Opioid-Associated Hearing Loss: A 20-Year Review from the New Jersey Poison Center.

BACKGROUND: Opioid-associated ototoxicity is a known complication of opioid exposure, although the mechanism remains unclear. While historically most closely linked to heroin and oxycodone, evolving reports suggest that it may be a class effect of opioids. However, the evidence is limited to case reports. METHODS: A retrospective review of the New Jersey Poison Center records (ToxiCALL®) identified cases that included both hearing loss and recent opioid exposure between January 1, 1999, and September 21, 2018. RESULTS: Forty-one cases were identified, mean age 29.4 years, 51% (n = 21) were male. Reported heroin exposures comprised 51% (n = 22), 18 of which were heroin alone. The next most commonly cited opioids were oxycodone (n = 7), methadone, (n = 4), and tramadol (n = 3). Hearing loss was described as tinnitus in 24% of cases, hypoacusis in 37% of cases, deafness in 29% of cases, and mixed tinnitus/hypoacusis in 10% of cases. Only 34% (n = 14) of cases were associated with a potential hypoxic event. Of the cases that documented resolution data, 21% (n = 4 of 19) reported no improvement at time of hospital discharge. DISCUSSION: Opioid-associated ototoxicity appears to be a hypoxia-independent adverse effect since most of the reported cases did not involve a known contributory hypoxic event. It occurs with a wide array of opioids, which supports an opioid receptor-mediated mechanism. The ototoxic effect may be self-limited in many patients. CONCLUSION: Opioid-associated ototoxicity was most commonly associated with heroin exposure and appeared independent of hypoxic events. Further investigation that clarifies the risk factors and long-term outcomes is needed.

Bismuth Subsalicylate Coagulopathy in a Patient with Chronic Liver Disease.

Bismuth subsalicylate (BSS) is the active ingredient in over-the-counter antacid and antidiarrheal medications. Coagulopathy in the setting of acetylsalicylic acid toxicity is well documented but not in setting of bismuth subsalicylate overuse. We present a case report of coagulopathy from BSS poisoning in a patient with underlying cirrhosis. The patient's high prothrombin time suggests inhibition of vitamin K-dependent coagulation factors. The patient had decreased factor V activity, which is responsible for converting prothrombin to thrombin. Patients with cirrhosis often have hypoprothrombinemia which may be exacerbated by salicylate-induced coagulopathy. Given the widespread use of BSS products, physicians should recognize coagulopathy as a possible manifestation of toxicity especially in patients with underlying liver disease.