Baiqiang Li

Hypertriglyceridemia is a risk factor for acute kidney injury in the early phase of acute pancreatitis.

Objective The aim of this study was to investigate the risk factors for acute kidney injury (AKI) in patients with acute pancreatitis (AP). Methods Patients with AP were retrospectively divided into AKI group and non-AKI group. To investigate the risk factors for AKI, logistic regression analysis was performed with demography, etiologies, and comorbidities. Mortalities of patients with different body mass indexes were compared. Results There were 43 patients with AKI and 202 patients without AKI. The risk factor for AKI in AP was hypertriglyceridemia (odds ratio, 2.964; 95% confidence interval, 1.485–5.915; P = 0.007). Forty-two patients developed AKI within the first 48 hours. The mortalities of normal weight, overweight, and obese groups in patients with AKI were 16.7%, 17.4%, and 62.5%, respectively. All the 4 patients who died in the non-AKI group were of normal weight. Conclusions Hypertriglyceridemia is an independent risk factor for AKI in the early phase of AP. Obesity does not increase mortality of patients without AKI. We hypothesize that the role of pancreatic enzymes on triglyceride accumulated in renal may be an explanation for AKI in the early phase of AP.

Development of a novel model of hypertriglyceridemic acute pancreatitis in mice

The morbidity rate of hypertriglyceridemic acute pancreatitis (HTG-AP) increased rapidly over the last decade. However an appropriate animal model was lacking to recapitulate this complicated human disease. We established a novel mice model of HTG-AP by poloxamer 407 (P-407) combined with caerulein (Cae). In our study, serum triglyceride levels of P-407 induced mice were elevated in a dose-dependent manner, and the pancreatic and pulmonary injuries were much severer in HTG mice than normal mice when injected with conventional dose Cae (50 ug/kg), what’s more, the severity of AP was positively correlative with duration and extent of HTG. In addition, we found that a low dose Cae (5 ug/kg) could induce pancreatic injury in HTG mice while there was no obvious pathological injury in normal mice. Finally, we observed that HTG leaded to the increased infiltrations of macrophages and neutrophils in mice pancreatic tissues. In conclusion, we have developed a novel animal model of HTG-AP that can mimic physiological, histological, clinical features of human HTG-AP and it could promote the development of therapeutic strategies and advance the mechanism research on HTG-AP.

The long-term quality of life in patients with persistent inflammation-immunosuppression and catabolism syndrome after severe acute pancreatitis: A retrospective cohort study

Purpose: To explore clinical characteristics and long‐term quality of life (QOL) in severe acute pancreatitis (SAP) patients with persistent inflammation‐immunosuppression and catabolism syndrome (PICS). Materials and methods: SAP patients admitted to ICU were eligible for the retrospective cohort study if they needed prolonged intensive care (> 14 days). Post‐ICU QOL was assessed by a questionnaire, including 36‐item Short Form Health Survey (SF‐36) and record of re‐work in a long‐term follow‐up. Results: 214 SAP patients were enrolled, in which 149 (69.6%) patients met the criteria of PICS. PICS patients had more complications and ICU days compared to non‐PICS patients (P < 0.001), and their post‐ICU mortality was higher (P = 0.046). When adjusted for confounders, PICS was independently associated with higher post‐ICU mortality (hazard ratio 4.5; 95% CI, 1.2 to 16.3; P = 0.024). The 36‐item Short Form Health Survey (SF‐36) score was lower for PICS group in six subscales (P < 0.001). Only 28.8% patients in the PICS group returned to work compared to 60% patients in the non‐PICS group (P = 0.001) Conclusions: SAP patients with prolonged ICU stay had a high morbidity of PICS, which was a risk factor for the post‐ICU mortality and poor long‐term QOL. HighlightsSAP patients with prolonged ICU stay had a high morbidity of PICS.PICS was correlated with poor clinical outcomes.PICS was a risk factor for the post‐ICU mortality and poor long‐term quality of life.

The prognostic value of the strong ion gap in acute pancreatitis

PURPOSE In this study, we aimed to evaluate the predictive value of Stewart-derived parameters for the development of severe type of acute pancreatitis (AP) and for AP-related mortality. METHODS We studied 186 patients admitted to the hospital with AP. We performed blood gas and biochemical analysis for each patient on admission. We calculated multiple metrics according to the Stewarts acid-base theory and assessed their accuracy as predictors of AP severity and mortality. RESULTS Of the 186 patients presenting with AP, 85 (45.7%) developed severe AP and 33 (17.7%) died during hospitalization. Patients with severe AP had significantly higher median strong ion gap (SIG) than did patients with mild or moderate AP (7.88 vs 2.11 mEq/L, P< .001). In multivariate logistic regression analysis, SIG had an odds ratio (OR) of 1.56 (P< .001). In addition, SIG had good predictive power for mortality (OR, 1.26; P= .014) as well as acute kidney injury (OR, 1.34; P< .001). CONCLUSIONS In a cohort of patients with AP, SIG was a strong independent predictor of severity and mortality. Besides, SIG might also be an early marker for acute kidney injury in AP patients. Additional research is needed to identify the nature of the unmeasured anions responsible for such findings.

Successful cardiopulmonary cerebral resuscitation in patient with severe acute pancreatitis.

Severe acute pancreatitis (SAP) is a critical illness in clinical practice, which is characterized by intensive inflammatory response in the early phase and infected pancreatic necrosis in the later phase. Despite the knowledge of SAP and critical care support technology got significant progress in recent years, SAP still carries approximately 30%mortality rate. Some SAP patients also have many other kinds of underlying disease such as hyperlipidemia, hypertension, coronary atherosclerotic heart disease, and heart rhythm abnormalities, which are related to cardiopulmonary arrest to some extent. Thus, the incidence of unpredictive cardiopulmonary arrest is high. Recently, a SAP patient in our intensive care unit had sudden cardiac arrest. After 52 minutes of cardiopulmonary resuscitation, she had return of spontaneous circulation and regained consciousness within 2 hours. To our knowledge, there is no successful report after such long resuscitation in SAP patients. She was receiving continuous renal replacement therapy (CRRT) and continuous veno-venous hemofiltration, in the event of cardiopulmonary arrest. No study reported what kind of role CRRT can play when cardiac arrest occurs. Usually, we would stop existing CRRT when cardiac arrest occurred.We would not start CRRT for the complexity of operation and additional loss of blood. This time, we used CRRT to regulate electrolyte and acid-base imbalance and implement hypothermia brain protection, which played an important role in the patient that we report here.We strongly recommended a prolonged cardiopulmonary cerebral resuscitation in some not quite old SAP patients and continue to use existing CRRT but not remove it.

INT-777, a bile acid receptor agonist, extenuates pancreatic acinar cells necrosis in a mouse model of acute pancreatitis

Bile acids receptor TGR5 and its agonist INT-777, which has been found to be involved in the NLRP3 inflammasome pathway, play an important role in inflammatory diseases. However, the role of INT-777 in acute pancreatitis (AP) has not been reported. In this present study, we found that TGR5 was expressed in pancreatic tissue and increased after AP onset induced by caerulein and further evaluated the impact of INT-777 on the severity of AP. The results showed that INT-777 could reduce the severity of AP in mice, which was manifested as decreased pancreatic tissue damage as well as the decrease of serum enzymes (amylase and lipase), pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) and the expression of necrosis related proteins (RIP3 and p-MLKL). Furthermore, we found that INT-777 reduced the reactive oxygen species (ROS) production in pancreatic acinar cells and inhibited the activation of NLRP3 inflammasome pathway. In conclusion, our data showed that INT-777 could protect pancreatic acinar cell against necrosis and reduce the severity of AP, which may be mediated by inhibiting ROS/NLRP3 inflammasome pathway.

Intercostal artery damage and massive hemothorax after thoracocentesis by central venous catheter: A case report

Central venous catheters (CVCs) are widely used in various puncture and drainage operations in intensive care units (ICUs) in recent years. Compared to conventional operating devices, CVC was welcomed by clinicians because of the advantages of easy use, less damage to the body and convenient fixation process. We came across a patient with severe acute pancreatitis (SAP) who developed cardiac arrest due to thoracic cavity massive bleeding 24 h after thoracocentesis with CVC. Thoracotomy surgery was carried out immediately, which confirmed an intercostal artery injury. The patient was discharged from hospital without any neurological complications two months later. Here we report this case to remind all the emergency department and ICU physicians to pay more attention to the complication of thoracic cavity bleeding following thoracocentesis conducted by CVC.