Management patterns of multiple magnet ingestion reported to New Jersey Poison Information and Education System.

BACKGROUND: Ingestion of multiple high-powered neodymium rare-earth magnets poses a significant risk for gastrointestinal (GI) injury such as bowel perforation or ischemia. Given the rising incidence of rare earth magnetic ingestions and the corresponding increase in serious injuries in children, published guidelines recommend urgent endoscopic removal of all magnets within endoscopic reach in cases involving ingestions of two or more magnets. RESEARCH QUESTION: Do management patterns for multiple magnet ingestion align with current practice guidelines, and does hospital length of stay (LOS) differ based on the initial emergency department (ED) approach? METHODS: This is a retrospective chart review of consecutive patient encounters reported to the New Jersey Poison Information and Education System (NJPIES) between January 2021 and April 2022 involving multiple magnet ingestion. Potential cases were retrieved from the NJPIES TOXICALL® database, using substance codes relating to magnet or foreign body ingestion. Two-sample T tests were used to determine the statistical difference in the hospital LOS between the group of patients receiving early emergent esophagogastroduodenoscopy (EGD) versus those receiving expectant management on initial presentation. RESULTS: There was a difference in the average LOS of 2.7 days (p = 0.023) longer in the expectant management group with no medical complications in either group. Twenty-five percent or 2 out of 8 cases deviated from guidelines. CONCLUSION: The initial ED decision to pursue expectant management instead of attempting emergent EGD removal of magnets may result in prolonged hospitalization, increased risk for readmission, and delayed definitive removal of magnets due to nonprogression along the GI tract.

The Poison Center as a pandemic response: establishment and characteristics of a COVID-19 hotline through the New Jersey Poison Center.

BACKGROUND: Poison Centers are uniquely positioned to respond to an unprecedented public health threat such as the COVID-19 pandemic, as fully operational 24-h hotlines already staffed with healthcare professionals. METHODS: On January 27, 2020 the New Jersey Poison Information and Education System (NJPIES) agreed to operate the New Jersey Coronavirus Hotline. Call patterns, subject matter, and staffing and infrastructure strategies that were implemented to meet the demand are described. In addition, a sample of 1500 individual calls were collected and analyzed in an endeavor to describe call times, call days, area from which the call originated, callers to the hotline, primary language of the caller, and why a call was placed to the hotline. Binomial regression analysis was utilized in an attempt to identify significant patterns. RESULTS: Since the inception of the hotline through October 31, NJPIES responded to 57,579 calls for COVID-19 information. Most calls (68.7%) were regarding testing for COVID-19 and for general questions/symptoms. Call types varied when they were analyzed by time of day with calls for general questions/symptoms and where to get tested for COVID-19 showing a significant association for the early morning hours, how to obtain test results being significantly associated with the afternoon hours, and how to renew or obtain a medical license showing a significant association to the evening hours. We additionally noted that specific call types became significant when analyzed on a week-to-week basis and as specific events, like the enactment of the CARES Act of 2020, occurred. CONCLUSION: Although not the traditional role of a regional Poison Control Center, pandemic response synergizes with the workflow of this hotline because the infrastructure, staffing, and healthcare expertise are already present. Poison centers can rapidly adapt through scaling and process change to meet the needs of the public during times of public health threats.

A review of the existing literature on buprenorphine pharmacogenomics.

Buprenorphine is an effective treatment for opioid dependence; however, it demonstrates individual variability in efficacy. Pharmacogenomics may explain this drug response variability and could allow for tailored therapy on an individual basis. The Food and Drug Administration and the Clinical Pharmacogenomics Implementation Consortium have guidelines on pharmacogenomic testing for some opioids (e.g., codeine); however, no guidelines exist for the partial opioid agonist buprenorphine. Pharmacogenomic testing targets for buprenorphine include pharmacodynamic genes like the mu-opioid receptor (MOP receptor) and catechol-O-methyltransferase (COMT), as well as the pharmacokinetic genes like the CYP enzymes. In this review we identified genotypes in patients with opioid addiction receiving buprenorphine that may result in altered therapeutic dosing and increased rate of relapse. The OPRM1 A118G single nucleotide polymorphism (SNP rs1799971) gene variant encoding the N40D MOP receptor has been associated with variable efficacy and response to treatment in both adult and neonatal patients receiving buprenorphine for treatment of opioid withdrawal. An SNP associated with rs678849 of OPRD1, coding for the delta opioid receptor, was associated with opioid relapse as indicated by opioid positive urine drug screens; there was also sex specific SNP identified at rs581111 and rs529520 in the European American population. COMT variability, particularly in rs4680, has been associated with length of stay and need for opioid treatment in patients with neonatal abstinence syndrome. Variations of the pharmacokinetic gene for CYP3A4 showed that the ultrarapid metabolizer phenotype required higher doses of buprenorphine. Genotyping of patients may allow us to appropriately tailor buprenorphine therapy to individual patients and lead to improved patient outcomes; however, further research on the pharmacogenomics of buprenorphine is needed.

Ketamine Implicated in New Onset Seizure.

Ketamine is used widely in emergency departments for a variety of purposes, including procedural sedation and pain management. A major benefit of using ketamine is the rapid onset and lack of respiratory depression. The known side effects include emergence reactions, hallucinations, hypertension, dizziness, nausea, and vomiting. Recent studies have shown the benefit of ketamine for refractory status epilepticus; however, this application of the drug is still being studied. We present a case where ketamine likely induced a seizure in a patient on whom it was used as a single agent in procedural sedation. Seizure is not a known side effect of ketamine in patients without a seizure history. Given the eagerness over additional uses for ketamine, this novel case of a seizure following procedural sedation with ketamine should be of interest to emergency providers.

Pulmonary Edema Occurring after Nitric Acid Exposure.

Nitric acid (HNO3) is a strong acid and oxidizing agent used for various applications including production of ammonium nitrate in the fertilizer industry. Nitrogen oxides formed when nitric acid interacts with the environment have been implicated in inhalation injuries. This describes a case of a 49-year-old male who presented to the emergency department complaining of an acute onset of shortness of breath approximately 12 hours after being exposed to nitric acid fumes. He presented with a room air oxygen saturation of 80 percent with moderate to severe respiratory distress. His plain film chest radiograph showed bilateral pulmonary infiltrates and pulmonary edema. Over a seven-day hospital course, he had an improvement in his clinical status and chest X-ray with normal pulmonary function tests one month after discharge. Although exposure to the fumes of nitric acid is known to cause delayed pulmonary edema, it is rarely reported in the medical literature. This case serves as a reminder to consider exposure to fumes of nitric acid in a patient presenting with pulmonary edema and highlights the importance of obtaining a work history.

A Rare and Lethal Complication: Cerebral Edema in the Adult Patient with Diabetic Ketoacidosis.

Commonly seen in the emergency department, diabetic ketoacidosis is a potentially lethal sequela of uncontrolled diabetes mellitus. In the adult population, a rare complication of diabetic ketoacidosis is cerebral edema. This case report discusses a 26-year-old male with new onset diabetes mellitus who developed cerebral edema leading to death.

Quantitative analysis of Pac1/LIS1-mediated dynein targeting: Implications for regulation of dynein activity in budding yeast.

LIS1 is a critical regulator of dynein function during mitosis and organelle transport. Here, we investigated how Pac1, the budding yeast LIS1 homologue, regulates dynein targeting and activity during nuclear migration. We show that Pac1 and Dyn1 (dynein heavy chain) are dependent upon each other and upon Bik1 (budding yeast CLIP-170 homologue) for plus end localization, whereas Bik1 is independent of either. Dyn1, Pac1 and Bik1 interact in vivo at the plus ends, where an excess amount of Bik1 recruits approximately equal amounts of Pac1 and Dyn1. Overexpression of Pac1 enhanced plus end targeting of Dyn1 and vice versa, while affinity-purification of Dyn1 revealed that it exists in a complex with Pac1 in the absence of Bik1, leading us to conclude that the Pac1-Dyn1 complex preassembles in the cytoplasm prior to loading onto Bik1-decorated plus ends. Strikingly, we found that Pac1-overexpression augments cortical dynein activity through a mechanism distinct from loss of She1, a negative regulator of dynein-dynactin association. While Pac1-overexpression enhances the frequency of cortical targeting for dynein and dynactin, the stoichiometry of these complexes remains relatively unchanged at the plus ends compared to that in wild-type cells (∼3 dynein to 1 dynactin). Loss of She1, however, enhances dynein-dynactin association at the plus ends and the cell cortex, resulting in an apparent 1:1 stoichiometry. Our results reveal differential regulation of cortical dynein activity by She1 and Pac1, and provide a potentially new regulatory step in the off-loading model for dynein function.