Trends in opioid exposures among young children reported to United States poison centers from 2016 to 2023.

INTRODUCTION: The objective of this study was to update and expand on previous studies of opioid exposures among young children reported to America's Poison Centers, and to describe how fentanyl and medications for opioid use disorder have contributed. METHODS: This retrospective study investigated 34,632 reports of single-substance opioid exposure from 2016 to 2023 involving pediatric patients aged one month to six years old. Descriptive statistics, tests for data normality, and significance testing were performed where applicable. RESULTS: Of 34,632 reported exposures, 96.7% were unintentional. The median age of exposure was 2.0 years (IQR 1.33-3.0 years). Reported exposures decreased by 57.5% over the study period (r = -0.96; P < 0.001). However, there was a 300% absolute increase in deaths and major effects (r = 0.96; P < 0.001). Exposures resulting in minor, no effect, not followed, or unable to follow decreased 66.2% (r = -0.99; P < 0.001). Buprenorphine was most frequently involved, comprising 23.4% of reported exposures. Buprenorphine (OR 1.93; P < 0.001) and methadone (OR 14.98; P < 0.001) were associated with an increased risk of severe effects when compared to other prescription drugs (OR: 1). There was an absolute increase of 512% over time in reports of heroin, fentanyl, synthetic non-pharmaceutical opioids (r = 0.92; P < 0.001), which were also associated with severe effects (OR 20.1; P < 0.001). DISCUSSION: Pediatric opioid exposures have previously been reported to be relatively stable. It is likely the 57.5% reduction is exaggerated due to underreporting from health care providers. However, decreases in exposures are presumed to be balanced throughout the dataset and, therefore, without differential impact on other points of analysis. Our study highlights the continued need for enhanced poisoning prevention strategies. CONCLUSIONS: The relative severity of poisonings reported to poison centers worsened over the study period. The opioids implicated have shifted away from hydrocodone, oxycodone, and tramadol, and towards fentanyl and buprenorphine.

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.