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Purpose: To elucidate whether fluid balance and body weight change are associated with failed planned extubation. Materials and Methods: Patients who received invasive mechanical ventilation for over 24 hours were enrolled and divided into extubation success and extubation failure groups. Fluid balance and body weight fluctuation within 24 and 48 hours before extubation and from admission to planned extubation were calculated. The primary outcome was extubation failure (ie, all-cause reintubation within 72 hours). The association of extubation failure with fluid balance and body weight change was assessed via logistic regression analysis. Results: Extubation failure occurred in 12(7.4%)/161 patients. The extubation success group had a significantly lower fluid balance within 24 hours before extubation than did the extubation failure group (-276 mL [-1111 to 456] vs 1217 mL [503 to 1875], P = .002). However, fluid balance within 48 hours before extubation, cumulative fluid balance, and body weight change were not significantly different between the 2 groups. The sensitivity and specificity of water balance þ1000 mL within 24 hours before extubation for the extubation failure group were 0.54 and 0.84, respectively, based on the receiver operating characteristic curve. Logistic regression analysis showed that fluid balance within 24 hours before extubation was associated with extubation failure (odds ratio: 22.9, 95% confidence interval: 4.1-128.4). Conclusions: A larger fluid balance within 24 hours before extubation is associated with extubation failure. Thus, fluid balance may be a good indicator of extubation outcome. [ABSTRACT FROM AUTHOR]

We report a severe case of Chromobacterium haemolyticum pneumonia associated with near-drowning and detail the investigation of the pathogen and river water. Our genomic and environmental investigation demonstrated that river water in a temperate region can be a source of C. haemolyticum causing human infections. [ABSTRACT FROM AUTHOR]

Background: Hyperfibrinolysis is a critical complication in severe trauma. Hyperfibrinolysis is traditionally diagnosed via elevated D-dimer or fibrin/fibrinogen degradation product levels, and recently, using thromboelastometry. Although hyperfibrinolysis is observed in patients with severe isolated traumatic brain injury (TBI) on arrival at the emergency department (ED), it is unclear which factors induce hyperfibrinolysis. The present study aimed to investigate the factors associated with hyperfibrinolysis in patients with isolated severe TBI.Methods: We conducted a multicentre retrospective review of data for adult trauma patients with an injury severity score ≥ 16, and selected patients with isolated TBI (TBI group) and extra-cranial trauma (non-TBI group). The TBI group included patients with an abbreviated injury score (AIS) for the head ≥ 4 and an extra-cranial AIS < 2. The non-TBI group included patients with an extra-cranial AIS ≥ 3 and head AIS < 2. Hyperfibrinolysis was defined as a D-dimer level ≥ 38 mg/L on arrival at the ED. We evaluated the relationships between hyperfibrinolysis and injury severity/tissue injury/tissue perfusion in TBI patients by comparing them with non-TBI patients.Results: We enrolled 111 patients in the TBI group and 126 in the non-TBI group. In both groups, patients with hyperfibrinolysis had more severe injuries and received transfusion more frequently than patients without hyperfibrinolysis. Tissue injury, evaluated on the basis of lactate dehydrogenase and creatine kinase levels, was associated with hyperfibrinolysis in both groups. Among patients with TBI, the mortality rate was higher in those with hyperfibrinolysis than in those without hyperfibrinolysis. Tissue hypoperfusion, evaluated on the basis of lactate level, was associated with hyperfibrinolysis in only the non-TBI group. Although the increase in lactate level was correlated with the deterioration of coagulofibrinolytic variables (prolonged prothrombin time and activated partial thromboplastin time, decreased fibrinogen levels, and increased D-dimer levels) in the non-TBI group, no such correlation was observed in the TBI group.Conclusions: Hyperfibrinolysis is associated with tissue injury and trauma severity in TBI and non-TBI patients. However, tissue hypoperfusion is associated with hyperfibrinolysis in non-TBI patients, but not in TBI patients. Tissue hypoperfusion may not be a prerequisite for the occurrence of hyperfibrinolysis in patients with isolated TBI. [ABSTRACT FROM AUTHOR]

Hemorrhage is the most important contributing factor of acute-phase mortality in trauma patients. Previously, traumatologists and investigators identified iatrogenic and resuscitation-associated causes of coagulopathic bleeding after traumatic injury, including hypothermia, metabolic acidosis, and dilutional coagulopathy that were recognized as primary drivers of bleeding after trauma. However, the last 10 years has seen a widespread paradigm shift in the resuscitation of critically injured patients, and there has been a dramatic evolution in our understanding of trauma-induced coagulopathy. Although there is no consensus regarding a definition or an approach to the classification and naming of trauma-associated coagulation impairment, trauma itself and/or traumatic shockinduced endogenous coagulopathy are both referred to as acute traumatic coagulopathy (ATC), and multifactorial trauma-associated coagulation impairment, including ATC and resuscitation-associated coagulopathy is recognized as trauma-induced coagulopathy. Understanding the pathophysiology of trauma-induced coagulopathy is vitally important, especially with respect to the critical issue of establishing therapeutic strategies for the management of patients with severe trauma. [ABSTRACT FROM AUTHOR]

Achieving a balance between organ perfusion and hemostasis is critical for optimal fluid resuscitation in patients with severe trauma. The concept of "permissive hypotension" refers to managing trauma patients by restricting the amount of resuscitation fluid and maintaining blood pressure in the lower than normal range if there is continuing bleeding during the acute period of injury. This treatment approach may avoid the adverse effects of early, high-dose fluid resuscitation, such as dilutional coagulopathy and acceleration of hemorrhage, but does carry the potential risk of tissue hypoperfusion. Current clinical guidelines recommend the use of permissive hypotension and controlled resuscitation. However, it is not mentioned which subjects would receive most benefit from this approach, when considering factors such as age, injury mechanism, setting, or the presence or absence of hypotension. Recently, two randomized clinical trials examined the efficacy of titrating blood pressure in younger patients with shock secondary to either penetrating or blunt injury; in both trials, overall mortality was not improved. Another two major clinical trials suggest that controlled resuscitation may be safe in patients with blunt injury in the pre-hospital setting and possibly lead to improved outcomes, especially in patients with pre-hospital hypotension. Some animal studies suggest that hypotensive resuscitation may improve outcomes in subjects with penetrating injury where bleeding occurs from only one site. On the other hand, hypotensive resuscitation in blunt trauma may worsen outcomes due to tissue hypoperfusion. The influence of these approaches on coagulation has not been sufficiently examined, even in animal studies. The effectiveness of permissive hypotension/ hypotensive resuscitation and restricted/controlled resuscitation is still inconclusive, even when examining systematic reviews and meta-analyses. Further investigation is needed to elucidate the effectiveness of these approaches, so as to develop improved treatment strategies which take into account coagulopathy in the pathophysiology of trauma. [ABSTRACT FROM AUTHOR]

Background: Alarmins, including high-mobility group box 1 (HMGB-1), can be released from damaged tissues and activated cells as inflammatory mediators. We aimed to evaluate HMGB-1 and mitochondrial DNA dynamics and estimate the prognostic value for neurological outcome in patients with post-cardiac arrest syndrome after out-of-hospital cardiac arrest. Methods: We evaluated the dynamics of HMGB-1, mitochondrial DNA, and other variables in patients with return of spontaneous circulation after out-of-hospital cardiac arrest. Patients were divided into two groups according to the cerebral performance category at 30 days: the favourable outcome group (cerebral performance categories 1 and 2) and unfavourable group (≥3). Results: Twenty-one patients were included, and 11 demonstrated favourable outcomes. HMGB-1 levels and mitochondrial DNA on day 1 were significantly higher than on days 2, 3, 5, and 7. Plasma levels of HMGB-1 on day 1 correlated with prognostic parameters (estimated interval to return of spontaneous circulation, lactate, and NH3), tissue damage, systemic inflammation, and disease severity. HMGB-1 on day 1 in the unfavourable group was significantly higher than in the favourable group (median [interquartile range] 15.5 [6.65-18.7], 39.4 [17-69.5], P = 0.009). These findings were not observed regarding mitochondrial DNA. Regarding HMGB-1 prediction accuracy for a good neurological outcome, the area under the receiver operating characteristic curve was 0.864 (95 % confidence interval 0.702, 1.000). Conclusions: HMGB-1 may be involved in acute-phase post-cardiac arrest syndrome pathophysiology, and an increase in plasma levels may be associated with a poor neurological outcome. The study was registered with the University Hospital Medical Information Network Clinical Trials Registry ID: UMIN000006714. [ABSTRACT FROM AUTHOR]

Background: Hepatic portal venous gas associated with non-occlusive mesenteric ischemia is indicative of a serious pathology that leads to bowel necrosis and it has a high mortality rate. Although non-occlusive mesenteric ischemia is acknowledged as a condition that requires early surgical treatment, it has been reported that bowel necrosis and surgical resection of the gangrenous lesion may be avoided if the condition is identified quickly and the cause is detected at an early phase. However, no reports or guidelines have been published that describe the management of patients in whom bowel necrosis and surgical treatment were avoided. We report the case of a patient who presented with non-occlusive mesenteric ischemia who was managed with non-resectional treatment at an early phase and had a delayed small-bowel stricture. Case presentation: A 24-year-old man presented to the hospital with fever, abdominal pain, and vomiting. Abdominal computed tomography confirmed a diffuse gaseous distention with small-bowel pneumatosis and hepatic portal venous gas. An urgent laparotomy was performed, because septic shock associated with diffuse peritonitis and bowel necrosis was strongly suspected. Although we found purulent ascites and a perforated appendix at the time of surgery, gangrenous and transmural ischemic changes were not evident in the small bowel and colon. We performed an appendectomy without a bowel resection, and the patient was discharged on an oral diet. However,he was re-admitted to hospital, because 4 days after discharge he developed postoperative paralytic ileus. Non-operative management was chosen, but his symptoms did not improve. We decided to perform a laparotomy 40 days after the initial operation, and a considerable adhesion was detected. Therefore, only a synechotomy was performed. On day 57, he experienced symptoms that were associated with bowel obstruction once again. On day 59, a partial resection of the jejunum was performed. Severe luminal strictures were apparent within the jejunum, and marked structural changes were evident. Conclusion: While non-surgical management can be chosen for selected patients with non-occlusive mesenteric ischemia, continuous observation to evaluate the development of delayed strictures that lead to bowel obstructions is required in patients who undergo non-resectional treatment. [ABSTRACT FROM AUTHOR]

Introduction Abnormal body temperatures (Tb) are frequently seen in patients with severe sepsis. However, the relationship between Tb abnormalities and the severity of disease is not clear. This study investigated the impact of Tb on disease severity and outcomes in patients with severe sepsis. Methods We enrolled 624 patients with severe sepsis and grouped them into 6 categories according to their Tb at the time of enrollment. The temperature categories (⩽35.5°C, 35.6-36.5°C, 36.6- 37.5°C, 37.6-38.5°C, 38.6-39.5°C, ⩾39.6°C) were based on the temperature data of the Acute Physiology and Chronic Health Evaluation II (APACHE II) scoring. We compared patient characteristics, physiological data, and mortality between groups. Results Patients with Tb of ⩽36.5°C had significantly worse sequential organ failure assessment (SOFA) scores when compared with patients with Tb >37.5°C on the day of enrollment. Scores for APACHE II were also higher in patients with Tb ⩽35.5°C when compared with patients with Tb >36.5°C. The 28-day and hospital mortality was significantly higher in patients with Tb ⩽36.5°C. The difference in mortality rate was especially noticeable when patients with Tb ⩽35.5°C were compared with patients who had Tb of >36.5°C. Although mortality did not relate to Tb ranges of ⩾37.6°C as compared to reference range of 36.6- 37.5°C, relative risk for 28-day mortality was significantly greater in patients with 35.6- 36.5°C and ⩽35.5°C (odds ratio; 2.032, 3.096, respectively). When patients were divided into groups based on the presence (⩽36.5°C, n = 160) or absence (>36.5°C, n = 464) of hypothermia, disseminated intravascular coagulation (DIC) as well as SOFA and APACHE II scores were significantly higher in patients with hypothermia. Patients with hypothermia had significantly higher 28-day and hospital mortality rates than those without hypothermia (38.1% vs. 17.9% and 49.4% vs. 22.6%, respectively). The presence of hypothermia was an independent predictor of 28-day mortality, and the differences between patients with and without hypothermia were observed irrespective of the presence of septic shock. Conclusions In patients with severe sepsis, hypothermia (Tb ⩽36.5°C) was associated with increased mortality and organ failure, irrespective of the presence of septic shock. Trial registration UMIN-CTR ID UMIN000008195 [ABSTRACT FROM AUTHOR]

Introduction: The Berlin definition divides acute respiratory distress syndrome (ARDS) into three severity categories. The relationship between these categories and pulmonary microvascular permeability as well as extravascular lung water content, which is the hallmark of lung pathophysiology, remains to be elucidated. The aim of this study was to evaluate the relationship between extravascular lung water, pulmonary vascular permeability, and the severity categories as defined by the Berlin definition, and to confirm the associated predictive validity for severity. Methods: The extravascular lung water index (EVLWi) and pulmonary vascular permeability index (PVPI) were measured using a transpulmonary thermodilution method for three consecutive days in 195 patients with an EVLWi of ⩾10 mL/kg and who fulfilled the Berlin definition of ARDS. Collectively, these patients were seen at 23 ICUs. Using the Berlin definition, patients were classified into three categories: mild, moderate, and severe. Results: Compared to patients with mild ARDS, patients with moderate and severe ARDS had higher acute physiology and chronic health evaluation II and sequential organ failure assessment scores on the day of enrollment. Patients with severe ARDS had higher EVLWi (mild, 16.1; moderate, 17.2; severe, 19.1; P <0.05) and PVPI (2.7; 3.0; 3.2; P <0.05). When categories were defined by the minimum PaO2/FIO2 ratio observed during the study period, the 28-day mortality rate increased with severity categories: moderate, odds ratio: 3.125 relative to mild; and severe, odds ratio: 4.167 relative to mild. On independent evaluation of 495 measurements from 195 patients over three days, negative and moderate correlations were observed between EVLWi and the PaO2/FIO2 ratio (r = -0.355, P<0.001) as well as between PVPI and the PaO2/FIO2 ratio (r = -0.345, P <0.001). ARDS severity was associated with an increase in EVLWi with the categories (mild, 14.7; moderate, 16.2; severe, 20.0; P <0.001) in all data sets. The value of PVPI followed the same pattern (2.6; 2.7; 3.5; P <0.001). Conclusions: Severity categories of ARDS described by the Berlin definition have good predictive validity and may be associated with increased extravascular lung water and pulmonary vascular permeability. [ABSTRACT FROM AUTHOR]

Introduction To test the hypothesis that the administration of antithrombin concentrate improves disseminated intravascular coagulation (DIC), resulting in recovery from DIC and better outcomes in patients with sepsis, we conducted a prospective, randomized controlled multicenter trial at 13 critical care centers in tertiary care hospitals. Methods We enrolled 60 DIC patients with sepsis and antithrombin levels of 50% to 80% in this study. The participating patients were randomly assigned to an antithrombin arm receiving antithrombin at a dose of 30 IU/kg per day for three days or a control arm treated with no intervention. The primary efficacy end point was recovery from DIC on day 3. The analysis was conducted with an intention-to-treat approach. DIC was diagnosed according to the Japanese Association for Acute Medicine (JAAM) scoring system. The systemic inflammatory response syndrome score, platelet count and global markers of coagulation and fibrinolysis were measured on day 0 and day 3. Results Antithrombin treatment resulted in significantly decreased DIC scores and better recovery rates from DIC compared with those observed in the control group on day 3. The incidence of minor bleeding complications did not increase, and no major bleeding related to antithrombin treatment was observed. The platelet count significantly increased; however, antithrombin did not influence the Sequential Organ Failure Assessment score or markers of coagulation and fibrinolysis on day 3. Conclusions Moderate doses of antithrombin improve DIC scores, thereby increasing the recovery rate from DIC without any risk of bleeding in DIC patients with sepsis. Trial registration UMIN Clinical Trials Registry (UMIN-CTR) UMIN000000882 [ABSTRACT FROM AUTHOR]

Introduction: Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by features other than increased pulmonary vascular permeability. Pulmonary vascular permeability combined with increased extravascular lung water content has been considered a quantitative diagnostic criterion of ALI/ARDS. This prospective, multi-institutional, observational study aimed to clarify the clinical pathophysiological features of ALI/ARDS and establish its quantitative diagnostic criteria. Methods: The extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI) were measured using the transpulmonary thermodilution method in 266 patients with PaO2/FiO2 ratio ≤ 300 mmHg and bilateral infiltration on chest radiography, in 23 ICUs of academic tertiary referral hospitals. Pulmonary edema was defined as EVLWI ≥ 10 ml/kg. Three experts retrospectively determined the pathophysiological features of respiratory insufficiency by considering the patients' history, clinical presentation, chest computed tomography and radiography, echocardiography, EVLWI and brain natriuretic peptide level, and the time course of all preceding findings under systemic and respiratory therapy. Results: Patients were divided into the following three categories on the basis of the pathophysiological diagnostic differentiation of respiratory insufficiency: ALI/ARDS, cardiogenic edema, and pleural effusion with atelectasis, which were noted in 207 patients, 26 patients, and 33 patients, respectively. EVLWI was greater in ALI/ ARDS and cardiogenic edema patients than in patients with pleural effusion with atelectasis (18.5 ± 6.8, 14.4 ± 4.0, and 8.3 ± 2.1, respectively; P < 0.01). PVPI was higher in ALI/ARDS patients than in cardiogenic edema or pleural effusion with atelectasis patients (3.2 ± 1.4, 2.0 ± 0.8, and 1.6 ± 0.5; P < 0.01). In ALI/ARDS patients, EVLWI increased with increasing pulmonary vascular permeability (r = 0.729, P < 0.01) and was weakly correlated with intrathoracic blood volume (r = 0.236, P < 0.01). EVLWI was weakly correlated with the PaO2/FiO2 ratio in the ALI/ARDS and cardiogenic edema patients. A PVPI value of 2.6 to 2.85 provided a definitive diagnosis of ALI/ARDS (specificity, 0.90 to 0.95), and a value < 1.7 ruled out an ALI/ARDS diagnosis (specificity, 0.95). Conclusion: PVPI may be a useful quantitative diagnostic tool for ARDS in patients with hypoxemic respiratory failure and radiographic infiltrates. [ABSTRACT FROM AUTHOR]

Abstract  Procalcitonin serum level has been recommended as a new marker of bacterial infectious diseases. The aim of this prospective, multicenter study was to determine the clinical usefulness of procalcitonin in differentiating patients with sepsis from those with severe sepsis. Eighty-two patients were enrolled: 20 without systemic inflammatory response syndrome (SIRS), 9 with SIRS, 34 with sepsis, and 19 with severe sepsis. The patients with severe sepsis had significantly higher procalcitonin levels (median, 36.1 ng/ml) than those with sepsis (median, 0.6 ng/ml). With a procalcitonin cutoff value of 2.0 ng/ml, sensitivity for the detection of severe sepsis and specificity for the detection of sepsis were 94.7% and 78.1%, respectively. A good correlation was found between the serum procalcitonin level and the Sepsis-Related Organ Failure Assessment (SOFA) score (r = 0.680), although no correlation was found between the C-reactive protein (CRP) level and the SOFA score. In conclusion, the procalcitonin serum level may be useful not only for aiding the diagnosis of sepsis but also for discriminating between sepsis and severe sepsis. [ABSTRACT FROM AUTHOR]

Abstract The clinical significance of serum procalcitonin (PCT) for discriminating between bacterial infectious disease and nonbacterial infectious disease (such as systemic inflammatory response syndrome (SIRS)), was compared with the significance of endotoxin, ß-D-glucan, interleukin (IL)-6, and C-reactive protein (CRP) in a multicenter prospective study. The concentrations of PCT in patients with systemic bacterial infection and those with localized bacterial infection were significantly higher than the concentrations in patients with nonbacterial infection or noninfectious diseases. In addition, PCT, endotoxin, IL-6, and CRP concentrations were significantly higher in patients with bacterial infectious disease than in those with nonbacterial infectious disease (P < 0.001, P < 0.005, P < 0.001, and P < 0.001, respectively). The cutoff value of PCT for the discrimination of bacterial and nonbacterial infectious diseases was determined to be 0.5?ng/ml, which was associated with a sensitivity of 64.4% and specificity of 86.0%. Areas under the receiver operating characteristic curves (POCs) were 0.84 for PCT, 0.60 for endotoxin, 0.77 for IL-6, and 0.78 for CRP in the combined group of patients with bacterial infectious disease and those with nonbacterial infectious disease, and the area under the ROC for PCT was significantly higher than that for endotoxin (P < 0.001). In patients diagnosed with bacteremia based on clinical findings, the positive rate of diagnosis with PCT was 70.2%, while that of blood culture was 42.6%. PCT is thus essential for discriminating bacterial infection from SIRS, and is superior in this respect to conventional serum markers and blood culture. [ABSTRACT FROM AUTHOR]