Michael G. Rockemann

Prophylactic use of epidural mepivacaine/morphine, systemic diclofenac, and metamizole reduces postoperative morphine consumption after major abdominal surgery

Background Surgical trauma induces nociceptive sensitization leading to amplification and prolongation of postoperative pain. While preemptive analgesic treatment with numerous agents has been successful in experimental animals, results of human studies remain conflicting. The authors used a multimodal approach for preemptive analgesia before abdominal surgery: diclofenac and metamizole inhibit prostaglandin synthesis, thus influencing peripheral sensitization; epidural local anesthetics induce conduction block, epidural opioids inhibit nociceptive synaptic transmission, and metamizole induces descending inhibition. The interaction of these drugs might suppress spinal nociceptive sensitization and postoperative analgesic demand. Methods One hundred forty-two patients scheduled for major abdominal surgery were randomly assigned to one of three groups and studied prospectively. Epidural catheters in groups 1 and 2 were placed at interspaces T8-T10, the position of the catheter was confirmed by epidurography, and sensory testing after administration of 5 ml mepivacaine 1%. Group 1 received 75 mg intramuscular diclofenac, 1000 mg intravenous metamizole, 5.3+/-1 mg epidural morphine, and 15-20 ml mepivacaine 1% 85+/-41 min before skin incision. Epidural analgesia was maintained by injections of 0.1 ml *symbol* kg sup -1 *symbol* h sup -1 mepivacaine 1%. Group 2 patients received the balanced analgesia regimen before wound closure (221+/-86 min after skin incision). Group 3 patients did not receive any study substances. General anesthesia was induced with 5 mg/kg thiopental and 2 micro gram/kg fentanyl and maintained with enflurane and nitrous oxide. Postoperative analgesia consisted of patient-controlled intravenous morphine over 5 days. Results Median visual analog scale pain intensities were < 3 cm and did not differ among the groups. Morphine consumption per hour on postoperative day 2 was 0.8+/-0.1 mg/h (group 1) < 1.2+/- 0.1 mg/h (group 2) = 1.1+/-0.1 mg/h (group 3) and cumulative morphine consumption (in mg) on the morning of day 5 was 95+/-9 (group 1) < 111+/-11 (group 2) < 137+/-10 (group 3). Conclusions A significant reduction of patient-controlled analgesia requirements could be achieved by our preincisional balanced analgesia regimen compared to application before wound closure. The more distinct difference between patients receiving balanced analgesia and those in the control group is based on the analgesic action of the study substances, which lasted about 14 h.

Effect of 7.2% Hypertonic Saline/6% Hetastarch on Left Ventricular Contractility in Anesthetized Humans

Background Although a positive inotropic effect of hypertonic saline has been demonstrated in isolated cardiac tissue as well as in animal preparations, no information exists about a possible positive inotropic action of hypertonic saline in humans. The aim of this investigation was to determine whether a clinically relevant positive inotropic effect can be demonstrated in humans. Methods Twenty-six patients without cardiovascular disease were randomized to receive 4 ml/kg of either 7.2% hypertonic saline/6% hetastarch or 6% hetastarch (control) at a rate of 1 ml *symbol* kg sup -1 *symbol* min sup -1 while under general endotracheal anesthesia. Transesophageal echocardiography was used to evaluate left ventricular function. Arterial pressure, heart rate, and left ventricular end-systolic and end-diastolic diameter, area, and wall thickness were measured immediately before and after administration of either solution. Fractional area change, end-systolic wall stress, and the area under the end-systolic pressure-length relationship curve (ESPLRarea) were calculated. ESPLRarea was used to assess left ventricular contractility. Results Administration of hypertonic saline/hetastarch resulted in a significant decrease of mean arterial pressure and end-systolic wall stress from 77 plus/minus 14 (mean plus/minus SD) to 64 plus/minus 17 mmHg (P < 0.01) and from 52 plus/minus 14 to 32 plus/minus 11 103 dyne/cm2 (P > 0.01), respectively. End-diastolic area and fractional area change increased from 16.5 plus/minus 2.9 to 21.7 plus/minus 3.3 cm2 (P < 0.01) and from 0.53 plus/minus 0.07 to 0.70 plus/minus 0.06 (P < 0.01), respectively, whereas there was only a minor change of ESPLRarea from 38 plus/minus 13 to 44 plus/minus 13 mmHg.cm (P < 0.05). Conclusions The apparent improvement of left ventricular systolic function in response to hypertonic saline/hetastarch is caused mainly by the combined effect of increased left ventricular preload and reduced left ventricular afterload. A possible positive inotropic action of hypertonic saline/hetastarch is not likely to be clinically relevant.

Analgesic and hemodynamic effects of epidural clonidine, clonidine/morphine, and morphine after pancreatic surgery--a double-blind study.

This study characterizes analgesia and hemodynamics after epidural clonidine 8 micro gram/kg (Group C) or clonidine 4 micro gram/kg + morphine 2 mg (Group CM) in comparison to epidural morphine 50 micro gram/kg (Group M).Forty-five patients scheduled for pancreatectomy in combined general/epidural anesthesia were studied. The study drugs were administered 75 min postoperatively and for 10 h pain intensity (visual analog scale [VAS]), heart rate (HR), mean arterial pressure (MAP), and cardiac output (CO) were measured; filling pressures were kept >5 mm Hg. Adequate analgesia could be achieved within 1 h in all patients of Groups C and CM, but only in six patients of Group M (P < 0.001). Quality of analgesia was comparable in all groups (VAS reduction 82% +/- 20%, mean +/- SD) but duration of analgesic action was longer in Groups CM (586 +/- 217 min) and M (775 +/- 378 min) compared to Group C (336 +/- 119 min) (P < 0.001). In Group M, no hemodynamic alterations occurred. In Groups C and CM, HR, CO, and MAP were reduced significantly compared to baseline within the first 15-90 min, while stroke volume and systemic vascular resistance remained stable. We conclude, that hemodynamic alteration after epidural clonidine under conditions of stable filling pressures is caused mainly by a decrease in HR. It is not an effect of analgesia but of the intrinsic antihypertensive action of clonidine. (Anesth Analg 1995;80:869-74)

The effects of thoracic epidural anesthesia on hepatic blood flow in patients under general anesthesia.

BACKGROUND: Hepatic hypoperfusion is regarded as an important factor in the pathophysiology of perioperative liver injury. Although epidural anesthesia (EDA) is a widely used technique, no data are available about the effects on hepatic blood flow of thoracic EDA with blockade restricted to thoracic segments in humans. METHODS: In 20 patients under general anesthesia, we assessed hepatic blood flow index in the right and middle hepatic vein by use of multiplane transesophageal echocardiography before and after induction of EDA. The epidural catheter was inserted at TH7-9, and mepivacaine 1% with a median (range) dose of 10 (8–16) mL was injected. Norepinephrine (NE) was continuously administered to patients who demonstrated a decrease in mean arterial blood pressure below 60 mm Hg after induction of EDA (EDA-NE group). The other patients did not receive any catecholamine during the study period (EDA group). A further 10 patients without EDA served as controls (control group). RESULTS: In five patients, administration of NE was necessary to avoid a decrease in mean arterial blood pressure below 60 mm Hg. Thus, the EDA-NE group consisted of five patients and the EDA group of 15. In the EDA group, EDA was associated with a median decrease in hepatic blood flow index of 24% in both hepatic veins (P < 0.01). In the EDA-NE group, all five patients showed a decrease in the blood flow index of the right (median decrease 39 [11–45] %) and middle hepatic vein (median decrease 32 [7–49] %). Patients in the control group showed a constant blood flow index in both hepatic veins. Reduction in blood flow index in the EDA group and the EDA-NE group was significant in comparison with the control group (P < 0.05). In contrast to hepatic blood flow, cardiac output was not affected by EDA. CONCLUSIONS: We conclude that, in humans, thoracic EDA is associated with a decrease in hepatic blood flow. Thoracic EDA combined with continuous infusion of NE seems to result in a further decrease in hepatic blood flow.

The effect of ephedrine bolus administration on left ventricular loading and systolic performance during high thoracic epidural anesthesia combined with general anesthesia.

We investigated the effect of ephedrine on left ventricular function in patients without cardiovascular disease under high thoracic epidural anesthesia combined with general anesthesia. Because the epidural block was extended to all cardiac segments, ephedrine was assumed to be deprived of its centrally mediated actions. Left ventricular (LV) function was assessed using transesophageal echocardiography. We measured arterial pressure (AP), heart rate (HR), LV end-systolic and end-diastolic diameter and area (ESA, EDA), wall thickness, and LV ejection time before and after intravenous ephedrine bolus administration. We calculated area ejection fraction (EFA), end-systolic wall stress (ESWS), and mean velocity of circumferential fiber shortening (mVcfc). Ephedrine had a biphasic effect on left ventricular function. It transiently decreased EDA from 18.9 to 16.5 cm2 (mean), whereas EFA and mVcfc were increased from 33% to 49%, and from 1.88 to 2.67 circumferences/s, respectively. During the second phase, ephedrine increased mean arterial pressure (MAP) from a baseline value of 62 to 87 mm Hg, EDA was restored to 19.3 cm2, and EFA and mVcfc remained above baseline (52% and 2.64 circumferences/s, respectively). ESWS was not significantly increased from baseline. We conclude that ephedrine improves left ventricular contractility, even in the presence of high thoracic epidural anesthesia, without causing relevant changes of left ventricular afterload.

Effect of Phenylephrine Bolus Administration on Left Ventricular Function During High Thoracic and Lumbar Epidural Anesthesia Combined with General Anesthesia

The effect of phenylephrine (PHE) boluses on left ventricular (LV) function was examined in patients without cardiovascular disease who developed arterial hypotension during high thoracic epidural anesthesia (TEA) combined with general anesthesia (GA) (group 1) or lumbar epidural anesthesia (LEA) combined with GA (group 2). LV function was assessed by transesophageal echocardiography (TEE) before and after central venous injection of 1 microgram/kg PHE. Fractional diameter shortening (FDS), end-systolic wall stress (ESWS), and rate-corrected velocity of circumferential fiber shortening (mVcfc) were determined. PHE effectively restored arterial blood pressure in both groups with a peak effect between 30 and 45 s after injection. FDS was reduced from 38% to 25% (mean, P < 0.01) in group 1 and remained unchanged in group 2. ESWS increased from 70 to 143 x 10(3) dyne.cm-2 (P < 0.01) and from 57 to 86 x 10(3) dyne.cm-2 (P < 0.05), in groups 1 and 2, respectively. mVcfc was significantly reduced from 1.11 to 0.80 circ/s (P < 0.05) in group 1 and was not altered in group 2. The authors conclude that PHE given as an intravenous bolus to patients under high TEA plus general anesthesia causes a transient impairment of LV function.

Epidural bolus clonidine/morphine versus epidural patient-controlled bupivacaine/sufentanil: quality of postoperative analgesia and cost-identification analysis.

We compared the costs, quality of analgesia, and side effects of postoperative patient-controlled epidural analgesia (PCEA) with bupivacaine/sufentanil versus an epidural bolus (BOLUS) of clonidine/morphine in 68 patients with pancreatic surgery. Postoperative pain treatment was performed over 4 days: the PCEA pump was filled with bupivacaine 0.25% and sufentanil 2 micro g/mL and set to 3-mL bolus and 10-min lockout time. BOLUS patients received injections of clonidine 150 micro g plus morphine 2 mg on demand. Visual analog scale (VAS) score at rest and during coughing, heart rate (HR), systolic arterial pressure (SAP), incidence of postoperative nausea and vomiting, pruritus, duration of intestinal paralysis, hospital treatment, and costs for personnel and material were recorded. VAS scores during coughing (3 +/- 2.5 vs 5 +/- 3, P <0.001) was higher, and HR (79 +/- 13 vs 89 +/- 15, P <0.001), and SAP (110 +/- 18 vs 124 +/- 23, P <0.001) were lower, in the BOLUS compared with the PCEA group. The incidence of hypotension (SAP <80 mm Hg) was greater (6 vs 0, P <0.001) in the BOLUS group. The incidence of all other side effects was comparable. The costs of personnel (

Kardioprotektion durch thorakale Periduralanästhesie

204 +/-

[Cardioprotection by thoracic epidural anesthesia? : meta-analysis].

40 vs

Changes in Gastric Intramucosal pH following Mesenteric Traction in Patients Undergoing Pancreas Surgery

166 +/-