Abstract
Otogenic brain abscesses account for 31.4% of all cerebral abscesses: bone erosion due to coalescent otomastoiditis or cholesteatomas, osteothrombophlebitis, and hematogenous spreading are the most frequent pathways of infection. We briefly reported and discussed the first case of otogenic brain abscess due to infectious labyrinthitis that (likely) spread intracranially through a dehiscence of the superior semicircular canal.
1
Introduction
Bacterial brain abscesses are life-threatening infections diagnosed in approximately 1500 to 2500 patients each year in the United States . Otogenic brain abscesses account for a large proportion of all cerebral abscesses (31.4%) , carrying a mortality rate of 3.8% . Bone erosion due to coalescent otomastoiditis or cholesteatomas, osteothrombophlebitis, and hematogenous spreading are the most frequent pathways of infection; but the increasing quality of neuroradiologic examinations enables other, less common diffusion routes to be detected.
2
Case report
A 53-year-old man was admitted to the Otolaryngology Section of Padova University complaining of a frontal headache, left ear fullness, and severe objective vertigo. Otoscopy was negative except for mild hyperemia of the left tympanic membrane (at the handle of the malleus). Neurovestibular examination revealed a spontaneous, right-beating, grade II horizontal nystagmus with an counter-clockwise rotary component and rotation of the body’s axis to the left on the Unterberger’s stepping test. Pure tone audiometry identified left anacusis. The left tympanogram was A type. Laboratory investigations showed no leukocytosis (leukocytes, 6.08 × 10 9 /L) and a normal C-reactive protein level (5.2 mg/L). A saline solution with 10% glycerol (250 mL once a day), pentoxifylline (500 mg in 100 mL of saline solution, twice a day), and betamethasone disodium phosphate (4 mg twice a day) was administered intravenously. The vestibular signs and symptoms persisted so the patient underwent contrast-enhanced magnetic resonance imaging (MRI) of the brain 10 days after the onset of his clinical symptoms, which disclosed a left temporal ring enhancing lesion ( Fig. 1 A ) close to the petrous bone with marked enhancement of the contiguous dura mater. The lesion was characterized by severe perilesional edema and a necrotic core that was hyperintense on diffusion-weighted imaging (not shown), consistent with a pyogenic abscess. High-resolution sequences (slice 1-mm thick) showed a marked enhancement of the left membranous labyrinth ( Fig. 1 B) and a mild T2-weighted hypointensity of the left cochlea and vestibule ( Fig. 1 C). Inflammatory changes in the tympanic cavity and a few petromastoid cells were also noted. Computerized tomography (CT) of the temporal bone confirmed the integrity of the tegmen tympani, a minimal involvement of contiguous petrous air cells and the superior semicircular canal dehiscence (SSCD) ( Fig. 1 D). Intravenous antibiotic therapy was started (ceftriaxone 2 g twice a day and metronidazole 500 mg 3 times a day), and the patient slowly but constantly improved in terms of his vestibular symptoms, whereas his anacusis remained. The case was discussed with the neurosurgeon who ruled out any attempt to approach the brain abscess surgically. The patient was discharged after 6 weeks and continued with IM ceftriaxone 2 g twice a day. Brain MRI control showed a significant reduction in the size of the abscess ( Fig. 1 E) with the disappearance of the purulent component and a decrease in the perilesional edema, whereas enhancement of the labyrinth persisted. Plugging of the SSCD via a middle fossa approach was planned.
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