OBJECTIVE: This study describes the histopathologic findings of a patient with severe bilateral sensorineural hearing loss after perinatal and postnatal hypoxia and asphyxia. STUDY DESIGN: Histopathologic examination on the temporal bones. SETTING: The study was performed at the Elizabeth McCullough Knowles Otopathology Laboratory, Division of Otopathology, Department of Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. RESULTS: Histopathologic examination on the left temporal bone revealed severe atrophy of the organ of Corti throughout the entire cochlea, decrease in the number of the spiral ganglion cells especially in the basal turn, and mild atrophy of saccular macula. In the right temporal bone, similar abnormalities were observed in the inner ear, but the changes were milder than those in the left temporal bone. No other distinct pathologic finding was observed in either ear. CONCLUSION: These findings suggest that the presence of severe hypoxic ischemia causes cochleosaccular atrophy. To our knowledge, this is the first histopathologic case report describing the long-term effect of perinatal and postnatal hypoxia and asphyxia that produced cochleosaccular abnormalities in the human inner ear.
OBJECTIVE: This study describes the histopathologic findings of a patient with severe bilateral sensorineural hearing loss after perinatal and postnatal hypoxia and asphyxia. STUDY DESIGN: Histopathologic examination on the temporal bones. SETTING: The study was performed at the Elizabeth McCullough Knowles Otopathology Laboratory, Division of Otopathology, Department of Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. RESULTS: Histopathologic examination on the left temporal bone revealed severe atrophy of the organ of Corti throughout the entire cochlea, decrease in the number of the spiral ganglion cells especially in the basal turn, and mild atrophy of saccular macula. In the right temporal bone, similar abnormalities were observed in the inner ear, but the changes were milder than those in the left temporal bone. No other distinct pathologic finding was observed in either ear. CONCLUSION: These findings suggest that the presence of severe hypoxic ischemia causes cochleosaccular atrophy. To our knowledge, this is the first histopathologic case report describing the long-term effect of perinatal and postnatal hypoxia and asphyxia that produced cochleosaccular abnormalities in the human inner ear.