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Background: Acute kidney injury (AKI) and multiple organ failure (MOF) are leading causes of mortality in trauma injuries. Early diagnosis of AKI and MOF is vital to improve outcomes, but current diagnostic criteria rely on laboratory markers that are delayed or unreliable. In this study, we investigated whether damage associated molecular patterns such as high-mobility group box 1 (HMGB1), syndecan-1 (SDC-1) and C3a correlate with the development of trauma-induced AKI and MOF. Methods: Thirty-nine swine underwent smoke inhalation and severe burns, then received critical care for 72 hours or until death. AKI was defined by the KDIGO (Kidney Disease: Improving Global Outcomes) criteria, which labels AKI when a 1.5-fold increase in blood creatinine levels from baseline or a urine output < 0.5 mL/kg/h for 6 hours or more occurs. MOF was defined by the presence of both AKI and acute respiratory distress syndrome (PaO2/FiO2<300 for 4 hours). Results: Eight of 39 pigs developed AKI and seven of those developed MOF. Pathological analysis revealed that polytrauma induces significantly higher kidney injury scores compared to sham controls. The average time from injury to KDIGO AKI was 24 hours (interquartile range: 22.50-32.25). Twelve hours after injury, HMGB1 levels were significantly increased in animals that went on to develop AKI compared to those that did not (73.07 ± 18.66 ng/mL vs. 31.64 ± 4.15 ng/mL, p <0.01), as well as in animals that developed MOF compared to those that did not (81.52±19.68 ng/mL vs. 31.19 ± 3.972 ng/mL, p <0.05). SDC-1 and C3a levels were not significantly different at any time point between groups. ROC analysis revealed that HMGB1 levels at 12 hours post-injury were predictive of both AKI and MOF development (AKI: AUROC=0.81, cut-off value=36.41 ng/mL; MOF: AUROC=0.89, cut-off value=36.41 ng/mL). Spearman's correlation revealed that HMGB1 levels at 12 hours correlated with multiple parameters of AKI, including blood urea nitrogen, blood creatinine, and blood myoglobin. Conclusion: Twelve-hour post-injury HMGB1 levels predict AKI and MOF in a smoke inhalation and burn swine model. Further research is needed to validate this result in other polytrauma models and in critical combat causalities. [ABSTRACT FROM AUTHOR]

Skin injuries are a major healthcare problem that are not well understood or prevented in the critically ill, suggesting that underappreciated variables are contributing. This pilot study tested the hypothesis that perfusion-related factors contribute to skin injuries diagnosed as hospital-acquired pressure injuries (HAPIs). A total of 533 adult patients were followed over 2574 critical care days (mean age 62.4, standard deviation (SD) 14.3 years, mean body mass index 30.4 (SD 7.4) kg/m2, 36.4% female). This was a secondary analysis of prospective, non-randomised clinical data from an intensive care unit at a large urban teaching hospital. Factors related to perfusion, specifically two or more infusions of vasopressors/inotropes, temporary mechanical circulatory support (MCS), extracorporeal membrane oxygenation, and durable MCS, were analysed to determine whether they were more strongly associated with HAPIs than immobility due to prolonged mechanical ventilation (>72 h) or operating room time (>6 h). Patients diagnosed with a HAPI had a statistically significant higher risk of being exposed to variables related to perfusion and immobility (P < 0.05 for each variable). Perfusion-related variables, except durable MCS, had a larger effect on skin breakdown (number needed to harm (NNH) 4–10) than immobility-associated variables (NNH 12–17). The finding that perfusion-related variables predicted HAPIs may warrant consideration of alternative diagnoses, such as skin failure due to impaired perfusion as a pathophysiological process that occurs concurrently with multisystem organ failure. Differentiation of skin injuries primarily from circulatory malfunction, rather than external pressure, may guide the development of more effective treatment and prevention protocols. This pilot study suggests that the contribution of perfusion to skin injuries should be explored further. [ABSTRACT FROM AUTHOR]

Sepsis is a life-threatening organ dysfunction caused by a disorder in the regulation of a body's response to infection. If sepsis is not recognized at an early stage and treatment is not started, it can lead to septic shock, multiple organ failure, and death. Sepsis diagnostics, traditionally based on the clinical picture and the detection of etiologically significant microorganisms in the blood and foci, has been improved in recent years through the search for and the implementation of various biomarkers. One of promising sepsis biomarkers is 3-(4-hydroxyphenyl)lactic acid (4-HPLA). In this work, an amperometric sensor modified with a molecularly imprinted polymer (MIP) of hydroxyphenyllactic acid is developed, and a fundamental possibility of determining 4-HPLA in model aqueous solutions using this sensor is demonstrated. Molecularly imprinted polymers are widely used in substance separation processes and in the fabrication of selective sensors. Among a variety of selective materials, polyimides are of particular interest. In this regard, MIP sensors with imprints of 4-hydroxyphenyllactic acid were developed based on a copolymer of 1,2,4,5-benzenetracarboxylic acid with 4,4'-diaminodiphenyl oxide. The sensors are obtained in two stages (stage I at 80°C, stage II at 180°C) using the non-covalent imprinting method. The high selectivity of the MIP sensors with respect to the target molecules was established. The analytical range of the acid is 0.0002−0.2 mg/L. The experimentally established limit of detection for 4-hydroxyphenyllactic acid is 4.5 × 10–5 mg/L. [ABSTRACT FROM AUTHOR]

Background: Deep sedation may be indicated in the intensive care unit (ICU) for the management of acute organ failure, but leads to sedative‐induced delirium. Whether processed electroencephalography (p‐EEG) is useful in this setting is unclear. Aim: To describe the PSI index in deeply sedated critically ill patients with acute organ failure, and to examine a potential association between low PSI values and ICU delirium. [Correction added on 16 October 2024, after first online publication: Aim subsection in Abstract has been added on this version.] Methods: We conducted a single‐centre observational study of non‐neurological ICU patients sedated according to a standardized guideline of deep sedation (Richmond Agitation Sedation Scale [RASS] between −5 and −4) during the acute phase of respiratory and/or cardio‐circulatory failure. The SedLine (Masimo Incorporated, Irvine, California) was used to monitor the Patient State Index (PSI) (ranging from 0 to 100, <25 = very deep sedation and >50 = light sedation to full awareness) during the first 72 h of care. Delirium was assessed with the Confusion Assessment Method for the Intensive Care Unit (CAM‐ICU). Results: The median duration of PSI monitoring was 43 h. Patients spent 49% in median of the total PSI monitoring duration with a PSI <25. Patients with delirium (n = 41/97, 42%) spent a higher percentage of total monitored time with PSI <25 (median 67% [19–91] vs. 47% [12.2–78.9]) in non‐delirious patients (p.047). After adjusting for the cumulative dose of analgesia and sedation, increased time spent with PSI <25 was associated with higher delirium (odds ratio 1.014; 95% CI 1.001–1.027, p =.036). Conclusions: A clinical protocol of deep sedation targeted to RASS at the acute ICU phase may be associated with prolonged EEG suppression and increased delirium. Whether PSI‐targeted sedation may help reducing sedative dose and delirium deserves further clinical investigation. Relevance to Clinical Practice: Patients requiring deep sedation are at high risk of being over‐sedated and developing delirium despite the application of an evidence‐based sedation guideline. Development of early objective measures are essential to improve sedation management in these critically ill patients. [ABSTRACT FROM AUTHOR]

Mechanical circulatory support devices have profoundly transformed the management of severe cardiothoracic disorders. While heart transplantation is the gold standard therapy for end-stage heart disease, long-term mechanical support devices are a viable alternative for those ineligible and/or those awaiting organ availability. Major technological advancements were made over first 5 decades of development, resulting in improved durability and survival with reduced adverse events. However, gains have tapered recently for various complications (e.g., internal bleeding, multisystem organ failure), which collectively represent a significant proportion of disability and/or mortality. Further, in light of mature ventricular assist devices failing during clinical trials or even after clinical approval (class I withdrawals), it is timely to consider: Are our preclinical assessment protocols vital in the design and development of mechanical circulatory support devices, providing a realistic and reliable profile of future clinical performance? This commentary explores this question and analyses development pathways through the lens of the various disciplines involved in the preclinical assessment of mechanical circulatory support technologies: Limitations in approaches to benchtop blood testing, computational design and simulation, and animal testing are discussed as likely contributors to some of the common hemocompatibility-related adverse events (HRAEs). While it is acknowledged that some shortcomings are pragmatic in nature, possible solutions are presented that will only be realized through truly transdisciplinary and open approaches that challenge the current nature of medical device development. We suggest that these can and must be overcome to diminish HRAEs and will potentially demarcate the fourth generation of cardiac assist devices. [ABSTRACT FROM AUTHOR]

Introduction: Most patients on extracorporeal membrane oxygenation (ECMO) decease during therapy on the system. However, the actual causes of death have not been studied sufficiently. This study analyses the etiology, prevalence, and risk factors for the outcome variable death during ongoing ECMO for all patients and divided according to venoarterial (VA) or venovenous (VV) support. Methods: We retrospectively analysed all patients receiving ECMO support at our institution between March 2006 to January 2021. Only the patients deceased during ongoing support were included. Results: 2016 patients were placed on VA (n = 1168; 58%) or VV (n = 848; 42%) ECMO; 759 patients (37.7%) deceased on support. The causes of death differed between the support types: VA ECMO patients mostly died from cerebral ischemia (34%), low-cardiac output (LCO; 24.1%) and multi-organ failure (MOF; 21.6%), whereas in VV ECMO cases, refractory respiratory failure (28.2%), and sepsis (20.4%) dominated. Multivariate regression analysis revealed cardiopulmonary resuscitation (CPR) and acidosis prior to ECMO as risk factors for dying on VA ECMO, while high inotropic doses pre-ECMO, a high fraction of inspired oxygen on day 1, elevated lactate dehydrogenase, and international normalized ratio levels lead to an unfavourable outcome in VV ECMO patients. Conclusion: Even in highly experienced centers, ECMO mortality remains high and occurs mainly on support or 24 h after its termination. The causes of death differ between VV and VA ECMO, depending on the underlying diseases responsible for the need of extracorporeal support. [ABSTRACT FROM AUTHOR]

Clinical manifestations of congenital syphilis (CS) include liver disease with/without impaired liver function, identified as syphilitic hepatitis. Hepatic involvement may be dramatic; therefore, early diagnosis is crucial to provide treatment and prevent fatal outcomes. A new resurgence of CS cases has been described in recent years worldwide. We reported our experience with a case series of infants hospitalized for liver disease with a final diagnosis of CS, highlighting the wide spectrum of liver involvement, the rapid progression in cases with late diagnosis, and the pitfalls of the management of this forgotten but reemerging disease. A retrospective analysis of CS patients with hepatic presentation in the period 2008–2023 was conducted. We collected five cases (three female) with a median age of 13.8 days (range 1–84 days). In three cases, mothers were not screened for syphilis during pregnancy, and in two cases, they were seronegative in the first trimester screening. None practiced specific therapy during pregnancy. Hepatic involvement was characterized by hepatosplenomegaly, in four cases associated with cholestatic jaundice and in three cases with liver failure. Rapid plasma reagin (RPR) and Treponema pallidum hemagglutination assay (TPHA) were positive in all cases in mothers and infants. CS presented with multiorgan involvement and was fatal in one case. Conclusions: It is important to consider CS in infants with cholestasis and acute liver failure, but also in sick infants with isolated hepatomegaly. Early recognition of infants with CS is critical to identify missed cases during pregnancy and to start early treatment. What is known: • In recent years, it has been seen an increase of congenital syphilis cases in both low- and middle-income countries. • In most cases, infants born to mothers untreated for syphilis appear normal without signs of infection at birth but may develop manifestations of the disease after months or years if left untreated. • What is new: • Congenital syphilis is an emerging problem that may result in multiorgan involvement with liver disease predominant at onset. • It is important to consider congenital syphilis in infants with cholestasis and liver failure, but also in sick infants with isolated hepatomegaly. [ABSTRACT FROM AUTHOR]

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Sepsis is a life-threatening syndrome of organ dysfunction, characterized by uncontrolled inflammatory response and immune dysregulation, often leading to multiple organ failure and even death. Specialized pro-resolving mediators (SPMs), which are typically thought to be formed via consecutive steps of oxidation of polyenoic fatty acids, have been shown to suppress inflammation and promote timely resolution of inflammation. They are mainly divided into four categories: lipoxins, resolvins, protectins, and maresins. The SPMs may improve the prognosis of sepsis by modulating the immune and inflammatory balance, thereby holding promise for clinical applications. However, their biosynthetic and pharmacological properties are very complex. Through a literature review, we aim to comprehensively elucidate the protective mechanisms of different SPMs in sepsis and its organ damage, in order to provide sufficient theoretical basis for the future clinical translation of SPMs. [ABSTRACT FROM AUTHOR]

Acute lung injury (ALI) is a serious acute respiratory disease that can cause alveolar-capillary barrier disruption and pulmonary edema, respiratory failure and multiple organ dysfunction syndrome. However, there is no effective drugs in clinic until now. GSK3179106 has been reported can alleviate intestinal stress syndrome, but the protective effect of GSK3179106 on ALI has not been elucidated. The present study will evaluate the pharmacological activity of GSK3179106 on lipopolysaccharide (LPS)-induced inflammation and lung injury and clarify its underlying mechanism. We found that GSK3179106 significantly attenuated LPS-induced lung injury in vivo, accompanied by inhibited infiltration of inflammatory cells and reduced expression of inflammatory cytokines. Meanwhile, GSK3179106 dose-dependently reduced the LPS-induced IL-6 expression both in protein and gene levels in macrophages. Mechanistically, GSK3179106 could inhibited the phosphorylation of P38 MAPK induced by LPS. Importantly, results showed that there is a direct combination between GSK3179106 and P38 MAPK. Together, our findings not only clarified the anti-inflammatory activity of GSK3179106 but also discovered its new clinical indications. Therefore, compound GSK3179106 may be a potential candidate for the treatment of acute inflammatory diseases. [ABSTRACT FROM AUTHOR]

Background: Despite the progress made in recent years in the treatment of Acute Heart Failure (AHF), its prognosis remains poor in the developing country. The objective of this study is to analyze the survival and predictors of mortality of patients with acute heart failure in the cardiology department of the Basse Terre Hospital Center in Guadeloupe. Methods: this was a historical cohort study carried out over a period from June 2021 to June 2022, targeting all acute heart failure patients undergoing cardiac monitoring in the cardiology department of the Basse Terre Hospital Center in Guadeloupe. Sociodemographic, clinical, biological characteristics and outcome (recovery or death) were studied. Survival was described using the Kaplan Meier method α = 5%. Results: this study involved 242 acute heart failure patients whose median age was 75 years and the majority were male (sex ratio 2 M/1F). Among these patients, 14.9% died, the most common cause of death was cardiogenic shock (52.8%). After adjustment, tobacco consumption (aHR: 2.90; 95% CI: 1.36–8.09), Chronic Kidney Disease (aHR: 2.52; 95% CI: 1.22–5.20), infection (aHR: 2.14; 95CI %: 1.99–4.58), hyponatremia (aHR: 1.90; 95% CI: 1.10–2.86), mitral regurgitation (aHR: 3.04; 95% CI: 1.98–9.47) and N-terminal pro Brain Natriuretic Peptide > 10000ng/ml (aHR: 2.57; 95% CI: 1.21–5.49) were independently associated with the risk of death in heart failure patients. Conclusion: Acute heart failure leads to high mortality, mainly due to cardiogenic shock and factors of multiple organ failure. [ABSTRACT FROM AUTHOR]

Background: Helsmoortel–Van der Aa syndrome is a neurodevelopmental disorder in which patients present with autism, intellectual disability, and frequent extra-neurological features such as feeding and gastrointestinal problems, visual impairments, and cardiac abnormalities. All patients exhibit heterozygous de novo nonsense or frameshift stop mutations in the Activity-Dependent Neuroprotective Protein (ADNP) gene, accounting for a prevalence of 0.2% of all autism cases worldwide. ADNP fulfills an essential chromatin remodeling function during brain development. In this study, we investigated the cerebellum of a died 6-year-old male patient with the c.1676dupA/p.His559Glnfs*3 ADNP mutation. Results: The clinical presentation of the patient was representative of the Helsmoortel–Van der Aa syndrome. During his lifespan, he underwent two liver transplantations after which the child died because of multiple organ failure. An autopsy was performed, and various tissue samples were taken for further analysis. We performed a molecular characterization of the cerebellum, a brain region involved in motor coordination, known for its highest ADNP expression and compared it to an age-matched control subject. Importantly, epigenome-wide analysis of the ADNP cerebellum identified CpG methylation differences and expression of multiple pathways causing neurodevelopmental delay. Interestingly, transcription factor motif enrichment analysis of differentially methylated genes showed that the ADNP binding motif was the most significantly enriched. RNA sequencing of the autopsy brain further identified downregulation of the WNT signaling pathway and autophagy defects as possible causes of neurodevelopmental delay. Ultimately, label-free quantification mass spectrometry identified differentially expressed proteins involved in mitochondrial stress and sirtuin signaling pathways amongst others. Protein–protein interaction analysis further revealed a network including chromatin remodelers (ADNP, SMARCC2, HDAC2 and YY1), autophagy-related proteins (LAMP1, BECN1 and LC3) as well as a key histone deacetylating enzyme SIRT1, involved in mitochondrial energy metabolism. The protein interaction of ADNP with SIRT1 was further biochemically validated through the microtubule-end binding proteins EB1/EB3 by direct co-immunoprecipitation in mouse cerebellum, suggesting important mito-epigenetic crosstalk between chromatin remodeling and mitochondrial energy metabolism linked to autophagy stress responses. This is further supported by mitochondrial activity assays and stainings in patient-derived fibroblasts which suggest mitochondrial dysfunctions in the ADNP deficient human brain. Conclusion: This study forms the baseline clinical and molecular characterization of an ADNP autopsy cerebellum, providing novel insights in the disease mechanisms of the Helsmoortel–Van der Aa syndrome. By combining multi-omic and biochemical approaches, we identified a novel SIRT1-EB1/EB3-ADNP protein complex which may contribute to autophagic flux alterations and impaired mitochondrial metabolism in the Helsmoortel–Van der Aa syndrome and holds promise as a new therapeutic target. Highlights: The ADNP patient mutation affects genome-wide methylation and leads to neurodevelopmental abnormalities. The ADNP brain transcriptome reveals impaired neuronal differentiation and cellular homeostasis by aberrant signaling of the WNT pathway and autophagy process. ADNP forms a complex with SIRT1 through the microtubule end-binding proteins EB1 and EB3. Mitochondrial gene expression is impaired in the ADNP brain and patient-derived cellular models. [ABSTRACT FROM AUTHOR]

We report a case of T‐B+NK+ severe combined immunodeficiency disease (SCID) caused by IL2RG gene mutation (NM_000206.3 [IL2RG]: c.925‐2A > G). The patient, a 2‐month‐old male, experienced multiple infections and decreased white blood cells in the early postnatal period. Antibiotic treatment was ineffective and ultimately resulted in multiple organ failure. The second‐generation gene sequencing of patient showed that the IL2RG gene had a hemizygous mutation NM_000206.3 (IL2RG): c.925‐2A > G, indicating a classical splice site mutation. According to the guidelines of the American College of Medical Genetics (ACMG), NM_00206.3 (IL2RG): c.925‐2A > G variants can be classified as pathogenic (PVS1&PM1&PM6). [ABSTRACT FROM AUTHOR]

Objective: To summarize the causes of death and clinical characteristics of systemic lupus erythematosus (SLE) hospitalized patients in the last 20 years to improve SLE survival rates by detecting critical SLE early. Methods: In this case-control study, 218 SLE death cases were retrospectively analyzed from January 2002 to December 2022, with 110 SLE inpatients chosen at random as controls. The clinical symptoms, causes of death, and risk factors in patients with SLE were investigated. Results: There were 218 deaths among 9538 patients with SLE, including 188 women and 30 men. The death rate fell steadily from 4.14% in 2002 to 1.96% in 2013 and remained at 1.84% from 2014 to 2022. The standardized mortality ratio (SMR) was 4.98 [95% CI (4.06-5.89)] from 2002 to 2012 and 3.39 [95% CI (2.74-4.04)] from 2013 to 2022. Infection, lupus-induced multiple organ failure syndrome (MODS), and neuropsychiatric lupus (NPLE) were the leading causes of death, accounting for 31.19%, 15.14%, and 11.47% of overall deaths. Age had a significant association with the major causes of death. Logistic regression analysis showed NPLE[OR = 10.772,95% CI (3.350,34.633), p < 0.001], lupus pulmonary involvement (LP)[OR = 3.844,95%CI (1.547,9.552), p = 0.004], pneumonia[OR = 3.439,95%CI(1.552,7.621), p = 0.002], thrombocytopenia[OR = 14.941,95%CI (4.088,54.604), p < 0.001], creatinine>177 μmol/L[OR = 8.644,95%CI (2.831,26.388), p < 0.001], glutamic transaminase(AST) > 60U/L[OR = 5.762,95%CI (2.200,15.088), p < 0.001], total bilirubin > 34 μmol/L[OR = 16.701,95%CI (3.349,83.294), p = 0.001], higher SLE Disease Activity Index (SLEDAI)[OR = 1.089,95%CI (1.032,1.149), p = 0.002] and SLE Damage Index (SDI)[OR = 3.690,95%CI (2.487,5.474), p < 0.001] correlated positively with death. Conclusion: From 2002 to 2013, the mortality rate among patients with SLE fell steadily but remained unchanged from 2014 to 2022. Patients with SLE had significantly higher SMR than the general population. Childhood-onset SLE had a poorer prognosis than adult-onset SLE. Infection, MODS, and NPLE were the three leading causes of death. Major organ involvement and high disease activity were risk factors for mortality. [ABSTRACT FROM AUTHOR]

ABSTRACT Background Aims Methods Results Conclusions Acute‐on‐chronic liver failure (ACLF) is a syndrome of patients with chronic liver disease presenting with multiple organ failures. Recently, Sundaram‐ACLF‐LT Mortality (SALT‐M) score has been developed to predict 1‐year post‐liver transplantation mortality. We validated the SALT‐M score in a large‐volume, Asian single‐centre cohort.We validated the SALT‐M score in a large‐volume, Asian single‐centre cohort.We analysed 224 patients of ACLF grade 2–3. Area under the receiver operating characteristic curve (AUROC) and concordance index (c‐index) were used to assess and compare the predictability of posttransplant mortality of SALT‐M and other scores. Moreover, we compared the survivals of patients with high and low SALT‐M, in conjunction with MELD score and ACLF grade.The AUROC for prediction of 1‐year post‐LT survival was higher in SALT‐M (0.691) than in MELD, MELD‐Na, MELD 3.0 and delta‐MELD. Similarly, the c‐index of the SALT‐M (0.650) was higher than aforementioned MELD systems. When categorised by the cut‐off of SALT‐M ≥ 20 and MELD ≥ 30, patients with high SALT‐M exhibited lower post‐LT survival than those with low SALT‐M scores regardless of high or low MELD (40.0% for high SALT‐M/high MELD vs. 42.9% for high SALT‐M/low MELD vs. 73.8% for low SALT‐M/high MELD vs. 63.7% for low SALT‐M/low MELD, p < 0.001). In patients with ACLF grade 3, SALT‐M effectively stratified the posttransplant mortality (39.4% for high SALT‐M vs. 63.1% for low SALT‐M, p = 0.018).SALT‐M outperformed previous MELD systems for predicting posttransplant mortality in Asian LT cohort with severe ACLF. Transplantability for patients with severe ACLF could be determined based on SALT‐M. [ABSTRACT FROM AUTHOR]

Background: Peripheral veno-arterial extracorporeal membrane oxygenation (pECMO) has become the first-line device in refractory cardiogenic shock (rCS). Some pECMO complications can preclude any bridging strategies and a peripheral-to-central ECMO (cECMO) switch can be considered as a bridge-to-decision. We conducted this study to appraise the in-hospital survival and the bridging strategies in patients undergoing peripheral-to-central ECMO switch. Methods: This retrospective monocenter study included patients admitted to a ECMO-dedicated intensive care unit from February 2006 to January 2023. Patients with rCS requiring pECMO switched to cECMO were included. Patients were not included when the cECMO was the first mechanical circulatory support. Results: Eighty patients, with a median [IQR25-75] age of 44 [29–53] years at admission and a female-to-male sex ratio of 0.6 were included in the study. Refractory pulmonary edema was the main switching reason. Thirty patients (38%) were successfully bridged to: heart transplantation (n = 16/80, 20%), recovery (n = 10/80, 12%) and ventricle assist device (VAD, n = 4/30, 5%) while the others died on cECMO (n = 50/80, 62%). The most frequent complications were the need for renal replacement therapy (76%), hemothorax or tamponade (48%), need for surgical revision (34%), mediastinitis (28%), and stroke (28%). The in-hospital and one-year survival rates were 31% and 27% respectively. Myocardial infarction as the cause of the rCS was the only variable independently associated with in-hospital mortality (HR 2.5 [1.3–4.9], p = 0.009). Conclusions: The switch from a failing pECMO support to a cECMO as a bridge-to-decision is a possible strategy for a very selected population of young patients with a realistic chance of heart function recovery or heart transplantation. In this setting, cECMO allows patients triage preventing from wasting expensive and limited resources. [ABSTRACT FROM AUTHOR]

Background: Complications of pancreatitis can lead to admission to the intensive care unit (ICU) with invasive mechanical ventilation. Reducing the duration of mechanical ventilation is challenging for critical care practitioners. Respiratory muscle weakness hinders the weaning process, thereby increasing the duration of mechanical ventilation and hindering pulmonary rehabilitation. Methods: We evaluated the effect of transcutaneous neuromodulation on predictors of extubation failure. The patient was a 51-year-old male with a history of type 2 diabetes, obesity (body mass index=35), and regular alcohol consumption of 40 g/day. The patient was admitted to ICU with a diagnosis of severe acute pancreatitis and multi-organ failure. Maximum inspiratory pressure (MIP), airway occlusion pressure at 100 ms (P0.1), rapid shallow breathing index (RSBI), and diaphragmatic thickening fraction (DTf) were measured. Results: The results demonstrated an improvement in all the parameters. Show an increase in MIP from -18 cmH2O to -37 cmH2O and a reduction in P0.1 from -5.7 cmH2O to -3.1 cmH2O. RSBI decreased from 107 to 72, and DTf increased from 20% to 35%. The patient was extubated successfully and discharged to the ward after a 28-day ICU stay. Conclusions: The application of transcutaneous neuromodulation led to an improvement in the predictive parameters of extubation failure in patients with severe acute pancreatitis, which was ultimately confirmed by ventilatory support not being required after extubation. Transcutaneous neuromodulation application helps improve respiratory parameters and systemic improvement of the patient until he is released from ICU. Transcutaneous neuromodulation should be used in combination with other physiotherapy techniques and should be included in a comprehensive rehabilitation protocol rather than as an isolated therapy. [ABSTRACT FROM AUTHOR]

Background: Kratom, also known as Mitragyna speciosa, is a plant that originates in Southeast Asia and possesses unique pharmacological characteristics. It is commonly consumed in the form of tea made by boiling the leaves or using the leaves to create the powder. According to its pain-relieving effects, the prevalence of kratom use around the world has increased, which has various implications for healthcare providers. Mitragynine is a well-known active compound in kratom. Objective: This review aims to provide a comprehensive perspective on the cardiovascular effects of mitragynine and its potential cardiotoxicity through the literature. Method: Authors searched PubMed, Scopus, and Google Scholar databases using appropriate search strategies for each database. After the screening, all relevant studies were included. Results: Although kratom may have the potential for therapeutic benefits, it has been associated with multi-organ damage and cardiac toxicity in some cases. According to the available data, tachycardia and hypertension are the most common adverse effects. Other possible cardiovascular effects include atherosclerosis, ventricular arrhythmia, cardiomyopathy, dose-dependent prolonged QTc interval, myocarditis, cardiomegaly, and cardiopulmonary arrest. Conclusion: While prior research has indicated the possible negative effects of mitragynine overdose on the cardiovascular system, there are no definitive conclusions, and additional investigations are needed. [ABSTRACT FROM AUTHOR]

Although toxicity from excessive exogenous vitamin D supplementation is rare, a range of symptoms can occur, most of which result from hypercalcemia. We report a novel case of posterior reversible encephalopathy syndrome (PRES) in a young child who required intensive care after presenting with hypercalcemia, hypertensive emergency, acute kidney injury, and hypercarbic respiratory failure, which ultimately were attributed to vitamin D toxicity (VDT). We report a young child who developed PRES in association with VDT. Our report informs pediatric outpatient, hospitalist, and intensivist providers about rare but lifethreatening complications from hypervitaminosis D, adds VDT to the differential diagnosis for children with similar presentations, and highlights the importance of vitamin supplementation safety guidance for families. [ABSTRACT FROM AUTHOR]

Objectives Systemic lupus erythematosus (SLE) is a complex autoimmune disease with varying symptoms and multi-organ damage. Relapse-remission cycles often persist for many patients for years with the current treatment. Improved understanding of molecular changes caused by SLE flare and intensive treatment may result in more targeted therapies. Methods RNA sequencing was performed on peripheral blood mononuclear cells (PBMCs) from 65 SLE patients in flare, collected both before (SLE1) and after (SLE2) in-hospital treatment, along with 15 healthy controls (HC). Differentially expressed genes (DEGs) were identified among the three groups. Enriched functions and key molecular signatures of the DEGs were analysed and scored to elucidate the transcriptomic changes during treatment. Results Few upregulated genes in SLE1 vs HC were affected by treatment (SLE2 vs SLE1), mostly functional in interferon signalling (IFN), plasmablasts and neutrophils. IFN and plasmablast signatures were repressed, but the neutrophil signature remained unchanged or enhanced by treatment. The IFN and neutrophil scores together stratified the SLE samples. IFN scores correlated well with leukopenia, while neutrophil scores reflected relative cell compositions but not cell counts. Conclusions In-hospital treatment significantly relieved SLE symptoms with expression changes of a small subset of genes. Notably, IFN signature changes matched SLE flare and improvement, while enhanced neutrophil signature upon treatment suggested the involvement of low-density granulocytes (LDG) in disease development. [ABSTRACT FROM AUTHOR]

The article focuses on a teenage male who was admitted to the pediatric intensive care unit (PICU) after a mixed overdose, presenting with severe symptoms including low Glasgow Coma Scale (GCS), fixed dilated pupils, and metabolic and respiratory acidosis. Topics include the patient's clinical presentation and initial lab findings, the management of his overdose with intubation and supportive care, and the subsequent monitoring of his vital signs and neurological status in the PICU.

We describe a case of autochthonous human Babesia divergens infection in an immunocompetent woman in England. The patient had fever, hemolysis, multiorgan failure, and 18% parasitemia. We confirmed B. divergens by 18S rDNA PCR and sequencing. Clinicians should consider babesiosis as a differential diagnosis in patients with unexplained hemolysis. [ABSTRACT FROM AUTHOR]

West Nile virus (WNV) is the most common cause of human arboviral disease in the contiguous United States, where only lineage 1 (L1) WNV had been found. In 2023, an immunocompetent patient was hospitalized in Nebraska with West Nile neuroinvasive disease and multisystem organ failure. Testing at the Centers for Disease Control and Prevention indicated an unusually high viral load and acute antibody response. Upon sequencing of serum and cerebrospinal fluid, we detected lineage 3 (L3) and L1 WNV genomes. L3 WNV had previously only been found in Central Europe in mosquitoes. The identification of L3 WNV in the United States and the observed clinical and laboratory features raise questions about the potential effect of L3 WNV on the transmission dynamics and pathogenicity of WNV infections. Determining the distribution and prevalence of L3 WNV in the United States and any public health and clinical implications is critical. [ABSTRACT FROM AUTHOR]

A 68-year-old male presented with a one-month history of progressive proptosis and vision loss in the left eye. Examination of the left eye showed visual acuity of NLP, marked relative proptosis of 10 mm, and complete external ophthalmoplegia. CT orbits showed an extensive left orbital lesion with proptosis. Urgent orbital biopsy was undertaken. Intraoperatively, the patient developed new atrial flutter and fever. Bloodwork revealed metabolic derangements suggestive of tumor lysis syndrome. Systemic evaluation revealed a large tumor burden involving the retroperitoneal space. Histopathology of the orbital specimen showed non-germinal center diffuse large B-cell lymphoma. The patient passed away 3 days postoperatively due to rapidly progressive multisystem organ failure. Our case demonstrates an unusually aggressive presentation of DLBCL in which orbital mass was the first presentation of spontaneous tumor lysis syndrome owing to large systemic tumor burden. [ABSTRACT FROM AUTHOR]

Multi-organ transplantation involves the transplant of two or more organs from a single donor into a single recipient; in most cases, one of these organs is a kidney. Multi-organ transplantation is uncommon in pediatric transplantation but can be life-saving or significantly life-improving for children with rare diseases, including primary heart, liver, pancreas, or intestinal failure with secondary kidney failure, metabolic disorders, and genetic conditions causing multi-organ dysfunction. This manuscript reviews the current state of pediatric multi-organ transplantation that includes a kidney, with a focus on indications, evaluation, and key differences in management compared to kidney-alone transplantation. Guidelines and consensus statements for pediatric multi-organ transplantation are nonexistent; this review condenses reported statistics and peer-reviewed expert opinion while highlighting areas in need of further research. [ABSTRACT FROM AUTHOR]

Paediatric acute liver failure (PALF) is often characterised by its rapidity of onset and potential for significant morbidity and even mortality. Patients often develop multiorgan dysfunction/failure, including severe acute kidney injury (AKI). Whilst the management of PALF focuses on complications of hepatic dysfunction, the associated kidney impairment can significantly affect patient outcomes. Severe AKI requiring continuous kidney replacement therapy (CKRT) is a common complication of both PALF and liver transplantation. In both scenarios, the need for CKRT is a poor prognostic indicator. In adults, AKI has been shown to complicate ALF in 25–50% of cases. In PALF, the incidence of AKI is often higher compared to other critically ill paediatric ICU populations, with reports of up to 40% in some observational studies. Furthermore, those presenting with AKI regularly have a more severe grade of PALF at presentation. Observational studies in the paediatric population corroborate this, though data are not as robust—mainly reflecting single-centre cohorts. Perioperative benefits of CKRT include helping to clear water-soluble toxins such as ammonia, balancing electrolytes, preventing fluid overload, and managing raised intracranial pressure. As liver transplantation often takes 6–10 h, it is proposed that these benefits could be extended to the intraoperative period, avoiding any hiatus. Intraoperative CKRT (IoCKRT) has been shown to be practicable, safe and may help sicker recipients tolerate the operation with outcomes analogous with less ill patients not requiring IoCKRT. Here, we provide a comprehensive guide describing the rationale, practicalities, and current evidence base surrounding IoCKRT during transplantation in the paediatric population. [ABSTRACT FROM AUTHOR]

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Plasma plays a crucial role in maintaining health through regulating coagulation and inflammation. Both are essential to respond to homeostatic threats such as traumatic injury or microbial infection; however, left unchecked, they can themselves cause damage. A well‐functioning plasma regulatory milieu controls the location, intensity, and duration of the response to injury or infection. In contrast, plasma failure can be conceptualized as a state in which these mechanisms are overwhelmed and unable to constrain coagulation and inflammation appropriately. This dysregulated state causes widespread tissue damage and multiple organ dysfunction syndrome. Unlike plasma derangements caused by individual factors, plasma failure is characterized by a heterogeneous set of plasma component deficiencies and excesses. Targeted therapies such as factor replacement or recombinant antibodies are thus inadequate to restore plasma function. Therapeutic plasma exchange offers the unique ability to remove harmful factors and replete exhausted components, thereby reestablishing appropriate regulation of coagulation and inflammation. [ABSTRACT FROM AUTHOR]