No abstract

Sepsis develops when an infection surpasses local tissue containment. A series of dysregulated physiological responses are generated, leading to organ dysfunction and a 10% mortality risk. When patients with sepsis demonstrate elevated serum lactates and require vasopressor therapy to maintain adequate blood pressure in the absence of hypovolemia, they are in septic shock with an in-hospital mortality rate >40%. With improvements in intensive care treatment strategies, overall sepsis mortality has diminished to ~20% at 30 days; however, mortality continues to steadily climb after recovery from the acute event. Traditionally, it was thought that the complex interplay between inflammatory and anti-inflammatory responses led to sepsis-induced organ dysfunction and mortality. However, a closer examination of those who die long after sepsis subsides reveals that many initial survivors succumb to recurrent, nosocomial, and secondary infections. The comorbidly challenged, physiologically frail diabetic individuals suffer the highest infection rates. Recent reports suggest that even after clinical “recovery” from sepsis, persistent alterations in innate and adaptive immune responses exists resulting in chronic inflammation, immune suppression, and bacterial persistence. As sepsis-associated immune defects are associated with increased mortality long-term, a potential exists for immune modulatory therapy to improve patient outcomes. We propose that diabetes causes a functional immune deficiency that directly reduces immune cell function. As a result, patients display diminished bactericidal clearance, increased infectious complications, and protracted sepsis mortality. Considering the substantial expansion of the elderly and obese population, global adoption of a Western diet and lifestyle, and multidrug resistant bacterial emergence and persistence, diabetic mortality from sepsis is predicted to rise dramatically over the next two decades. A better understanding of the underlying diabetic-induced immune cell defects that persist following sepsis are crucial to identify potential therapeutic targets to bolster innate and adaptive immune function, prevent infectious complications, and provide more durable diabetic survival.

Background: The coronavirus disease 2019 pandemic has negatively affected the training of general surgery chief residents during the last trimester of their residency. Our goal was to evaluate the educational concerns of graduating general surgery chief residents during the coronavirus disease 2019 pandemic. Methods: An anonymous web-based survey was distributed between March 31 and April 7, 2020 to all current general surgery chief residents from 6 academic medical centers in Boston, Massachusetts. Interviews were also conducted with attending surgeons from participating institutions. Results: A total of 24 of 39 general surgery chief residents participated in our survey (61.5% response rate). General surgery chief residents were most concerned about the potential delay in the date of board examinations, followed by not feeling adequately prepared for the board examinations and a possible delay in the graduation date. Whereas not having enough cases to feel ready for fellowship or job and not achieving a sufficient number of cases to meet the requirements for graduation were only moderately concerning to chief residents, attending surgeons stressed a greater importance on the loss of the operative experience as nearly all (93.3%) of them suggested a personalized approach for additional general surgery training during fellowship or job onboarding. Conclusion: In addition to the dramatic impact on public health, the coronavirus disease 2019 outbreak has also caused unprecedented changes to surgical education. Therefore, creative interventions are needed to help general surgery chief residents successfully transition into the next phase of their surgical career.