Epidural combination of ropivacaine with sufentanil for postoperative analgesia after total knee replacement: a pilot study.

BACKGROUND AND OBJECTIVE: We assessed the analgesic efficacy of postoperative epidural infusions of ropivacaine 0.1 and 0.2% combined with sufentanil 1 microg mL(-1) in a prospective, randomized, double-blinded study. METHODS: Twenty-two ASA I-III patients undergoing elective total-knee replacement were included. Lumbar epidural blockade using ropivacaine 0.75% was combined with either propofol sedation or general anaesthesia for surgery. After surgery, the epidural infusion was commenced. Eleven patients in each group received either an epidural infusion of ropivacaine 0.1% with 1 microg mL(-1) sufentanil (Group 1) or ropivacaine 0.2% with 1 microg mL(-1) sufentanil (Group 2) at a rate of 5-9 mL h(-1). All patients had access to intravenous pirinatrimide (piritramide) via a patient-controlled analgesia (PCA) device. RESULTS: Motor block was negligible for the study duration in both groups. There was no significant difference with the 100 mm visual analogue scale (VAS) scores, with the consumption of rescue analgesia or with patient satisfaction. Patients in Group 1 experienced significantly less nausea (P < 0.05) than those in Group 2. Both treatment regimens provided effective postoperative analgesia with only a minimal use of supplemental opioid PCA. CONCLUSIONS: We recommend the use of ropivacaine 0.1% with 1 microg mL(-1) sufentanil for postoperative analgesia after total knee replacement as it provides efficient pain relief with no motor block of the lower limbs. In addition, compared with 0.2% ropivacaine with sufentanil, the mixture reduces local anaesthetic consumption without compromise in patient satisfaction or VAS scores. Patients even experience less nausea.

H1-antagonism improves intestinal mucosal pH and heart function in porcine hypodynamic endotoxic shock.

Porcine hypodynamic shock was induced by continuous infusion of 5 micrograms lipopolysaccharide/kg per hour. This resulted in a decrease of cardiac output from baseline values of 3.5 +/- .9 L/min to 1.5 +/- .8 L/min and a reduced left ventricular stroke work index in the endotoxin-group (n = 6 animals). Pretreatment with the H1-antagonist dimethindene (2 mg/kg) in a second group (n = 6) significantly prevented these effects. Furthermore animals pretreated with the H1-antagonist showed a stable mean arterial blood pressure, whereas the control endotoxin-treated group revealed a drastic reduction in mean arterial blood pressure (99 +/- 4.7 mmHg versus 65.8 +/- 10 mmHg after 240 min, respectively). Pulmonary function and systemic vascular resistance were not ameliorated by the H1-antagonist in hypodynamic shock. Gastrointestinal mucosal pH (pHi), which indicates oxygenation of the mucosa, was decreased by endotoxin-infusion (7.45 +/- .32 baseline value to 6.92 +/- .24 after 120 min). This parameter as well as base excess values and lactate levels were significantly improved by dimethindene-pretreatment (p < .05). These results may indicate a beneficial effect of H1-antagonist-pretreatment on endotoxin-induced deterioration of the microcirculation. Furthermore our results clearly demonstrated that only pretreatment before endotoxemia with H1-antagonism is effective, since infusion of H1-antagonist in hypodynamic shock 45 min after addition of endotoxin (n = 6 animals) did not improve the cardiovascular system or the microcirculation.

Effect of H1-antagonism on cardiovascular, pulmonary, and immunological dysfunction in porcine endotoxic shock.

The definite role of histamine in early hyperdynamic septic shock is not yet clear. Therefore a randomized, controlled, blind trial was performed to investigate the effect of the H1-antagonist dimethindene in hyperdynamic porcine shock. Lipopolysaccharide (LPS) infusion (5 micrograms/kg/h) in anesthetized pigs (n = 6) in the control-group induced a hyperdynamic shock state with a decrease in mean arterial blood pressure, and systemic vascular resistance (SVR), and an increase in mean arterial pulmonary pressure and pulmonary vascular resistance (PVR). In the verum group (n = 6) dimethindene (2 mg/kg) administered 15 min before LPS application prevented the decrease in SVR significantly (p < .05) and ameliorated the increase in MPAP and PVR. The impairment in pulmonary function, as measured by the oxygenation ratio (PaO2/FiO2) in LPS-treated animals, was reduced by the H1-antagonist (p = .01). Tissue oxygenation was ameliorated by the H1-antagonist treatment, as demonstrated by plasma lactate levels and base excess values (p < .05, control group versus dimethindene group). The increase in tumor necrosis factor alpha by LPS infusion was not influenced by H1-antagonist pretreatment. The early decrease in SVR did not correlate with an enhanced nitric oxide formation, as measured by nitrate/nitrite plasma levels.