Management of Symptomatic Gallstone Disease during COVID-19 Lockdown in a High-Resource Setting: Is There a Need for Treatment Alterations?

Introduction: Cholecystectomy (CCE) is the treatment of choice of symptomatic gallstones. Due to the SARS-CoV-2 pandemic, operating room (OR) capacities have been reduced. The goal of this study was to evaluate the duration of symptoms of patients presenting with gallstone disease during a lockdown, the surgical management, and the severity grade of their disease. Materials and Methods: A cohort study of 353 CCEs performed at a university hospital over two 10-week periods during 2 pandemic lockdowns in Germany compared to corresponding periods in 2018 and 2019. Results: During the lockdowns, 101 CCEs were performed compared to 252 in the prior years. The number of elective CCEs was reduced to save OR capacities (p < 0.001), and the most common indication for CCE was acute cholecystitis. The median time to CCE after symptom onset was 3 days in both groups for acute cholecystitis. The severity of cholecystitis was comparable (p = 0.760). The time to CCE after choledocholithiasis was shorter during the lockdowns (median of 4 days vs. 9 days; p = 0.006). Conclusions: The incidence and severity of acute cholecystitis during the lockdowns were comparable to the prior years. Acute care surgery was provided at the expense of elective procedures, and there was no need for treatment alterations.

Role of Hemorrhagic Shock in Experimental Polytrauma.

Hemorrhagic shock (HS) after tissue trauma increases the complication and mortality rate of polytrauma (PT) patients. Although several murine trauma models have been introduced, there is a lack of knowledge about the exact impact of an additional HS. We hypothesized that HS significantly contributes to organ injury, which can be reliably monitored by detection of specific organ damage markers. Therefore we established a novel clinically relevant PT plus HS model in C57BL/6 mice which were randomly assigned to control, HS, PT, or PT+HS procedure (n = 8 per group). For induction of PT, anesthetized animals received a blunt chest trauma, head injury, femur fracture, and soft tissue injury. HS was induced by pressure-controlled blood drawing (mean arterial blood pressure of 30 mmHg for 60 min) and mice then resuscitated with ionosterile (4 × volume drawn), monitored, and killed for blood and organ harvesting 4 h after injury. After HS and resuscitation, PT+HS mice required earlier and overall more catecholamine support than HS animals to keep their mean arterial blood pressure. HS significantly contributed to the systemic release of interleukin-6 and high mobility group box 1 protein. Furthermore, the histological lung injury score, pulmonary edema, neutrophil influx, and plasma clara cell protein 16 were all significantly enhanced in PT animals in the presence of an additional HS. Although early morphological changes were minor, HS also contributed functionally to remote acute kidney injury but not to early liver damage. Moreover, PT-induced systemic endothelial injury, as determined by plasma syndecan-1 levels, was significantly aggravated by an additional HS. These results indicate that HS adds to the systemic inflammatory reaction early after PT. Within hours after PT, HS seems to aggravate pulmonary damage and to worsen renal and endothelial function which might overall contribute to the development of early multiple organ dysfunction.