Undertreatment of opioid use disorder in patients hospitalized with injection drug use-associated infections.

OBJECTIVE: To evaluate the association between medication for opioid use disorder (MOUD) initiation and addiction consultation and outcomes for patients hospitalized with infectious complications of injecting opioids. METHOD: This was a retrospective cohort study performed at four academic medical centers in the United States. The participants were patients who had been hospitalized with infectious complications of injecting opioids in 2018. Three hundred and twenty-two patients were included and their individual patient records were manually reviewed to identify inpatient receipt of medication for opioid use disorder (MOUD), initiation of MOUD, and addiction consultation. The main outcomes of interest were premature discharge, MOUD on discharge, linkage to outpatient MOUD, one-year readmission and death. RESULTS: Three hundred and twenty-two patients were predominately male (59%), white (66%), and median age 38 years, with 36% unstably housed, and 30% uninsured. One hundred and forty-five (45%) patients received MOUD during hospitalization, including only 65 (28%) patients not on baseline MOUD. Discharge was premature for 64 (20%) patients. In the year following discharge, 27 (9%) patients were linked to MOUD, and 159 (50%) patients had at least one readmission. Being on MOUD during hospitalization was significantly associated with higher odds of planned discharge [odds ratio (OR) 3.87, P  < 0.0001], MOUD on discharge (OR 129.7, P  < 0.0001), and linkage to outpatient MOUD (OR 1.25, P  < 0.0001), however, was not associated with readmission. Study limitations were the retrospective nature of the study, so post-discharge data are likely underestimated. CONCLUSION: There was dramatic undertreatment with MOUD from inpatient admission to outpatient linkage, and high rates of premature discharge and readmission. Engagement in addiction care during hospitalization is a critical first step in improving the care continuum for individuals with opioid use disorder; however, additional interventions may be needed to impact long-term outcomes like readmission.

Alpha Lipoic Acid Toxicity: The First Reported Mortality in an Adult Patient After Multiorgan Failure.

BACKGROUND: Alpha lipoic acid (ALA) is an anti-oxidant found in many over-the-counter supplements and is used in treatments for diabetes, hypertension, and obesity. Although it is a safe oral molecule, there have been eight cases of ALA toxicity reported. Three reported cases were among adult patients and five were among pediatric patients. A 14-year-old girl died after ingestion of 6 g of ALA leading to multi-organ failure. CASE REPORT: A 42-year-old woman presented to the emergency department 4 h after an intentional overdose of 10 tablets of ALA 600 mg each (6 g, 92.3 mg/kg). She developed refractory seizures, metabolic acidosis, thrombocytopenia, rhabdomyolysis, depressed cardiac contractility, kidney injury, and supraventricular tachycardia. Her condition deteriorated and she developed multi-organ failure. The patient was started on dual pressors, anti-epileptic medications, high-dose insulin and euglycemia protocol, and methylene blue (1 mg/kg). Despite aggressive resuscitation, she required intubation and died. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This was the ninth case and the first reported adult mortality from ALA toxicity with multi-organ failure. Our case shared some similar findings with previously reported cases, including refractory seizures, metabolic acidosis, thrombocytopenia, and rhabdomyolysis. Refractory supraventricular tachycardia and severe agitation have not been reported with ALA toxicity previously. The range of toxicity of ALA is not well established. A reported dose of 6 g caused death in a pediatric patient as well as our patient, but others survived doses of 6 g and 18 g. Toxicologists and emergency physicians should be prepared for clinical deterioration and consider aggressive resuscitation in severe ALA toxicity.

Adult opioid poisonings by drug, intent, and resource use from the United States National Poison Data System from 2005-2018.

INTRODUCTION: Deaths due to an opioid overdose nearly doubled from 2013 to 2017. Our objective is to describe the trends in intent, healthcare resource use, and clinical outcomes among adults with opioid exposures. MATERIALS AND METHODS: This study is a retrospective analysis of data from the 55 U.S. poison control centers. Adults, >19 years, with an opioid as the primary poisoning agent between 2005 and 2018 were included. These years were divided into three epochs (2005-2009, 2010-2014, and 2015-2018) to describe the trends in frequency, intent, severity, healthcare resource use, and regional differences in U.S. adults affected by prescription and illicit opioid exposures. RESULTS: A total of 546,049 (54.4%) of the 1,002,947 opioid-related cases reported to the U.S. poison centers met inclusion criteria. The percentage of patients with a moderate/major clinical effect increased in each epoch (24.4, 29.13, and 35.3%) as did the proportion of patients with illicit opioids (coded as heroin) as their primary substance (2.89, 5.47, and 13.95%). Illicit opioid use was associated with increased frequency of moderate/major clinical effects (54.2 vs. 27.4%), need for an ICU procedure (11.4 vs. 6.8%), and death (3.9 vs. 1.2%) compared with prescription opioid use. Suicidal intent (34.88%) followed by misuse/abuse (26.26%) were the most frequent intents. Misuse/abuse increased in frequency over each epoch in the study period (23.1 vs. 26.12 vs. 30.3%). Discussion and conclusions: The severity of clinical effects and death following acute opioid poisonings increased over the study period, driven by suicidal intent and an increasing proportion of illicit opioid cases. This study highlights the importance of developing strategies to address suicide prevention in addition to the continued focus on opioid use disorder.

Elevated Methemoglobin Levels in a Patient Treated with Hydroxocobalamin After Suspected Cyanide Exposure.

BACKGROUND: Cyanide (CN) toxicity commonly occurs during enclosed-space fires. Historically, the first step in treating CN toxicity utilized amyl nitrite and sodium nitrite to induce methemoglobinemia, which can be dangerous in this population. Hydroxocobalamin (OHCob), which binds to CN to form the nontoxic metabolite cyanocobalamin, is now the first-line antidote for CN toxicity, and has the advantage of not inducing methemoglobinemia. CASE REPORT: A 62-year-old man presented to the Emergency Department (ED) after a house fire. He was intubated for respiratory distress and hypoxia with an initial carboxyhemoglobin of 1.3%, methemoglobin 0.3%, and anion gap 19. Eleven hours after presentation, his serum lactic acid was 9 mmol/L. Given his continued deterioration, 14 h after arrival he received OHCob 5 g i.v. for presumed CN toxicity. Methemoglobin concentration 4 min prior to OHCob administration was 0.7%, and 2 h after administration was 4.2%. This subsequently increased to 14.3% (16 h after OHCob administration) and peaked at 16.3% (47 h after OHCob administration), at which time he was administered a dose of methylene blue 50 mg i.v., 60 h after ED arrival. His methemoglobin concentrations fluctuated until a consistent downward trend starting at 92 h from ED arrival. He continued to deteriorate and expired on hospital day 5 with a methemoglobin concentration of approximately 6.0%. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: CN toxicity requires immediate recognition and treatment. The antidote, OHCob, is believed to not induce methemoglobinemia. However, this potential side effect must be considered by emergency physicians when treating suspected CN toxicity, especially if the patient does not improve after antidotal therapy.

Bongkrekic Acid-a Review of a Lesser-Known Mitochondrial Toxin.

INTRODUCTION: Bongkrekic acid (BA) has a unique mechanism of toxicity among the mitochondrial toxins: it inhibits adenine nucleotide translocase (ANT) rather than the electron transport chain. Bongkrekic acid is produced by the bacterium Burkholderia gladioli pathovar cocovenenans (B. cocovenenans) which has been implicated in outbreaks of food-borne illness involving coconut- and corn-based products in Indonesia and China. Our objective was to summarize what is known about the epidemiology, exposure sources, toxicokinetics, pathophysiology, clinical presentation, and diagnosis and treatment of human BA poisoning. METHODS: We searched MEDLINE (1946 to present), EMBASE (1947 to present), SCOPUS, The Indonesia Publication Index ( http://id.portalgaruda.org/ ), ToxNet, book chapters, Google searches, Pro-MED alerts, and references from previously published journal articles. We identified a total of 109 references which were reviewed. Of those, 29 (26 %) had relevant information and were included. Bongkrekic acid is a heat-stable, highly unsaturated tricarboxylic fatty acid with a molecular weight of 486 kDa. Outbreaks have been reported from Indonesia, China, and more recently in Mozambique. Very little is known about the toxicokinetics of BA. Bongkrekic acid produces its toxic effects by inhibiting mitochondrial (ANT). ANT can also alter cellular apoptosis. Signs and symptoms in humans are similar to the clinical findings from other mitochondrial poisons, but they vary in severity and time course. Management of patients is symptomatic and supportive. CONCLUSIONS: Bongkrekic acid is a mitochondrial ANT toxin and is reported primarily in outbreaks of food-borne poisoning involving coconut and corn. It should be considered in outbreaks of food-borne illness when signs and symptoms manifest involving the liver, brain, and kidneys and when coconut- or corn-based foods are implicated.

A Common Source Outbreak of Severe Delirium Associated with Exposure to the Novel Synthetic Cannabinoid ADB-PINACA.

BACKGROUND: Since 2009, synthetic cannabinoid (SC) use has emerged as a growing public health threat in the United States (US). Several outbreaks of unexpected, severe toxicity linked to SC use have been reported since 2012. Reports of varied and significant morbidity after SC use are expected to increase because newer compounds enter the marketplace more frequently as manufacturers attempt to circumvent regulatory efforts. CASE REPORT: We report a cluster of 7 patients who experienced a spectrum of anxiety, delirium, psychosis, and aggressive behaviors after smoking the same SC-containing product at a party. An 8th patient with the same exposure source presented with delayed onset seizures. Biologic samples were analyzed for novel, newly identified SCs belonging to the FUBINACA family of compounds. A previously unknown SC, N-(1-amino-3,3-dimethyl-1-oxobutan-2-yl)-1-pentyl-1H-indazole-3-carboxamide (ADB-PINACA) was identified in biologic samples from 7 of the individuals. ADB-PINACA was identified in the SC-containing product ("Crazy Clown") seized by law enforcement and identified as the product smoked by the 8 patients in the reported cluster. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The information compiled using this cluster of cases, and a similar reported outbreak of altered mental status in Colorado, implicating the same SC (ADB-PINACA) and brands of SC-containing products, aided the US Drug Enforcement Administration in its temporary scheduling of ADB-PINACA and three other SCs. In this outbreak, close cooperation between public health and law enforcement allowed for a rapid intervention, which halted the outbreak by interrupting the common source and accelerated regulatory efforts to prevent further morbidity and mortality.