Background. Major bleeding has been a common and serious complication with poor outcomes in ECMO patients. With a novel, less-invasive cannulation approach and closer coagulation monitoring regime, the incidence of major bleeding is currently not determined yet. Our study aims to examine the incidence of major bleeding, its determinants, and association with mortality in peripheral-ECMO patients. Method. We conducted a single-center retrospective study on adult patients undergoing peripheral-ECMO between January 2019 and January 2020 at a tertiary referral hospital. Determinants of major bleeding were defined by logistic regression analysis. Risk factors of in-hospital mortality were determined by Cox proportional hazard regression analysis. Results. Major bleeding was reported in 33/105 patients (31.4%) and was associated with higher in-hospital mortality [adjusted hazard ratio (aHR) 3.56, 95% confidence interval (CI) 1.63–7.80, ). There were no significant difference in age, sex, ECMO indications, ECMO modality, pre-ECMO APACHE-II and SOFA scores between two groups with and without major bleeding. Only APTT >72 seconds [adjusted odds ratio (aOR) 7.10, 95% CI 2.60–19.50, ], fibrinogen <2 g/L [aOR = 7.10, 95% CI 2.60–19.50, ], and ACT >220 seconds [aOR = 3.9, 95% CI 1.20–11.80, ] on days with major bleeding were independent predictors. Conclusions. In summary, major bleeding still had a fairly high incidence and poor outcome in peripheral-ECMO patients. APTT > 72 seconds, fibrinogen < 2 g/L were the strongest predicting factors for major bleeding events.

Background. During ECMO, anticoagulants, in particular, unfractionated heparin (UFH), are commonly used and monitored by laboratory tests, including ACT, APTT, and anti-Xa level. Method. A single-center retrospective observational study was conducted on adult patients undergoing ECMO between January 2019 and January 2020 at a tertiary hospital. The correlations between ACT, APTT, anti-Xa, antithrombin, and UFH dose were assessed. Results. 129 sets of measurements from 37 patients were obtained including ACT, APTT, anti-Xa, antithrombin, and UFH dose measured simultaneously. 102 out of 129 sets of values were interpreted as antithrombin deficiencies. The correlation coefficient between APTT and anti-Xa; ACT and anti-Xa are 0.72 and 0.33, respectively, $p<0.001$ . The patients with normal antithrombin levels exhibited a significant correlation between APTT and anti-Xa (r = 0.80, $p<0.001$ ). ACT, on the other hand, was poorly correlated with UFH dose, whether there is AT deficiency or not. Anti-Xa and APTT are only moderately correlated with UFH dose in the group without antithrombin deficiency, with correlation coefficients of 0.62 and 0.57, respectively, $p<0.05$ . Conclusion. APTT value is strongly correlated with anti-Xa value, particularly in patients with normal antithrombin levels. However, the ACT value was poorly correlated with anti-Xa and not with the UFH dose. In groups without antithrombin deficiency, APTT and anti-Xa values only moderately correlated with UFH dose.

Chúng tôi mô tả một trường hợp nhiễm Salmonella có biểu hiện nặng và hiếm gặp ở bệnh nhân nam 26 tuổi, với các triệu chứng của nhiễm trùng tiêu hóa, tổn thương thận cấp và sốc nhiễm khuẩn. Triệu chứng lâm sàng và hình ảnh học cho thấy bệnh nhân có tình trạng tắc ruột non. Bệnh nhân được ưu tiên hồi sức nội khoa, trì hoãn phẫu thuật, theo dõi sát tình trạng bụng. Sau hồi sức tích cực 12 giờ với kháng sinh, bù dịch, lọc máu liên tục tình trạng bệnh nhân cải thiện nhanh. Cấy máu và cấy phân chỉ ra tác nhân là vi khuẩn Salmonella. Bệnh nhân được điều trị nội khoa thành công và xuất viện sau 14 ngày.

Hyperammonemic encephalopathy is a rare but serious condition often linked to hepatic dysfunction or metabolic disorders. Thyroid storm is an endocrine emergency that can cause profound metabolic disturbances, though its relationship with hyperammonemia remains unclear. We report a unique case of a 33‐year‐old previously healthy male who developed progressive fatigue, nausea, and vomiting, followed by acute neurological deterioration. Initial evaluation revealed hyperammonemia (284 μ mol/L) and thyrotoxicosis (fT4: 27 pmol/L and TSH: 0.007 μ IU/mL), with no hepatic dysfunction. His neurological status declined from GCS 12 to GCS 7 within hours. Brain MRI and cerebrospinal fluid analysis were unremarkable. The patient was diagnosed with coma in the setting of hyperammonemic encephalopathy and thyroid storm. Management included propylthiouracil, Lugol’s iodine, propranolol, hydrocortisone, and continuous renal replacement therapy (CRRT). His ammonia levels significantly improved within 48 h, leading to rapid clinical improvement and extubation. This case highlights the importance of recognizing hyperammonemia as a potential cause of altered mental status, even in the absence of hepatic dysfunction, and raises questions about potential but unestablished links between thyroid dysfunction and ammonia metabolism.

Background: Persistent severe acute kidney injury (PS‐AKI)—recently standardized as Kidney Disease: Improving Global Outcomes (KDIGO) Stage 3 persisting ≥ 72 h, or renal replacement therapy/death after Stage 3 diagnosis—has emerged as a trajectory‐based phenotype complementing conventional KDIGO staging. Evidence in contemporary intensive care unit (ICU) cohorts remains limited. Methods: We retrospectively studied adults admitted to a tertiary ICU (January 2024–June 2025). Acute kidney injury (AKI) was staged per KDIGO 2012, with trajectories classified as Stage 1 AKI, transient AKI (Stage 2‐3 resolving within 48 h), persistent mild–moderate AKI, or PS‐AKI. The primary outcome was in‐hospital mortality; secondary outcomes included renal recovery. Predictors of PS‐AKI were explored using logistic regression and gradient boosting with SHAP attribution. Results: Among 139 ICU patients with AKI screened, 106 met criteria. Most AKI was community‐acquired (97/106, 91.5%). PS‐AKI accounted for 23% (24/106) and carried the worst outcomes, with in‐hospital mortality 54% and renal recovery 17%. Within Stage 2‐3, PS‐AKI was associated with substantially worse outcomes than non‐PS trajectories (mortality 54% vs 10.8%; adjusted HR for death 2.23, 95% CI 0.69–7.21; adjusted OR for renal recovery 0.07, 95% CI 0.01–0.24). A 72‐h landmark analysis showed similar but nonsignificant trends. Inflammatory profiles distinguished PS‐AKI, with higher neutrophil‐to‐lymphocyte ratio (NLR), C‐reactive protein (CRP), and lower platelets. The composite NLR‐to‐platelet ratio (NLR/PLT) was independently associated with PS‐AKI (adjusted OR 2.51 per doubling, 95% CI 1.52–4.12; AUC 0.86), while the systemic immune‐inflammation index (SII) showed no significant association. Conclusions: In this predominant community‐acquired ICU cohort, PS‐AKI was common and strongly associated with poor in‐hospital outcomes. The co‐occurrence of inflammation and thrombocytopenia, summarized by NLR/PLT, may represent a simple exploratory signal for early‐risk appraisal. These findings support further research into trajectory‐based AKI phenotypes and the potential utility of inflammation–hematologic markers in predicting persistence.

Melioidosis is endemic in Southeast Asia and northern Australia and can resemble various conditions. Soft tissue involvement is usually limited to localise