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Purpose Acute gastrointestinal (GI) dysfunction and failure have been increasingly recognized in critically ill patients. The variety of definitions proposed in the past has led to confusion and difficulty in comparing one study to another. An international working group convened to standardize the definitions for acute GI failure and GI symptoms and to review the therapeutic options. Methods The Working Group on Abdominal Problems (WGAP) of the European Society of Intensive Care Medicine (ESICM) developed the definitions for GI dysfunction in intensive care patients on the basis of the available evidence and current understanding of the pathophysiology. Results Definitions for acute gastrointestinal injury (AGI) with its four grades of severity, as well as for feeding intolerance syndrome and GI symptoms (e.g. vomiting, diarrhoea, paralysis, high gastric residual volumes) are proposed. AGI is a malfunctioning of the GI tract in intensive care patients due to their acute illness. AGI grade I = increased risk of developing GI dysfunction or failure (a self-limiting condition); AGI grade II = GI dysfunction (a condition that requires interventions); AGI grade III = GI failure (GI function cannot be restored with interventions); AGI grade IV = dramatically manifesting GI failure (a condition that is immediately life-threatening). Current evidence and expert opinions regarding treatment of acute GI dysfunction are provided. Conclusions State-of-the-art definitions for GI dysfunction with gradation as well as management recommendations are proposed on the basis of current medical evidence and expert opinion. The WGAP recommends using these definitions for clinical and research purposes.

ObjectiveTo estimate the incidence of acute mesenteric ischaemia (AMI), proportions of its different forms and short-term and long-term mortality.DesignSystematic review and meta-analysis.Data sourcesMEDLINE (Ovid), Web of Science, Scopus and Cochrane Library were searched until 26 July 2022.Eligibility criteriaStudies reporting data on the incidence and outcomes of AMI in adult populations.Data extraction and synthesisData extraction and quality assessment with modified Newcastle-Ottawa scale were performed using predeveloped standard forms. The outcomes were the incidence of AMI and its different forms in the general population and in patients admitted to hospital, and the mortality of AMI in its different forms.ResultsFrom 3064 records, 335 full texts were reviewed and 163 included in the quantitative analysis. The mean incidence of AMI was 6.2 (95% CI 1.9 to 12.9) per 100 000 person years. On average 5.0 (95% CI 3.3 to 7.1) of 10 000 hospital admissions were due to AMI. Occlusive arterial AMI was the most common form constituting 68.6% (95% CI 63.7 to 73.2) of all AMI cases, with similar proportions of embolism and thrombosis.Overall short-term mortality (in-hospital or within 30 days) of AMI was 59.6% (95% CI 55.5 to 63.6), being 68.7% (95% CI 60.8 to 74.9) in patients treated before the year 2000 and 55.0% (95% CI 45.5 to 64.1) in patients treated from 2000 onwards (p<0.05). The mid/long-term mortality of AMI was 68.2% (95% CI 60.7 to 74.9). Mortality due to mesenteric venous thrombosis was 24.6% (95% CI 17.0 to 32.9) and of non-occlusive mesenteric ischaemia 58.4% (95% CI 48.6 to 67.7). The short-term mortality of revascularised occlusive arterial AMI was 33.9% (95% CI 30.7 to 37.4).ConclusionsIn adult patients, AMI is a rarely diagnosed condition with high mortality, although with improvement of treatment results over the last decades. Two thirds of AMI cases are of occlusive arterial origin with potential for better survival if revascularised.PROSPERO registration numberCRD42021247148.

Liver cirrhosis and ascites are risk factors for intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS); however, data is scarce. We aimed to determine the prevalence of IAH/ACS in a population of critically ill cirrhotic patients with acute medical illness in intensive care and to assess for risk factors and clinical outcomes. This was a multicentric retrospective cohort study including two general ICUs and pooled data from a multicentric study between January 2009 and October 2019. A total of 9,345 patients were screened, and 95 were included in the analysis. Mean age was 56.7±1.3 years, and 79% were male. Liver cirrhosis etiology included alcohol in 45.3% and alcohol plus hepatitis C virus in 9.5%. Precipitating events included infection in 26% and bleeding in 21% of cases. Mean severity score MELD and SAPS II were 26.2±9.9 and 48.5±15.3, respectively, at ICU admission. The prevalence of IAH and ACS was respectively 82.1% and 23.2% with a mean value of maximum IAP of 16.0±5.7 mmHg and IAH grades: absent 17.9%, I 26.3%, II 33.7%, III 17.9%, and IV 4.2%. Independent risk factors for IAH were alcoholic cirrhosis (p = 0.01), West-Haven score (p = 0.01), and PaO2/FiO2 ratio (p = 0.02); as well as infection (p = 0.048) for ACS. Overall, 28-day mortality was 52.6% associated with higher IAP and ACS, and independent risk factors were MELD (p = 0.001), white blood cell count (p = 0.03), PaO2/FiO2 ratio (p = 0.03), and lactate concentration (p = 0.04) at ICU admission. This study demonstrates a very high prevalence of IAH/ACS in the critically ill cirrhotic patient in intensive care. Increased IAP and ACS were associated with severity of disease and adverse outcomes and independent risk factors for IAH were alcoholic cirrhosis, hepatic encephalopathy and PO2/FiO2 ratio, as well as infection for ACS. Early diagnosis, prevention, and treatment of IAH/ACS might improve outcome in critically ill cirrhotic patients.

Computed tomography (CT) is widely used in diagnosing acute mesenteric ischemia (AMI), but robust identification of distinctive subtypes and stages of progression is lacking. Systematic literature search in PubMed, Cochrane Library, Web of Science and Scopus was conducted in May 2024. Studies including at least 10 adult patients and reporting radiological diagnosis of AMI versus no AMI or transmural ischemia versus no transmural ischemia were included. Meta-analyses on sensitivity and specificity of different radiological features in diagnosing AMI were conducted. From 2628 titles, 490 studies underwent full text review, and 81 were included in 14 meta-analyses. Diagnostic accuracy of CT angiography (CTA) was high - sensitivity of 92.0% and specificity of 98.8% (I 2 45% and 79%, respectively), but lower for other CT protocols (sensitivity 75.8 and specificity 90.5; I 2 83%). In most included studies, distinction of subtypes and severity of AMI (non-transmural or transmural) was not possible. Amongst the non-vascular features, absent/reduced bowel wall enhancement provided the best prognostic value (sensitivity 57.9 and specificity 90.1). CTA is the method of choice for diagnosing AMI with high diagnostic accuracy. None of the non-vascular features alone is sufficiently reliable to diagnose AMI or its progression to transmural necrosis, whereas a combination of different radiological features conveys a potential.

Background Acute mesenteric ischaemia (AMI) is a disease with different pathophysiological mechanisms, leading to a life-threatening condition that is difficult to diagnose based solely on clinical signs. Despite widely acknowledged need for biomarkers in diagnosis of AMI, a broad systematic review on all studied biomarkers in different types of AMI is currently lacking. The aim of this study was to estimate the diagnostic accuracy of all potential biomarkers of AMI studied in humans. Methods A systematic literature search in PubMed, The Cochrane Library, Web of Science and Scopus was conducted in December 2022. Studies assessing potential biomarkers of AMI in (at least 10) adult patients and reporting their diagnostic accuracy were included. Meta-analyses of biomarkers’ sensitivity, specificity, and positive and negative likelihood ratios were conducted. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed, and the study quality was assessed with the QUADAS-2 tool. Results Seventy-five studies including a total of 9914 patients assessed 18 different biomarkers in serum/plasma and one in urine (each reported in at least two studies), which were included in meta-analyses. None of the biomarkers reached a conclusive level for accurate prediction. The best predictive value overall (all studies with any type and stage of AMI pooled) was observed for Ischaemia-modified albumin (2 studies, sensitivity 94.7 and specificity 90.5), interleukin-6 (n = 4, 96.3 and 82.6), procalcitonin (n = 6, 80.1 and 86.7), and intestinal fatty acid-binding protein (I-FABP) measured in serum (n = 16, 73.9 and 90.5) or in urine (n = 4, 87.9 and 78.9). In assessment of transmural mesenteric ischaemia, urinary I-FABP (n = 2, 92.3 and 85.2) and D-dimer (n = 3, 87.6 and 83.6) showed moderate predictive value. Overall risk of bias was high, mainly because of selected study populations and unclear timings of the biomarker measurements after onset of symptoms. Combinations of biomarkers were rarely studied, not allowing meta-analyses. Conclusions None of the studied biomarkers had sufficient sensitivity and specificity to diagnose AMI, although some biomarkers showed moderate predictive accuracy. Future studies should focus on timing of measurements of biomarkers, distinguishing between early stage and transmural necrosis, and between different types of AMI. Additionally, studies on combinations of biomarkers are warranted. PROSPERO registration : CRD42022379341.

Background Acute mesenteric ischaemia (AMI) is a life-threatening disease where early diagnosis is critical to avoid morbidity and mortality from extensive irreversible bowel necrosis. Appropriate prediction of presence of bowel necrosis is currently not available but would help to choose the optimal method of treatment. The study aims to identify combinations of biomarkers that can reliably identify AMI and distinguish between potentially reversible and irreversible bowel ischaemia. Methods This is a prospective multicentre study. Adult patients with clinical suspicion of AMI ( n  = 250) will be included. Blood will be sampled on admission, at and after interventions, or during the first 48 h of suspicion of AMI if no intervention undertaken. Samples will be collected and the following serum or plasma biomarkers measured at Tartu University Hospital laboratory: intestinal fatty acid-binding protein (I-FABP), alpha-glutathione S-transferase (Alpha- GST), interleukin 6 (IL-6), procalcitonin (PCT), ischaemia-modified albumin (IMA), D-lactate, D-dimer, signal peptide-CUB-EGF domain-containing protein 1 (SCUBE-1) and lipopolysaccharide-binding protein (LBP). Additionally, more common laboratory markers will be measured in routine clinical practice at study sites. Diagnosis of AMI will be confirmed by computed tomography angiography, surgery, endoscopy or autopsy. Student’s t or Wilcoxon rank tests will be used for comparisons between transmural vs. suspected (but not confirmed) AMI (comparison A), confirmed AMI of any stage vs suspected AMI (comparison B) and non-transmural AMI vs transmural AMI (comparison C). Optimal cut-off values for each comparison will be identified based on the AUROC analysis and likelihood ratios calculated. Positive likelihood ratio > 10 (> 5) and negative likelihood ratio < 0.1 (< 0.2) indicate high (moderate) diagnostic accuracy, respectively. All biomarkers with at least moderate accuracy will be entered as binary covariates (using the best cutoffs) into the multivariable stepwise regression analysis to identify the best combination of biomarkers for all comparisons separately. The best models for each comparison will be used to construct a practical score to distinguish between no AMI, non-transmural AMI and transmural AMI. Discussion As a result of this study, we aim to propose a score including set of biomarkers that can be used for diagnosis and decision-making in patients with suspected AMI. Trial registration NCT06212921 (Registration Date 19–01-2024).

Background Vascular surgery patients have reduced tissues` blood supply, which may lead to mitochondrial dysfunction and accumulation of acylcarnitines (ACs). It has been suggested that remote ischaemic preconditioning (RIPC) has its organ protective effect via promoting mitochondrial function. The aim of this study was to evaluate the effect of RIPC on the profile of ACs in the vascular surgery patients. Methods This is a randomised, sham-controlled, double-blinded, single-centre study. Patients undergoing open surgical repair of abdominal aortic aneurysm, surgical lower limb revascularisation surgery or carotid endarterectomy were recruited non-consecutively. The RIPC protocol consisting of 4 cycles of 5 min of ischaemia, followed by 5 min of reperfusion, was applied. A blood pressure cuff was used for RIPC or a sham procedure. Blood was collected preoperatively and approximately 24 h postoperatively. The profile of ACs was analysed using the AbsoluteIDQp180 kit (Biocrates Life Sciences AG, Innsbruck, Austria). Results Ninety-eight patients were recruited and randomised into the study groups and 45 patients from the RIPC group and 47 patients from the sham group were included in final analysis. There was a statistically significant difference between the groups regarding the changes in C3-OH ( p  = 0.023)—there was a decrease (− 0.007 µmol/L, ± 0.020 µmol/L, p  = 0.0233) in the RIPC group and increase (0.002 µmol/L, ± 0.015 µmol/L, p  = 0.481) in the sham group. Additionally, a decrease from baseline to 24 h after surgery ( p  < 0.05) was detected both in the sham and the RIPC group in the levels of following ACs: C2, C8, C10, C10:1, C12, C12:1, C14:1, C14:2, C16, C16:1, C18, C18:1, C18:2. In the sham group, there was an increase ( p  < 0.05) in the levels of C0 (carnitine) and a decrease in the level of C18:1-OH. In the RIPC group, a decrease ( p  < 0.05) was noted in the levels of C3-OH, C3-DC (C4-OH), C6:1, C9, C10:2. Conclusions It can be concluded that RIPC may have an effect on the levels of ACs and might therefore have protective effects on mitochondria in the vascular surgery patients. Further larger studies conducted on homogenous populations are needed to make more definite conclusions about the effect of RIPC on the metabolism of ACs. Trial registration ClinicalTrials.gov database, NCT02689414. Registered 24 February 2016—Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT02689414 .

Background Protein intake is recommended in critically ill patients to mitigate the negative effects of critical illness-induced catabolism and muscle wasting. However, the optimal dose of enteral protein remains unknown. We hypothesize that supplemental enteral protein (1.2 g/kg/day) added to standard enteral nutrition formula to achieve high amount of enteral protein (range 2–2.4 g/kg/day) given from ICU day 5 until ICU discharge or ICU day 90 as compared to no supplemental enteral protein to achieve moderate amount enteral protein (0.8–1.2 g/kg/day) would reduce all-cause 90-day mortality in adult critically ill mechanically ventilated patients. Methods The REPLENISH (Replacing Protein Via Enteral Nutrition in a Stepwise Approach in Critically Ill Patients) trial is an open-label, multicenter randomized clinical trial. Patients will be randomized to the supplemental protein group or the control group. Patients in both groups will receive the primary enteral formula as per the treating team, which includes a maximum protein 1.2 g/kg/day. The supplemental protein group will receive, in addition, supplemental protein at 1.2 g/kg/day starting the fifth ICU day. The control group will receive the primary formula without supplemental protein. The primary outcome is 90-day all-cause mortality. Other outcomes include functional and quality of life assessments at 90 days. The trial will enroll 2502 patients. Discussion The study has been initiated in September 2021. Interim analysis is planned at one third and two thirds of the target sample size. The study is expected to be completed by the end of 2025. Trial registration ClinicalTrials.gov Identifier: NCT04475666 . Registered on July 17, 2020.

Objective Coronary artery disease contributes to noncommunicable disease deaths worldwide. In order to make preventive methods more accurate, we need to know more about the development and progress of this pathology, including the genetic aspects. Humanin is a small peptide known for its cytoprotective and anti-apoptotic properties. Our study looked for genomic associations between humanin-like nuclear isoform genes and coronary artery disease using CARDIoGRAMplusC4D Consortium data. Results Lookup from meta-analysis datasets gave single nucleotide polymorphisms in all 13 humanin-like nuclear isoform genes with the lowest P value for rs6151662 from the MTRNR2L2 gene including the 50 kb flanking region in both directions (P-value = 0.0037). Within the gene region alone the top variant was rs78083998 from the MTRNR2L13 region (meta-analysis P-value = 0.042). None of the found associations were statistically significant after correction for multiple testing. Lookup for expression trait loci in these gene regions gave no statistically significant variants.