Cardiac Arrest Following Drug Overdose in the United States: An Analysis of the Cardiac Arrest Registry to Enhance Survival.

BACKGROUND: Given increases in drug overdose-associated mortality, there is interest in better understanding of drug overdose out-of-hospital cardiac arrest (OHCA). A comparison between overdose-attributable OHCA and nonoverdose-attributable OHCA will inform public health measures. METHODS AND RESULTS: We analyzed data from 2017 to 2021 in the Cardiac Arrest Registry to Enhance Survival (CARES), comparing overdose-attributable OHCA (OD-OHCA) with OHCA from other nontraumatic causes (non-OD-OHCA). Arrests involving patients <18 years, health care facility residents, patients with cancer diagnoses, and patients with select missing data were excluded. Our main outcome of interest was survival with good neurological outcome, defined as Cerebral Performance Category score 1 or 2. From a data set with 537 100 entries, 29 500 OD-OHCA cases and 338 073 non-OD-OHCA cases met inclusion criteria. OD-OHCA cases involved younger patients with fewer comorbidities, were less likely to be witnessed, and less likely to present with a shockable rhythm. Unadjusted survival to hospital discharge with Cerebral Performance Category score =1 or 2 was significantly higher in the OD-OHCA cohort (OD: 15.2% versus non-OD: 6.9%). Adjusted results showed comparable survival with Cerebral Performance Category score =1 or 2 when the first monitored arrest rhythm was shockable (OD: 28.9% versus non-OD: 23.5%, P=0.087) but significantly higher survival rates with Cerebral Performance Category score =1 or 2 for OD-OHCA when the first monitored arrest rhythm was nonshockable (OD: 9.6% versus non-OD: 3.1%, P<0.001). CONCLUSIONS: Among patients presenting with nonshockable rhythms, OD-OHCA is associated with significantly better outcomes. Further research should explore cardiac arrest causes, and public health efforts should attempt to reduce the burden from drug overdoses.

Soybean polyenylphosphatidylcholine (PPC) is beneficial in liver and extrahepatic tissue injury: An update in experimental research.

Polyenylphosphatidylcholine (PPC) is a purified polyunsaturated phosphatidylcholine extract of soybeans. This article updates PPC's beneficial effects on various forms of liver cell injury and other tissues in experimental research. PPC downregulates hepatocyte CYP2E1 expression and associated hepatotoxicity, as well as attenuates oxidative stress, apoptosis, lipoprotein oxidation and steatosis in alcoholic and nonalcoholic liver injury. PPC inhibits pro-inflammatory cytokine production, while stimulating anti-inflammatory cytokine secretion in ethanol or lipopolysaccharide-stimulated Kupffer cells/macrophages. It promotes M2-type macrophage polarization and metabolic reprogramming of glucose and lipid metabolism. PPC mitigates steatosis in NAFLD through inhibiting polarization of pro-inflammatory M1-type Kupffer cells, alleviating metabolic inflammation, remodeling hepatic lipid metabolism, correcting imbalances between lipogenesis and lipolysis and enhancing lipoprotein secretion from hepatocytes. PPC is antifibrotic by preventing progression of alcoholic hepatic fibrosis in baboons and also prevents CCl4-induced fibrosis in rats. PPC supplementation replenishes the phosphatidylcholine content of damaged cell membranes, resulting in increased membrane fluidity and functioning. Phosphatidylcholine repletion prevents increased membrane curvature of the endoplasmic reticulum and Golgi and decreases sterol regulatory element binding protein-1-mediated lipogenesis, reducing steatosis. PPC remodels gut microbiota and affects hepatic lipid metabolism via the gut-hepatic-axis and also alleviates brain inflammatory responses and cognitive impairment via the gut-brain-axis. Additionally, PPC protects extrahepatic tissues from injury caused by various toxic compounds by reducing oxidative stress, inflammation, and membrane damage. It also stimulates liver regeneration, enhances sensitivity of cancer cells to radiotherapy/chemotherapy, and inhibits experimental hepatocarcinogenesis. PPC's beneficial effects justify it as a supportive treatment of liver disease.

Kidney-specific biomarkers for predicting acute kidney injury following cardiac arrest.

AIM: To evaluate the performance of kidney-specific biomarkers (neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and cystatin-C) in early detection of acute kidney injury (AKI) following cardiac arrest (CA) when compared to serum creatinine. METHODS: Adult CA patients who had kidney-specific biomarkers of AKI collected within 12 h of return of spontaneous circulation (ROSC) were included. The association between renal biomarker levels post-ROSC and the development of KDIGO stage III AKI within 7 days of enrollment were assessed as well as their predictive value of future AKI development, neurological outcomes, and survival to discharge. RESULTS: Of 153 patients, 54 (35%) developed stage III AKI within 7 days, and 98 (64%) died prior to hospital discharge. Patients who developed stage III AKI, compared to those who did not, had higher median levels of creatinine, NGAL, and cystatin-C (p < 0.001 for all). There was no statistically significant difference in KIM-1 between groups. No biomarker outperformed creatinine in the ability to predict stage III AKI, neurological outcomes, or survival outcomes (p > 0.05 for all). However, NGAL, cystatin-C, and creatinine all performed better than KIM-1 in their ability to predict AKI development (p < 0.01 for all). CONCLUSION: In post-CA patients, creatinine, NGAL, and cystatin-C (but not KIM-1) measured shortly after ROSC were higher in patients who subsequently developed AKI. No biomarker was statistically superior to creatinine on its own for predicting the development of post-arrest AKI.

Fatal Air Medical Accidents in the United States (2000-2020).

INTRODUCTION: Currently, many airplanes and helicopters are used as air ambulances to transport high-acuity patients. Unfortunately, civilian air medical transport in the United States has experienced a significant number of serious and fatal accidents. At the moment, additional research is needed to identify what factors affect air medical safety. METHODS: Accident reports from the National Transportation Safety Board (NTSB) were queried. Accident reports were analyzed if the accident occurred from 2000 through 2020, involved a helicopter or airplane on an air medical flight (as identified by the NTSB), and had at least one fatality. The date of the accident, the model of aircraft involved, and NTSB-determined probable causes of the accident were examined. RESULTS: Eighty-seven (87) accidents and 239 fatalities took place from January 2000 through December 2020. Nearly three-fourths (72.4%) of fatalities occurred on helicopters, while just 27.6% occurred on airplanes. Interpreting the NTSB findings, various human factors probably contributed to 87.4% of fatalities. These include pilot disorientation, pilot errors, maintenance errors, impairment, fatigue, or weather misestimation. Nighttime-related factors probably contributed to 38.9% of fatalities, followed by weather-related factors (35.6%), and various mechanical failures (17.2%). CONCLUSION: These data show that the probable causes of fatal air medical accidents are primarily human factors and are, therefore, likely preventable. Developing a safety-first culture with a focus on human factors training has been shown to improve outcomes across a wide range of medical specialties (eg, anesthesia, surgery, and resuscitation). While there have been fewer fatal accidents in recent years, a continued emphasis on various training modalities seems warranted.