[Facial nerve paralysis as a sequelae of chronic suppurative otitis].

BACKGROUND

Facial palsy can be a consequence of untreated chronic suppurative otitis media. This disease can last for many years manifesting as partial deafness and ear effusion resulting in palsy after spreading of pathological process in the surrounding cranial structures. The patient with facial palsy cannot rise his forehead, nor close his eye on the involved side, while his cheek and lips just fall.

METHODS

This retrospective research included patients operated for chronic suppurative otitis media with facial palsy during the last ten years. We have examined data on duration of disease, time of development of facial palsy and relations with other otogenic complications.

RESULTS

We described 19 patients with this otogenic complication. Most of them--13 (68%) had symptoms of chronic suppurative otitis media for several years. In some cases, we found other otogenic complications, like acute mastoiditis in 4 (21%), meningitis in 4 (21%), cerebral abscesses in 1 (5%) and cerebellar abscesses in 1 (5%). All patients were operated and the pathological process was completely removed. During operation we found polypoid formations in 9 (47%) patients, granulation tissue in 8 (42%) and cholesteatoma in 7 (37%) cases. In 16 (84.2%) we did not find any visible defects on facial nerve canal, in 2 (10%) cases pathological process destroyed the canal in the tympanic region, and in 1 (5%) facial nerve was partially bare in tympanic and mastoid region. 16 (84.2%) patients have fully recovered, in 2 (10%) cases sequelae remained and in 1 (5%) patient, who had meningitis and cerebral abscess, there were no signs of recovery.

CONCLUSIONS

Facial paralysis as an otogenic complication, can originate from acute otitis media and secretory otitis media. The pathological process in chronic suppurative otitis media causes changes in mucous of middle ear, manifested by edema, submucous fibrosis and infiltration with chronic inflammation cells. Progressive spreading of these inflammation changes causes osteitis, which provokes invasion and bone destruction of inner ear, durae or facial canal and development of palsy. The sex of patients is not relevant. The significant data concern the duration of disease since 13 (68%) patients have suffered from chronic otitis for several years. This points out the silent character of the disease. The clinical picture of all patients with peripheral facial palsy is identical, no matter of etiology, so they are often wrongly classified and treated as Bell's palsy. That is the reason for imperative examination of middle ear in every patient with respective symptoms. Late and inadequate treatment is a common cause of further progressiveness of disease, which causes development of other otogenic complications that can jeopardize life of patient. Acute mastoiditis is the most frequently mentioned, but we also recorded the most severe complications as otogenic meningitis and cerebral and cerebellar abscesses. It is possible that bacterial toxins penetrate and provoke neuritis with bigger or smaller edema. On the other side, it is commonly considered that facial palsy appears with cholesteatoma of middle ear. Cholesteatoma directly distracts bones and provokes inflammation and also makes compression on nerve itself. Our research showed that there were no visible bone defects in most of the cases 16 (84%), but process developed through cracks, and only in 2 (10%) defect was in tympanic part of canal and in 1 (5.8%) facial nerve was bare in tympanic and partially in mastoid part two centimeters in length. Pathological process was operationally removed without opening the facial canal, because removal of the process provides decompression and relieve of nerve. Operation is followed by medicamentous treatment (antibiotics, corticosteroids). This treatment succeeded with full recovery in 16 (84.2%) patients, partial recovery in 2 (10%) and only one did not have any signs of recovery.

CONCLUSIONS

Otogenic facial