[Cardioprotection by thoracic epidural anesthesia? : meta-analysis]. / Kardioprotektion durch thorakale Periduralanästhesie? : Metaanalyse.

BACKGROUND: Thoracic epidural analgesia (EDA) is thought to provide cardioprotective effects in patients undergoing noncardiac surgery. The results of two previous meta-analysis showed controversial conclusions regarding the impact of EDA on perioperative survival. The purpose of the present meta-analysis was to evaluate, whether thoracic EDA has the potential to reduce perioperative cardiac morbidity or mortality on the basis of available randomized controlled trials. PATIENTS AND METHODS: A systematic literature search was conducted in medical databases (Med-Line, EBM-Reviews, Embase, Biosis and Biological Abstracts) and relevant clinical trials including patients undergoing noncardiac surgery were evaluated by two independent investigators. All randomized controlled trials investigating the effects of thoracic EDA on perioperative outcome, published from 1980 up to the end of 2008 were included into this quantitative systematic review. Calculations were performed using the statistics program Review Manager 4.1 using a fixed-effects model. RESULTS: Nine studies with a total of 2,768 patients were included in the meta-analysis. Thoracic EDA did not reduce perioperative mortality [odds ratio (Peto OR): 1.08; 95% confidence interval (CI) 0.74-1.58]. Patients receiving thoracic EDA demonstrated a tendency to a lower rate of perioperative myocardial infarction. However, this effect of thoracic EDA did not reach statistical significance (Peto OR: 0.65; 95% CI 0.4-1.05). CONCLUSIONS: The present meta-analysis did not prove any positive influence of thoracic EDA on perioperative in-hospital mortality in patients undergoing noncardiac surgery. Furthermore, it remains questionable if thoracic EDA has the potential to reduce the rate of perioperative myocardial infarction.

[Intraoperative bronchospasm during paranasal sinus surgery -- indicator of aspirin intolerance syndrome?]. / Intraoperativer Bronchospasmus bei Nasennebenhöhlen-Operationen -- Hinweis auf ein Analgetikaintoleranz-Syndrom?

BACKGROUND: The aim of this study was to evaluate whether an intraoperative bronchospasm is more frequent in sinus surgery than in non-sinus surgery, whether its appearance after application of a non-steroidal anti-inflammatory drug (NSAID) is an indicator of an aspirin intolerance syndrome, and whether its appearance can be interpreted as an aspirin provocation test. METHODS: Anaesthesia charts from 5 years were retrospectively analysed whether anaphylactic/allergic reactions or bronchospasm were observed intraoperatively. In these cases the ENT charts of the patients were analysed and the occurrence of an analgesic-induced bronchospasm was assumed according to a probability algorithm. PATIENTS: All operations in general anaesthesia of an otorhinolaryngology clinic were analysed. RESULTS: An intraoperative bronchospasm was observed significantly more often in patients undergoing sinus surgery than during other ENT operations. In 17 of 23 patients a possible/probable analgesic-induced bronchospasm after application of NSAID was found. Diclofenac was intraoperatively given in 3 patients, diclofenac and metamizole in 5 patients, metamizole in 7 patients, paracetamol in 1 patient, and paracetamol and metamizole in 1 patient. CONCLUSIONS: An intraoperative bronchospasm during sinus surgery is not a clear indicator of an aspirin intolerance syndrome. An analgesic-induced bronchospasm can also be observed after paracetamol and metamizole. It can not be interpreted analogous to an aspirin provocation test.

[The ASA-score as a comorbidity index in patients with cancer of the oral cavity and oropharynx]. / Der ASA-Score als Komorbiditätsindex bei Mundhöhlen- und Mundrachenkarzinomen.

BACKGROUND: The American Society of Anesthesiologists Physical Status Scores (ASA-Score) may serve as a valuable indicator of comorbidity in head and neck cancer patients. METHODS: In 135 patients with squamous cell carcinoma of the oral cavity and/or oropharynx, the relation of disease free and overall survival and the ASA-score was evaluated in a univariate (logrank-test) and a Cox regression model. In the Cox model, age, tumor site and stage, and therapeutic modality served as covariates. RESULTS: In the univariate model, overall 5 year survival in ASA I and II patients was 44 %, and in ASA III and IV patients, it was 16 % (p < 0.005). The ASA-score also significantly influenced survival in the multivariate model. The hazard ratio (ASA I and II vs. ASA III and IV) was 2.1 (95 % confidence interval 1.3 to 3.4; p < 0,005). This corresponds to a 8 times higher risk to die, even when the effects of age, tumor site and stage, and therapeutic modalities are compensated for. CONCLUSION: The ASA-score is a valuable indicator of comorbidity in patients with oral cavity and oropharyngeal tumors. An essential advantage is its easy availability in most clinical settings.

[Delta(9)-tetrahydrocannabinol and the opioid receptor agonist piritramide do not act synergistically in postoperative pain]. / Keine synergistische Wirkung der Kombination von Delta(9)-Tetrahydrocannabinol und Piritramid bei postoperativen Schmerzen.

BACKGROUND: It is concluded from animal experiments that cannabinoid receptor and mu-opioid receptor agonists act synergistically with respect to antinociception. In order to demonstrate this effect under clinical conditions, we conducted a randomized double blind trial with patients after radical prostatectomy. PATIENTS AND METHODS: From the evening before the operation until the morning of the second postoperative day, all patients received eight oral doses of either placebo or 5 mg Delta(9)-tetrahydrocannabinol (dronabinol). Postoperatively patients had access to patient-controlled analgesia with the micro-opioid agonist piritramide for 48 h. We expected patients receiving dronabinol to require significantly less piritramide compared to patients on placebo. RESULTS: The consumption of piritramide was recorded in 100 patients after radical retropubic prostatectomy with regional lymphadenectomy. Patients in the placebo group consumed 74 mg (median), interquartile range (IQR) 44-90 mg, patients in the verum group consumed 54 mg (median) IQR 46-88 mg. The difference between groups was not statistically significant. Plasma concentrations of Delta(9)-THC were measurable in all patients in the verum group. The levels (median) were 1.5 ng/ml (IQR 0.6-2.3), 1.3 ng/ml (IQR 0.5-2.2) and 1.9 ng/ml (IQR 0.8-2.7) on the day of operation, the first and second postoperative day, respectively. CONCLUSION: We found neither a synergistic nor even an additive antinociceptive interaction between Delta(9)-tetrahydrocannabinol and the micro-opioid agonist piritramide in a setting of acute postoperative pain.

Changes in gastric intramucosal pH following mesenteric traction in patients undergoing pancreas surgery.

BACKGROUND/AIM: During major abdominal surgery, mesenteric traction (MT) may result in hemodynamic instability mainly due to endogenous prostacyclin release. Gastric intramucosal pH (pHi) and PiCO2 are indicators of splanchnic tissue perfusion with a predictive value for the postoperative outcome. We investigated the influence of MT on gastric pHi and on postoperative outcome in patients undergoing pancreas surgery. METHODS: Forty-six consecutive patients scheduled for pancreas surgery were investigated. We registered hemodynamics and pHi by gastric tonometry and documented postoperative outcome (complications, hospital stay). Baseline data (T0) were recorded after skin incision. Further assessments followed 30, 60 and 120 min after intentional MT (T1-3) and at the end of surgery (T4). RESULTS: Thirty-three patients demonstrated a decrease in mean arterial pressure (MAP) following MT, whereas 13 patients showed entirely stable hemodynamics. The significant reduction in MAP in patients with an MT response was not associated with changes in pHi as compared to patients with no response (stable MAP) (T0 7.34 +/- 0.08 vs. 7.35 +/- 0.06; T1 7.34 +/- 0.05 vs. 7.32 +/- 0.07; T2 7.32 +/- 0. 05 vs. 7.31 +/- 0.08; T3 7.32 +/- 0.05 vs. 7.32 +/- 0.07; T4 7.26 +/- 0.1 vs. 7.27 +/- 0.08; mean +/- SD, MT response vs. no response). Neither MT response nor gastric intramucosal acidosis as evidenced by a pHi <7.32 at the end of surgery predicted postoperative complications or longer hospital stay. CONCLUSION: No deterioration of gastric pHi was found, which could reflect acceptable splanchnic perfusion and oxygenation despite systemic blood pressure reactions in patients experiencing an MT response.

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

UNLABELLED: 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 micrograms/mL and set to 3-mL bolus and 10-min lockout time. BOLUS patients received injections of clonidine 150 micrograms 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 ($204 +/- $40 vs $166 +/- $38, P < 0.001) were higher in the BOLUS group, but the costs of material ($51 +/- $17 vs $87 +/- $18, P < 0.001) were higher in the PCEA group. Total costs ($62 +/- $9 vs $62 +/- $11 per day, P = 0.9) were comparable. We conclude that because of superior analgesia and reduced side effects at analogous costs, PCEA is preferable to the BOLUS technique for the treatment of postoperative pain. IMPLICATIONS: An epidural clonidine/morphine bolus technique resulted in inferior analgesia, more side effects, and comparable costs compared with a bupivacaine/sufentanil patient-controlled regimen in a randomized controlled trial after abdominal surgery.

The impact of prostanoids on pulmonary gas exchange during abdominal surgery with mesenteric traction.

We investigated the effect of intravenous (iv) ibuprofen on prostanoid release and on pulmonary gas exchange after abdominal mesenteric traction (MT) during either abdominal aortic surgery or pancreas resection. In a prospective, randomized, double-blind study, 400 mg ibuprofen (pancreas n = 13, aorta n = 13) or a placebo (pancreas n = 13, aorta n = 13) was administered iv before skin incision. MT was applied uniformly. The prostanoid plasma concentrations, venous admixture (Q(va)/Q(t)), and PaO2/FIO2 ratio were determined at baseline (before MT) and 5, 15, 45, and 90 min after MT. Patients who underwent aortic surgery were older and exhibited a lower preoperative PaO2 than those who underwent pancreas resection. Placebo-treated patients revealed a 30-fold peak increase in 6-keto-prostaglandin F1alpha (stable metabolite of prostacyclin) levels after intentional MT during aortic as well as pancreatic operations. This response was accompanied by an increase in Q(va)/Q(t) (ibuprofen: pancreas 7% +/- 1%, aorta 14% +/- 2%; placebo: pancreas 16% +/- 3%, aorta 26% +/- 3%/15 min after MT [mean +/- SEM, P < 0.05, placebo vs ibuprofen]), which resulted in decreased PaO2/ FIO2 ratio only in the aortic surgery patients (ibuprofen: 310 +/- 19; placebo: 237 +/- 24 15 min after MT, [mean +/- SEM, P < 0.05]). The authors conclude that ibuprofen-pretreated patients demonstrated almost constant prostanoid levels without changes in pulmonary gas exchange after MT.

[Differential indications for non-opioids for postoperative analgesia III. Analgesic effect of perioperative administration of metamizole plus diclofenac after spinal anesthesia]. / Untersuchungen zum differenzierten Einsatz von Nichtopioiden zur postoperativen Analgesie III. Analgetischer Effekt einer perioperativen Gabe von Metamizol plus Dicllofenac nach Spinalanästhesien.

PURPOSE: In a previous study we investigated the analgesic efficacy of a combination of metamizol plus diclofenac after general anaesthesia. After minor orthopaedic surgery postoperative opioid requirements were reduced by 73% during the first 24 h after surgery. In the present study, we have investigated the efficacy of this analgesic combination after minor orthopaedic operations performed in spinal anaesthesia. METHODS: Seventy four patients, scheduled for minor orthopaedic surgery, participated in this double-blind, randomised, placebo-controlled study. The setting was comparable to our previous study. Before induction of spinal anaesthesia, verum-treated patients received a diclofenac suppository (100 mg), and metamizol (1 g/100 ml NaCl 0.9% intravenously over 15 min). These infusions were repeated at 6 h and 12 h. In addition to the third infusion, the patients received a further diclofenac suppository (100 mg). Cumulated doses of buprenorphine (PCA, patient-controlled analgesia), pain scores (0-10), blood pressure, heart rate and side effects were recorded during the first 6 h and again at 24 h. RESULTS: After spinal anaesthesia had subsided, all patients required increasing doses of buprenorphine. Verum-treated patients required significantly lower doses during the first 24 h after surgery (median -29%). CONCLUSIONS: The combination of metamizol and diclofenac causes a clinically relevant reduction in opioid requirements after minor orthopaedic surgery in spinal anaesthesia.

[Effectiveness, side effects and costs of postoperative pain therapy: intravenous and epidural patient-controlled analgesia (PCA)]. / Wirksamkeit, Nebenwirkungen und Kosten postoperativer Schmerztherapie: Intravenöse und epidurale patientenkontrollierte Analgesie (PCA).

PURPOSE: Improvement of the quality of analgesia, reduction of side effects and costs by application of epidural (PCEA) in comparison to intravenous patient-controlled analgesia (PCA) in postoperative pain treatment. METHODS: 62 patients with upper abdominal surgery took part in this randomised prospective study which was approved by the local ethics committee. Epidural catheters were inserted at T 8/9 (group PCEA). General anaesthesia was performed with propofol, sufentanil 2 micrograms/kg, pancuronium, enflurane and O2:N2O = 1:2. Postoperative analgesia consisted of epidural bupivacaine 0.25% + sufentanil 2 micrograms/ml (BS). (bolus 0.05 ml/kg, lockout 10 min) in group PCEA, or of intravenous morphine (bolus 2 mg. lockout 10 min) in group PCA. The following parameters were recorded until the evening of postoperative day 4: pain intensity at rest (VASR, 1-10) and on coughing (VASH, 1-10), blood pressure, heart rate, blood gas analysis, ability to ambulate, pruritus, nausea/vomiting (PONV), patient satisfaction (0-4), time and expenses for postoperative pain treatment. RESULTS: Median VASR (1 vs 2) and VASH (3 vs 4.5) were lower, cough intensity (2 vs 1) and patient satisfaction score (4 vs 3) were higher in PCEA compared to PCA. Ability to ambulate, pruritus, PONV, haemodynamics, paO2 and paCO2 were comparable. Postoperative pain treatment with PCEA was more time-consuming (407 vs 299 min) and expensive (71 vs 40 S/day) than PCA. CONCLUSION: PCEA in comparison to PCA after major abdominal surgery provides superior analgesia with comparable side effects at approximately 80% higher costs.

Reduced postoperative analgesic demand after inhaled anesthesia in comparison to combined epidural-inhaled anesthesia in patients undergoing abdominal surgery.

We studied the effect of epidural/general combination anesthesia, in comparison to inhaled anesthesia, on postoperative pain and analgesic consumption in patients undergoing upper abdominal surgery. Anesthesia was induced with propofol and maintained with enflurane in 70% N2O as necessary to maintain arterial blood pressure within 20% of baseline. Group I received bupivacaine 0.25% 0.2 mL/kg and sufentanil 1 microgram/kg 65 +/- 3 min before dermal incision and 0.1 mL/kg bupivacaine 0.25% + sufentanil 2 micrograms/mL (BS) every hour thereafter. Group II received 0.2 mL/kg of BS 316 +/- 15 min after dermal incision in the recovery room. Postoperative patient-controlled epidural analgesia (PCEA) with BS was provided. Pain intensities and consumption of PCEA BS were recorded on postoperative days (PODs) 1 to 5. Inspiratory fraction of enflurane was lower (0.5% +/- 0.01% vs 1.6% +/- 0.04%; P < 0.001) in Group I compared with Group II. Cumulative postoperative consumption of PCEA BS was higher in Group I compared with Group II from the evening of POD 2 until the end of the study (301 +/- 19 mL vs 249 +/- 17 mL; P < 0.001), while pain intensities were comparable at all times. The intraoperative effects of combined BS and enflurane/N2O (inspiratory fraction [Fi] approximately 1 minimum alveolar anesthetic concentration [MAC]) did not preempt postoperative pain in contrast to enflurane/N2O anesthesia (Fi approximately 2.8 MAC).

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.kg-1.h-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 micrograms/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.

[Epidural and intrathecal administration of alpha 2-adreno-ceptor agonists for postoperative pain relief]. / Epidurale und intrathekale Anwendung von alpha2-Adrenozeptor-Agonisten zur postoperativen Analgesie.

Spinal clonidine interacts with pre- and postsynaptic alpha(2)-adrenoceptors on afferent neurons in the superficial dorsal horn of the spinal cord: it causes analgesia by inhibition of the synaptic and electrotonic neurotransmission of nociceptive impulses. Epidural doses higher than 4 microg/kg have an analgesic onset time of less than 30 min, reduce pain by more than 70 %; these effects last for 4-5 h. Epidural clonidine analgesia is accompanied by a reduction in heart rate, cardiac output and blood pressure of approximately 20 % compared with baseline. The haemodynamic side effects mean close supervision is needed during the first hour after epidural application and limit the use of epidural clonidine to patients who are refractory to the analgesic effects of epidural opioid or local anaesthetics. In these patients excellent results can be achieved either with clonidine alone or with a combination of clonidine and an opioid or a local anaesthetic to exploit the additive or supra-additive interactions of these drugs.

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.kg-1.min-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 +/- 14 (mean +/- SD) to 64 +/- 17 mmHg (P < 0.01) and from 52 +/- 14 to 32 +/- 11 10(3) dyne/cm2 (P > 0.01), respectively. End-diastolic area and fractional area change increased from 16.5 +/- 2.9 to 21.7 +/- 3.3 cm2 (P < 0.01) and from 0.53 +/- 0.07 to 0.70 +/- 0.06 (P < 0.01), respectively, whereas there was only a minor change of ESPLRarea from 38 +/- 13 to 44 +/- 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 an hemodynamics after epidural clonidine 8 micrograms/kg (Group C) or clonidine 4 micrograms/kg+morphine 2 mg (Group CM) in comparison to epidural morphine 50 micrograms/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.

[The effect of changes in lung compliance on ventilation in newborns. Results of animal experiments with two different respirators]. / Einfluss von Störungen der Lungencompliance auf die Ventilation von Neugeborenen. Tierexperimentelle Untersuchung mit zwei verschiedenen Respiratoren.

In most ventilators used in anaesthesia tidal volume delivered during mechanical ventilation is different from the tidal volume preset at the respirator on the basis of respirator and circuit compliance and gas compression during inspiration. The error in ventilation due to the compressed volume is especially significant clinically when the tidal volume is very small or when the airway pressure is very high. In newborns and neonates in particular, decreasing lung compliance during a surgical procedure may contribute to marked hypoventilation. We therefore investigated ventilation in newborn piglets during decreasing lung compliance induced by tension pneumothorax. We used the anaesthesia ventilator CICERO (Dräger, Lübeck, Germany) and the SERVO 900 C ventilator (Siemens-Elema, Sweden). MATERIALS AND METHODS. Two anaesthesia ventilators, the CICERO (group I, n = 8) and the SERVO ventilators (group II, n = 8) were investigated following randomized selection in a group of 16 newborn piglets (Table 1). After normoventilation for 60 min a tension pneumothorax at +10 mbar was induced. After 15 min the pneumothorax was increased to +20 mbar and maintained at this level for the rest of the study. When hypercapnia (PaCO2 > 45 mmHg) resulted, the respiratory rate was increased by +10/min after 15 min with pneumothorax at +20 mbar. When hypercapnia continued, the respiratory rate was increased again 25 min and if necessary also 35 min after the induction of pneumothorax at +20 mbar. After normoventilation for 60 min (T1) (Table 2), after 15 min with pneumothorax at +10 mbar (T2) and after 15 min (T3), 25 min (T4), 35 min (T5) and 45 min (T6) with pneumothorax at +20 mbar the following parameters were obtained: central venous (CVP) and mean arterial pressure (MAP), heart rate (HR), arterial (PaCO2) and end-tidal CO2 tension (PetCO2), peak inspiratory pressure (PIP), respiratory frequency (RF) and expiratory tidal (Vtex) and minute volume (VE). RESULTS. In group I the pneumothorax resulted in a significantly smaller increase in PaCO2 (43.3 +/- 6.2 mmHg) than in group II (Fig. 1), and hypercapnia was present in only 3 piglets. Vtex (Fig. 2), VE (Fig. 3) and PIP (Fig. 5) increased significantly, with significantly higher values than in group II, while PetCO2 (Fig. 6) decreased significantly. In group II the pneumothorax was attributed to a significant increase in PaCO2 and a marked hypercapnia in all piglets (PaCO2 61.2 +/- 5.9 mmHg) (Fig. 1). Vtex (Fig. 2) and VE (Fig. 3) remained unchanged, while PIP (Fig. 5) and PetCO2 (Fig. 6) increased. Following the increase in RF (Fig. 4) in all piglets, Vtex and VE increased and PaCO2 and PetCO2 decreased. CONCLUSIONS. During ventilation of neonates with the SERVO ventilator a decrease in lung compliance will cause hypoventilation and hypercapnia. This reflected by an increase in peak inspiratory pressure and can be corrected by increasing the respiratory rate. In contrast, the CICERO is able to preserve ventilation by an internal correction for gas compression, but it does not guarantee normoventilation in all cases. In neither group does the end-tidal PCO2 reflect the true ventilation during decreasing lung compliance, so that arterial blood gas analysis seems to be mandatory for the diagnosis of hypercapnia in such situations.

[The effect of thoracic epidural anesthesia on the pathophysiology of the eventration syndrome]. / Einfluss der thorakalen Epiduralanästhesie auf die Pathophysiologie des Eventrationssyndroms.

Abdominal mesenteric traction (MT) results in decreased mean arterial pressure (MAP), systemic vascular resistance (SVR) and increased cardiac output (CO). This response is induced by a considerable release of prostacyclin (PGI2). Precipitous falls in systemic arterial pressure related to central and/or autonomic nervous reflex arcs also have been described during operations on the upper abdominal viscera. Those hypotensive responses to visceral traction appear to be transmitted along afferent fibres contained within the splanchnic nerves. We investigated the influence of supplementary thoracic epidural anaesthesia on mesenteric traction response during major abdominal surgery. METHODS. With the approval of the Human Investigation Review Board we studied 40 patients scheduled for major abdominal surgery (infrarenal aortic, gastrointestinal and pancreatic surgery) according to a prospective, randomized double-blinded protocol. Patients were randomized to two different anaesthetic regimens. Patients in group 1 received general anaesthesia (GA n = 20) with 0.1-0.15 mg/kg midazolam and 10 micrograms/kg fentanyl prior to skin incision. Maintenance included 65% nitric oxide in oxygen and 0.1 mg increments of fentanyl as required. Group 2 patients (EA n = 20) underwent a combined technique of dose-reduced general anaesthesia and supplementary continuous, thoracic epidural anaesthesia (bupivacaine 0.25%, sensory blockade T4 to L1-3). In both anaesthesia groups ibuprofen (400 mg i.v.) or a placebo equivalent was administered 15 min before the induction of anaesthesia. MT was applied in a uniform fashion. Baseline values preceded the incision of the peritoneum. Further assessments followed 5, 15 and 30 min after MT. The plasma concentrations of 6-keto-PGF1 alpha (stable metabolite of PGI2), TXB2 (stable metabolite of thromboxane), PGF2 alpha, KH2-PGF2 alpha (stable metabolite of PGF2 alpha) were determined by radioimmunoassay. At all assessments we recorded systolic and diastolic blood pressure, heart rate and measured arterial blood gases. Statistical analyses were performed using three-factor ANOVA for repeated measurements after log(x) transformation. A P-value of less than 0.05 was considered significant when the Bonferroni-Holm adjustment was applied. RESULTS. Patients with supplementary epidural anaesthesia demonstrated lower systolic (P = 0.0001) and diastolic (P = 0.006) blood pressure than those in the GA group. Nevertheless, in untreated patients in the EA and GA group there was a significant decrease of about 20-30% in systolic and diastolic blood pressure (P = 0.0001) after mesenteric traction. Irrespective of the anaesthetic procedure, paO2 (P = 0.0001) decreased after mesenteric traction in the placebo group. The control patients in the GA group exhibited a more pronounced increase in heart rate after MT. After traction on the mesentery a significant 20- to 30-fold increase in 6-keto-PGF1 alpha plasma concentrations occurred in the placebo group: GA group 1950/58 (5 min), 1574/59 (15 min) 858/66 (30 min) ng/l, P < 0.0001; EA group: 2002/106 (5 min), 2955/107 (15 min) 1807/70 (30 min) ng/l, P < 0.0001, for placebo vs ibuprofen. There was no statistically significant difference between the two anaesthetic procedures used. In ibuprofen-pretreated patients haemodynamics and paO2 values were stable, while 6-keto-PGF1 alpha plasma concentrations remained within the normal range. CONCLUSION. Our data clearly indicate that the mesenteric traction response consists in relevant haemodynamic alterations and a significant decrease of paO2. Stable haemodynamics and paO2 following cyclooxygenase inhibition signify an action mediated by prostacyclin. Deafferentation of the splanchnic nerves by supplementary thoracic epidural anaesthesia did not influence either prostacyclin release or the decrease in blood pressure and paO2 after traction on the mesentery root...

[Analgesia and hemodynamics under 8 mu/kg clonidine for pain therapy following major abdominal surgery]. / Analgesie und Hämodynamik unter 8 mu/kg Clonidin epidural zur Schmerztherapie nach grossen abdominellen Eingriffen.

OBJECTIVE: To characterise the haemodynamic profile after epidural injection of high-dose clonidine for postoperative pain management and to establish recommendations for the therapy of haemodynamic instabilities. DESIGN: 20 patients with major surgery on pancreas, stomach or infrarenal aorta took part in the study. Anaesthesia was a combined epidural/inhalational regimen with bupivacaine 0.25%, enflurane, oxygen/nitrous oxide, fentanyl 0.1 mg and pancuronium. Postoperative analgesia consisted of morphine 50 micrograms/kg in 10 ml NaCl 0.9% for the first 12 postoperative hours; if pain > = 5 points on the VAS occurred after > 12 h postoperatively clonidine 8 micrograms/kg in 10 ml NaCl 0.9% was injected epidurally and the pain intensity (self-assessment by the patient using the visual analog scale) and circulation (invasive pressure monitoring, pulmonary artery catheter) was monitored for 60 minutes in ten minutes intervals. RESULTS: The reduction of the initial VAS score of 6 was 50% after 20 minutes and 100% after 60 minutes. We observed a significant decline in heart rate (87 +/- 11 (t0), 74 +/- 10 min-1 (t60)), mean arterial pressure (97 +/- 17 (t0), 72 +/- 15 mmHg (t60)) and cardiac output (8.7 +/- 1.3 (t0), 7.0 +/- 1.3 l.min-1 (t60)) (all p < 0.001) and no change of systemic vascular resistance. Filling pressures (CVP and PCWP) remained stable. In 9 patients the mean arterial pressure fell below 60 mmHg (always within the first 40 min); 6 of these patients responded to infusion of a colloid (500 ml of hydroxyethyl starch at > = 2 ml/kg.min) whereas the other 3 patients needed a bolus injection of a betamimetic catecholamine (theodrenaline/cafedrine, Akrinor). CONCLUSION: Epidural clonidine 8 micrograms/kg causes rapid and intense analgesia. Haemodynamic instability is a consequence of a drop in heart rate and has to be treated accordingly. The application of a pure vasopressor does not seem to be indicated taking in account the fact that the total peripheral resistance remains unchanged and in the normal range.

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.

[Influence of postoperative pain on morbidity and mortality.]. / Beeinflußt die Schmerztherapie postoperative Morbidität und Letalität?

Postoperative pain can intensify the sympathoadrenergic reaction, which is commonly seen after surgery, and thus possibly pave the way for certain complications, such as coronary ischemia, bronchopneumonia, intestinal stasis, thromboembolism, infection, sepsis, and metabolic disturbances. Investigations of cardiovascular, respiratory, gastrointestinal, metabolic, and immunologic function indicate that high-quality pain relief can diminish postoperative organ impairment and failure. Some aspects of the improvements attributed to the quality of analgesia, such as prevention of tachycardia and hypertension, attenuation of hyperglycemia and catabolism, improvement of gastrointestinal motility and cellular immunity cannot be definitely distinguished from the effects of sympathetic blockade due to epidural analgesia with local anesthetics, however. There is another aspect of the problem. The better the quality of postoperative pain relief, the more likely it is that analgesia-related complications, such as respiratory depression (opioids), cardiovascular depression (epidural local anesthetics), renal failure (NSAIDs) and bladder dysfunction (epidural opioids and local anesthetics) will occur. The question of whether postoperative morbidity and mortality can be reduced by effective analgesia has been investigated in the past few years. Some studies indicate that better analgesia is advantageous for the patient, especially with respect to postoperative complications, hospital stay, long-term well being, and costs. In other clinical trials incorporating more patients, however, this hypothesis had to be rejected. At present, therefore, we cannot state that effective pain relief influences postoperative morbidity and mortality.