Effects of sevoflurane on postoperative liver functions in morbidly obese as compared to the non-obese patients

To assess the effect of sevoflurane anesthesia on hepatic function in morbidly obese versus non-obese patients undergoing abdominal surgeries. We prospectively evaluated the levels of the serum concentration of liver enzymes aspartate aminotransferase [AST], alanine aminotransferase [ALT], lactate dehydrogenase [LDH], gamma glutamyl transferase [GGT], alkaline phosphatase [ALP], and total bilirubin [TBil], in 42 morbidly obese and 40 non obese patients who were scheduled for elective abdominal surgery under sevoflurane anesthesia at the Jordan University Hospital, Amman, Jordan. Measurement of liver enzymes was done in the recovery room, and on the first, 3 and 7 days after sevoflurane anesthesia, and the results were compared between the morbidly obese and non obese patients. ALT, AST, GGT and LDH increased significantly in the morbidly obese than they did in non obese patients. In morbidly obese patients TBil increased gradually peaking 7 days after anesthesia, LDH increased in the recovery room, AST and ALT increased in the recovery room and first day, while GGT increased 7th day after anesthesia. In non obese patients, AST, LDH increased in the recovery. ALP did not change in both groups. Sevoflurane induces elevation of the serum liver enzymes in morbidly obese patients with variable onsets

Intravenous dexmedetomidine prolongs bupivacaine spinal analgesia

The prolongation of spinal anesthesia by using clonidine through the oral, intravenous and spinal route has been known. The new ?2 agonist, dexmedetomidine has been proved to prolong the spinal anesthesia through the intrathecal route. We hypothesized that dexmedetomidine when administered intravenously following spinal block, also prolongs spinal analgesia. 48 patients were randomly allocated into two equal groups following receiving spinal isobaric bupivacaine 12.5 mg. Patients in group D received intravenously a loading dose of 1 microg/kg dexmedetomidine over 10 min and a maintenance dose of 0.5 microg/kg/hr. Patients in group C [the control group] received normal saline. The regression times to reach S1 sensory level and Bromage 0 motor scale, hemodynamic changes and the level of sedation were recorded. The duration of sensory block was longer in intravenous dexmedetomidine group compared with control group [261.5 +/- 34.8 min versus 165.2 +/- 31.5 min, P < 0.05]. The duration of motor block was longer in dexmedetomidine group than control group [199 +/- 42.8 min versus 138.4 +/- 31.3 min, P < 0.05]. Intravenous dexmedetomidine administration prolonged the sensory and motor blocks of bupivacaine spinal analgesia with good sedation effect and hemodynamic stability