Person:

Santos, Felipe

Objective: Lipochoristomas comprise 0.1% of all cerebellopontine angle tumors and may be misdiagnosed as vestibular schwannomas. We describe a lipochoristoma of the internal auditory canal (IAC) and present the salient features of the evaluation, diagnosis, and management. Study Design and Methods Retrospective case review. Results (Case Report) A 51-year-old woman presented with left-sided severe hearing loss, tinnitus, mild episodic vertigo, and facial paresthesias progressive over 1 year. Magnetic resonance imaging (MRI) demonstrated a small (5 × 4 mm) T1 hyperintense lobulated lesion in the distal internal auditory canal. With fat-suppressed images, there was no enhancement of the lesion. A diagnosis of IAC lipochoristoma was made. Conservative management was recommended, and on 17-month follow-up there was no interval growth. The patient remains symptomatically stable with improved equilibrium but persistent left-sided hearing loss. Conclusions: Differential diagnosis of an enhancing lesion in the IAC includes acoustic neuroma, meningioma, epidermoid and arachnoid cysts, lipochoristoma, and metastatic tumors. Fat-suppressed MRI sequences aid in a definitive diagnosis of lipochoristomas. Because lipochoristomas may have a tendency for more indolent growth and intimate involvement of the auditory nerve, conservative management with interval imaging is recommended. Surgical treatment is reserved for growing lesions or those with disabling vestibular symptoms.

Objectives: To describe the human temporal bone pathology in two patients who incurred furosemide induced ototoxicity. Patients 1) A 46‐year‐old woman in acute liver and renal failure treated with high doses of furosemide for anasarca who developed a rapidly progressive severe‐to‐profound asymmetric sensorineural hearing loss. 2) A 65‐year‐old woman with undifferentiated small cell carcinoma of the lung who received intravenous furosemide 1 day prior to death for pulmonary edema. Interventions Removal of temporal bones, histologic processing, and light microscopy of temporal bones. Main Outcome Measures: Temporal bone histopathology and correlation with clinical and audiometric data. Results: All three temporal bones demonstrated edema and cystic changes in the stria vascularis. In the first case the furosemide exposure was associated with hearing loss and the pathological changes were more extensive including cystic changes in the Hensen's cells, collapse of Reissner's membrane and the tectorial membrane and diffuse loss of inner and outer hair cells with only modest reduction in the spiral ganglion cell population. In the second case, without attributable hearing loss, there was only modest reduction in hair cell and spiral ganglion cell counts. Pathological changes were not observed in the ampullae of the semicircular canals or epithelium of the saccular or utricular maculae in either case. Conclusions: The temporal bone pathologic correlate for furosemide‐induced ototoxicity is edema and cystic degeneration of the stria vascularis. The degree of degenerative change appears dose‐dependent. We infer that pathological changes may occur in the absence of a measurable immediate clinical effect. Level of Evidence NA.