Do It to Them, Not to Me: Doctors' and Nurses' Personal Preferences Versus Recommendations for End-of-Life Care.

BACKGROUND: The emotional toll and financial cost of end-of-life care can be high. Existing literature suggests that medical providers often choose to forego many aggressive interventions and life-prolonging therapies for themselves. To further investigate this phenomenon, we compared how providers make medical decisions for themselves versus for relatives and unrelated patients. METHODS: Between 2016 and 2019, anonymous surveys were emailed to physicians (attendings, fellows, and residents), nurse practitioners, physician assistances, and nurses at two multifacility tertiary medical centers. Participants were asked to decide how likely they would offer a tracheostomy and feeding gastrostomy to a hypothetical patient with a devastating neurological injury and an uncertain prognosis. Participants were then asked to reconsider their decision if the patient was their own family member or if they themselves were the patient. The Kruskal-Wallis H, Mann-Whitney U, and Tukey tests were used to compare quantitative data. Statistical significance was set at P < 0.05. RESULTS: Seven hundred seventy-three surveys were completed with a 10% response rate at both institutions. Regardless of professional identity, age, or gender, providers were significantly more likely to recommend a tracheostomy and feeding gastrostomy to an unrelated patient than for themselves. Professional identity and age of the respondent did influence recommendations made to a family member. CONCLUSIONS: We demonstrate that medical practitioners make different end-of-life care decisions for themselves compared with others. It is worth investigating further why there is such a discrepancy between what medical providers choose for themselves compared with what they recommend for others.

Risk Factors for Early Readmission After Acute Pancreatitis: Importance of Timely Interventions.

BACKGROUND: Despite improvements in the diagnosis and care of acute pancreatitis, the mortality, morbidity, and long-term complications of this disease currently account for an annual cost of $10 billion in the United States. Lack of high-quality consolidated clinical data about this ever-increasing national and global burden makes it challenging to be able to recognize at-risk populations and intervene to avoid early readmission (ER) (i.e., readmission within 30 d of hospital discharge or ER). METHODS: We reviewed the National Readmission Database for 2016. We retrieved 25,476 ER out of a total of 188,757 patients admitted with acute pancreatitis (ICD-10 diagnosis of K85), alive at discharge. Patients younger than 18 at the time of initial admission were excluded. Diagnostic characteristics and procedures performed were extracted from ICD-10 data. Based on patient demographics and the diagnostic and procedural profiles from their initial admission, we identified clusters of risk factors for ER using agglomerative hierarchical clustering. These are depicted in a correlation matrix. RESULTS: Acute pancreatitis is associated with a 13.5% overall ER rate. Certain pre-existing chronic diseases, particularly cardiovascular disease diagnoses and interventions at initial presentation increase the odds of ER. In contrast to interventions on the pancreas, interventions on the biliary system correlated with lower odds of ER. Furthermore, the earlier the biliary system intervention was performed during the initial hospitalization, the lower the odds of ER. We identified five clusters of interrelationships: age/comorbidity cluster, cirrhosis cluster, sepsis/pulmonary complication cluster, biliary intervention cluster, and high-risk of mortality cluster. CONCLUSIONS: We identified several potentially modifiable risk factors for ER of patients hospitalized with acute pancreatitis, which included timing of biliary interventions. Furthermore, we identified clusters of interrelationships that further illuminate which complications tend to occur concomitantly and ultimately contribute to ER. By identifying risk factors and elucidating their interactions, we have improved our understanding of this highly morbid disease and offer potential points of intervention to reduce ER.

Growth arrest-specific protein 6 protects against renal ischemia-reperfusion injury.

BACKGROUND: Renal injury caused by ischemia-reperfusion (I/R) often occurs after shock or transplantation. Growth arrest-specific protein 6 (Gas6) is a secreted protein that binds to the TAM-Tyro3, Axl, Mer-family tyrosine kinase receptors, which modulate the inflammatory response and activate cell survival pathways. We hypothesized that Gas6 could have a protective role in attenuating the severity of renal injury after I/R. MATERIALS AND METHODS: Adult mice were subjected to 45 min of bilateral renal ischemia. Recombinant mouse Gas6 (rmGas6, 5 µg per mouse) or normal saline (vehicle) was administered intraperitoneally 1 h before ischemia and all subjects were sacrificed at 23 h after I/R for blood and tissue analysis. The expression of protein and messenger RNA (mRNA) was assessed by Western blotting and quantitative polymerase chain reaction, respectively. RESULTS: Treatment with rmGas6 significantly decreased serum levels of creatinine and blood urea nitrogen by 29% and 27%, respectively, improved the renal histologic injury index, and reduced the apoptosis in the kidneys, compared with the vehicle. Renal mRNA levels of interleukin 1ß, interleukin 6, tumor necrosis factor α, keratinocyte-derived chemokine and macrophage inflammatory protein 2 were decreased significantly by 99%, 60%, 53%, 58%, and 43%, with rmGas6 treatment, respectively. After I/R, renal I-kappa-B α levels were reduced by 40%, whereas they returned to sham levels with rmGas6 treatment. The mRNA levels of inducible nitric oxide synthase and cyclooxygenase 2 were reduced by 79% and 70%, respectively, whereas the expression of cyclin D1 was increased by 2.1-fold in the rmGas6-treated group, compared with the vehicle. CONCLUSIONS: Gas6 suppresses the nuclear factor κB pathway and promotes cell proliferation, leading to the reduction of inflammation and protection of renal injury induced by I/R.

Growth arrest-specific protein 6 attenuates neutrophil migration and acute lung injury in sepsis.

Sepsis is an acute inflammatory condition that can result in multiple organ failure and acute lung injury. Growth arrest-specific protein 6 (Gas6) is a broad regulator of the innate immune response involved with the nuclear factor κB signaling pathway. We hypothesized that Gas6 could have a protective role in attenuating the severity of acute lung injury and sepsis. Male mice were subjected to sepsis by cecal ligation and puncture (CLP) after which recombinant murine Gas6 (rmGas6; 5 µg/mouse) or normal saline (vehicle) was administered intravenously. Blood and lung tissues were collected at 20 h after CLP for various measurements. Treatment with rmGas6 significantly reduced serum levels of the injury markers aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase, as well as proinflammatory cytokines interleukin 6 (IL-6) and IL-17, compared with the vehicle group (P < 0.05). The parenchyma of the lungs damaged by CLP was attenuated by rmGas6 treatment. Lung mRNA levels of tumor necrosis factor α, IL-1ß, IL-6, IL-17, and macrophage inflammatory protein 2 (MIP-2) were decreased by 60%, 86%, 82%, 93%, and 82%, respectively, with rmGas6 treatment as determined by real-time reverse transcriptase-polymerase chain reaction (P < 0.05). The degradation of IκB-α induced by CLP in the lungs was inhibited by rmGas6 treatment. The number of neutrophils and myeloperoxidase activity in the lungs were significantly reduced in the rmGas6 group. Moreover, rmGas6 reduced the in vitro migration of differentiated human promyelocytic HL60 cells by 64%. Finally, the 10-day survival rate of mice subjected to CLP was increased from 31% in the vehicle group to 67% in the rmGas6 group (P < 0.05). Thus, Gas6 has potential to be developed as a novel therapeutic agent to treat patients with sepsis and acute lung injury.