Acute High-Output Heart Failure with Pulmonary Hypertension and Severe Liver Injury Caused by Amlodipine Poisoning: A Case Report.

Acute high-output heart failure (HOHF) with pulmonary hypertension and liver injury caused by amlodipine poisoning is very rare. We report a 52-year-old woman who suffered from severe shock after an overdose of amlodipine. Hemodynamic monitoring showed that while her left ventricular systolic function and cardiac output were elevated, her systemic vascular resistance decreased significantly. At the same time, the size of her right heart, her central venous pressure, and the oxygen saturation of her central venous circulation all increased abnormally. The patient's circulatory function and right ventricular dysfunction gradually improved after large doses of vasopressors and detoxification measures. However, her bilirubin and transaminase levels increased significantly on hospital day 6, with a CT scan showing patchy, low-density areas in her liver along with ascites. After liver protective treatment and plasma exchange, the patient's liver function gradually recovered. A CT scan 4 months later showed all her liver abnormalities, including ascites, had resolved. The common etiologies of HOHF were excluded in this case, and significantly reduced systemic vascular resistance caused by amlodipine overdose was thought to be the primary pathophysiological basis of HOHF. The significant increase in venous return and pulmonary blood flow is considered to be the main mechanism of right ventricular dysfunction and pulmonary hypertension. Hypoxic hepatitis caused by a combination of hepatic congestion and distributive shock may be the most important factors causing liver injury in this patient. Whether amlodipine has other mechanisms leading to HOHF and pulmonary hypertension needs to be further studied. Considering the significant increase of right heart preload, aggressive fluid resuscitation should be done very cautiously in patients with HOHF and shock secondary to amlodipine overdose.

Management of regional citrate anticoagulation for continuous renal replacement therapy: guideline recommendations from Chinese emergency medical doctor consensus.

Continuous renal replacement therapy (CRRT) is widely used for treating critically-ill patients in the emergency department in China. Anticoagulant therapy is needed to prevent clotting in the extracorporeal circulation during CRRT. Regional citrate anticoagulation (RCA) has been shown to potentially be safer and more effective and is now recommended as the preferred anticoagulant method for CRRT. However, there is still a lack of unified standards for RCA management in the world, and there are many problems in using this method in clinical practice. The Emergency Medical Doctor Branch of the Chinese Medical Doctor Association (CMDA) organized a panel of domestic emergency medicine experts and international experts of CRRT to discuss RCA-related issues, including the advantages and disadvantages of RCA in CRRT anticoagulation, the principle of RCA, parameter settings for RCA, monitoring of RCA (mainly metabolic acid-base disorders), and special issues during RCA. Based on the latest available research evidence as well as the paneled experts' clinical experience, considering the generalizability, suitability, and potential resource utilization, while also balancing clinical advantages and disadvantages, a total of 16 guideline recommendations were formed from the experts' consensus.

High-flow nasal cannula oxygen therapy versus noninvasive ventilation for patients with blunt chest trauma: protocol for a randomized controlled trial.

BACKGROUND: High-flow nasal cannula oxygen therapy (HFNC) is recommended by some scholars as an optimized respiratory support method for blunt chest trauma (BCT) patients. The basis of this recommendation is limited, however, and the efficacy of HFNC or noninvasive ventilation (NIV) in BCT patients has not yet been rigorously explored. This study aims to determine if HFNC is non-inferior to NIV in reducing treatment failure in moderate to severe BCT patients with acute respiratory failure. METHODS: This will be a prospective, open-label, multicenter, non-inferiority, randomized controlled trial. Moderate to severe BCT patients with acute respiratory failure (100mmHg < PaO2/FiO2 ≦ 200mmHg) who do not need immediate intubation will be randomized to HFNC or NIV within 48 h after trauma. The primary outcome is treatment failure, defined as invasive ventilation or a switch in respiratory support modality (from HFNC to NIV or vice-versa). Secondary outcomes include arterial blood gas analysis and vital signs at 2 and 12 h after initiating HFNC or NIV treatment, as well as patients' comfort scores, dyspnea scores, daily number of nursing airway care interventions, incidence of pneumonia or pneumothorax, facial skin breakdown, duration of NIV or HFNC, 28-day mortality, and total ICU and hospital lengths of stay. Based on an α error of 5% and a ß error of 80%, with a non-inferiority limit of 9%, a sample size of 562 will be required to accomplish the trial goal, considering potential patient dropouts and nonparametric analysis. DISCUSSION: We hypothesize that HFNC will be non-inferior to NIV in reducing treatment failure in moderate to severe BCT with acute respiratory failure. The results should be useful for judging whether HFNC could be an effective alternative to NIV to treat moderate to severe BCT patients, especially for those who do not tolerate or have contraindications for NIV. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR1800017313 . Registered on July 24, 2018.

A Nomogram Model for Predicting Type-2 Myocardial Infarction Induced by Acute Upper Gastrointestinal Bleeding.

OBJECTIVE: To examine the independent risk factors of type-2 myocardial infarction (T2MI) elicited by acute upper gastrointestinal bleeding (AUGIB), and to establish a nomogram model for the prediction of AUGIB-induced T2MI. METHODS: A nomogram model was established on the basis of a retrospective study that involved 533 patients who suffered from AUGIB in the Department of Critical Care Medicine (CCM) or Emergency Intensive Care Unit (EICU) of Renmin Hospital of Wuhan University, Wuhan, China, from January 2017 to December 2020. The predictive accuracy and discriminative power of the nomogram were initially evaluated by internal validation, which involved drawing the receiver operating characteristic (ROC) curve, calculating the area under the curve (AUC), plotting the calibration curve derived from 1000 resampled bootstrap data sets, and computing the root mean square error (RMSE). The predictive ability of the nomogram was further validated through the prospective and multicenter study conducted by the investigators, which enrolled 240 AUGIB patients [including 88 cases from Renmin Hospital of Wuhan University, 73 cases from Qilu Hospital of Shandong University (Qingdao), and 79 cases from Northern Jiangsu People's Hospital)], who were admitted to the Department of CCM or EICU, from February 2021 to July 2021. RESULTS: Among the 533 patients in the training cohort, 78 (14.6%) patients were assigned to the T2MI group and 455 (85.4%) patients were assigned to the non-T2MI group. The multivariate analysis revealed that age >65, hemorrhagic shock, cerebral stroke, heart failure, chronic kidney disease, increased blood urea nitrogen, decreased hematocrit, and elevated D-Dimer were independent risk factors for AUGIB-induced T2MI. All these factors were incorporated into the nomogram model. The AUC for the nomogram for predicting T2MI was 0.829 (95% CI, 0.783-0.875) in the internal validation cohort and 0.848 (95% CI, 0.794-0.902) in the external validation cohort. The calibration curve for the risk of T2MI exhibited good consistency between the prediction by the nomogram and the actual clinical observation in both the internal validation (RMSE=0.016) and external validation (RMSE=0.020). CONCLUSION: The nomogram was proven to be a useful tool for the risk stratification of T2MI in AUGIB patients, and is helpful for the early identification of AUGIB patients who are prone to T2MI for early intervention, especially in emergency departments and intensive care units.

Xuebijing Injection Ameliorates H2S-Induced Acute Respiratory Distress Syndrome by Promoting Claudin-5 Expression.

OBJECTIVE: To investigate the protective effects and underlying mechanisms of Xuebijing Injection (XBJ) on the lung endothelial barrier in hydrogen sulfide (H2S)-induced acute respiratory distress syndrome (ARDS). METHODS: Sprague-Dawley rats were exposed to H2S (300 ppm) to establish ARDS model, while human pulmonary microvascular endothelial cells (HPMECs) were incubated with NaHS (a H2S donor, 500 µmol/L) to establish cell model. H2S and XBJ were concurrently administered to the rat and cell models. Lung hematoxylin and eosin staining, immunohistochemistry, transmission electron microscopy and wet/dry ratio measurement were used to confirm ARDS induced by H2S in vivo. The expression levels of claudin-5, phosphorylated protein kinase B (p-AKT)/t-AKT and p-forkhead box transcription factor O1 (FoxO1)/t-FoxO1 in vivo and in vitro were also assessed. Paracellular permeability and transepithelial electrical resistance (TEER) were measured to evaluate endothelial barrier function in the cell model. RESULTS: The morphological investigation showed that XBJ attenuated H2S-induced ARDS in rats. XBJ significantly ameliorated both the reduction in TEER and the increased paracellular permeability observed in NaHS-treated HPMECs (P<0.05). The protective effects of XBJ were blocked by LY294002, a phosphatidylinositol 3-kinase (PI3K)/AKT/FoxO1 pathway antagonist (P<0.05). Furthermore, XBJ promoted the expression of claudin-5 and increased the levels of p-AKT and p-FoxO1 in vivo and in vitro (P<0.05). CONCLUSIONS: XBJ ameliorated H2S-induced ARDS by promoting claudin-5 expression via the PI3K/AKT/FoxO1 signaling pathway.

Pulse oximetry waveform: A non-invasive physiological predictor for the return of spontaneous circulation in cardiac arrest patients ---- A multicenter, prospective observational study.

OBJECTIVE: This study aimed to investigate the predictive value of pulse oximetry plethysmography (POP) for the return of spontaneous circulation (ROSC) in cardiac arrest (CA) patients. METHODS: This was a multicenter, observational, prospective cohort study of patients hospitalized with cardiac arrest at 14 teaching hospitals cross China from December 2013 through November 2014. The study endpoint was ROSC, defined as the restoration of a palpable pulse and an autonomous cardiac rhythm lasting for at least 20 minutes after the completion or cessation of CPR. RESULTS: 150 out-of-hospital cardiac arrest (OHCA) patients and 291 in-hospital cardiac arrest (IHCA) patients were enrolled prospectively. ROSC was achieved in 20 (13.3%) and 64 (22.0%) patients in these cohorts, respectively. In patients with complete end-tidal carbon dioxide (ETCO2) and POP data, patients with ROSC had significantly higher levels of POP area under the curve (AUCp), wave amplitude (Amp) and ETCO2 level during CPR than those without ROSC (all p < 0.05). Pairwise comparison of receiver operating characteristic (ROC) curve analysis indicated no significant difference was observed between ETCO2 and Amp (p = 0.204) or AUCp (p = 0.588) during the first two minutes of resuscitation. CONCLUSION: POP may be a novel and effective method for predicting ROSC during resuscitation, with a prognostic value similar to ETCO2 at early stage.

Oxyberberine Prevented Lipopolysaccharide-Induced Acute Lung Injury through Inhibition of Mitophagy.

Acute lung injury (ALI) is a serious respiratory syndrome characterized with uncontrolled inflammatory response. Oxyberberine has strong potential for clinical usage since it showed strong anti-inflammatory, antifungal, and antiarrhythmic effects in various diseases. In the present study, we evaluated whether oxyberberine can inhibit lipopolysaccharide- (LPS-) induced ALI in vivo and further evaluated the possible involvement of mitophagy in vitro by using A549 cells, a human lung epithelial cell line. Our in vivo study shows that oxyberberine significantly inhibited LPS-induced lung pathological injury and lung edema, as indicated by the changes in lung wet/dry ratio and total protein levels in the BALF in mice. Moreover, oxyberberine inhibited inflammation, as indicated by the changes of neutrophil accumulation and production of proinflammatory cytokines including tumor necrosis factor α (TNF-α), interleukin 1ß (IL-1ß), and IL-6 in both the lung and bronchoalveolar lavage fluid (BALF) in ALI mice. Our in vitro study shows that LPS significantly decreased the protein level of mitochondrial proteins, including cytochrome c oxidase subunit IV (COX IV), p62, and mitofusin-2 (Mfn2) in A549 cells. In addition, LPS induced significant Parkin1 translocation from cytoplasm to mitochondria. These changes were significantly inhibited by oxyberberine. Notably, the inhibitory effect of oxyberberine was almost totally lost in the presence of lysosome fusion inhibitor bafilomycin A1 (Baf), a mitophagy inhibitor. In conclusion, the present study demonstrated that oxyberberine alleviated LPS-induced inflammation in ALI via inhibition of Parkin-mediated mitophagy.

High-flow nasal cannula oxygen therapy versus non-invasive ventilation for chronic obstructive pulmonary disease patients after extubation: a multicenter, randomized controlled trial.

BACKGROUND: High-flow nasal cannula (HFNC) oxygen therapy is being increasingly used to prevent post-extubation hypoxemic respiratory failure and reintubation. However, evidence to support the use of HFNC in chronic obstructive pulmonary disease (COPD) patients with hypercapnic respiratory failure after extubation is limited. This study was conducted to test if HFNC is non-inferior to non-invasive ventilation (NIV) in preventing post-extubation treatment failure in COPD patients previously intubated for hypercapnic respiratory failure. METHODS: COPD patients with hypercapnic respiratory failure who were already receiving invasive ventilation were randomized to HFNC or NIV at extubation at two large tertiary academic teaching hospitals. The primary endpoint was treatment failure, defined as either resumption of invasive ventilation or switching to the other study treatment modality (NIV for patients in the NFNC group or vice versa). RESULTS: Ninety-six patients were randomly assigned to the HFNC group or NIV group. After secondary exclusion, 44 patients in the HFNC group and 42 patients in the NIV group were included in the analysis. The treatment failure rate in the HFNC group was 22.7% and 28.6% in the NIV group-risk difference of - 5.8% (95% CI, - 23.8-12.4%, p = 0.535), which was significantly lower than the non-inferior margin of 9%. Analysis of the causes of treatment failure showed that treatment intolerance in the HFNC group was significantly lower than that in the NIV group, with a risk difference of - 50.0% (95% CI, - 74.6 to - 12.9%, p = 0.015). One hour after extubation, the mean respiratory rates of both groups were faster than their baseline levels before extubation (p < 0.050). Twenty-four hours after extubation, the respiratory rate of the HFNC group had returned to baseline, but the NIV group was still higher than the baseline. Forty-eight hours after extubation, the respiratory rates of both groups were not significantly different from the baseline. The average number of daily airway care interventions in the NIV group was 7 (5-9.3), which was significantly higher than 6 (4-7) times in the HFNC group (p = 0.006). The comfort score and incidence of nasal and facial skin breakdown of the HFNC group was also significantly better than that of the NIV group [7 (6-8) vs 5 (4-7), P < 0.001] and [0 vs 9.6%, p = 0.027], respectively. CONCLUSION: Among COPD patients with severe hypercapnic respiratory failure who received invasive ventilation, the use of HFNC after extubation did not result in increased rates of treatment failure compared with NIV. HFNC also had better tolerance and comfort than NIV. TRIAL REGISTRATION: chictr.org ( ChiCTR1800018530 ). Registered on 22 September 2018, http://www.chictr.org.cn/usercenter.aspx.

[Xuebijing injection attenuates hydrogen sulfide-induced endothelial barrier dysfunction by upregulating claudin-5 expression].

OBJECTIVE: To study the new mechanism of Xuebijing injection improving the function of pulmonary vascular barrier from the perspective of claudin-5 protein. METHODS: Acute lung injury (ALI) model was induced by hydrogen sulfide (H2S) exposure. (1) In vivo study: Sprague-Dawley (SD) rats were divided into control group, H2S exposure group (exposure to 300×10-6 H2S for 3 hours), Xuebijing control group (Xuebijing injection 4 mL/kg , twice a day, for 3 days), and Xuebijing intervention group (H2S exposure after pretreatment of Xuebijing injection) according to random number method, with 6 rats in each group. At different time points (0, 6, 12 and 24 hours) after the model was made successfully, the total protein content in plasma and bronchoalveolar lavage fluid (BALF) of rats were detected respectively, and the pulmonary permeability index (PPI) was calculated (PPI = protein content in BALF/protein content in plasma), lung dry/wet weight ratio (W/D) was detected, and claudin-5 mRNA expression in lung tissue was measured by real time-polymerase chain reaction. (2) In vitro test: human pulmonary microvascular endothelial cells (HPMECs) were divided into blank control group, NaHS treatment group (co-incubated with 500 µmol/L NaHS for 12 hours), Xuebijing control group (2 g/L Xuebijing injection for 24 hours), and Xuebijing intervention group (2 g/L Xuebijing injection pre-treated for 24 hours, then co-incubated with 500 µmol/L NaHS for 12 hours). The HPMECs claudin-5 protein expression and monolayer permeability changes were measured at different co-incubation time (1, 3, 6, 12 and 24 hours) by Western Blot and fluoresceinsodium. RESULTS: (1) In vivo study: compared with the control group, the lung W/D ratio increased significantly at 6 hours and peaked at 12 hours after H2S exposure in rats (4.67±0.11 vs. 4.26±0.06, P < 0.01). The expression of claudin-5 mRNA in lung tissue was significantly decreased, which was 89% of control group 6 hours after exposure (P < 0.01). The total protein content in BALF and PPI at 12 hours after exposure were significantly higher than those in the control group [total protein content (mg/L): 262.31±14.24 vs. 33.30±3.09, PPI: (11.72±0.57)×10-3 vs. (1.21±0.08)×10-3, both P < 0.01], while the results in Xuebijing intervention group were significantly decreased [total protein content (mg/L): 153.25±7.32 vs. 262.31±14.24, PPI: (5.79±0.23)×10-3 vs. (11.72±0.57)×10-3, both P < 0.01]. (2) In vitro test: compared with the blank control group, after incubating HPMECs with NaHS, the permeability of monolayer endothelial cells gradually increased, reaching the highest level in 12 hours, about twice of that in the blank control group, while claudin-5 protein expression decreased to the lowest level at 12 hours (claudin-5/ß-actin: 0.42±0.03 vs. 1.03±0.05, P < 0.01). After intervention with Xuebijing, the permeability of endothelial cells was significantly improved (fluorescence intensity of fluorescein sodium: 1.46±0.10 vs. 1.89±0.11, P < 0.01), and the decrease of claudin-5 protein was reduced (claudin-5/ß-actin: 0.68±0.04 vs. 0.38±0.03, P < 0.01). CONCLUSIONS: Xuebijing injection may improve pulmonary vascular barrier function in ALI by upregulating claudin-5 expression.

Involvement of claudin-5 in H2S-induced acute lung injury.

Acute exposure to hydrogen sulfide (H2S) can cause fatal acute lung injury (ALI). However, the mechanisms of H2S-induced ALI are still not fully understood. This study aims to investigate the role of the tight junction protein claudin-5 in H2S-induced ALI. In our study, Sprague-Dawley (SD) rats were exposed to H2S to establish the ALI model, and in parallel, human pulmonary microvascular endothelial cells (HPMECs) were incubated with NaHS (a H2S donor) to establish a cell model. Lung immunohistochemistry and electron microscopy assays were used to identify H2S-induced ALI, and the expression of claudin-5, p-AKT/t-AKT and p-FoxO1/t-FoxO1 was detected. Our results show that H2S promoted the formation of ALI by morphological investigation and decreased claudin-5 expression. Dexamethasone (Dex) could partly attenuate NaHS-mediated claudin-5 downregulation, and the protective effects of Dex could be partially blocked by LY294002, a PI3K/AKT/FoxO1 pathway antagonist. Moreover, as a consequence of the altered phosphorylation of AKT and FoxO1, a change in claudin-5 with the same trend was observed. Therefore, the tight junction protein claudin-5 might be considered a therapeutic target for the treatment of ALI induced by H2S and other hazardous gases.

Duration of cardiac arrest requires different ventilation volumes during cardiopulmonary resuscitation in a pig model.

There are few studies examining the ventilation strategies recommended by current CPR guidelines. We investigated the influence of different minute volume applying to untreated cardiac arrest with different duration, on resuscitation effects in a pig model. 32 Landrace pigs with 4 or 8 min (16 pigs each) ventricular fibrillation (VF) randomly received two ventilation strategies during CPR. "Guideline" groups received mechanical ventilation with a tidal volume of 7 ml/kg and a frequency of 10/min, while "Baseline" groups received a tidal volume (10 ml/kg) and a frequency used at baseline to maintain an end-tidal PCO2 (PETCO2) between 35 and 40 mmHg before VF. Mean airway pressures and intrathoracic pressures (PIT) in the Baseline-4 min group were significantly higher than those in the Guideline-4 min group (all P < 0.05). Similar results were observed in the 8 min pigs, except for no significant difference in minimal PIT and PETCO2 during 10 min of CPR. Venous pH and venous oxygen saturation were significantly higher in the Baseline-8 min group compared to the Guideline-8 min group (all P < 0.05). Aortic pressure in the Baseline-8 min group was higher than in the Guideline-8 min group. Seven pigs in each subgroup of 4 min VF models achieved the return of spontaneous circulation (ROSC). Higher ROSC was observed in the Baseline-8 min group than in the Guideline-8 min group (87.5% vs. 37.5%, P = 0.039). For 4 min VF but not 8 min VF, a guideline-recommended ventilation strategy had satisfactory results during CPR. A higher minute ventilation resulted in better outcomes for subjects with 8 min of untreated VF through thoracic pump.

High flow nasal cannula oxygen therapy versus non-invasive ventilation for chronic obstructive pulmonary disease with acute-moderate hypercapnic respiratory failure: an observational cohort study.

Background: High-flow nasal cannula (HFNC) oxygen therapy in acute hypoxic respiratory failure is becoming increasingly popular. However, evidence to support the use of HFNC in acute respiratory failure (ARF) with hypercapnia is limited. Methods: Chronic obstructive pulmonary disease (COPD) patients with moderate hypercapnic ARF (arterial blood gas pH 7.25-7.35, PaCO2>50 mmHg) who received HFNC or non-invasive ventilation (NIV) in the intensive care uint from April 2016 to March 2018 were analyzed retrospectively. The endpoint was treatment failure, defined as either invasive ventilation, or a switch to the other study treatment (NIV for patients in the NFNC group, and vice-versa), and 28-day mortality. Results: Eighty-two COPD patients (39 in the HFNC group and 43 in the NIV group) were enrolled in this study. The mean age was 71.8±8.2 and 54 patients (65.9%) were male. The treatment failed in 11 out of 39 patients with HFNC (28.2%) and in 17 of 43 patients with NIV (39.5%) (P=0.268). No significant differences were found for 28-day mortality (15.4% in the HFNC group and 14% in the NIV group, P=0.824). During the first 24 hrs of treatment, the number of nursing airway care interventions in the HFNC group was significantly less than in the NIV group, while the duration of device application was significantly longer in the HFNC group (all P<0.05). Skin breakdown was significantly more common in the NIV group (20.9% vs 5.1%, P<0.05). Conclusion: Among COPD patients with moderate hypercarbic ARF, the use of HFNC compared with NIV did not result in increased rates of treatment failure, while there were fewer nursing interventions and skin breakdown episodes reported in the HFNC group.

[Benefits and risks of stress ulcer prevention with proton pump inhibitors for critical patients: an observational cohort study with 1 972 patients].

OBJECTIVE: To investigate the benefits and risks of stress ulcer prevention (SUP) using proton pump inhibitors (PPI) for critical patients. METHODS: The clinical data of adult critically ill patients admitted to the intensive care unit (ICU) of Northern Jiangsu People's Hospital from January 2016 to December 2018 were retrospectively analyzed. All patients who were treated with PPI for SUP within the first 48 hours after ICU admission were enrolled in the SUP group. Those who not received PPI were enrolled in the control group. A one-to-one propensity score matching (PSM) was performed to control for potential biases. The gender, age, underlying diseases, main diagnosis of ICU, drug use before ICU admission, sequential organ failure score (SOFA) at ICU admission, risk factors of stress ulcer (SU) and PPI usage were recorded. The end point was the incidence of gastrointestinal bleeding, hospital acquired pneumonia, Clostridium difficile infection and 30-day mortality. Kaplan-Meier survival curves were plotted, and survival analysis was performed using the log-rank test. RESULTS: 1 972 critical patients (788 in the SUP group and 1 184 in the control group) were enrolled, and each group enrolled 358 patients after PSM. Prior to PSM, compared with the control group, the SUP group had older patients, more underlying diseases, higher proportion of acute coronary syndrome (ACS), acute cerebrovascular disease, acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and poisoning in main diagnosis of ICU, more serious illness, and more risk factors of SU, indicating that ICU physicians were more likely to prescribe SUP for these patients. The incidence of gastrointestinal bleeding in the SUP group was significantly lower than that in the control group [1.8% (14/788) vs. 3.7% (44/1 184), P < 0.05], while the incidence of hospital acquired pneumonia and 30-day mortality were significantly higher than those in the control group [6.6% (52/788) vs. 3.5% (42/1 184), 17.9% (141/788) vs. 13.1% (155/1 184), both P < 0.01]. There was no significant difference in the incidence of Clostridium difficile infection between the SUP group and the control group [2.9% (23/788) vs. 1.8% (21/1 184), P > 0.05]. After the propensity scores for age, underlying diseases, severity of illness and SU risk factors were matched, there was no significant difference in the incidence of gastrointestinal bleeding or 30-day mortality between the SUP group and the control group [2.2% (8/358) vs. 3.4% (12/358), 15.9% (57/358) vs. 13.7% (49/358), both P > 0.05], but the incidence of hospital acquired pneumonia in the SUP group was still significantly higher than that in the control group [6.7% (24/358) vs. 3.1% (11/358), P < 0.05]. Kaplan-Meier survival curve analysis showed that the 30-day cumulative survival rate of the SUP group was significantly lower than that of the control group before the PSM (log-rank test: χ2 = 9.224, P = 0.002). There was no significant difference in the 30-day cumulative survival rate between the two groups after PSM (log-rank test: χ2 = 0.773, P = 0.379). CONCLUSIONS: For critical patients, the use of PPI for SUP could not significantly reduce the incidence of gastrointestinal bleeding and mortality, but increase the risk of hospital acquired pneumonia.

A meta-analysis of early oral refeeding and quickly increased diet for patients with mild acute pancreatitis.

BACKGROUND/AIM: The objective of the study is to clarify whether early oral refeeding (EORF) and quickly increasing diet (QID) are of benefit to patients with mild acute pancreatitis compared with a traditional oral refeeding strategy. MATERIALS AND METHODS: Studies were searched in PubMed, Cochrane library, ScienceDirect, SpringerLink, China Biology Medicine disc and Embase. A meta-analysis was then performed, using relapse of abdominal pain, nausea/vomiting, and length of hospital stay (LOHS) as the evaluation indices. RESULTS: Eight trials met the inclusion criteria. For the oral refeeding time group, EORF could significantly decrease the LOHS (mean deviation [MD] -1.97; 95% confidence interval (CI) -3.32 to -0.62;P = 0.004), and there was no significant difference for relapse of abdominal pain (relative risk [RR] 1.17; 95% CI 0.69-2.00;P = 0.56) or nausea/vomiting (RR 1.30; 95% CI 0.19-8.82;P = 0.79) when compared with conventional oral refeeding. For the oral refeeding material group, there was no significant difference for relapse of abdominal pain (RR 0.86; 95% CI 0.53-1.40;P = 0.54), nausea/vomiting (risk difference -0.01; 95% CI -0.19-0.18;P = 0.94), or LOHS (MD -0.88; 95% CI -2.24-0.48;P = 0.20) between the QID and stepwise increasing diet groups. CONCLUSION: Pure EORF or QID caused no damage to patients with mild acute pancreatitis, and EORF could significantly decrease the LOHS.

Full recovery after prolonged resuscitation from cardiac arrest due to propafenone intoxication: A case report.

RATIONALE: The prognosis of cardiac arrest (CA) induced by propafenone intoxication was thought to be very poor. The maximal duration of cardiopulmonary resuscitation (CPR) for propafenone induced CA is unknown. PATIENT CONCERNS: We describe a case that was successfully resuscitated after prolonged CPR (totaling 340 minutes during one hospital visit) for propafenone intoxication without subsequent neurological sequela. DIAGNOSES: A previously healthy 36-year-old female who developed multiple and prolonged CAs after consuming 98 tablets of 50mg propafenone. The CPR duration of this case, to the best of our knowledge, is the longest of all existing propafenone-induced CPR events to still have full recovery. We also analyse the contributing factors to this successful CPR. INTERVENTIONS: Sodium bicarbonate, inotropic drugs and pacemaker application did not prevent the occurrence of CA. A full recovery was eventually achieved after prolonged CPR with a mechanical CPR device, blood purification and other aggressive supportive treatments. OUTCOMES: Full recovery without neurological sequela. LESSONS: Prolonged CPR including the application of mechanical CPR devices should be considered in propafenone-related CA, especially in young patients without significant comorbidities and delayed resuscitation.

[Predictive value of continuous monitoring end-tidal carbon dioxide partial pressure on in-hospital resuscitation outcome: secondary analysis of the data from a multicenter observational study].

OBJECTIVE: To approach the predictive value of continuous monitoring end-tidal carbon dioxide partial pressure (PETCO2) on the outcome of in-hospital cardiopulmonary resuscitation (CPR), and explored the indicators of termination of resuscitation. METHODS: A secondary analysis of a multicenter observational study data was conducted. The screening aim was adult non-traumatic in-hospital CPR patients whose PETCO2 were recorded within 30 minutes of CPR. Clinical information was reviewed. The mean PETCO2 in restoration of spontaneous circulation (ROSC) and non-ROSC patients was recorded. The outcome of CPR was continuously assessed by PETCO2 ≤ 10 mmHg (1 mmHg = 0.133 kPa) for 1, 3, 5, 8, 10 minutes. Receiver operating characteristic (ROC) curve was plotted, and the predictive value of PETCO2 ≤ 10 mmHg for different duration on the outcome of CPR was evaluated. RESULTS: A total of 467 recovery patients, including 419 patients with complete recovery were screened. Patients who were out-of-hospital resuscitation, non-adults, traumatic injury, had no PETCO2 value, PETCO2 value failed to explained the clinical conditions, or patients had not monitored PETCO2 within 30 minutes of resuscitation were excluded, and finally 120 adult patients with non-traumatic in-hospital resuscitation were enrolled in the analysis. The mean PETCO2 in 50 patients with ROSC was significantly higher than that of 70 non-ROSC patients [mmHg: 17 (11, 27) vs. 9 (6, 16), P < 0.01]. ROC curve analysis showed that the area under ROC curve (AUC) of PETCO2 during the resuscitation for predicting recovery outcome was 0.712 [95% confidence interval (95%CI) = 0.689-0.735]; when the cut-off was 10.5 mmHg, the sensitivity was 57.8%, and the specificity was 78.0%, the positive predictive value (PPV) was 84.6%, and negative predictive value (NPV) was 46.9%. The duration of PETCO2 ≤ 10 mmHg was used for further analysis, which showed that with PETCO2 ≤10 mmHg in duration, the prediction of the sensitivity of the patients failed to recover decreased from 58.2% to 28.2%, but specificity increased from 39.4% to 100%; PPV increased from 40% to 100%, and NPV decreased from 57.5% to 34.2%. CONCLUSIONS: For adult non-traumatic in-hospital CPR patients, continuous 10 minutes PETCO2 ≤10 mmHg may be an indicate of termination of CPR.

Postoperative acute respiratory failure caused by adult-onset Pompe disease.

Pompe disease, which leads to dysfunction of the enzyme acid a-glucosidase, is a genetic disorder seen in 1 in 40000 births. Adult-onset Pompe disease is known as a slowly progressive myasthenia with or without respiratory dysfunction. We herein report two cases of adult-onset Pompe disease, in which postoperative acute respiratory failure was the the initial manifestation. The two patients showed no symptoms of ambulatory and respiratory dysfunction before operation. The diagnosis of Pompe disease was determined by muscle biopsy and acid a-glucosidase assay in the blood. Rapid deterioration of already struggling diaphragmatic function induced by stress of surgery and anesthesia were thought to be the main reason of postoperative acute respiratory failure. Physicians should be aware of the existence of an adult form of Pompe disease which may present with postoperative acute respiratory failure.

[Experimental study on effect of airway pressure on cardiopulmonary resuscitation].

OBJECTIVE: To observe the effect of different airway pressure on ventilation, organ perfusion and return of spontaneous circulation (ROSC) of cardiac arrest (CA) pigs during cardiopulmonary resuscitation (CPR), and to explore the possible beneficial mechanism of positive airway pressure during CPR. METHODS: Twenty healthy landrace pigs of clean grade were divided into low airway pressure group (LP group, n = 10) and high airway pressure group (HP group, n = 10) with random number table. The model of ventricular fibrillation (VF) was reproduced by electrical stimulation, and mechanical chest compressions and mechanical ventilation (volume-controlled mode, tidal volume 7 mL/kg, frequency 10 times/min) were performed after 8 minutes of untreated VF. Positive end expiratory pressure (PEEP) in LP group and HP group was set to 0 cmH2O and 6 cmH2O (1 cmH2O = 0.098 kPa) respectively. Up to three times of 100 J biphasic defibrillation was delivered after 10 minutes of CPR. The ROSC of animals were observed, and the respiratory parameters, arterial and venous blood gas and hemodynamic parameters were recorded at baseline, 5 minutes and 10 minutes of CPR. RESULTS: The number of animals with ROSC in the HP group was significantly more than that in the LP group (8 vs. 3, P < 0.05). Intrathoracic pressure during chest compression relaxation was negative in the HP group, and its absolute value was significantly lower than that in LP group at the same time [intrathoracic negative pressure peak (cmH2O): -4.7±2.2 vs. -10.8±3.5 at 5 minutes, -3.9±2.8 vs. -6.5±3.4 at 10 minutes], however, there was significantly difference only at 5 minutes of CPR (P < 0.01). Intrathoracic pressure variation during CPR period in the HP group were significantly higher than those in the LP group (cmH2O: 22.5±7.9 vs. 14.2±4.4 at 5 minutes, 23.1±6.4 vs. 12.9±5.1 at 10 minutes, both P < 0.01). Compared to the LP group, arterial partial pressure of oxygen [PaO2 (mmHg, 1 mmHg = 0.133 kPa): 81.5±10.7 vs. 68.0±12.1], venous oxygen saturation (SvO2: 0.493±0.109 vs. 0.394±0.061) at 5 minutes of CPR, and PaO2 (mmHg: 77.5±13.4 vs. 63.3±10.5), arterial pH (7.28±0.09 vs 7.23±0.11), SvO2 (0.458±0.096 vs. 0.352±0.078), aortic blood pressure [AoP (mmHg): 39.7±9.5 vs. 34.0±6.9], coronary perfusion pressure [CPP (mmHg): 25.2±9.6 vs. 19.0±7.6], and carotid artery flow (mL/min: 44±16 vs. 37±14) at 10 minutes of CPR in the HP group were significantly higher (all P < 0.05). Arterial partial pressure of carbon dioxide (PaCO2) in the HP group was significantly lower than that in the LP group at 10 minutes of CPR (mmHg: 60.1±9.7 vs. 67.8±8.6, P < 0.05). CONCLUSIONS: Compared to low airway pressure, a certain degree of positive airway pressure can still maintain the negative intrathoracic pressure during relaxation of chest compressions of CPR, while increase the degree of intrathoracic pressure variation. Positive airway pressure can improve oxygenation and hemodynamics during CPR, and is helpful to ROSC.