Management Options of Giant Colonic Lipomas.

Colonic lipomas are rare, benign neoplasms, typically asymptomatic, and predominantly found incidentally during autopsy or routine surveillance. Symptomatic lesions are usually those greater than 2 cm in diameter while "giant" lesions are characterized as those over 4 cm. Presentations can vary from asymptomatic to more severe sequelae, including obstruction, gastrointestinal bleeding, or intussusception. Resection of these lesions has historically been restricted to large or symptomatic lesions. However, recent reports suggest lipomas may retain the ability to grow and can become symptomatic over time despite being inconsequential initially. This series provides a review of the clinical manifestations of colonic lipomas, radiographic characteristics, and a treatment recommendation for management of these lesions using minimally invasive surgical techniques whilst advocating for consideration of resection prior to the development of symptoms or more emergent complications.

Rapid Adoption of an Interdisciplinary Care Team Model for Surgical Residents Managing Coronavirus Disease-19.

Introduction: Patients infected with SARS-Cov-2, the causative virus behind the coronavirus disease-19 (COVID-19) pandemic, have been increasing rapidly in New York City. New York City has the highest incidence in the United States and fully 45% of all deaths from COVID-19. Our medical center is located within a high-density region of cases in south Brooklyn and, in fact, three of our neighborhood zip codes are in the top seven in New York in incidence. As a result, our center has experienced a dramatic increase in hospitalizations, particularly respiratory distress secondary to COVID-19, which rapidly exceeded the capacity of our internal medicine service. This necessitated the formation of new COVID-19 units throughout the hospital, replacing all former service lines. These units employed management teams composed of residents from many medical and surgical disciplines, including general surgery residents. Methods: Our general surgery residency program established a surgical COVID-19 (SCOVID) management team. Initially, 4 surgical residents (2 senior and 2 junior), 1 attending surgeon, and 1 attending internal medicine physician were allocated to the initial SCOVID team. On day 3 of implementation, to achieve more rapid competence in the complex management of these patients, a senior medicine resident with direct experience in the care of COVID-19 patients was added in an advisory capacity. Results: The addition of an experienced senior medical resident and attending allowed for the quick adoption of uniform management protocols by surgical residents and attendings. Discussion: We describe a protocol for the establishment of COVID-19 management teams staffed with general surgical residents, as well as a strategy for the achievement of rapid increases in competency. The addition of a senior internal medicine resident and attending to our SCOVID team allowed for rapid achievement of competency in the care of COVID-19 patients in our large institution at the epicenter of the COVID-19 pandemic.

Loss of signal transducer and activator of transduction 4 or 6 signaling contributes to immune cell morbidity and mortality in sepsis.

OBJECTIVE: The role of signal transducer and activator of transduction (STAT) 4 vs. 6 has been assessed thus far only in a model of high mortality strongly driven by proinflammation alone. Their role in a low-mortality (LD25) model of sepsis remains unclear. DESIGN AND SETTING: Prospective controlled animal study in a research laboratory. SUBJECTS: STAT4 and STAT6 knockout mice. INTERVENTIONS: We induced sepsis by cecal ligation and puncture (CLP) or sham CLP in three groups of mice: (a) STAT4-/-, (b) STAT6-/-, (c) BALB/c. Splenic T cells or macrophages were then harvested 24 h after CLP, and their ability to produce cytokines was assessed. RESULTS: Following CLP T-cells from BALB/c mice were suppressed in the ability to release the Th1 cytokines interleukin (IL) 2 and interferon gamma. The release of Th2 cytokine IL-10 was increased. The Th1 response of STAT4-deficient animals was not only markedly lower in shams but was further suppressed by CLP. The Th2 cytokine response was elevated even more than that of the septic BALB/c. This was associated with lower survival than in the BALB/c. STAT6 deficiency resulted in a stronger Th1 response and a suppressed Th2 response to CLP. A similar difference between IL-12 and IL-10 release was seen in macrophages from these mice. Interestingly, while this resulted in improved survival, compared to STAT4-/- mice, the STAT6-/- animals still had a higher mortality than the BALB/c. CONCLUSIONS: These data suggest that contributions from both STAT4 driven processes as well as STAT6 responses are needed in a balanced fashion to maximize the animals' ability to survive septic challenge.

Inhibition of CD1d activation suppresses septic mortality: a role for NK-T cells in septic immune dysfunction.

BACKGROUND: Studies indicate that following septic insult there is development of generalized immune dysfunction in T cells, B cells and phagocytes, which is thought to contribute to morbidity and mortality. Specifically, there is a shift in the lymphocytes of septic animals toward an increased release of Th2 cytokines. NK-T cells have been shown to contribute to propagation of the Th2 response. The influence of NK-T cells on the immune response to septic challenge is poorly understood. In this study, we examine whether NK-T cells contribute to the immune dysfunction seen following the onset of polymicrobial sepsis, as produced by cecal ligation and puncture (CLP). MATERIALS AND METHODS: Male 129S1/SvImJ mice were pretreated with either rat IgG (isotypic control) or monoclonal antibody to CD1d (clone 1B1) (0.5 mg), which blocks signaling/antigen presentation via the CD1d cell surface receptor, thereby, ablating the activation and differentiation of the NK-T cells. Septic survival with and without anti-CD1d (CLP/CD1d) pretreatment was assessed. Mice sacrificed 24 h after CLP were assessed for change in splenic %NK-T cell (via flourescense activated cell sector) and for splenic, hepatic, and lymphoid/macrophage production of pro-inflammatory or anti-inflammatory cytokines (via enzyme-linked immunosorbent assay). RESULTS: Administration of anti-CD1d reduced septic mortality 35% at 6-10 d (n = 23 mice/group) (P <.05). There was a consistent increase in the %CD3(+) NK1.1(+) cell population (NK-T cells) in septic mice (1.706%), which was markedly suppressed by pretreatment with anti-CD1d (0.592%). IL-6 and IL-10 levels were suppressed by anti-CD1d in the spleen and blood. CONCLUSIONS: Together these findings imply not only that NK-T cells may play a role in mediating the immune suppression seen in bacterial sepsis, but that inhibition of their activation promotes survival to septic challenge.

PATHOLOGICAL ASPECTS OF THE ANTI-INFLAMMATORY/IMMUNE SUPPRESSIVE RESPONSE IN SEPSIS AND SHOCK.

Despite the recent advances in contemporary therapeutic, operative as well as supportive care sepsis and its associated co-morbidity/mortality are still a common occurrence in the critically ill trauma/surgical patient. Thus, it remains important to continue to expand our understanding of pathological components which drive the development of immune dysfunction contributing to subsequent multiple organ failure. Here we overview some of the immuno-pathological processes, cells and mediators which may play a role in the development of this immune dysfunctional condition.