Prevention of postoperative nausea and vomiting by continuous infusion of subhypnotic propofol in female patients receiving intravenous patient-controlled analgesia

In this prospective, randomized, double-blind, placebo-controlledstudy, the use of continuous subhypnotic propofol infusion asan antiemetic in fentanyl intravenous patient-controlled analgesia(i.v. PCA) was investigated during the first 24 h after surgery.One hundred female patients, ASA I–II, aged 20–71yr, undergoing major gynaecological or orthopaedic surgery,were included. Either propofol 10 mg or placebo (1 ml of Intralipid)was given and one of the following five regimens was maintainedfor 24 h: propofol 5, 10, 15 or 20 µg kg^–1 min^–1or Intralipid 1 ml h^–1 as a placebo. Fentanyl i.v. PCAwas started in the postanaesthesia care unit for postoperativeanalgesia. Significantly more of the patients given propofol15 and 20 µg kg^–1 min^–1 experienced no nauseaor vomiting compared with those given placebo (65% and 70% versus25%; P<0.05). Patients given propofol 20 µg kg^–1min^–1 reported more sedation than those in the other groups4 h after surgery (P<0.05). Br J Anaesth 2000; 85: 898–900     

Analgesic effects of parecoxib following total abdominal hysterectomy

Background. Forty-eight ASA I–II patients undergoing totalabdominal hysterectomy (TAH) were studied in a double blind,randomized placebo controlled trial of parecoxib for postoperativeanalgesia. Methods. All patients were given propofol 2–4 mg kg^–1i.v., a non-depolarizing muscle relaxant, morphine 10 mg i.v.and prochlorperazine 12.5 mg i.m. intraoperatively. Their lungswere ventilated with nitrous oxide and isoflurane 1–1.5%in oxygen. Morphine was self-administered for postoperativeanalgesia via a patient controlled analgesia (PCA) device. Patientswere allocated randomly to receive either parecoxib 40 mg i.v.or normal saline on induction of anaesthesia. Results. Twelve patients did not complete the study. Of theremaining 36 patients, there was no significant difference betweenthe treatment groups in age, weight, ASA status, duration ofsurgery, or intraoperative dose of morphine. However, mean (95%CI) 24 h morphine consumption of 54 (42–65) mg in theparecoxib group was significantly (P=0.04) lower than that of72 (58–86) mg in the placebo group. Pain intensity scoreson sitting up were significantly lower (P=0.02) in the parecoxibgroup compared with placebo. There was no significant differencebetween the treatment groups in pain intensity scores at restand on deep inspiration, or in nausea, total number of vomitingepisodes, median number of rescue antiemetic doses, and sedationscores. Conclusions. Parecoxib 40 mg i.v. may be recommended in patientshaving TAH as it provides morphine-sparing analgesia. Br J Anaesth 2003; 90: 746–9     

Intrathecal morphine and clonidine for coronary artery bypass grafting

Background. After cardiac surgery adequate postoperative analgesiais necessary. We assessed analgesia using intrathecal morphineand clonidine. Methods. In a double-blind randomized study, 45 patients havingcoronary artery bypass graft surgery were allocated randomlyto receive i.v. patient-controlled analgesia (PCA) morphine(bolus, 1 mg; lock-out interval, 7 min) (control group), eitheralone or combined with intrathecal morphine 4 µg kg^–1or with both intrathecal morphine 4 µg kg^–1and clonidine 1 µg kg^–1. Intrathecal injectionswere performed before the induction of general anaesthesia.Pain was measured after surgery using a visual analogue scale(VAS). We recorded i.v. PCA morphine consumption during the24 h after operation. Results. Morphine dosage [median (25th–75th percentiles)]was less in the first 24 h in the patients who were given intrathecalmorphine + clonidine [7 (0–37) mg] than in other patients[40.5 (15–61.5) mg in the intrathecal morphine group and37 (30.5–51) mg in the i.v. morphine group]. VAS scoreswere lower after intrathecal morphine + clonidine compared withthe control group. Time to extubation was less after intrathecalmorphine + clonidine compared with the i.v. morphine group [225(195–330) vs 330 (300–360) min, P<0.05]. Conclusion. Intrathecal morphine and clonidine provide effectiveanalgesia after coronary artery bypass graft surgery and allowearlier extubation. Br J Anaesth 2003; 90: 300–3     

Effects of three different dose regimens of magnesium on propofol requirements, haemodynamic variables and postoperative pain relief in gynaecological surgery

Background. In this double-blind, randomized, placebo-controlledstudy we compared the effects of three different dose regimensof magnesium on intraoperative propofol and atracurium requirements,and postoperative morphine consumption in patients undergoinggynaecological surgery. Methods. Eighty women were allocated to four equal groups. Thecontrol group received normal saline; magnesium groups received40 mg kg^–1 of magnesium before induction of anaesthesia,followed by i.v. infusion of normal saline, magnesium 10 mgkg^–1 h^–1 or magnesium 20 mg kg^–1 h^–1for the next 4 h. Propofol infusion was targeted to keep bispectralindex values between 45 and 55. Postoperative analgesia wasachieved using PCA with morphine. Results. Magnesium groups required significantly less propofol[mean (SD) 121.5 (13.3), 102.2 (8.0) and 101.3 (9.7) µgkg^–1 min^–1 respectively] than the control group(140.7 (16.5) µg kg^–1 min^–1). Atracurium usewas significantly higher in the control group than magnesiumgroups [0.4 (0.06) vs 0.34 (0.06), 0.35 (0.04), 0.34 (0.06)mg kg^–1 h^–1 respectively]. Morphine consumptionwas significantly higher in control group than magnesium groupson the first postoperative day [0.88 (0.14) vs 0.73 (0.17),0.59 (0.23), 0.53 (0.21) mg kg^–1 respectively]. The heartrate was lower in magnesium groups and 20 mg kg^–1 h^–1infusion group demonstrated the lowest values. Conclusion. Magnesium 40 mg kg^–1 bolus followed by 10mg kg^–1 h^–1 infusion leads to significant reductionsin intraoperative propofol, atracurium and postoperative morphineconsumption. Increasing magnesium dosage did not offer any advantages,but induced haemodynamic consequences.     

Propofol pharmacokinetics in children with biliary atresia

We studied the pharmacokinetics of an i.v. bolus dose of propofol2.5–3.0 mg kg^–1 in eight children (age 4–24months) with biliary atresia and in six control (ASA I) children(age 11–43 months). Blood samples were obtained for 4h after administration of propofol. Blood concentrations ofpropofol were measured by high pressure liquid chromatography.Systemic clearance of propofol (Cl) and volume of distributionat steady state (V^ss) showed a highly significant correlationwith body weight. Propofol Cl and V^ss, normalized for body weight,were similar in children with biliary atresia (mean 37.5 (SD8.3) ml min^–1 kg^–1 and 3.5 (1.6) litre kg^–1,respectively) compared with control children (38.7 (6.8) mlmin^–1 kg^–1 and 2.4 (0.8) litre^–1 kg^–1,respectively). We conclude that in children with biliary atresiathe pharmacokinetics of propofol are similar to those of healthychildren.     

Parecoxib sodium has opioid-sparing effects in patients undergoing total knee arthroplasty under spinal anaesthesia

Background. This multicentre, double-blind, placebo-controlledstudy compared the opioid-sparing effectiveness and clinicalsafety of parecoxib sodium over 48 h, in 195 postoperativepatients after routine total knee replacement surgery. Methods. Elective total primary knee arthroplasty was performedunder spinal anaesthesia, with a single dose of spinal bupivacaine10–20 mg, and intraoperative sedation with midazolam0.5–1.0 mg i.v., or propofol <6 mg kg^–1h^–1. Patients were randomized to receive either parecoxibsodium 20 mg twice daily (bd) i.v. (n=65), parecoxib sodium40 mg bd i.v. (n=67), or placebo (n=63) at the completionof surgery, and after 12, 24, and 36 h. Morphine (1–2 mg)was taken by patient-controlled analgesia or by bolus dosesafter 30 min. Results. Patients receiving parecoxib sodium 20 mg bd and40 mg bd consumed 15.6% and 27.8% less morphine at 24 hthan patients taking placebo (both P<0.05). Both doses ofparecoxib sodium administered with morphine provided significantlygreater pain relief than morphine alone from 6 h (P<0.05).A global evaluation of study medication demonstrated a greaterlevel of satisfaction among patients taking parecoxib sodiumthan those taking placebo. Parecoxib sodium administered incombination with morphine was well tolerated. However, a reductionin opioid-type side-effects was not demonstrated in the parecoxibsodium groups. Conclusion. Parecoxib sodium provides opioid-sparing analgesiceffects in postoperative patients. Br J Anaesth 2003; 90: 166–72     

Effects of intramuscular administration of lidocaine or bupivacaine on induction and maintenance doses of propofol evaluated by bispectral index

Background. Interest in combining local and general anaesthesiahas lead to studies investigating possible interactions. Ina prospective, randomized, double-blind study, we tested whetherlocal anaesthetics administered i.m. potentiate the hypnoticeffect of propofol. Methods. Sixty patients (three groups, n=20) undergoing lowerabdominal surgery with total i.v. propofol anaesthesia wereinvestigated. Patients in Group B received i.m. bupivacaine(5 mg ml^–1) 1 mg kg^–1, patients in Group Lreceived i.m. lidocaine (100 mg ml^–1) 2 mg kg^–1and patients in Group C received i.m. saline 5 ml beforeoperation. Hypnosis was measured with bispectral index (BIS). Results. The induction (BIS <45), and the maintenance dosesof propofol (BIS between 40 and 50) were significantly lessin Group B and Group L compared with the control group. Inductiondoses were 1.58 (SD 0.39), 1.56 (0.24) and 2.03 (0.33) mg kg^–1respectively; P<0.0001. Maintenance doses were 6.33 (2.06),7.08 (1.23) and 9.95 (2.02) mg kg^–1 respectively in thefirst hour; P<0.0001. Groups B and L were associated withan attenuated haemodynamic response to both induction and intubation. Conclusion. I.M. administered local anaesthetics are associatedwith a decrease in both the induction and maintenance dosesof propofol during total i.v. anaesthesia and a reduction inhaemodynamic responses. Br J Anaesth 2002; 89: 849–52     

Effects of magnesium sulphate on intraoperative anaesthetic requirements and postoperative analgesia in gynaecology patients receiving total intravenous anaesthesia

Background: This randomized, double-blind, prospective study was undertakento evaluate the effects of magnesium sulphate on anaestheticrequirements and postoperative analgesia in patients undergoingtotal i.v. anaesthesia (TIVA). Methods: Fifty patients who underwent gynaecological surgery were randomlydivided into two groups. Before induction of anaesthesia, themagnesium group (Group M) received magnesium sulphate 50 mgkg^–1 i.v. as a bolus and then 15 mg kg^–1 h^–1i.v. by continuous infusion. The control group (Group S) receivedthe same amount of isotonic saline. TIVA (propofol+remifentanil)was administered under bispectral index monitoring during anaesthesiainduction and maintenance. Rocuronium was administered beforeorotracheal intubation and during surgery when the train-of-fourcount was 2 or more. After operation, patient-controlled analgesiawith a solution of ketorolac and morphine was used and the consumptionof this solution was recorded. Pain scores at rest and uponmovement were evaluated 30 min, 4, 24, and 48 h after surgery. Results: Patients in Group M required less rocuronium than those in GroupS [mean (SD) 0.44 (0.09) vs 0.35 (0.07) µg kg^–1min^–1, P<0.05]. The total amounts of propofol and remifentaniladministered were similar in the two groups. Postoperative painscores, cumulative analgesic consumption, and shivering incidentswere significantly lower in Group M (P<0.05). Mean arterialpressure just after intubation and during the immediate postoperativeperiod was also significantly lower in Group M (P<0.05). Conclusions: I.V. magnesium sulphate during TIVA reduced rocuronium requirementand improved the quality of postoperative analgesia.     

Does tolerance develop to the anaesthetic effects of propofol in rats?

We have studied the development of tolerance to the anaestheticeffects of propofol in rats. In the first set of experiments,three groups of rats (A, B and C) received i.v. propofol 10mg kg^–1, 15 mg kg^–1 and 20 mg kg^–1, respectively.The durations of anaesthesia were recorded, the rats were killedand blood was collected to measure the concentrations of propofol.In a second set of experiments, rats received propofol 10 mgkg^–1 i.v. repeated 24 h (group D), 48 h (group E) or 72h (group F) later. Sleeping times were recorded after the firstand the second administration and concentrations of propofolat awakening were measured after the second dose, when ratswere killed. Sleeping times were significantly longer in groupsB (22.4 min) and C (25.9 min) compared with group A (13.7 min)(P < 0.001 for both). Durations of anaesthesia in groupsD, E and F were 14.7, 14.5 and 14.3 min, respectively, afterthe first dose of propofol and 11.6, 12.1, and 14.9 min, respectively,after the second dose. The rats in groups D and E exhibitedshorter sleeping times after the second dose of propofol thanafter the first (P < 0.01 for both). Concentrations of propofolat awakening did not differ between groups A, B and C or betweengroups D, E and F. The results suggest lack of changes in susceptibilityof the CNS to the anaesthetic effects of propofol. (Br. J. Anaesth.1994; 72: 127–128)     

Interactions between opioid drugs and propofol in laboratory models of seizures

Propofol (i.v. and i.p.) exhibited anticonvulsant activity inthree models of seizure in the mouse, induced by bicuculline,kainic acid and N-methyl-DL-aspartic acid (NMDLA). Morphine,pethidine and fentanyl, which showed a biphasic doseresponserelationship with respect to seizure modulation, abolished theanticonvulsant activity of propofol to exhibit their own intrinsicactivity in proconvulsant doses. This occurred with very lowdoses of fentanyl and pethidine (15µgkg^–1 and 0.5mg kg^–1, respectively) in the NMDLA model. Thus it appearsthat propofol has anticonvulsant activity only when a convulsionis elicited directly; it does not prevent the actions of compoundsthat lower seizure thresholds to convulsant stimuli. The anticonvulsantdoses of morphine and fentanyl did not summate with the anticonvulsantactivity of propofol. However, there was some evidence of summationof anticonvulsant activity between pethidine and propofol inthe NMDLA model. (Br. J. Anaesth. 1995; 74: 311–314)     

Use of ketorolac in the prevention of suxamethonium myalgia

We have evaluated the effect of ketorolac in the preventionof suxamethonium myalgia. Sixty ASA I patients who presentedfor extraction of wisdom teeth as day cases were allocated randomlyto one of three equal groups. Patients received either 0.9%saline (placebo), atracurium 0.05 mg kg^–1 i.v. or ketorolac10 mg i.v., 3 min before induction of anaesthesia. Follow-uppostal questionnaires (97% response rate) at 48 h showed noreduction in the incidence of myalgia after ketorolac pretreatmentcompared with saline. The use of atracurium reduced the incidenceof myalgia by 60% (P < 0.001) and the severity of fasciculations(P < 0.001). There was no difference in the severity of fasciculationsbetween the saline and ketorolac groups. Intubating conditionswere comparable in the three groups.     

Double-blind randomized controlled trial of caudal versus intravenous S(+)-ketamine for supplementation of caudal analgesia in children

Background. The postoperative analgesic efficacy of S(+)-ketamineafter caudal or i.v. administration following sub-umbilicalsurgery in children was studied to investigate its principalsite of analgesic action. Methods. Sixty children undergoing caudal block during generalanaesthesia for hernia repair or orchidopexy were prospectivelyrandomized to one of three groups: the bupivicaine group receivedplain bupivacaine 0.25% 1 ml kg^–1; the caudal ketaminegroup received caudal plain bupivacaine 0.25% 1 ml kg^–1with S(+)-ketamine 0.5 mg kg^–1; the i.v. ketamine groupreceived caudal plain bupivacaine 0.25% 1 ml kg^–1 plusS(+)-ketamine 0.5 mg kg^–1 i.v.. Postoperative measurementsincluded analgesic requirements and modified objective painscore for the first 24 h. Results. The median time to first analgesia was significantlylonger in the caudal ketamine group (10 h) than in the i.v.ketamine (4.63 h) or bupivacaine (4.75 h) groups (P=0.01). Significantlyfewer doses of analgesia were required over the first postoperative24 h by subjects in the caudal ketamine group (median 1) comparedwith the i.v. ketamine (median 2) or bupivacaine (median 2.5)groups (P<0.05). There was no difference between the groupsin the incidence of postoperative nausea and vomiting or psychomotorreactions. Conclusions. We have demonstrated that the addition of caudalS(+)-ketamine to bupivacaine prolongs the duration of postoperativeanalgesia. However, the same dose of i.v. S(+)-ketamine combinedwith a plain bupivacaine caudal provides no better analgesiathan caudal bupivacaine alone, indicating that the principalanalgesic effect of caudal S(+)-ketamine results from a localneuroaxial rather than a systemic effect. Br J Anaesth 2004; 92: 344–7     

Effect of intraoperative intravenous crystalloid infusion on postoperative nausea and vomiting after gynaecological laparoscopy: comparison of 30 and 10 ml kg(-1)

Background. I.V. fluid administration has been shown to reducepostoperative nausea and vomiting (PONV). The optimum dose isunknown. We tested the hypothesis that administration of i.v.crystalloid of 30 ml kg^–1 would reduce the incidence ofPONV compared with 10 ml kg^–1 of the same fluid. Methods. A total of 141 ASA I female patients undergoing electivegynaecological laparoscopy were randomized, in double-blindfashion, to receive either 10 ml kg^–1 (n=71; CSL-10 group)or 30 ml kg^–1 (n=70; CSL-30 group) of i.v. compound sodiumlactate (CSL). Results. In the first 48 h after anaesthesia, the incidenceof vomiting was lower in the CSL-30 group than in the CSL-10group (8.6% vs 25.7%, P=0.01). Anti-emetic use was less in theCSL-30 group at 0.5 h (2.9% vs 14.3%, P=0.04). The incidenceof severe nausea was significantly reduced in the treatmentgroup at awakening (2.9% vs 15.7%, P=0.02), 2 h (0.0% vs 8.6%,P=0.04) and cumulatively (5.7% vs 27.1%, P=0.001). The numbersneeded to treat to prevent vomiting, severe nausea and antiemeticuse in the first 48 h were 6, 5 and 6, respectively. Conclusion. I.V. administration of CSL 30 ml kg^–1 to healthywomen undergoing day-case gynaecological laparoscopy reducedthe incidence of vomiting, nausea and anti-emetic use when comparedwith CSL 10 ml kg^–1.     

Questioning the cardiocirculatory excitatory effects of opioids under volatile anaesthesia

Background. Opioid-induced hyperalgesia has been demonstratedin awake animals. We observed an increased haemodynamic reactivityin response to noxious stimuli in rats under sevoflurane anaesthesiatreated with a very low dose of sufentanil. The aim of thisinvestigation was to determine whether the two phenomena sharea common origin: an opioid-induced excitatory reaction. To addressthis, we administered several drugs with proven efficacy inopioid hyperalgesia to rats presenting with haemodynamic hyper-reactivity. Methods. The MACbar of sevoflurane was measured in controlsand in animals treated with sufentanil 0.005 µg kg^–1min^–1 before and after administration of i.v. (0.25, 0.5mg kg^–1) and intrathecal (i.t.) (250 µg) ketamine,i.v. (0.5, 1 mg kg^–1) and i.t. (30 µg) MK-801(NMDAantagonist), i.v. (0.1, 0.5 mg kg^–1) naloxone, i.v. (10mg kg^–1) and i.t. (50, 100 µg) ketorolac or i.t.(100, 150 µg) meloxicam (COX-2 inhibitor). Results. Sufentanil 0.005 µg kg^–1 min^–1 significantlyincreased MACbar (3.2 (SD 0.3) versus 1.9 (0.3) vol%). Withthe exception of naloxone, all drugs displayed a significantMACbar-sparing effect (>50%) in controls. Naloxone completelyprevented haemodynamic hyperactivity. Two patterns of reactionwere recorded for the other drugs: either hyper-reactivity wassuppressed and the MACbar-sparing effect was maintained (i.t.ketamine, i.t. MK-801, i.t. ketorolac [100 µg], i.t. meloxicam[150 µg]) or hyper-reactivity was blocked but MACbar-sparingeffect was lost (i.v. ketamine [0.5 mg kg^–1], i.v. MK-801[0.5, 1 mg kg^–1], i.v. ketorolac [10 µg kg^–1],i.t. ketorolac [50 µg], i.t. meloxicam [100 µg]). Conclusions. We have demonstrated that low-dose sufentanil-inducedhaemodynamic hyper-reactivity is an excitatory µ-opiate-relatedphenomenon. This effect is reversed by drugs effective in treatingopiate-induced hyperalgesia.     

DOSE REQUIREMENTS OF PROPOFOL BY INFUSION DURING NITROUS OXIDE ANAESTHESIA IN MAN: I: Patients Premedicated with Morphine Sulphate

The study was performed to determine the ED₅₀ and ED₉₅ of acontinuous infusion of the emulsion formulation of propofolduring 67% nitrous oxide anaestheisa in 57 patients premed-icatedwith morphine sulphate 0.15 mg kg^–1. Anaesthesia was inducedwith propofol 2 mg kg^–1, and maintained before incisionwith a fixed-rate infusion of propofol to supplement nitrousoxide. The response to the first surgical incision, made atleast 30 min after induction of anaesthesia, was observed. TheED₅₀; was 53.5 µg kg^–1 min^–1 and the ED₉₅was 112.2 µg kg^–1 min^–1. At the time of thefirst surgical incision, the venous whole blood concentrationsof propofol at the ED₅₀ and ED₉₅ infusion rates (EC₅₀and EC₉₅were 1.66 µg ml^–1 and 3.39 fig ml^–1 respectively.The satisfactory maintenance of anaesthesia provided by nitrousoxide supplemented with propofol was associated with stabilityand rapid, uncomplicated recovery.     

Role of propofol and its solvent,intralipid, in nitric oxide-induced peripheral vasodilatation in dogs

Background. The commercial propofol preparation in an intralipidsolution causes marked vasodilatation. Both propofol and itssolvent seem to stimulate the nitric oxide (NO) pathway. Therole of intralipid in cardiac and regional haemodynamic changesinduced by propofol and their respective interactions with theNO pathway was assessed. Methods. Dogs were instrumented to record arterial pressure,heart rate, cardiac output, dP/dt (the first derivative of leftventricular pressure) and vertebral, carotid, coronary, mesenteric,hepatic, portal and renal blood flows. Experimental groups wereas follows. Group 1 (control; n=11): N-methyl-L-arginine (L-NMA)20 mg kg^–1 i.v.; Group 2 (n=8): propofol (10mg ml^–1) 4 mg kg^–1 i.v. bolus followedby 0.6 mg kg^–1 min^–1; Group 3 (n=6):intralipid 0.25 ml kg^–1 bolus followed by 0.06ml kg^–1 min^–1. After 60 min, L-NMAwas injected in Groups 2 and 3. Results. Propofol induced increases in heart rate, coronaryand carotid blood flows, and decreases in systemic vascularresistance and dP/dt. Intralipid increased renal blood flow,carotid vascular resistance and mesenteric vascular resistance.In the presence of intralipid, L-NMA-induced pressor responseand systemic, carotid and renal vasoconstriction were more pronouncedthan in control dogs. Conclusions. Except for the coronary and carotid circulations,intralipid modulates the NO pathway in cardiac and regionalblood flow. Br J Anaesth 2002; 89: 492–8     

COMPARISON OF PROPOFOL WITH THIOPENTONE FOR TREATMENT OF BUPIVACAINE-INDUCED SEIZURES IN RATS

Thirty Sprague-Dawley rats were paralysed with pancuronium andtheir lungs ventilated mechanically with 70% nitrous oxide and0.5% halothane in oxygen. Bupivacaine 2 mg kg^–1 min^–1was infused continuously i.v. until the animals died. At theonset of seizures, animals were given an i.v. bolus of propofol1 mg kg^–1 (n=10), thiopentone 2 mg kg^–1 (n=10) orlipid vehicle (n=10). Administration of propofol or thiopentonewas repeated each time seizures restarted and lipid vehicleadministrations were repeated at 2-min intervals until the electroencephalogrambecame isoelectric. All animals developed seizures, arrhythmias,iso-electric EEG and asystole. Administration of lipid vehicleinduced no obvious changes in ongoing epileptiform activity.The initial doses of thiopentone and of propofol stopped epileptiformactivity in all animals, usually within 6s after administration.The seizure-free period after the initial administration ofthiopentone and of propofol lasted, on average, 0.98 min and1.72 min, respectively. We conclude that propofol may have valuein treating seizures induced by bupivacaine. (Br. J. Anaesth.1993; 71: 715–719)     

Tramadol does not modify the Bispectral Index during anaesthesia with sevoflurane and remifentanil

Background. The aim of this study was to investigate the effectsof tramadol administered with ketorolac on the Bispectral Index(BIS) during anaesthesia with sevoflurane and remifentanil. Methods. Forty-six adult patients, ASA I–III, scheduledfor elective minor surgical procedures were studied. Patientswere premedicated with remifentanil infusion 0.4 µg kg^–1min^–1 and anaesthesia was induced 4–5 min laterwith propofol 1.5 mg kg^–1 and maintained with air–oxygen( 0.4), remifentanil 0.1–0.15 µg kg^–1 min^–1 and sevoflurane, adjusted to keep theBIS between 40 and 50. After 20 min of stable anaesthesia, thesubjects were allocated randomly to receive i.v. tramadol 1.5mg kg^–1 and i.v. ketorolac 0.3 mg kg^–1 (tramadolgroup) or saline (control group). BIS values, mean arterialpressure, heart rate and end-tidal carbon dioxide were recordedevery 5 min for 20 min. Results. Mean BIS values after tramadol administration werenot significantly different from those recorded in patientsreceiving saline throughout the period of observation. Therewere no patients who presented explicit recall of events underanaesthesia. No significant changes in mean arterial pressure,heart rate and end-tidal carbon dioxide were noted after tramadolinjection. Conclusion. Tramadol, given with ketorolac to prevent postoperativepain, during anaesthesia maintained with sevoflurane and remifentanilat BIS between 40 and 50, does not modify the BIS value.     

Analgesic efficacy of tramadol 2 mg kg(-1) for paediatric day-case adenoidectomy

We studied the analgesic efficacy of tramadol 2 mg kg^–1for post-operative analgesia after day-case adenoidectomy inchildren aged 1–3 yr. Eighty children were allocatedrandomly to receive tramadol 2 mg kg^–1 i.v.or placebo immediately after induction of anaesthesia. Anaesthesiawas induced with alfentanil 10 µg kg^–1and propofol 4 mg kg^–1 followed by mivacurium0.2 mg kg^–1 for tracheal intubation. Anaesthesiawas continued with sevoflurane in nitrous oxide and oxygen.All children were given ibuprofen rectally at approximately10 mg kg^–1 before the start of surgery. Post-operativepain and recovery assessments were performed by a nurse blindedto the analgesic treatment using the Aldrete recovery score,the pain/discomfort scale and measurement of recovery times.Rescue medication (pethidine in increments of 5 mg i.v.)was administered according to the pain scores. A post-operativequestionnaire was used to evaluate the need for analgesia athome up to 24 h after operation. Rescue analgesic at homewas rectal or oral ibuprofen 125 mg. Children in the tramadolgroup required fewer pethidine doses than those in the placebogroup (P=0.014). Forty-five per cent of children receiving tramadoldid not require post-operative analgesia at all compared with15% of children receiving placebo (P=0.003). Recovery timesand the incidence of adverse effects were similar in the twogroups in the recovery room and at home. The requirement forrectal ibuprofen at home did not differ between groups. Br J Anaesth 2001; 86: 572–5     

Ketoprofen for pain after hip and knee arthroplasty

In a double-blind, randomized study, we have compared the effectsof i.v. ketoprofen 200 mg followed by 12.5 mg h^–1 over13 h, with those of extradural morphine 4 mg in 32 patientsafter hip and knee arthroplasty. A visual analogue scale wasused to score pain before analgesic administration (first complaintafter operation), 1 h after and every 2 h subsequently. Painreduction 1 h after the start of analgesia was mean 44% (SEM17%) in the extradural morphine group and 54% (9%) in the ketoprofengroup (ns). There were no significant differences between groupsin pain scores, pain reduction and additional analgesia requirement(i.v. paracetamol). Naloxone 5 µg kg^–1 h^–1was required for hypercapnia exceeding 6.0 kPa in three patientsin the extradural morphine group (vs none in the ketoprofengroup; ns). There were no differences between groups in sideeffects, except for urinary retention, which was more frequentin the extradural morphine group (P < 0.05). As there werefew differences between i.v. ketoprofen and extradural morphine,we conclude that ketoprofen may be an efficient alternativeto extradural morphine after hip and knee arthroplasty. (Br.J. Anaesth. 1994; 72: 383–387)