Transient conductive hearing loss as a notable and rare manifestation of preeclampsia: a case report.

OBJECTIVE: To report a case of transient conductive hearing loss secondary to secretory otitis media (SOM) in a patient with preeclampsia, highlight its unique pathophysiological link, and emphasize the importance of recognizing this potential complication.

CASE PRESENTATION: Preeclampsia is a severe, pregnancy-specific multisystem disorder characterized by new-onset hypertension and proteinuria after 20 weeks of gestation. While endothelial dysfunction and vasospasm are central to its pathophysiology, its clinical manifestations are diverse. Auditory dysfunction, particularly conductive hearing loss, is infrequently reported. We present a case of a 25-year-old gravida 2, para 0 woman diagnosed with preeclampsia at 33 weeks of gestation. She had persistent proteinuria (24-hour urinary protein 1244.7 mg), unstable hypertension (148-165/95-107mmHg) managed with labetalol (100 mg every 8 h, suboptimal adherence), and gestational diabetes. She had no prior history of ear disease, trauma, or ototoxic medication use.At 35w5d gestation, the patient developed sudden bilateral hearing loss, accompanied by mild chest tightness and an elevated brain natriuretic peptide (BNP) level (346.1 pg/ml). Otolaryngology consultation was performed, and otoendoscopic examination revealed bilateral intratympanic fluid. Pure tone audiometry confirmed bilateral conductive hearing loss with significant air-bone gaps (left 30 dB, right 13 dB). Bone conduction thresholds were within normal limits (left 15 dB, right 16 dB), ruling out sensorineural hearing loss. Acoustic immittance audiometry showed bilateral B-type tympanograms, indicative of middle ear effusion. Alternative causes of conductive hearing loss (e.g. upper respiratory infection-related eustachian tube dysfunction, barotrauma, tympanic membrane pathology, middle ear mass) were excluded through clinical evaluation, negative inflammatory markers (C-reactive protein: <0.5 mg/l, white blood cell count: 12.9 × 10^9), and absence of relevant symptoms. Given her deteriorating condition, an emergent Cesarean section was performed at 36 weeks of gestation, delivering a healthy male infant. Postoperatively, supportive management with combined diuretics (furosemide and spironolactone) led to rapid and complete resolution of her hearing deficits within three days. She was discharged on continued antihypertensive therapy and was well at one-month follow-up.

CONCLUSION: Transient conductive hearing loss due to SOM is a rare manifestation of preeclampsia, likely driven by hypertension-induced increased vascular permeability and altered fluid dynamics. Severe proteinuria may exacerbate systemic fluid imbalance, contributing to middle ear effusion. Early recognition via audiometric and tympanometric evaluation, exclusion of alternative etiologies, and targeted management (e.g. fluid overload reduction) can ensure prompt recovery and improve maternal outcomes. Early recognition and management can improve maternal outcomes by addressing fluid dysregulation and potentially preventing further complications.