Bispectral index for monitoring anesthetic depth in patients with severe burns receiving target-controlled infusion of remifentanil and propofol.

This study evaluated the feasibility and effectiveness of using the bispectral index (BIS) to monitor anesthetic depth in patients with severe burns receiving intravenous target-controlled infusion (TCI) of remifentanil and propofol. We randomly assigned 80 patients undergoing elective escharectomy (<1 week) to BIS (A) and control (B) groups. All patients received remifentanil and propofol as intravenous TCI anesthesia. Clinical data were recorded at different time points. The time from drug withdrawal to eye opening upon the patient hearing his/her name called and upon reaching an Aldrete score of 9 points was also recorded. During anesthesia maintenance, the target concentrations of remifentanil and propofol in group A were significantly lower than that in group B (2.12 ± 0.35 vs 2.50 ± 0.21 ng/mL and 2.54 ± 0.22 vs 2.86 ± 0.31 µg/mL, respectively; P < 0.01). The time from drug withdrawal to eye opening upon the patient hearing his/her name called and reaching an Aldrete score of 9 points in group A was considerably shorter than that in group B (7.90 ± 0.58 vs 8.35 ± 0.66 min and 9.15 ± 0.69 vs 11.13 ± 0.96 min, respectively; P < 0.01). In both groups, mean arterial pressure and heart rate values at each time point after loss of consciousness were significantly lower than the baseline values (P < 0.05), with the exception of 2 min after intubation. The use of BIS to monitor anesthetic depth in patients with severe burns receiving TCI of remifentanil and propofol during the perioperative period reduces propofol consumption and shortens the consciousness recovery time in patients.

Prevalence of antibodies to hepatitis C virus in Chinese patients with viral hepatitis and hepatic failure.

Anti-HCV assay with ORTHO kits was done in 100 blood donors and recipients and 374 cases of viral hepatitis, including 65 cases of fulminant, subacute and chronic hepatic failure. None of the 100 blood donors and recipients showed positive anti-HCV response. Anti-HCV was positive in 7.6% of the patients with chronic persistent hepatitis, 9.7% of the patients with chronic active hepatitis and 23.1% of the patients with liver cirrhosis. High prevalence of anti-HCV was observed in subacute hepatic failure (60.8%) and chronic hepatic failure (53.9%). Fifty-two (83.9%) of 62 anti-HCV positive cases were infected concurrently with HBV. The incidence of HBV replicating marker in patients with HCV or co-infected with HBV was lower than that of those with HBV alone. It is suggested that HCV might inhibit the replication of hepatitis B virus. The mortality rate of patients with anti-HCV positive hepatic failure was higher than that of those with HBV infection. Therefore, anti-viral therapy for anti-HCV positive hepatic failure should be considered.

Serum tumor necrosis factor (TNF) in the pathogenesis of clinical hepatic failure of HCV and/or HBV infection.

Serum TNF and IL-6 levels were measured in 48 patients with liver disease positive for anti-HCV only or concurrent HBV infection. High serum TNF levels were observed in patients with liver disease positive for anti-HCV and/or HBV infection (P < 0.001). Serum TNF levels varied with the severity of liver disease. Serum TNF levels of anti-HCV positive patients with hepatic failure were higher than those with CAH (P < 0.01). Serum TNF levels of patients infected with HCV or concurrent HBV were also significantly higher than those with HBV infection alone (P < 0.001). However, no difference in serum IL-6 levels was observed in either group of patients. Serum TNF in the deceased patients with hepatic failure induced by HBV and HCV infection was higher than in those who survived (P < 0.05), and it also seemed significantly different in patients with and without multiple organ failure (P < 0.05). In vitro, HSS showed marked inhibitory activity on TNF production from PBM induced by endotoxin, but had no significant effect on the TNF cytotoxicity of L929 cells. It seems that high serum TNF level is an important mediator in the pathogenesis of liver necrosis and failure of microcirculation in HCV and/or HBV infection. These observations favor the attempt to treat hepatic failure with HSS or anti-TNF. Encouraging results were achieved using HSS in the treatment of subacute liver necrosis in our institute.(ABSTRACT TRUNCATED AT 250 WORDS)

[Tumor necrosis factor and interleukin 6 in hepatitis C virus infection].

Tumor necrosis factor (TNF) was determined with ELISA in 72 patients with hepatitis C and hepatitis B virus infections. Interleukin 6 (IL-6) was determined at the same time. TNF and IL-6 were significantly increased in patients with hepatitis C virus infections when compared with normal subjects and hepatitis B patients. There was a significant positive correlation between TNF and IL-6. It is suggested that increased TNF and IL-6 may play an important role in pathogenesis of hepatitis C virus infection.