中田 孝明

Objective: Physiological parameters are crucial for the caring of trauma patients. There is a significant loss of prehospital vital signs data of patients during handover between prehospital and in-hospital teams. Effective strategies for reducing the loss remain a challenging research area. We tested whether the newly developed electronic automated prehospital vital signs chart sharing system would increase the amount of prehospital vital signs data shared with a remote trauma center prior to hospital arrival. Methods: Fifty trauma patients, transferred to a level I trauma center in Japan, were studied. The primary outcome variable was the number of prehospital vital signs shared with the trauma center prior to hospital arrival. Results: The prehospital vital signs chart sharing system significantly increased the number of prehospital vital signs, including blood pressure, heart rate, and oxygen saturation, shared with the in-hospital team at a remote trauma center prior to patient arrival at the hospital (P <.0001). There were significant differences in prehospital vital signs during ambulance transfer between patients who had severe bleeding and non-severe bleeding within 24 hours after injury onset. Conclusions: Vital signs data collected during ambulance transfer via patient monitors could be automatically converted to easily visible patient charts and effectively shared with the remote trauma center prior to hospital arrival. The prehospital vital signs chart sharing system increased the number of precise vital signs shared prior to patient arrival at the hospital, which can potentially contribute to better trauma care without increasing labor and reduce information loss during clinical handover. (C) 2015 Elsevier Inc. All rights reserved.

Background: Systemic immune response to injury plays a key role in the pathophysiological mechanism of blunt trauma. We tested the hypothesis that increased blood interleukin-6 (IL-6) levels of blunt trauma patients on emergency department (ED) arrival are associated with poor clinical outcomes, and investigated the utility of rapid measurement of the blood IL-6 level. Methods: We enrolled 208 consecutive trauma patients who were transferred from the scene of an accident to a level I trauma centre in Japan and admitted to the intensive care unit (ICU). Blood IL-6 levels on ED arrival were measured by using a rapid measurement assay. The primary outcome variable was prolonged ICU stay (length of ICU stay > 7 days). The secondary outcomes were 28-day mortality, probability of survival and Abbreviated Injury Scale (AIS) scores. Results: Patients with prolonged ICU stay had significantly higher blood IL-6 levels on ED arrival than the patients without prolonged ICU stay (P < 0.0001). The receiver-operating characteristic curves produced an area under the curve of 0.75 (95 % confidence interval [CI], 0.66-0.84; P < 0.0001) for prolonged ICU stay. The patients who had increased blood IL-6 levels on ED arrival had increased 28-day mortality (P = 0.021) and decreased probability of survival (P < 0.0001). The AIS scores for the thorax, abdomen, extremity, and external body regions independently correlated with blood IL-6 levels (unstandardized coefficients [95 % CI] for the thorax: 23.8 [12.6-35.1]; P < 0.0001; abdomen: 42.7 [23.8-61.7]; P < 0.0001; extremity: 19.0 [5.5-32.4]; P = 0.0060; external body regions: 62.9 [13.2-112.7]; P = 0.030); the standardized coefficients for the thorax (0.27) and abdomen (0.28) were larger than those for the extremity (0.18) and external body regions (0.15). Conclusions: Increased blood IL-6 level on ED arrival was significantly associated with prolonged length of ICU stay. Blood IL-6 level on ED arrival independently correlated with the AIS scores for the abdomen and thorax, and, to a lesser extent, those for the extremity and external body regions. The rapid measurement of blood IL-6 level on ED arrival can be utilized as a fast screening tool to improve assessment of injury severity and prediction of clinical outcomes in the initial phase of trauma care.

Hereditary angioedema (HAE) is a rare genetic disease caused by a deficiency of functional C1 esterase inhibitor that causes swelling attacks in various body tissues. We hereby report a case of out-of-hospital cardiac arrest due to airway obstruction in HAE. Cutaneous swelling and abdominal pain attacks caused by gastrointestinal wall swelling are common symptoms in HAE, whereas laryngeal swelling is rare. Emergency physicians may have few chances to experience cases of life-threatening laryngeal edema resulting in a delay from symptom onset to the diagnosis of HAE. Hereditary angioedema is diagnosed by performing complement blood tests. Because safe and effective treatment options are available for the life-threatening swellings in HAE, the diagnosis potentially reduces the risk of asphyxiation in patients and their blood relatives.

Introduction: Previous studies evaluating whether subsequent conversion to shockable rhythms in patients who had initially non-shockable rhythms was associated with altered clinical outcome reported inconsistent results. Therefore, we hypothesized that subsequent shock delivery by emergency medical service (EMS) providers altered clinical outcomes in patients with initially non-shockable rhythms.Methods: We tested for an association between subsequent shock delivery in EMS resuscitation and clinical outcomes in patients with initially non-shockable rhythms (n = 11,481) through a survey of patients after out-of-hospital cardiac arrest in the Kanto region (SOS-KANTO) 2012 study cohort, Japan. The primary investigated outcome was 1-month survival with favorable neurological functions. The secondary outcome variable was the presence of subsequent shock delivery. We further evaluated the association of interval from initiation of cardiopulmonary resuscitation to shock with clinical outcomes.Results: In the univariate analysis of initially non-shockable rhythms, patients who received subsequent shock delivery had significantly increased frequency of return of spontaneous circulation, 24-hour survival, 1-month survival, and favorable neurological outcomes compared to the subsequent not shocked group (P < 0.0001). In the multivariate logistic regression analysis, subsequent shock was significantly associated with favorable neurological outcomes (vs. not shocked; adjusted P = 0.0020, odds ratio, 2.78; 95 % confidence interval, 1.45-5.30). Younger age, witnessed arrest, initial pulseless electrical activity rhythms, and cardiac etiology were significantly associated with the presence of subsequent shock in patients with initially non-shockable rhythms.Conclusions: In this study of cardiac arrest patients with initially non-shockable rhythms, patients who received early defibrillation by EMS providers had increased 1-month favorable neurological outcomes.

Liver abscess remains a life-threatening disease, particularly when it results in systemic organ failure necessitating intensive care. Only few cases of respiratory failure caused by liver abscess and treated with veno-venous extracorporeal membrane oxygenation (ECMO) have been reported. Here we present a case of liver abscess with rapid progression of multiple organ dysfunction, including severe acute respiratory failure on admission to the intensive care unit (ICU). Upon admission, we immediately initiated artificial organ support systems, including ventilator, continuous renal replacement therapy, and cardiovascular drug infusion for septic multiple organ failure and source control. Despite this initial management, respiratory failure deteriorated and V-V ECMO was introduced. The case developed abdominal compartment syndrome, for which we performed a bedside decompressive laparotomy in the ICU. The case gradually recovered from multiple organ failure and was discharged from the ICU on day 22 and from the hospital on day 53. Since liver abscess is potentially lethal and respiratory failure on admission is an additional risk factor of mortality, V-V ECMO may serve as an adjunctive choice of artificial organ support for cases of severe acute respiratory failure caused by liver abscess.

ObjectivesWhether sex affects the mortality of trauma patients remains unknown. The hypothesis of this study was that sex was associated with altered mortality rates in trauma. MethodsA retrospective review of trauma patients' records in the Japan Trauma Data Bank was conducted (n=80,813) from 185 major emergency hospitals across Japan. The primary outcome variable was in-hospital mortality within 28days. Secondary outcome variables included serious injuries to different body regions with an Abbreviated Injury Scale of 3. ResultsIn the analysis of 80,813 trauma patients, males had significantly greater 28-day mortality compared to females (adjusted p=0.0072, odds ratio [OR]=1.14, 95% confidence interval [CI]=1.06 to 1.23) via logistic regression analysis adjusted for age, mechanism, Injury Severity Score, Revised Trauma Score, and potential preexisting risk factors. Of 10 injury categories examined, sex significantly affected in-hospital 28-day mortality rate in falls (adjusted p&lt;0.0001, OR= 1.34, 95% CI=1.19 to 1.52). Further analysis of three fall subcategories by falling distance revealed that male patients who fell from ground level had significantly higher 28-day mortality (adjusted p&lt;0.0001, OR= 1.75, 95% CI=1.43 to 2.14) and a significantly greater frequency of serious injury to the head, thorax, abdomen, and spine, but a lower frequency of serious injury to the extremities, compared to female patients. ConclusionsCompared to female trauma patients, male trauma patients had greater 28-day mortality. In particular, ground-level falls had a significant sex difference in mortality, with serious injury to different body regions. Sex differences appeared to be important for fatalities from ground-level falls.

Objectives: Mortality from septic shock is highly heritable. The identification of causal genetic factors is insufficient. To discover key contributors, we first identified nonsynonymous single-nucleotide polymorphisms in conserved genomic regions that are predicted to have significant effects on protein function. We then test the hypothesis that these nonsynonymous single-nucleotide polymorphisms across the genome alter clinical outcome of septic shock. Design: Genetic-association study plus in vitro experiment using primary cells plus in silico analysis using genomic DNA and protein database. Setting: Twenty-seven ICUs at academic teaching centers in Canada, Australia, and the United States. Patients: Patients with septic shock of European ancestry (n = 520). Interventions: Patients with septic shock were genotyped for 843 nonsynonymous single-nucleotide polymorphisms in conserved regions of the genome and are predicted to have damaging effects from the protein sequence. Measurements and Main Results: The primary outcome variable was 28-day mortality. Secondary outcome variables were organ dysfunction. Productions of adhesion molecules including interleukin-8, growth-regulated oncogene-alpha, monocyte chemoattractant protein-1, and monocyte chemoattractant protein-3 were measured in human umbilical vein endothelial cells after SVEP1 gene silencing by RNA interference. Patients with septic shock having the SVEP1 C allele of nonsynonymous single-nucleotide polymorphism, SVEP1 c.2080A&gt;C (p. Gln581His, rs10817033), had a significant increase in the hazard of death over the 28 days (hazard ratio, 1.72; 95% CI, 1.31-2.26; p = 9.7 x 10-5) and increased organ dysfunction and needed more organ support (p &lt; 0.05). Silencing SVEP1 significantly increased interleukin-8, growth-regulated oncogene-alpha, monocyte chemoattractant protein-1, monocyte chemoattractant protein-3 production in human umbilical vein endothelial cells under lipopolysaccharide stimulation (p &lt; 0.01). Conclusions: C allele of SVEP1 c.2080A&gt;C (p. Gln581His) single-nucleotide polymorphism, a non-synonymous single-nucleotide polymorphism in conserved regions and predicted to have damaging effects on protein structure, was associated with increased 28-day mortality and organ dysfunction of septic shock. SVEP1 appears to regulate molecules of the leukocyte adhesion pathway.

Background: Genetic variations contribute to septic shock mortality. To discover a novel locus, we performed in vitro genome-wide association studies (GWAS) and further tested the result in a cohort of septic shock patients. Methods: Two in vitro GWAS using a quantitative trait locus analysis of stimulated IL-6 production in lymphoblastoid cells from 60 individuals of European ancestry were performed. VPS13D rs6685273 was genotyped in European ancestry patients (n = 498). The VPS13D gene was silenced in vitro. Results: Two GWAS using lymphoblastoid cells identified the locus of VPS13D rs6685273 that was significant in the same direction in both GWAS. The VPS13D rs6685273 C allele was associated with increased IL-6 production. Patients with septic shock who had the VPS13D rs6685273 CC genotype had an increased 28-day mortality (p = 0.023) and more organ failure (p &lt; 0.05) compared to the CT/TT genotypes. VPS13D in vitro gene silencing in the HeLa cell line increased IL-6 production. Furthermore, the rs6685273 genotype was associated with differential VPS13D splice variant expression. Conclusions: The VPS13D rs6685273 C allele was associated with increased IL-6 production in vitro. The patients with the VPS13D rs6685273 CC genotype had increased 28-day mortality and increased organ failure. VPS13D appears to regulate IL-6 production. (C) 2015 S. Karger AG, Basel

Subclavian arterial injury is rare and potentially life-threatening, particularly when it leads to arterial occlusion, causing limb ischemia, retrograde thromboembolization and cerebral infarction within hours after injury. Here we report a blunt trauma case with subclavian arterial injury, upper extremity ischemia, and the need for urgent treatment to salvage the limb and prevent cerebral infarction. A 41-year-old man had a left, open, mid-shaft clavicle fracture and left subclavian artery injury accompanied by a weak pulse in the left radial artery, decreased blood pressure of the left arm compared to the right, and left hand numbness. Urgent debridement and irrigation of the open clavicle fracture was followed by angiography for the subclavian artery injury. The left distal subclavian artery had a segmental dissection with a thrombus. Urgent endovascular treatment using a self-expanding nitinol stent successfully restored the blood flow and blood pressure to the left upper extremity. Endovascular treatment is a viable option for cases of subclavian artery injury where there is a risk of extremity ischemia and cerebral infarction.

Purpose: The final decision for discharge from the intensive care unit (ICU) is uncertain because it is made according to various patient parameters; however, it should be made on an objective evaluation. Previous reports have been inconsistent and unreliable in predicting post-ICU mortality. To identify predictive factors associated with post-ICU mortality, we analyzed physiological and laboratory data at ICU discharge. Methods: Patients admitted to our ICU between September 2012 and August 2013 and staying for critical care. 2 days were included. Sequential Organ Failure Assessment (SOFA) score; systemic inflammatory response syndrome score; white blood cell count; and serum C reactive protein, procalcitonin (PCT), interleukin-6 (IL-6), lactate, albumin, and hemoglobin levels were recorded. The primary end point was 90-day mortality after ICU discharge. Two hundred eighteen patients were enrolled (195 survivors, 23 non-survivors). Results: Non-survivors presented a higher SOFA score and serum PCT, and IL-6 levels, as well as lower serum albumin and hemoglobin levels. Serum PCT, albumin, and SOFA score were associated with 90-day mortality in multiple logistic regression analysis. Hosmer-Lemeshow test showed chi-square value of 6.96, and P value of 0.54. The area under the curve (95% confidence interval) was 0.830 (0.771-0.890) for PCT, 0.688 (0.566-0.810) for albumin, 0.861 (0.796-0.927) for SOFA score, and increased to 0.913 (0.858-0.969) when these were combined. Serum PCT level at 0.57 ng/mL, serum albumin at 2.5 g/dL and SOFA score at 5.5 predict 90-day mortality, and high PCT, low albumin and high SOFA groups had significantly higher mortality. Serum PCT and SOFA score were significantly associated with survival days after ICU discharge in Cox regression analysis. Conclusions: Serum PCT level and SOFA score at ICU discharge predict post-ICU mortality and survival days after ICU discharge. The combination of these two and albumin level might enable accurate prediction.

A decrease in the activity of proprotein convertase subtilisin/kexin type 9 (PCSK9) increases the amount of low-density lipoprotein (LDL) receptors on liver cells and, therefore, LDL clearance. The clearance of lipids from pathogens is related to endogenous lipid clearance; thus, PCSK9 may also regulate removal of pathogen lipids such as lipopolysaccharide (LPS). Compared to controls, Pcsk9 knockout mice displayed decreases in inflammatory cytokine production and in other physiological responses to LPS. In human liver cells, PCSK9 inhibited LPS uptake, a necessary step in systemic clearance and detoxification. Pharmacological inhibition of PCSK9 improved survival and inflammation in murine polymicrobial peritonitis. Human PCSK9 loss-of-function genetic variants were associated with improved survival in septic shock patients and a decrease in inflammatory cytokine response both in septic shock patients and in healthy volunteers after LPS administration. The PCSK9 effect was abrogated in LDL receptor (LDLR) knockout mice and in humans who are homozygous for an LDLR variant that is resistant to PCSK9. Together, our results show that reduced PCSK9 function is associated with increased pathogen lipid clearance via the LDLR, a decreased inflammatory response, and improved septic shock outcome.

Purpose: Interleukin 6 (IL-6) is a proinflammatory cytokine produced during infections. We hypothesized that IL-6 levels in the cerebrospinal fluid (CSF) would be elevated in bacterial meningitis and useful for diagnosing and predicting neurologic outcomes. Materials and methods: For the differentiation of bacterial meningitis, serum and CSF samples were obtained from patients with an altered level of consciousness. Patients were classified into 3 groups: bacterial meningitis, nonbacterial central nervous system disease, and other site sepsis. Results: Of the 70 patients included in this study, there were 13 in the bacterial meningitis group, 21 in the nonbacterial central nervous system disease group, and 36 in the other site sepsis group. The CSF IL-6 level was significantly higher in the bacterial meningitis group than in the other 2 groups (P &lt; .0001). Of the 5 CSF parameters assessed, CSF IL-6 level exhibited the largest area under the receiver operating characteristic curve (0.962), with a cut-off value of 644 pg/mL (sensitivity, 92.3%; specificity, 89.5%). To examine a potential association between a high CSF level and neurologic outcome, CSF IL-6 levels were divided into 4 quartiles, and each level was compared with the frequency of a good neurologic outcome. The frequency of a good neurologic outcome was significantly lower in the highest CSF IL-6 quartile than in the other 3 quartiles (odds ratio, 0.18; 95% confidence interval, 0.05-0.69; P = .013). Conclusions: Measurement of the CSF IL-6 level is useful for diagnosing bacterial meningitis. (C) 2014 Elsevier Inc. All rights reserved.

The major symptoms of median arcuate ligament syndrome, celiac axis stenosis, or occlusion compressed by the median arcuate ligament include eating-associated abdominal pain and weight loss. Because celiac stenosis increases retrograde collateral blood flow from the superior mesenteric artery to the celiac artery via the pancreaticoduodenal arcade, a pancreaticoduodenal artery aneurysm could occur at a low incidence rate. Rupture of the pancreaticoduodenal artery aneurysm and hemorrhagic shock are rare. In this report, we present 3 cases of patients who had been well with no abdominal symptoms until the day of admission, when they experienced sudden-onset intra-abdominal hemorrhage and shock. These 3 patients were admitted to the emergency department, and contrast-enhanced computed tomography and radiographic selective catheter angiography revealed intra-abdominal hemorrhage, stenosis of the celiac arteries, and dilated pancreaticoduodenal arcade. Case 1 demonstrated severe hemorrhagic shock, whereas case 2 demonstrated moderate shock. We treated ruptured pancreaticoduodenal artery aneurysms with coil embolization. Case 3 demonstrated complete celiac occlusion and moderate hemorrhagic shock, and no aneurysm was detected.

Objective: Triggering receptor expressed on myeloid cells-1 (TREM-1) was reported to play a key roll in amplification of production of inflammatory cytokines. TREM-1 is suggested to be a specific biomarker for sepsis for this reason, but the clinical significance of TREM-1 has not been elucidated. We investigated TREM-1 expression on the cell-surface, and plasma levels of soluble TREM-1 (sTREM-1) in patients with non-infectious systemic inflammatory response syndrome (SIRS) and sepsis admitted to the ICU. Methods: Thirty-five patients with SIRS and 21 patients with sepsis admitted to ICU were subjected to the study. TREM-1 expressions on the surfaces of monocytes and neutrophils were measured by flow cytometry. Plasma sTREM-1 level and serum interleukin (IL)-6 level were measured. Results: Septic patients had decreased TREM-1 expression, clearly on neutrophils or to a lesser extent on monocyte compared to SIRS patients on ICU admission (neutrophils p&lt . 0.001, monocyte p&lt . 0.05). TREM-1 expression on neutrophils had a significant inverse correlation with serum IL-6 level (r= -0.64, p&lt . 0.0001). Plasma sTREM-1 level in septic patients was significantly higher than that in SIRS patients (p&lt . 0.05). Plasma sTREM-1 level positively correlated with severity score and non-survivors had increased plasma sTREM-1 level compared to survivors in all SIRS/sepsis patients (p&lt . 0.05). Conclusions: Patients with sepsis had increased soluble TREM-1 and decreased TREM-1 expression on neutrophil compared to SIRS patients. sTREM-1 may be useful to evaluate disease severity and outcome of patients with SIRS or sepsis. © 2012 Elsevier Ltd.

Background and Objective: Interleukin-8 (IL-8) is a central chemokine in acute respiratory distress syndrome (ARDS), and the IL-8 gene contains a functional single nucleotide polymorphism (SNP) -251A/T in its promoter region. We hypothesized that IL-8 -251A/T SNP is associated with PaO2/FiO(2) in critically ill patients. Methods: We conducted genetic-association studies in intensive care units at academic teaching centres using a derivation septic shock cohort (vasopressin and septic shock trial (VASST), n = 467) and a validation post-cardiopulmonary bypass surgery cohort (CPB, n = 739) of Caucasian patients. Patients in both cohorts were genotyped for IL-8 -251A/T. The primary outcome variable in both cohorts was the fraction of patients who had a PaO2/FiO(2) &lt; 200. IL-8 mRNA expression was measured in genotyped lymphoblastoid cells in vitro. Results: The frequency of the patients with PaO2/FiO(2) &lt; 200 was significantly greater in patients who had the AA genotype of -251A/T than in patients who had the AT or TT genotypes in both VASST (AA = 60.8% vs AT and TT = 53.8% and 48.0%, P = 0.038) and the CPB cohort (AA = 37.0% vs AT and TT = 27.0% and 26.0%, P = 0.039). Patients having the AA genotype had a higher probability to remain on mechanical ventilation (P = 0.047) in the first 14 days. Lymphoblastoid cells having the AA genotype had significantly higher IL-8 mRNA expression than cells having the AT or TT genotype (P = 0.022). Conclusions: Critically ill Caucasian patients who had the AA genotype of IL-8 -251A/T had an increased risk of PaO2/FiO(2) &lt; 200. The AA genotype was associated with greater IL-8 mRNA expression than the AT or TT genotypes.

Introduction: Genetic variation in the Protein C gene (PROC) is associated with altered risk of adverse outcome for a number of diseases. Common single nucleotide polymorphisms (SNPs) in the promoter region and the adjacent 5' region of PROC are associated with Protein C expression. We tested the hypothesis that common SNPs (minor allele frequency &gt;10%) between the frequently studied promoter SNPs -1654 (rs1799808) and -1641 (rs1799809), and the end of PROC intron 2 alter nuclear transcription factor binding. Materials and Methods: We used electrophoretic mobility shift assays with 25-mer oligonucleotides centered on each of the 10 SNPs assessed in this potential regulatory region of the Protein C gene to test for differential binding to nuclear factors isolated from Hep-G2 cells. Results: We found that the G-allele oligo of the intron 2 SNP rs2069915[G/A] bound nuclear factors more avidly than the A-allele (p = 1.9x10(-9), n = 24). Similarly, we found that the C-allele oligo of the intron 2 SNP rs2069916 [C/T] bound nuclear factors more avidly than the T-allele, (p = 3.7x10(-6), n = 19). Cold competition and supershift assays suggested that the protein differentially binding to the C-allele of rs2069916 was USF1. Notably, we observed minimal nuclear factor binding to oligos containing haplotypes of the previously reported -1654 and -1641 SNPs. Luciferase reporter assays that showed the A-T haplotype of rs2069915 and rs2069916 drives transcription significantly more than the C-G haplotype (t-test, P = 0.015, n = 12). Conclusion: Differential transcription factor binding occurs for common SNPs in the 5' intronic regions of PROC which may contribute to PROC regulation and reported PROC SNP - phenotype associations. (C) 2012 Elsevier Ltd. All rights reserved.

We hypothesized that lactate levels even within the normal range are prognostic and that low lactate levels predict a beneficial response to vasopressin infusion in septic shock. We conducted a retrospective analysis using the Vasopressin in Septic Shock Trial (VASST) as a derivation cohort (n = 665), then validated using another single-center septic shock cohort, St Paul's Hospital (SPH) cohort (n = 469). Lactate levels were divided into quartiles. The primary outcome variable was 28-day mortality in both cohorts. We used receiver operating characteristic (ROC) curve analysis to compare the prognostic value of lactate concentrations versus Acute Physiology and Chronic Health Evaluation II scores. We then explored whether lactate concentrations might predict beneficial response to vasopressin compared with noradrenaline in VASST. Normal lactate range is less than 2.3 mmol/L. At enrolment, patients in the second quartile (1.4 &lt; lactate &lt; 2.3 mmol/L) had significantly increased mortality and organ dysfunction compared with patients who had lactate &lt;= 1.4 mmol/L (quartile 1) (P &lt; 0.0001). Quartile 2 outcomes were as severe as quartile 3 (2.3 &lt;= lactate &lt; 4.4 mmol/L) outcomes. Baseline lactate values (area under the ROC curve = 0.63, 0.66; VASST, SPH) were as good as Acute Physiology and Chronic Health Evaluation II scores (area under the ROC curve = 0.66, 0.73; VASST, SPH) as prognostic indicators of 28-day mortality. Lactate concentrations of 1.4 mmol/L or less predicted a beneficial response in those randomized to vasopressin compared with noradrenaline in VASST (P &lt; 0.05). Lactate concentrations within the "normal" range can be a useful prognostic indicator in septic shock. Furthermore, patients whose lactate level is less than or equal to 1.4 mmol/L may benefit from vasopressin infusion.

Introduction: The aim of the present study was to investigate the relationship between the blood IL-6 level, the blood glucose level, and glucose control in septic patients.Methods: This retrospective observational study in a general ICU of a university hospital included a total of 153 patients with sepsis, severe sepsis, or septic shock who were admitted to the ICU between 2005 and 2010, stayed in the ICU for 7 days or longer, and did not receive steroid therapy prior to or after ICU admission. The severity of stress hyperglycemia, status of glucose control, and correlation between those two factors in these patients were investigated using the blood IL-6 level as an index of hypercytokinemia.Results: A significant positive correlation between blood IL-6 level and blood glucose level on ICU admission was observed in the overall study population (n = 153 r = 0.24, P = 0.01), and was stronger in the nondiabetic subgroup (n = 112 r = 0.42, P &lt 0.01). The rate of successful glucose control (blood glucose level &lt 150 mg/dl maintained for 6 days or longer) decreased with increase in blood IL-6 level on ICU admission (P &lt 0.01). The blood IL-6 level after ICU admission remained significantly higher and the 60-day survival rate was significantly lower in the failed glucose control group than in the successful glucose control group (P &lt 0.01 and P &lt 0.01, respectively).Conclusions: High blood IL-6 level was correlated with hyperglycemia and with difficulties in glucose control in septic patients. These results suggest the possibility that hypercytokinemia might be involved in the development of hyperglycemia in sepsis, and thereby might affect the success of glucose control. © 2012 Nakamura et al. licensee BioMed Central Ltd.

Introduction: The aim of the present study was to investigate the relationship between the blood IL-6 level, the blood glucose level, and glucose control in septic patients. Methods: This retrospective observational study in a general ICU of a university hospital included a total of 153 patients with sepsis, severe sepsis, or septic shock who were admitted to the ICU between 2005 and 2010, stayed in the ICU for 7 days or longer, and did not receive steroid therapy prior to or after ICU admission. The severity of stress hyperglycemia, status of glucose control, and correlation between those two factors in these patients were investigated using the blood IL-6 level as an index of hypercytokinemia. Results: A significant positive correlation between blood IL-6 level and blood glucose level on ICU admission was observed in the overall study population (n = 153; r = 0.24, P = 0.01), and was stronger in the nondiabetic subgroup (n = 112; r = 0.42, P &lt; 0.01). The rate of successful glucose control (blood glucose level &lt; 150 mg/dl maintained for 6 days or longer) decreased with increase in blood IL-6 level on ICU admission (P &lt; 0.01). The blood IL-6 level after ICU admission remained significantly higher and the 60-day survival rate was significantly lower in the failed glucose control group than in the successful glucose control group (P &lt; 0.01 and P &lt; 0.01, respectively). Conclusions: High blood IL-6 level was correlated with hyperglycemia and with difficulties in glucose control in septic patients. These results suggest the possibility that hypercytokinemia might be involved in the development of hyperglycemia in sepsis, and thereby might affect the success of glucose control.