Complicațiile otomastoidiene cauzate de otita medie cronică supurată în Clinica ORL a Spitalului ,,Timofei Moșneaga’’

Introduction

Chronic suppurative otitis media (CSOM) is a chro­nic, progressive, active inflammation of the mucoperiosteum of the middle ear, characterized by the presence of persistent otorrhea, perforation of the tympanic membrane, and hearing loss. According to WHO data, approximately 3-4.7% (65-330 million) of the population suffer from chronic suppurative otitis media, of which 60% (200 million) have moderate to severe hearing loss.

Chronic suppurative otitis media leads to the destruction of the facial nerve canal (FNCD) and the lateral semicircular canal (LSCC) over time. Facial nerve fibers become more vulnerable without their bony coverage. Destruction is more common in the tympanic segment, especially in tissues adjacent to the oval window, but it can also affect the geniculate ganglion and even the vertical segment.

Labyrinthine dehiscence is a rare complication of CSOM, being usually caused by cholesteatoma. In nearly 90% of cases, the labyrinthine fistula is located in the LSCC. Preoperative diagnosis with CT is useful, but confirmation of labyrinthine dehiscence can only be definitively made during surgery.

Methodology

A retrospective study was conducted on a group of 87 patients, aged between 18 and 82 years old, who presented to the ENT Clinic of the “Timofei Moșneaga” Republican Clinical Hospital with otomastoid complications caused by chronic suppurative otitis media.

We documented the primary examination, objective findings, local status, type of mastoidectomy (canal wall up, canal wall down, and radical mastoidectomy), information regarding the destruction of the Koerner septa, ossicular erosion, facial nerve destruction, and LSCC in patients operated on for chronic suppurative otitis media. We excluded patients with temporal bone fractures or temporal bone tumors, tympanoplasty without mastoidectomy, revision surgeries, stapedoplasty for otosclerosis, or exploratory cavotympanotomy.

We analyzed the erosion of the ossicular chain through direct inspection under high magnification. We investigated the destruction of the facial nerve canal and LSCC through direct inspection under high magnification using the operating microscope and by palpation with a blunt pick. We classified the FNCD into the labyrinthine, tympanic, and mastoid segments. We analyzed the prevalence of cholesteatoma in the pathology of chronic suppurative otitis media.

Results

Of the 87 patients, 43 were women (49.42%) and 44 were men (50.58%), with an average age of 50.8 ± 13 years old. From this sample, 11 patients underwent canal wall down mastoidectomy with CSL plasty and FNC, 45 patients underwent intact canal mastoidectomy, and 31 patients underwent canal wall down mastoidectomy (Figure 1). Furthermore, 52 of the 87 patients (59.77%) presented with clinical features of mastoiditis with mastoid reaction, detachment of the posterosuperior wall, and pulsatile otorrhea, while 35 (40.23%) were diagnosed with chronic suppurative otitis media with labyrinthitis.

Of the 87 patients, cholesteatoma was detected intraoperatively in 42 cases (48.27%), while 45 (51.73%) had chronic suppurative otitis media (mucosity, tympanosclerosis, etc.). Among the 45 (51.73%) patients, 25 (28.73%) had previously undergone surgical intervention for antromastoidotomy, and four of them (4.59%) developed complications such as destruction of the lateral semicircular canal and facial nerve paresis.

Among the 35 patients with labyrinthitis, 11 (12.6%) showed CSL involvement intraoperatively. In four patients (4.59), there was complete destruction of the CSL (Figure 2), and in seven patients (8.04%), there was destruction of the bony canal with preservation of the membranous canal of the CSL (Figure 3).

It should be corrected that six patients (6.8%) presented with facial nerve paresis, type II according to the House-Brackmann classification. Among them, intraoperatively, four patients had involvement of the tympanic segment, one patient had involvement of the mastoid segment, and one patient had involvement of both the tympanic segment and the geniculate ganglion. Furthermore, among the 87 patients, CT examination and intraoperative assessment revealed that 70 patients (80.45%) had destruction of the Koerner septa (Figure 4), and in 40 of the patients (45.9%), intraoperatively, ossicular chain erosion was observed (Table 1, Figure 5).

In all 11 patients with lateral semicircular canal and facial nerve dehiscence, fascia from the posterior auricular muscle was used for the plasty and protection of these anatomical structures (Figures 5 and 6).

Discussion

The maturation of the facial nerve canal begins at 21 weeks of gestation from the apical otic ossification centers and at 26 weeks of gestation from the ossification centers in the canaliculi, near the stapedius muscle. The two centers fuse postpartum near the region of the oval window. However, the exact moment at which the facial nerve canal is fully developed is not clearly defined. There is a report that suggests the canal’s development is completed by the age of 4 years old, both anatomically and radiologically.

In early childhood, middle ear inflammations may have a minimal impact on the development of the facial canal. The incidence of facial canal destruction varies between 0.5% and 74%, typically being higher in histological studies than in surgical studies. This result may be attributed to the destruction of the bones covering the facial nerve during the cadaveric processing or in the preparation of the temporal bone. Although facial canal dehiscences may be developmental due to insufficient ossification of the bony canal, they can also occur due to resorption caused by chronic otitis media, with or without cholesteatoma.    

Patients who had involvement of multiple ossicles generally had significant cholesteatoma in the tympanic cavity, therefore 85% of patients with lesions of the incus and stapes had cholesteatoma in the tympanic sinus, facial recess, oval window and round window.

Complications such as peripheral facial paralysis and labyrinthine fistulas were more frequent in patients with chronic otitis media with cholesteatoma than in those with chronic otitis media without cholesteatoma. We preferred to use the term “destruction of the canal” instead of “dehiscence of the canal”, as each case in this article had chronic otitis media. Although the mechanism of paralysis as a result of chronic otitis media is not fully understood, FNCD could be an underlying factor in the development of facial paralysis. Ossicular chain erosions in the retrospective analysis from the ENT clinic highlighted incudal necrosis and stapes head dislocation in approximately 80%, with malleus remnants and tympanic membrane remnants in 15-20%.

Additionally, chronic otitis media can cause destruction of the LSCC. The incidence of labyrinthine fistulas secondary to chronic otitis media in modern literature ranges between 3% and 13%.

Destruction of the semicircular canal was more frequently encountered in patients who had previously undergone surgical intervention to clear the otic infection focus, demonstrating the aggressiveness of the cholesteatoma focus and its tendency to spread to the compact bony structures. From the CT scan analysis perspective, these complications developed in patients with a sclerotic mastoid cellular structure and a compact external cortex.

In all 11 cases operated on in the ENT Clinic of the “Timofei Moșneaga” Republican Clinical Hospital, resulting in CSL destruction and dehiscence of the facial nerve canal, retroauricular muscle fascia or temporal muscle fascia was applied, and symptoms of balance loss, nausea, vomiting and signs of facial nerve paresis completely disappeared.

Conclusions

The purpose of this study is to show that destruction of the lateral semicircular canal and dehiscence of the facial nerve canal correlate with the aggressiveness of cholesteatoma in previously operated patients. The structure of the external cortex and the degree of pneumatization of the sclerotic and compact mastoid determined the spread of the process to these structures. Accidental lesions can lead to facial nerve damage if the surgeon does not pay sufficient attention to the area where bony defects of the facial canal are frequently expected. The risk of destruction of the facial and labyrinthine canal increases in a patient who has undergone radical tympanoplasty or canal wall down (CWD) tympanoplasty. Surgeons must be cautious about facial and labyrinthine canal destruction when deciding to perform radical mastoidectomy or CWD tympanoplasty.

Surgeons should ensure adequate drainage and permeability of the antrum when performing intact canal mastoidectomy. At the same time, ventilation of the auditory tube is a key factor in the recovery and cessation of the infectious process. A critical point is the blockage and occlusion of the auditory tube when the surgeon decides to perform CWD tympanoplasty, especially when the patient has a history of recurrent chronic rhinosinusitis.   

Corresponding authors: Iurie Noroc E-mail: iurie.noroc@mail.ru; Victor Enachi E-mail: victor.enachi@gmail.com

Conflict of interest: none declared.

Financial support: none declared.

This work is permanently accessible online free of charge and published under the CC-BY licence.