of facial palsy and accounts for 3.1% of all cases of facial palsy.  Facial palsy in CSOM can be acute or insidious. Further prognosis is varied because of different mechanisms of facial palsy in CSOM. Four cases of facial nerve paralysis secondary to CSOM are presented so as to illustrate the varying surgical situations and their management.
| Case Reports|| |
A 14-year-old male presented with left CSOM since 6 months and left facial palsy grade 3 since 15 days. Examination indicated a conductive hearing loss (PTA 50/15 B) and granulations in the posterosuperior quadrant with associated bony erosion of the canal wall. HRCT of the temporal bone revealed soft tissue involving the middle ear, mastoid antrum, and EAC with suspicious erosion of the LSCC dome. The patient underwent canal wall down (CWD) mastoidectomy and was found to have granulations involving the middle ear, attic, aditus, and antrum. There were granulations on the dome of the LSCC and the adjacent Fallopian canal More Details. Light palpation on the granulations indicated an underlying LSCC fistula (5 mm Χ 5 mm) and dehiscence of the fallopian canal. The granulations were left undisturbed as it was felt that surgical manipulation may jeopardize inner ear functions. Post-operatively, cochleovestibular function was preserved, and the facial nerve demonstrated steady improvement with return to normal function by the end of the 3 rd week.
An 18-year-old male presented with CSOM since 2 years associated with left facial weakness grade 2 since 7 days (PTA- left profound SNHL). The patient underwent CWD mastoidectomy and was found to have postero-superior retraction cholesteatoma involving the facial recess, sinus tympani, attic, aditus, and antrum. The LSCC was blue-lined by the cholesteatoma; the facial canal demonstrated no bony dehiscences. Post-operatively, the facial nerve status improved rapidly and by the 5 th day to grade 1.
A 35-year-old female presented with complaints of right ear discharge and hearing loss. She had a polypectomy in the right ear a month ago, and histopathology evaluation of the same had indicated simple granulation tissue. 15 days after the procedure, she developed right facial palsy (sudden onset and complete) with associated increase in pus discharge and right post-aural swelling, which improved partially with conservative treatment by her local practitioner. On presentation to us, a week from the onset of her facial paralysis, she demonstrated right profound SNHL and a postural abscess. The HRCT showed an expansile lytic locally invasive soft tissue opacification of the right mastoid with a promontory cochlear fistula, eroded SCCs, and LSCC fistula. An MRI indicated a large destructive right mastoid mass extending to EAC, ME, extradural MCF, and PCF erosion of labyrinth and vertical facial nerve with doubtful right sigmoid sinus thrombosis. The patient underwent an emergency radical mastoidectomy and intra-operatively was found to have a large cavity filled with cholesteatoma, which was eroding the dural plate and entire sinus plate, the Trautman's triangle and lying in direct contact with the posterior fossa dura. The disease was extending into the perifacial cells and eroding all the three SCCs, with only a small remnant of LSCC. The facial nerve was exposed from the first genu till the stylomastoid foramen with 360-degree exposure of the vertical facial nerve. There was a promontory cochlear fistula. Postoperatively, the patient developed grade 6 facial palsy, and there was breakdown of the postaural wound. 7 months in follow-up, her facial nerve function has recovered to grade 2, and she is planned for mastoid cavity obliteration to prevent any herniation of intracranial contents through the large dehiscence in the sinus plate. Her postoperative CT scans indicate she is otherwise disease-free, with a dry ear.
An 18-year-old female presented with complaints of bilateral CSOM since 10 years with bilateral severe impairment of hearing and left facial weakness grade VI since 7 years. She had developed the facial palsy 7 years ago with a left-sided post-aural abscess, which had spontaneously drained leaving a post-aural fistula and complete facial palsy. She underwent a CWD mastoidectomy and found to have cholesteatoma eroding all the 3 SCCs and a promontory cochlear fistula. There were no remnants of the facial nerve, only a soft tissue stump was found in the region of the first genu. Facial nerve repair was obviously inappropriate in this situation and she was, therefore, considered for alternate adynamic/static procedures. The patient's concern was primarily with the drooping of the angle of the mouth, and she had no significant asymmetry of the eye. She, therefore, underwent left malar suspension to pull up the paralyzed oral commisure and bring about symmetry at rest for the lower face.
| Discussion|| |
The incidence of facial palsy with OM/CSOM has a wide range as reported by various authors. Pollock and Brown  reported it to be 0.16% (2/1250), Kangsanarak et al.  reported it to be 0.29% in 13948 patients with CSOM, and Savic and Djeric  reported it as 5.1% in 1261 patients. The commonest cause of facial palsy is Bell's palsy. The incidence of facial palsy directly related to cholesteatoma in modern literature is around 0.04% to 0.16%.  There has been a definite decrease in the incidence of facial palsy due to CSOM, probably due to earlier diagnosis and treatment.
The facial nerve fills 35% to 65% of its canal and rest of the canal is filled by connective tissue and blood vessels without any empty space.  Facial canal dehiscence (75%) is thought to be a major factor in CSOM causing facial palsy by some authors. It can also be hidden from the surgeon's view e.g. dehiscence of the vestibular surface of the facial canal.  Various other factors include osteitis, bone erosion, external compression, edema, and inflammation of the nerve, interruption of the blood supply to the facial nerve, surgical trauma, and collagenase activity of cholesteatoma. On rare occasion, the nerve has been transected by cholesteatoma.  Cholesteatoma usually causes slow onset FNP, which accounts for 80% of such cases, whereas acute infections superimposed on CSOM tend to cause an acute FNP. It has been found that FNP does not occur until extrinsic compression results in disruption of>50% nerve fibers.  Thus, with an acute mastoiditis (with prior CSOM) and anatomical dehiscence/no dehiscence in facial canal, there might be acute paralysis (complete/incomplete) as in cases 1 and 2. Otherwise, with gradual spread of cholesteatoma and erosion of the facial canal, there might be gradual onset paralysis.
Despite a significant body of published literature on facial nerve paralysis in CSOM, clear recommendations on its management are nevertheless lacking. Altuntas et al.  described 20 cases of facial palsy, of whom 14 (70%) had cholesteatoma, 3 (15%) had granulation tissue, and 3 (15%) had polypoid tissue in their middle ear. They found a defect in the fallopian canal in 14 (70%) of the patients, 5/14 in the tympanic segment and 9/14 at the 2 nd genu and/or the vertical segment of the facial canal. Majority of the cases with fallopian canal defect had cholesteatoma (10), 2 had granulation tissue, and 2 had polypoid tissue in the middle ear. They decompressed the nerve from the first genu to the sylomastoid foramen and noted the facial nerve to be edematous in 14 cases and normal with no edema in the other 6. 75% of their patients i.e. 15 had complete recovery without synkinesis and 5 had an incomplete recovery. Yetiser et al.  in their report of 24 cases of FNP with CSOM found 18 patients had gradual onset FNP, of these 13/18 had cholesteatoma and 4 of the other 6 cases with sudden onset had cholesteatoma. All patients underwent FND from the 1 st genu to stylomastoid foramen along with anti-edema measures. 14/24 patients had very good recovery within 3 months. 6 had grade II and 2 patients had grade III facial paralysis, and 2 patients had grade II paresis with synkinesis at 1-year follow-up. Jackson recommends removal of all disease in the middle ear and mastoid and decompression of the involved segment of the nerve. In cases of long-standing paralysis, he recommends sectioning and grafting the nerve in attenuated nerves (under 2 yrs of paralysis). 
In our experience, when there is an incomplete paralysis, especially of acute onset, recovery may be anticipated with surgical removal of disease alone, and a formal facial nerve decompression (FND) may be unnecessary. If paralysis is complete and acute, then FND may help in recovery. When the nerve is dehiscent over a significant length, then only disease clearance may be sufficient. Three cases in this report had acute and incomplete paresis- they had surgical excision of disease in the middle ear and mastoid but did not undergo FND. Nevertheless, recovery was noted in all.
Granulations on the facial nerve deserve special mention as they indicate an ongoing inflammatory response from the tissues. Plucking of granulations from the facial nerve may, however, cause further injury to the nerve, and such situations present a surgical dilemma. In situations with acute/incomplete paralysis, it may be best to undertake complete disease clearance but to refrain from FND and institute anti-edema medical measures. Cases with long history and complete paralysis have a poorer prognosis, and more aggressive management (FND with granulation excision)  has been proposed but may not be universally acceptable to all workers. Despite surgical decompression, this subset may not do as well.  Dubey and Larawin decompressed 9 patients with otitic facial nerve palsy- 6/9 decompressed facial nerves had intact fallopian canal and recovered to House-Brackmann grade I postoperatively. 3/9 had erosion of the fallopian canal with granulation tissue over the facial nerve and postoperatively, their final facial nerve status was House-Brackmann grade III. 
Based on the literature and our experience in this report, a surgical scheme for the management of facial nerve paralysis is outlined in [Figure 1]. Patients with complete facial palsy of a few years (as in case 4 in this report) are unlikely to show recovery with FND alone and for them, a facial rehabilitation static or dynamic procedures is more appropriate.
|Figure 1: Proposed Scheme for the management of facial nerve paralysis related to Chronic Suppurative Otitis Media|
Click here to view
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