Rationale:Hydrofluoric acid (HF) is a highly corrosive agent and can cause corrosive burns. HF can penetrate deeply into tissues through intact skin and the lipid barrier, leading to painful liquefactive necrosis, and inducing hypocalcemia and hypomagnesemia. In this study, we hypothesize that continuous renal replacement therapy (CRRT) may be beneficial in addressing hemodynamic instability in cases of HF poisoning.Patient concerns:A 25-year-old man fell into an electroplating pool containing 10% HF and 50% nitric acid.Diagnoses:He had severe cutaneous injuries involving approximately 60% of his total body surface area including the head, face, neck, right upper arm, right hand, trunk, perineum, and both lower limbs and feet. Examination at admission showed the following electrolyte concentrations: ionic calcium 0.192 mmol/L, total calcium 0.72 mmol/L, magnesium 0.4 mmol/L, potassium 5.49 mmol/L, and sodium 136.8 mmol/L.Interventions:An initial 20 mL intravenous bolus of 10% calcium gluconate was followed by a continuous infusion at 6 g/h plus continuous intravenous drip 25% magnesium sulfate at 1.5 g/h. Continuous cardiac monitoring was performed in the intensive care unit. Extracorporeal membrane oxygenation (ECMO) was used to improve oxygenation function at 38 hours post exposure. Antibiotic therapy using imipenem/cilastin plus vancomycin was required.Outcomes:After treatment for 12 hours, electrolyte concentrations returned to normal. On day 11, the hemodynamic parameters were stable and oxygenation function had improved. On day 26, the patient was weaned off CRRT. One month later, the patient twice received skin grafting, then was discharged from the hospital without pulmonary, cardiac, or neurological complications 3 months later.Lessons:The present case study demonstrates that CRRT may be an effective and potentially lifesaving therapy after severe exposure to HF. Prolonged hemodialysis is recommended to remove delayed release fluoride ions to avoid delayed systemic injury. When conventional therapy can not improve oxygenation and/or carbon dioxide retention, ECMO should be performed as soon as possible.

Objective:We investigated the roles and mechanisms of IRF2 in sepsis-related acute kidney injury (S-AKI) in a lipopolysaccharide (LPS)-induced HK-2 cell line and caecal ligation and puncture (CLP)-induced IRF2 −/− mouse model. Methods: Quantitative real-time polymerase chain reaction assay was used to detect IRF2 in the serum of S-AKI patients and LPS-induced HK-2 cells. Cell proliferation, death, and apoptosis were analysed by CCK-8, lactate dehydrogenase release, and flow cytometry assays, respectively. The levels of interleukin (IL)-1β, IL-18, IL-6, tumour necrosis factor (TNF)-α, non-canonical inflammasomes, including caspase-4 and gasdermin-D (GSDMD), and canonical inflammasomes, such as caspase-1, NLR family pyrin domain containing 3 (NLRP3), and apoptosis-associated speck-like protein (ASC) in S-AKI cells or animal models were analysed by enzyme-linked immunosorbent assay or Western blotting. Results: IRF2 was upregulated in the serum of S-AKI patients and LPS-induced HK-2 cells. IRF2 downregulation promoted cell proliferation and inhibited cell death and apoptosis, respectively. IRF2 inhibition reduced the levels of IL-1β, IL-18, IL-6, and TNF-α in S-AKI cells and animal models. IRF2 knockdown inhibited LPS-treated HK-2 cell pyroptosis by decreasing the expression of caspase-4 and GSDMD, instead of affecting caspase-1, NLRP3, and ASC. An elevated survival rate and alleviated pathological features and scores were observed in the CLP-induced IRF2 −/− animal models. IRF2 deficiency also suppressed inflammation and pyroptosis by inhibiting non-canonical inflammasomes as indicated by the decreased expression of caspase-11 and GSDMD. Conclusion: Our findings suggest that IRF2 downregulation protects against S-AKI in vitro and in vivo.

Objectives To evaluate the value of chemotactic function of neutrophils in patients with severe infections. Methods A computer vision‐based cellular chemotaxis analysis platform was established for the dynamic assessment of neutrophil chemotaxis. Fifty‐three patients in the intensive care unit were eligible for the study. In parallel, 142 healthy volunteers were recruited to detect and establish the normal values for chemotactic function. Four chemotactic function indicators were determined–chemotaxis distance (CD), chemotaxis cell ratio (CCR), chemotaxis index (CI) and maximum speed of chemotaxis (Vmax). The chemotaxis function scores (CFS) were calculated for further correlation analysis with clinical data. Results The normal ranges of indicators were established as CD ≥ 1755.85 µm, CCR ≥ 3.34%, CI ≥ 39.63, Vmax ≥ 14.63 µm min−1 and CFS ≥ 15. We found that the chemotactic function of neutrophils in patients suffering from infections was significantly impaired. The mean values of CD, CCR, CI, Vmax and CFS were 1452.8 µm (P < 0.0001), 3.1% (P < 0.0001), 34.5 (P < 0.0001), 12.2 µm min−1 (P < 0.0001) and 9 (P < 0.0001), respectively. CD and CFS were significantly negatively correlated with the APACHE II score (rCD = −0.55, rCFS = −0.39), SOFA score (rCD = −0.68, rCFS = −0.56), procalcitonin concentration (rCD = −0.60, rCFS = −0.5) and the expression of P2RX1 (rCD = −0.76, rCFS = −0.56), respectively. Conclusions CD, CCR, CI and Vmax can well reflect the neutrophil chemotactic function in patients with severe infections. CFS systematically indicated neutrophil function and has promising clinical application prospects.

Objective: The aims of this study were to investigate and compare the clinical features and prognosis of chronic critical illness (CCI)/persistent inflammation immunosuppression and catabolism (PICS). Methods: This is a prospective observational clinical study. During this study period, we collect intensive care unit patients' data from Suzhou Municipal Hospital and Suzhou Ninth People's Hospital. All patients older than 18 years were included, and according to the corresponding exclusion and diagnostic criteria, they were divided into four groups: PICS group, CCI group, CCI and PICS group (CCI + PICS), and neither CCI nor PICS group (NCCI + NPICS) and collected and recorded age, sex, hospital time, hospital diagnosis, Acute Physiology and Chronic Health Evaluation II score, Sequential Organ Failure Assessment score, C-reactive protein, absolute value lymphocyte count, serum albumin, white blood cell count, absolute value neutrophil count, secondary infection, and 28-day case fatality rate separately. Results: A total of 687 patients were admitted to the intensive care unit during the study period. The hospitalization time less than 14 days were excluded, and 168 patients were eventually included. There are 17 in the PICS group, 71 in the CCI group, 50 in the CCI + PICS group, and 30 in the NCCI + NPICS group. Baseline characteristics showed statistically significant differences in Sequential Organ Failure Assessment, length of hospital stay, and 28-day mortality among four groups. Baseline main indicator and multiple comparisons showed that the CCI + PICS group had longer hospital stay, worse prognosis, and more adverse outcomes. Multivariate analysis showed that final age, C-reactive protein on days 14 and 21, and serum albumin on days 1 and 21 had an impact on the prognosis (P < 0.05). Conclusion: The clinical prognosis of the four groups decreased in order of NCCI + NPICS, CCI, PICS, and CCI + PICS. Our finding of clinically isolated PICS may indicate that PICS acts as an inducement or independent factor to worsen the prognosis of CCI.

Background Dexmedetomidine (DEX) had organ protection effects and could decrease mortality in animal models, but its association with mortality and length of stay (LOS) in ICU and hospital in critically ill patients was conflicting. Whether acute kidney injury (AKI) subgroup of critically ill patients could benefit from DEX was unknown. The present study aimed to evaluate the effects of DEX on clinical outcomes of critically ill patients with AKI. Methods Data were extracted from the Medical Information Mart for Intensive Care Ⅲ database (MIMIC Ⅲ). Propensity score matching (PSM) analysis (1:3), cox proportional hazards model, linear regression and logistic regression model were used to assess the effect of DEX on clinical outcomes. Results After PSM, 324 pairs of patients were matched between the patients with DEX administration and those without. DEX administration was associated with decreased in-hospital mortality [hazard ratio (HR) 0.287; 95% CI 0.151–0.542; P < 0.001] and 90-day mortality [HR 0.344; 95% CI 0.221–0.534; P < 0.001], and it was also associated with reduced length of stay (LOS) in ICU [4.54(3.13,7.72) versus 5.24(3.15,10.91), P < 0.001] and LOS in hospital [11.63(8.02,16.79) versus 12.09(7.83,20.44), P = 0.002]. Subgroup analysis showed the above associations existed only in mild and moderate AKI subgroups, but not in severe AKI subgroup. Nevertheless, DEX administration was not associated with the recovery of renal function [HR 1.199; 95% CI 0.851–1.688; P = 0.300]. Conclusions DEX administration improved outcomes in critically ill patients with mild and moderate AKI and could be a good choice of sedation.