Abstract

Background: Carbon monoxide (CO) is an odorless, colorless, flammable gas that is formed by the incomplete combustion of fuels and binds to hemoglobin with 200 to 250 times greater affinity compared to oxygen. As a result, blood oxygen-carrying capacity is reduced when CO is bound to hemoglobin. Reversible and irreversible unilateral or bilateral hearing loss due to CO poisoning has rarely been reported. We present a case of an 18-year-old previously healthy male with bilateral hearing loss after severe CO poisoning. Case Report: An 18-year-old male with no past medical history presented to the emergency department (ED) after being found unconscious with emesis in his vehicle. He failed to respond to Naloxone. In the ED, he was obtunded with vital signs significant only for tachycardia of 115 bpm. Initial workup revealed leukocytosis (WBC 16.0 10*3/uL), hyperglycemia (glucose 195 mg/dl ) and high sensitivity troponin elevation (131 ng/L). Electrocardiogram revealed sinus tachycardia with an incomplete right bundle branch block. Head CT and urine drug immunoassay were negative. Several hours after ED arrival, it was reported that the vehicle had a known problem with the exhaust pipe. The patient remained unresponsive for several hours. Approximately 6 hours after ED arrival, a carboxyhemoglobin level was ordered and returned at 9.5%. A non-rebreather oxygen mask was applied and the patient began waking up shortly after. Prior to receiving the first session of hyperbaric oxygen therapy (HBO2), the patient complained of bilateral hearing loss with tinnitus. Three sessions of HBO2 were done in the first 24 hours. The patient remained with bilateral hearing loss and tinnitus with minimal improvement over the three day hospitalization. A 3 day course of dexamethasone 10 mg daily was given. Audiological testing was not performed prior to discharge. Six months after discharge, he continued to have tinnitus and hearing loss though endorsed improvement. His audiogram shows moderate hearing loss. Discussion: CO poisoning is a rare cause of hearing loss. Tinnitus with hearing loss is reported even less. The mechanism for hearing loss in the setting of CO poisoning has not been identified however it is believed to be due to tissue hypoxia. The pattern of hearing loss after acute or chronic CO poisoning is typically sensorineural and could be unilateral or bilateral, reversible or irreversible. HBO2 is commonly used to treat severe CO poisoning, and occasionally to treat idiopathic sensorineural hearing loss (ISNHL). However, HBO2 has not been described for the sole purpose of treating CO-associated hearing loss. Corticosteroids have been shown to prevent delayed neuropsychiatric sequelae after CO poisoning and to treat ISNHL, but no reported cases with CO hearing loss. Due to the potential benefits of these relatively benign interventions, the patient was treated with HBO2 and corticosteroids with improvement in symptoms. Conclusion: Hearing loss is a rare clinical manifestation of carbon monoxide poisoning with few reported cases in the literature. Resulting hearing loss may be unilateral or bilateral, and reversible or irreversible.

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