Purpose: The aim of this study was to assess the accuracy of a continuous survival probability prediction using noninvasive measures of cardiac performance and tissue perfusion in severely injured pediatric patients. ...Purpose: The aim of this study was to assess the accuracy of a continuous survival probability prediction using noninvasive measures of cardiac performance and tissue perfusion in severely injured pediatric patients. Methods: Review of all patients entered into a prospective noninvasive monitoring protocol. Cardiac index (CI) was measured using a thoracic bioimpedance device and tissue perfusion was assessed by transcutaneous carbon dioxide (PtCO2) tension and oxygen tension indexed to the fraction of inspired oxygen (PtcO2FiO2). Survival probability (SP) was continuously calculated using a stochastic analysis program. Results: There were 45 patients with a total of 953 data sets. The mean age was 11 years (range, 1-16 years) with a mean Injury Severity Score of 24 (±16). There was no difference between survivors (n = 32) and nonsurvivors (n = 13) at study entry for heart rate, blood pressure, CI, or pulse oximetry (all P > .05). However, survivors demonstrated higher PtcCO2 (45 vs 35), higher PtcO2FiO2 (236 vs 156), and higher predicted SP (89%vs 62%) compared with nonsurvivors at study entry and throughout the monitoring period (all P < .01). For the entire data set, the strongest independent predictors of survival were PtcO2FiO2 and SP. The area under the receiver operating characteristic curve for mortality prediction was 0.83 for SP and 0.71 for PtcO2FiO2, compared with 0.6 for heart rate, 0.51 for blood pressure, and 0.53 for CI. Similar hemodynamic patterns were observed for all injury patterns with the exception of those with severe brain injury. Conclusions: Thoracic bioimpedance and transcutaneous monitoring give critical real-time hemodynamic and tissue perfusion data that can provide early identification of pathologic flow patterns and accurately predict survival.展开更多
Objective. In alcoholic liver disease (ALD), progression from initial steatosis, through hepatitis to cirrhosis is well described, resulting in 20,000 deaths in the UK annually. However, pathological mechanisms are no...Objective. In alcoholic liver disease (ALD), progression from initial steatosis, through hepatitis to cirrhosis is well described, resulting in 20,000 deaths in the UK annually. However, pathological mechanisms are not well understood and drug trials have led to conflicting results. It has been established that alcohol consumption increases hepatic free radical production and oxidant stress has been implicated in the disease process. Material and methods. Markers of lipid peroxidation, antioxidant status, hepatic fibrogenesis, inflammation and liver function were measured in blood and urine from 24 patients with established alcoholic cirrhosis and in 49 age-and sex-matched controls. Results. In the ALD group, lipid peroxidation markers 8-isoprostane and malondialdehyde were significantly increased (p < 0.001), as was the ratio of oxidized to reduced glutathione (p = 0.027). The antioxidants selenium, glutathione (whole blood and plasma) and vitamins A, C and E were all significantly decreased (p < 0.001); median plasma glutathione levels were only 19%of control levels. Type III procollagen peptide (PIIINP), a serum marker of hepatic fibrogenesis, and C-reactive protein (CRP) were both increased (p < 0.001). Urinary 8-isoprostane correlated positively with PIIINP, CRP and markers of cholestasis (alkaline phosphatase and bilirubin) and negatively with glutathione (whole blood), vitamins A and E and albumin. Conclusions. Oxidant stress, as reflected in blood and urine by a wide range of pro-and antioxidant markers, is a significant feature of alcoholic cirrhosis, providing a mechanism by which alcohol intake may be linked to hepatic inflammation and fibrosis. Non-invasive markers could prove valuable in monitoring response to treatment during clinical trials.展开更多
文摘Purpose: The aim of this study was to assess the accuracy of a continuous survival probability prediction using noninvasive measures of cardiac performance and tissue perfusion in severely injured pediatric patients. Methods: Review of all patients entered into a prospective noninvasive monitoring protocol. Cardiac index (CI) was measured using a thoracic bioimpedance device and tissue perfusion was assessed by transcutaneous carbon dioxide (PtCO2) tension and oxygen tension indexed to the fraction of inspired oxygen (PtcO2FiO2). Survival probability (SP) was continuously calculated using a stochastic analysis program. Results: There were 45 patients with a total of 953 data sets. The mean age was 11 years (range, 1-16 years) with a mean Injury Severity Score of 24 (±16). There was no difference between survivors (n = 32) and nonsurvivors (n = 13) at study entry for heart rate, blood pressure, CI, or pulse oximetry (all P > .05). However, survivors demonstrated higher PtcCO2 (45 vs 35), higher PtcO2FiO2 (236 vs 156), and higher predicted SP (89%vs 62%) compared with nonsurvivors at study entry and throughout the monitoring period (all P < .01). For the entire data set, the strongest independent predictors of survival were PtcO2FiO2 and SP. The area under the receiver operating characteristic curve for mortality prediction was 0.83 for SP and 0.71 for PtcO2FiO2, compared with 0.6 for heart rate, 0.51 for blood pressure, and 0.53 for CI. Similar hemodynamic patterns were observed for all injury patterns with the exception of those with severe brain injury. Conclusions: Thoracic bioimpedance and transcutaneous monitoring give critical real-time hemodynamic and tissue perfusion data that can provide early identification of pathologic flow patterns and accurately predict survival.
文摘Objective. In alcoholic liver disease (ALD), progression from initial steatosis, through hepatitis to cirrhosis is well described, resulting in 20,000 deaths in the UK annually. However, pathological mechanisms are not well understood and drug trials have led to conflicting results. It has been established that alcohol consumption increases hepatic free radical production and oxidant stress has been implicated in the disease process. Material and methods. Markers of lipid peroxidation, antioxidant status, hepatic fibrogenesis, inflammation and liver function were measured in blood and urine from 24 patients with established alcoholic cirrhosis and in 49 age-and sex-matched controls. Results. In the ALD group, lipid peroxidation markers 8-isoprostane and malondialdehyde were significantly increased (p < 0.001), as was the ratio of oxidized to reduced glutathione (p = 0.027). The antioxidants selenium, glutathione (whole blood and plasma) and vitamins A, C and E were all significantly decreased (p < 0.001); median plasma glutathione levels were only 19%of control levels. Type III procollagen peptide (PIIINP), a serum marker of hepatic fibrogenesis, and C-reactive protein (CRP) were both increased (p < 0.001). Urinary 8-isoprostane correlated positively with PIIINP, CRP and markers of cholestasis (alkaline phosphatase and bilirubin) and negatively with glutathione (whole blood), vitamins A and E and albumin. Conclusions. Oxidant stress, as reflected in blood and urine by a wide range of pro-and antioxidant markers, is a significant feature of alcoholic cirrhosis, providing a mechanism by which alcohol intake may be linked to hepatic inflammation and fibrosis. Non-invasive markers could prove valuable in monitoring response to treatment during clinical trials.
