The aim of the study was to investigate whether the COVID-19 pandemic caused an increased incidence of complicated appendicitis due to the late presentation when compared to the pre-COVID-19 period. Summary Background Data. Acute appendicitis is one of the most common surgical emergencies. During the coronavirus-19 (COVID-19) pandemic, there has been a reported delay in the presentation of some urgencies to the emergency hospital departments. Methods. A total of 427 patients who underwent surgical treatment due to suspected acute appendicitis from June 2019 to November 2020 were retrospectively included in this study. The patients were divided into two groups: the first (pre-COVID-19) group consisted of patients who had surgery before the onset of COVID-19 pandemic (n = 240), while the second (COVID-19) group consisted of those who were operated during the COVID-19 pandemic (n = 187). The primary outcome of the study was to compare the incidence of perforated appendicitis before and during the onset of COVID-19. Results. Overall, 84 patients (19.67%) were diagnosed with perforated appendicitis. We found a weak significance ( ) in the rate of perforated appendicitis between the pre-COVID-19 (17.08%) and the COVID-19 era (22.99%). Conclusions. We did not observe any significant difference in the complications of acute appendicitis before and during the COVID-19 pandemic in a university hospital in Rijeka. An emergent medical care should always be accessible.

Open-heart surgery with cardiopulmonary bypass (CPB) is a high-risk procedure with significant morbidity and mortality. CPB, tissue injury, blood loss, endotoxemia and ischemia–reperfusion injury induce a pronounced systemic inflammatory response, leading to endothelial glycocalyx (EG) damage and vascular endothelial dysfunction. Consequently, immune cells, reactive oxygen species, and enzymes gain free access to vascular endothelial cells, resulting in their dysfunction and enhancing inflammation, vascular permeability, and microvascular impairment. EG degradation is most commonly assessed by measuring the circulating levels of its degradation products. Additionally, CPB triggers an early inflammatory response that is characterized by the secretion of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor alpha, and IL-18, which play roles in initiating the process of EG injury. EG damage is further propagated by the sustained release of cytokines, inhibiting the regeneration of the glycocalyx layer. Heparanase and matrix metalloproteinases are enzymatic pathways involved in cytokine-mediated EG degradation after cardiac surgery, and the balance between the pro- and anti-inflammatory cytokines determines the magnitude and duration of the inflammatory response and EG impairment, which correlates with adverse clinical outcomes, including myocardial dysfunction, acute lung and kidney injury, neurological complications, and prolonged need for intensive care. Thus, identifying patients with an exaggerated cytokine response could potentially provide more personalized therapy based on the circulating biomarkers of EG shedding, and cytokine-directed preservation of EG represents a promising therapeutic strategy in vascular dysfunction prevention during and after open-heart surgery. In this review, we summarize the current knowledge on cytokine-mediated EG impairment following open-heart surgery with CPB.

Background/Objectives: The management of patients with severe systemic comorbidities undergoing radiologic interventional procedures presents a significant challenge for anesthesiologists. Selecting an appropriate combination of anesthetic drugs is crucial to ensure a safe, painless procedure, facilitate rapid recovery, and minimalize complications. Here, we present a case of a 68-year-old female patient of ASA V status with a history of diabetes, coronary artery disease, and severe chronic obstructive pulmonary disease due to lung emphysema and dependence on a home oxygenator, requiring sedation for CT-guided percutaneous drainage of the aortic graft infection. Methods: After on-site emergent patient preparation and several position adjustments, sedation was initiated and maintained using continuous infusions of remimazolam and esketamine. Results: Throughout the procedure, the patient remained sedated, comfortable, and free of unwanted movements. The patient was hemodynamically stable and maintained oxygen saturation between 92 and 96%. Conclusions: In our opinion, the combination of remimazolam and esketamine demonstrated an effective and safe profile for procedural sedation. This approach holds the potential to influence standard operating protocols, particularly for patients with severe and multiple comorbidities requiring personalized anesthetic management.

Background/Objectives: Cardiopulmonary bypass (CPB) induces a systemic inflammatory response that may contribute to postoperative organ dysfunction. However, the effects of pulsatile and non-pulsatile CPB on the inflammatory response remain incompletely understood. This study investigated the perioperative dynamics of interleukin (IL)-1β, IL-18, and IL-18 binding protein (IL-18BP), as pre-specified secondary inflammatory biomarker analysis of a prospective, multicentric, randomized trial (ISRCTN11243508), in patients undergoing cardiac surgery with pulsatile or non-pulsatile CPB and evaluated their relationships with routine inflammatory and myocardial injury biomarkers. Methods: In this study 142 patients undergoing elective cardiac surgery were randomized to pulsatile (Group P) or non-pulsatile (Group NP) CPB, and 129 were analyzed (pulsatile, n = 63; non-pulsatile, n = 66). Blood samples were collected before surgery and at five postoperative time points. Plasma concentrations of IL-1β, IL-18, and IL-18BP were measured by ELISA. Leukocyte count, C-reactive protein (CRP), procalcitonin (PCT), high-sensitivity cardiac troponin I (hsTnI), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were also analyzed. The trial was powered for its primary outcome; for these secondary outcomes the achieved sample size had 80% power to detect between-group ratios of geometric means of approximately 1.27 (IL-18), 1.41 (IL-18BP) and 1.38 (IL-1β). Results: Cardiac surgery with CPB induced a marked postoperative inflammatory response in both groups: leukocyte count, CRP, PCT, IL-18, IL-18BP, hsTnI and NT-proBNP increased significantly after surgery, whereas IL-1β remained essentially unchanged. In the pre-specified confirmatory comparison of postoperative peak concentrations, no biomarker differed significantly between groups. The 95% confidence intervals of this comparison exclude a pulsatile-flow effect on peak IL-18 larger than a 15% reduction or 19% increase, and on peak IL-18BP larger than a 26% reduction or 20% increase. A supporting mixed model for repeated measures showed no differential trajectory over time for any biomarker; its confidence intervals for the average postoperative effect were narrower (approximately ±10% for IL-18 and −9% to +15% for IL-18BP). The only exception was the leukocyte count, which was approximately 10% higher throughout the postoperative period in Group NP, without a differential trajectory shape. Conclusions: This pre-specified secondary analysis of a randomized trial found no evidence that pulsatile CPB reduces the early postoperative inflammatory or myocardial-injury response compared with non-pulsatile CPB for any of the eight biomarkers studied, apart from a modest difference in leukocyte count that did not survive correction for multiple comparisons. The confidence intervals obtained exclude only moderate-to-large between-group differences in IL-18 and IL-18BP; smaller true differences remain compatible with the data and cannot be ruled out at this sample size. These findings should not be interpreted as evidence of biochemical equivalence between pulsatile and non-pulsatile CPB, but they do not support a clinically important early anti-inflammatory advantage of pulsatile perfusion in this population.