Wulf Seeling

Evaluation of three risk scores to predict postoperative nausea and vomiting

Background: So far there are three different scores to predict postoperative vomiting (PV: Apfel et al., 1998) or postoperative nausea and vomiting (PONV: Koivuranta et al., 1997; Palazzo and Evans, 1993). All three scores used logistic regression analysis to identify and create weights for the risk factors for PV or PONV. In short, these were sex, age, history of previous PONV, motion sickness, duration of anaesthesia, and use of postoperative opioids. However, an external evaluation and a comparison of these scores has not been performed so far.

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.

Ginger does not prevent postoperative nausea and vomiting after laparoscopic surgery

IMPLICATIONS The potential antiemetic effect of two different oral doses of the herbal remedy ginger (Zingiber officinale) to prevent postoperative nausea and vomiting in 180 patients undergoing gynecologic laparoscopy was investigated in this randomized, double-blinded trial. Ginger failed to reduce the incidence of postoperative nausea and vomiting after these procedures.

Influence of high thoracic epidural anesthesia on left ventricular contractility assessed using the end-systolic pressure-length relationship

The effect of high thoracic epidural anesthesia (TEA) on left ventricular contractility was studied in a prospective clinical trial. Forty‐eight patients with ASA physical status 1 and 2 and without cardiovascular disease were included in the study. Thirty‐six patients scheduled for elective upper abdominal surgery were randomly assigned to Group 1 (TEA, bupivacaine 0.25%, n= 12), Group 2 (TEA, bupivacaine 0.5%, n = 12) or to Group 3 (control without TEA, n= 12). TEA induced a sensory block which extended over all cardiac segments. In order to assess the effect of systemically absorbed bupivacaine, we studied a separate group of patients who received lumbar epidural anesthesia without involvement of the cardiac segments: Group 4 (LEA, bupivacaine 0.5%, n= 10). Left ventricular contractility was assessed using the end‐systolic pressure‐length relationship. Left ventricular dimensions were measured by transesophageal echocardiography. All hemodynamic measurements were performed under general anesthesia. There was no significant difference in systolic or diastolic arterial pressure, heart rate, left ventricular end‐systolic and end‐diastolic cross‐sectional areas and left ventricular wall stress between the four groups. Left ventricular maximum elastance as a measure of left ventricular contractility was significantly (P<0.001) reduced in Groups 1 and 2 [8.1 (±3.5) and 9.6 (±4.4) kPa · cm‐1, respectively] as compared to Groups 3 and 4 [18.4 (±8.8) and 17.7 (±7.7) kPa · cm‐1, respectively]. No significant difference could be demonstrated between Groups 1 and 2 or between Groups 3 and 4. It is concluded that high TEA severely alters left ventricular contractility even in subjects without pre‐existing cardiac disease.

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)

Perioperative endotoxemia and bacterial translocation during major abdominal surgery. Evidence for the protective effect of endogenous prostacyclin

OBJECTIVE To investigate the potential role of endogenous prostacyclin (PGI2) released after mesenteric traction during major abdominal surgery on perioperative endotoxemia and bacterial translocation. DESIGN Prospective, randomized, double-blind clinical study. SETTING Operating room and surgical intensive care unit in a university hospital. PATIENTS Fifty consecutive patients scheduled for major abdominal surgery (pancreas resection, abdominal aortic surgery). INTERVENTIONS Fifteen minutes before skin incision, either 400 mg of ibuprofen or a placebo equivalent were administered intravenously. Immediately after peritoneal incision, eventration and action of the small bowel was intentionally performed in a uniform fashion. MEASUREMENTS AND MAIN RESULTS Baseline values were obtained before induction of anesthesia. Additional measurements, along with assessments of hemodynamics and gas exchange, were performed before incision of the peritoneum and at 5, 30, and 45 mins and 3, 6, and 24 hrs after mesenteric traction. Arterial plasma concentrations of 6-keto-prostaglandin F1 alpha and thromboxane B2 (stable metabolites of PGI2 and thromboxane A2) were determined by radioimmunoassay. Endotoxin was measured by limulus amebocyte lysate test. Mesenteric lymph nodes were sampled in 31 patients (ibuprofen n = 14, placebo n = 17) and sent for culture under sterile conditions. Transient hypotension and a marked increase of plasma 6-keto-prostaglandin F1 alpha concentrations occurred up to 6 hrs after mesenteric traction in untreated patients with median peak concentrations (2243 vs. 72 ng/L [p < .0001, placebo vs. ibuprofen], observed 5 mins after mesenteric traction). Endotoxemia occurred in both study groups. However, after mesenteric traction, plasma endotoxin concentrations were significantly higher in the ibuprofen group. Median peak concentrations (0.12 vs. 0.27 EU/mL [p < .001, placebo vs. ibuprofen]) were observed 3 hrs after mesenteric traction. Gram-negative bacteria in mesenteric lymph nodes were detected exclusively in the ibuprofen group (n = 5, p < .01). CONCLUSIONS In ibuprofen-pretreated patients, significantly higher endotoxin concentrations as well as bacterial translocation to mesenteric lymph nodes occurred, despite the absence of a transient decrease in mean arterial pressure that had been associated with PGI2 release. Therefore, we hypothesized that during major abdominal surgery, endogenous PGI2 released in response to mesenteric traction may play a crucial role in maintaining splanchnic microcirculation and thus preserving gut mucosal barrier function.

Dimenhydrinate and metoclopramide alone or in combination for prophylaxis of PONV

Purpose: Dimenhydrinate and metoclopramide are inexpensive antiemetic drugs. Metoclopramide, especially, has been stueied extensively in the past, but there are no studies on the combination of both drugs for prevention of postoperative nausea and vomiting (PONV).Methods: One hundred and sixty male inpatients undergoing endonasal surgery were randomized to receive one of four antiementic regimens in a double-blind manner: placebo, 1 mg·kg−1 dimenhydrinate, 0.3 mg·kg−1 metoclopramide, or the combination of both drugs was administered after induction of anesthesia. Patients received a second dose of these drugs six hours after the first administration to mitigate their short half-life. Standardized general anesthesia included benzodiazepine premedication, propofol, desflurane in N2O/O2 vecuronium, and a continuous infusion of remifentanil. Postoperative analgesia and antiemetic rescue medication were standardized. Episodes of vomiting, retching, nausea, and the need for additional antiedmetics were recorded for 24 hr. The incidences of PONV were analyzed witth Fisher’s Exact test and the severity of PONV (rated by a standardized scoring algorithm) with the Jonckheere- Terpestra-test.Results: The incidence of patients free from PONV was 62.5% in the placebo-group and increased to 72.5% in the metoclopramide-group (P=0.54), 75.0% in the dimenhydrinate-group (P=0.34), and 85.0% in the combination- group (P=0.025). In the latter group, the severity of PONV was reduced compared with placebo treatment (P=0.017; Jonckheere-Terpestra-test).Conclusion: Dimenhydrinate and metoclopramide were ineffective in reducing the incidence and the severity of PONV. Their combination reduced the incidence of PONV compared with placebo.RésuméObjectif: Le dimenhydrinate et le métoclopramide sont des antiémétiques pas chers. Beaucoup d’études ont déjà été faites, avec le métoclopramide surtout, mais aucune avec la combinaison des deux comme moyen de prévention des nausées et des vomissements postopératoires (NVPO).Méthode: Cent soixante patients masculins qui devaient subir une intervention endonasale ont consenti à participer à une étude prospective, randomisée et en double aveugle, et à recevoir un des quatre traitements antiémétiques suivants: un placebo; 1 mg·kg−1 de dimenhydrinate; 0,3 mg·kg−1 de métoclopramide ou une combinaison des deux médicaments après l’induction de l’anesthésie. Ceux qui ont reçu du dimenhydrinate ou les deux médicaments ont eu une seconde dose de dimenhydrinate six heures après la première étant donné la courte demi-vie de ce médicament. L’anesthésie générale standardisée comprenait une prémédication de benzodiazépine, du propofol, du desflurane dans un mélange de N2O/O2, du vécuronium et une perfusion continue de rémifentanil. L’analgésie postopératoire et les antiémétiques de rattrapage ont été standardisés. Les nausées, les vomissements, les efforts pour vomir et les demandses d’antkémétiques additionnels ont été enregistrés pendant 24 h. Les incidences de NVPO ont été analysées selon le test Exact de Fisher et la sévérité des NVPO (estimée avec un algorithme de cotation standardisé), avec le test de Jonckheere-Terpestra.Résultats: L’absence de NVPO a été de 62,5% dans le groupe placebo et a augmenté à 72,5 % parmi les patients qui ont reçu du métoclopramide (P=0,54); à 75,0 % chez ceux qui ont reçu du dimenhydrinate (P= 0,34) et à 85,0 % chez ceux qui ont reçu les deux médicaments (P= 0,025). La sévérité des NVPO a été réduite chez les patients recevant la combinaison de médicaments, comparés à ceux qui ont reçu le placebo (P=0,017; test de Jonckheere-Terpestra).Conclusion: Le dimenhydrinate et le métoclopramide n’ont pas réduit l’incidence et la sévérité des NVPO. Leur combinaison, comparée placebo, a diminué l’incidence de NVPO.

Vasopressor hormone response following mesenteric traction during major abdominal surgery

Background: We investigated the vasopressor hormone response following mesenteric traction (MT) with hypotension due to prostacyclin (PGI2) release in patients undergoing abdominal surgery with a combined general and epidural anesthesia.

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.