Facial Nerve Paralysis Following Transtympanic Penetrating Middle Ear Trauma

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Facial Nerve Paralysis Following Transtympanic Penetrating Middle Ear Trauma AlfredMarc Calo Iloreta, M.D., Benjamin D. Malkin, M.D. Department of Otolaryngology—Head and Neck Surgery, Mount Sinai School of Medicine, New York, NY INTRODUCTION Penetrating injuries violating the tympanic membrane and resulting in middle ear trauma may cause minor temporary symptoms or significant debilitation. Knowledge of the anatomy of the middle and inner ear is vital to proper diagnosis and appropriate treatment of these injuries. Initial work up of any facial nerve injury begins with a thorough history and physical exam with emphasis on the mechansim (penetrating vs. blunt trauma), timing (progressive vs. sudden loss) and associated symptoms such as vertigo or hearing loss. In addition, otoscopic evalution looking for canal lacerations, TM perforation or hemotympanum is key. Bedside Rinne and Weber tests can be used as the intial evaluation to estimate the type and magnitude of hearing loss. The facial muscles should be closely examined and their function classified by the HouseBrackmann grading system. Penetrating injuries are the second most common cause of perforations; these injuries are most often caused by objects such as Q-tips, bobby pins, keys and paper clips often used in attempts to clean the external ear canal.

CASE REPORT A 26-year old-woman without significant past medical history presented to our outpatient department with unilateral complete facial nerve paralysis and severe hearing loss. One day prior to presentation the patient had experienced a transtympanic penetrating middle ear trauma when she had fallen and a long earring was pushed into the left external auditory canal. Approximately 6 hours after the trauma she noticed the onset of facial nerve weakness, subsequently progressing to complete paralysis.

High-dose oral steroid therapy was initiated with a dose of 1 mg/kg/day of oral prednisone. Four days after the initial trauma the patient showed no improvement in facial motion. By twelve days after the event her facial nerve function had improved to a House-Brackmann grade IV. The patient did not return for further follow-up visits.

Common causes of penetrating middle ear trauma include: ¾ Foreign bodies ¾ Thermal injuries (e.g. slag burns) ¾ Blast injuries

Figure 1. Pure-tone audiogram showing maximal conductive hearing loss; also noted was a SDS of 100% bilaterally.



2. Lasak JM et al. Middle ear injury through the external auditory canal: a review of 44 cases. Ear Nose Throat J 2006; 85(11):722-8. 3. Snelling JD et al. Unusual middle-ear mischief: trans-tympanic trauma from a hair grip resulting in ossicular, facial nerve and oval window disruption. J Laryngol Otol 2006; 120(9):793-5. 4. Neuenschwander et al. Penetrating middle ear trauma: a report of 2 cases. Ear Nose Throat J 2005; 84(1):32-5.

Typical findings are: ¾ Tympanic membrane perforation ¾ Hearing loss and tinnitus ¾ Vertigo ¾ Otorrhea ¾ Ossicular injury ¾ Perilymph fistula ¾ Cholesteatoma (delayed) ¾ Facial nerve injury Perforating trauma to the posterosuperior quadrant of the tympanic membrane specifically places a number of middle ear structures at risk because of their anatomical alignment. These include all three ossicles, the facial nerve and the oval window. Thus, dislocation at the malleoincudal articulation, incudostapedial joint, or both, is possible and commonly occurs.

Here we report a case of facial nerve paralysis following transtympanic penetrating middle ear trauma, a situation that has been rarely reported in the literature.

1. Massa N, Westerberg BD. “Facial Nerve, Intratemporal Bone Trauma.” eMedicine. 26 Jan 2009. Web. 27 April 2010.

This case represents a rarely reported sequela of penetrating middle ear injury— facial paralysis. We postulate that either direct trauma from the earring itself or displacement of the incus into the tympanic segment of the facial nerve led to the development of edema and subsequent delayed-onset paralysis. No specific management guidelines are available for this type of injury, so we followed a typical strategy for facial paralysis secondary to temporal bone fractures. Because the paralysis was delayed in onset and the CT showed no gross abnormalities of the nerve, we proceeded with conservative management, including highdose steroid therapy.

Physical examination revealed a 40% superior tympanic membrane perforation, a posterior canal laceration and a HouseBrackmann grade VI paralysis. Initial tuning fork examination was consistent with a conductive hearing loss. An audiogram was performed confirming a maximal 60-dB left-sided conductive hearing loss (Figure 1). A high-resolution CT scan of the temporal bones showed significant ossicular displacement; there was no evidence of a fracture or penetrating bony spicule involving the tympanic segment of the facial nerve (Figure 2).


The concomitant facial nerve injury described here is a rare event, but should be kept in mind as a possible finding and treated aggressively. We propose that management should be similar to that for facial paralysis secondary to temporal bone fractures from external forces.



Figure 2. Axial (A, B) and coronal (C, D) cuts from a high-resolution CT scan showing separation of the incudomalleal and likely incudostapedial joints, with possible stapes displacement. The incus appears to be displaced towards the tympanic segment of the facial nerve, which is grossly normal.

AlfredMarc Calo Iloreta, Jr., M.D. Mount Sinai School of Medicine Department of Otolaryngology— Head and Neck Surgery One Gustave L. Levy Place New York, NY 10029 [email protected]

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