Purpose: Delirium is a common complication in postoperative critically ill patients. Although abnormal melatonin metabolism is thought to be one of the mechanisms of delirium, there have been few studies in which the association between alteration of perioperative plasma melatonin concentration and postoperative delirium was assessed.
Materials:We conducted a prospective observational study to assess the association of perioperative alteration of plasma melatonin concentration with delirium in 40 postoperative patients who required intensive care for more than 48 hours. We diagnosed postoperative delirium using CAM-ICU and measured melatonin concentration 4 times (before the operation as the preoperative value, 1 hour after the operation, POD 1 and POD 2).Results: Postoperative delirium occurred in 13 (33%) of the patients. Although there was no significant difference in preoperative melatonin concentration, delta melatonin concentration at 1 hour after the operation was significantly lower in patients with delirium than in those without delirium (-1.1 vs. 0 pg/ml, p=0.036). After adjustment of relevant confounders, delta melatonin concentration was independently associated with risk of delirium (odds ratio; 0.50, p=0.047).
Conclusions:Delta melatonin concentration at 1 hour after the operation has a significant independent association with risk of postoperative delirium.
BackgroundAcute kidney injury (AKI) after cardiac surgery in children with congenital heart disease is a common complication. AKI is also associated with high morbidity and mortality. The Kidney Diseases Improving Global Outcomes (KDIGO) criteria for AKI classification are now widely used for the definition of AKI. It is noteworthy that a statement about children was added to the criteria. Many studies aimed at finding useful biomarkers are now being performed by using these criteria. Clinicians should be aware of the recent progress in understanding AKI in children.Main contentsUnlike adult patients, young age is one of the major risk factors for AKI in pediatric cardiac surgery. The mechanism of the development of AKI in children might be different from that in adults because the surgical procedure and CPB technique in pediatric patients are greatly different from those in adult patients.There are many biomarkers for early detection of AKI, and some of them are widely used in hospitals. One of the major benefits of such biomarkers is the rapidness of expression for detecting increases in their expression levels. Neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, cystatin C, and albumin have been investigated in some studies, and the usefulness of these biomarkers for detection of AKI and diagnosis of disease severity has been shown.Although there are many interventions for preventing and treating AKI after cardiac surgery in children, there is still no specific effective treatment. Peritoneal dialysis is effective for only maintaining a negative fluid balance early after cardiac surgery. The long-term prognosis of AKI is an issue of interest. Although mortality and morbidity of AKI in the acute phase of disease remain high, the long-term condition in pediatric patients is relatively acceptable unlike in adults.ConclusionsKDIGO criteria are advocated as a diagnostic tool for common perception. Early recognition and intervention for AKI can be achieved by using several biomarkers. Further studies are needed to establish effective treatment for AKI.
BackgroundA change of serum lactate concentrations appeared to be useful for predicting outcomes in various acute ill settings. However, there is little information on intraoperative change of lactate level in pediatric cardiac surgery patients.MethodsWe conducted a retrospective observational study of 459 children who received pediatric cardiac surgery to determine the association between change of lactate level after cardiopulmonary bypass (CPB) and patient prognosis (length of ICU stay and incidence of postoperative serious adverse events (SAEs)). We defined change of lactate level after CPB (LAC⊿) as (final lactate level measurement in the operating room) – (lactate level measured at the end of CPB). To study the independent association of LAC⊿ with length of ICU stay, we used linear regression model.ResultsThere were 1145 lactate measurements after CPB in this study cohort. After weaning from CPB, the serum lactate levels significantly increased from 2.1 mmol/L to 2.5 mmol/L (p < 0.001). Patients with higher LAC⊿ had significantly longer stay in ICU (p = 0.017) and higher incidence of SAEs (p = 0.002). In multivariate linear regression analysis, higher LAC⊿ showed a significant independent association with longer length of ICU stay.ConclusionsIncreased lactate level after CPB was associated with the longer duration of ICU stay and increased risk of postoperative SAEs in pediatric cardiac surgery patients. Future studies should be conducted to determine the clinical utility of intraoperative trend of lactate levels.Electronic supplementary materialThe online version of this article (doi:10.1186/s12871-015-0007-y) contains supplementary material, which is available to authorized users.
Hemorrhagic shock followed by resuscitation (HSR) causes neutrophil sequestration in the lung which leads to acute lung injury (ALI). Neutrophil elastase (NE) is thought to play a pivotal role in the pathogenesis of ALI. This study investigated whether sivelestat, a specific NE inhibitor, can attenuate ALI induced by HSR in rats. Male Sprague-Dawley rats were subjected to hemorrhagic shock by withdrawing blood so as to maintain a mean arterial blood pressure of 30±5 mm Hg for 60 min followed by resuscitation with the shed blood. HSR-treated animals received a bolus injection of sivelestat (10 mg/kg) intravenously at the start of resuscitation followed by continuous infusion for 60 min (10 mg/kg/h) during the resuscitation phase, or the vehicle. Lung injury was assessed by pulmonary histology, lung wetweight to dry-weight (W/D) ratio, myeloperoxidase (MPO) activity, gene expression of tumor necrosis factor (TNF)-• and inducible nitric oxide synthase (iNOS), DNA binding activity of nuclear factor (NF)-κB, and immunohistochemical analysis of intercellular adhesion molecule (ICAM)-1. HSR treatment induced lung injury, as demonstrated by pulmonary edema with infiltration of neutrophils, the increase in lung W/D ratio, MPO activity, gene expression of TNF-• and iNOS, and DNA-binding activity of NF-κB, and enhanced expression of ICAM-1. In contrast, sivelestat treatment significantly ameliorated the HSR-induced lung injury, as judged by the marked improvement in all these indices. These results indicate that sivelestat attenuated HSR-induced lung injury at least in part through an inhibition of the inflammatory signaling pathway, in addition to the direct inhibitory effect on NE.
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