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This study aimed to determine the prevalence of adverse events in mechanically ventilated adults with COVID-19 who have undergone prone positioning. A total of 100 patients were included retrospectively; 60% were males, the mean age was 64.8 ± 9.1 years, and hospital mortality was 47%. In all, we recorded 118 removals of catheters and tubes in 66 patients; 29.6% were removals of a nasogastric tube, 18.6% of an arterial line, 14.4% of a urinary catheter, and 12.7% of a central venous catheter. Reintubation or repositioning of a tracheotomy tube was required in 19 patients (16.1%), and cardiopulmonary resuscitation in 2 patients (1.7%). We recorded a total of 184 pressure ulcers in 79 patients (on anterior face in 38.5%, anterior thorax in 23.3% and any extremity anteriorly in 15.2%). We observed that body weight (p = 0.021; β = 0.09 (CI95: 0.01–0.17)) and the cumulative duration of prone positioning (p = 0.005; β = 0.06 (CI95: 0.02–0.11)) were independently associated with the occurrence of any adverse event. The use of prone positioning in our setting was associated with a greater number of adverse events than previously reported. Body weight and cumulative duration of prone positioning were associated with the occurrence of adverse events; however, other factors during a COVID-19 surge, such as working conditions, staffing, and staff education, could also have contributed to a high prevalence of adverse events.

Angiotensin II is a recently introduced vasopressor, which has been available since 2017. The novelty and the relatively high cost of angiotensin II currently limit its broader application. It induces vasoconstriction by activating the renin–angiotensin–aldosterone system and is currently the sole vasopressor functioning through this pathway. Beyond vasoconstriction, angiotensin II also affects various other physiological processes. Current evidence supports its use in managing vasoplegic and cardiogenic shock in patients who are unresponsive to catecholamines and vasopressin. However, due to limited data, the optimal timing for initiating therapy with angiotensin II, strategies for combining it with other vasopressors, and strategies for its discontinuation remain unclear. Ongoing and planned studies aim to address some of these uncertainties. This article reviews the physiological and pathophysiological effects of angiotensin II, describes its pharmacology, and provides a narrative review of the current literature.

Background: Cardiac arrest remains one of the leading causes of death. After successful resuscitation of patients in cardiac arrest, post-cardiac arrest syndrome develops, part of it being an impaired cerebral blood flow autoregulation. Monitoring cerebral blood flow autoregulation after cardiac arrest is important for optimizing patient care and prognosticating patients’ survival, yet remains a challenge. There are still gaps in clinical implications and everyday use. In this article, we present a systematic review of studies with different methods of monitoring cerebral blood flow autoregulation after non-traumatic cardiac arrest. Methods: A comprehensive literature search was performed from 1 June 2024 to 27 June 2024 by using multiple databases: PubMed, Web of Science, and the Cochrane Central Register of Controlled Trials. Inclusion criteria were studies with an included description of the measurement of cerebral blood flow autoregulation in adult patients after non-traumatic cardiac arrest. Results: A total of 16 studies met inclusion criteria. Our data show that the most used methods in the reviewed studies were near-infrared spectroscopy and transcranial Doppler. The most used mathematical methods for calculating cerebral autoregulation were cerebral oximetry index, tissue oxygenation reactivity index, and mean flow index. Conclusions: The use of various monitoring and mathematical methods for calculating cerebral blood flow autoregulation poses a challenge for standardization, validation, and daily use in clinical practice. In the future studies, focus should be considered on clinical validation and transitioning autoregulation monitoring techniques to everyday clinical practice, which could improve the survival outcomes of patients after cardiac arrest.

BackgroundTraditionally, patients who are critically ill with infection and fever have been treated with antipyretics or even physically cooled. Presumed benefits of the reduction of body temperature are mostly based on decreased metabolic demands. However, it has been shown that decreasing body temperature in patients who are critically ill is not associated with improvement in treatment outcomes. Additionally, there is some data to support the use of temperature modulation (therapeutic hyperthermia) as an adjuvant treatment strategy in patients with infection. ObjectiveThis study aims to determine the effect of body temperature on the course of intensive care unit (ICU) treatment of patients who are mechanically ventilated with pneumonia, sepsis, and positive tracheal aspirates on admission. MethodsWe performed a single-center retrospective study. Core body temperature was measured in all patients. We analyzed associations between average temperatures in the first 48 hours after admission to ICU and ICU treatment parameters. Additionally, patients were divided into three groups: patients with negative tracheal aspirates 1 week after ICU admission (P-N group), patients with a different pathogen in tracheal aspirates 1 week after ICU admission (P-HAP group), and patients with a persisting pathogen in tracheal aspirates 1 week after ICU admission (P-P group). Differences in body temperature and interventions aimed at temperature modulation were determined. ResultsWe observed a significantly higher average temperature in the first 48 hours after admission to ICU in patients who survived to hospital discharge compared to nonsurvivors (mean 37.2 °C, SD 1 °C vs mean 36.9 °C, SD 1.6 °C; P=.04). We observed no associations between average temperatures in the first 48 hours after ICU admission and days of mechanical ventilation in the first 7 days of treatment (ρ=–0.090; P=.30), the average maximum daily requirement for noradrenaline in the first 7 days of treatment (ρ=–0.029; P=.80), average maximum FiO2 in the first 7 days of ICU treatment (ρ=0.040; P=.70), and requirement for renal replacement therapy in the first 7 days of ICU treatment (mean 37.3 °C, SD 1.4 °C vs mean 37.0 °C, SD 1.3 °C; P=.23). In an additional analysis, we observed a significantly greater use of paracetamol in the P-N group (mean 1.0, SD 1.1 g vs mean 0.4, SD 0.7 g vs mean 0.4, SD 0.8 g; P=.009), a trend toward greater use of active cooling in the first 24 hours after ICU admission in the P-N group (n=11, 44% vs n=14, 33.3% vs n=16, 32%; P=.57), and no other significant differences in parameters of ICU treatment between patient groups. ConclusionsWe observed better survival in patients who developed higher body temperatures in the first 48 hours after admission to the ICU; however, we observed no changes in other treatment parameters. Similarly, we observed greater use of paracetamol in patients with negative tracheal aspirates 1 week after ICU admission. Our results support the strategy of temperature tolerance in patients who are intubated with pneumonia and sepsis.

Background and Objectives: Survival with favorable neurologic outcomes after out-of-hospital cardiac arrest (OHCA) remains elusive. Post-cardiac arrest syndrome (PCAS) involves myocardial and neurological injury, ischemia-reperfusion response, and underlying pathology. Neurologic injury is a crucial determinant of survival and functional outcomes, with damage caused by free radicals among the responsible mechanisms. This study explores the feasibility of adding intravenous vitamin C to the treatment of OHCA survivors, aiming to mitigate PCAS. Vitamin C, a nutrient with antioxidative and free radical-scavenging properties, is often depleted in critically ill patients. Materials and Methods: This randomized, double-blinded trial was conducted at a tertiary-level university hospital with adult OHCA survivors. Participants received either standard care or the addition of 1.5 g of intravenous vitamin C every 12 h for eight consecutive doses. Neurologic injury was assessed using neuron-specific enolase (NSE) levels, with additional clinical and laboratory outcomes, such as enhanced neuroprognostication factors, inflammatory markers, and cardiac parameters. Results: NSE levels were non-significantly higher in patients who received vitamin C compared to the placebo group (55.05 µg/L [95% confidence interval (CI) 26.7–124.0] vs. 39.4 µg/L [95% CI 22.6–61.9], p > 0.05). Similarly, a non-significantly greater proportion of patients in the vitamin C group developed myoclonus in the first 72 h. We also observed a non-significantly shorter duration of mechanical ventilation, fewer arrhythmias, and reduced length of stay in the intensive care unit in the group of patients who received vitamin C (p = 0.031). However, caution is warranted in interpretation of our results due to the small number of participants. Conclusions: Our findings suggest that intravenous vitamin C should not be used outside of clinical trials for OHCA survivors. Due to the small sample size and conflicting results, further research is needed to determine the potential role of vitamin C in post-cardiac arrest care.