Ulinastatin reduces elevation of cytokines and soluble adhesion molecules during cardiac surgery

Purpose

To investigate whether ulinastatin pretreatment (6000 U · kg^?1 before CPB and before declamping of aorta) influenced the production of cytokines and adhesion molecules in the peripheral circulation.

Methods

This prospective randomized study was performed in 22 patients undergoing cardiac surgery. They were divided into two groups. Patients in Group I were untreated and in Group II treated with ulinastatin. The soluble intercellular adhesion molecule-1 (S-ICAM-1), soluble endothelial leukocyte adhesion molecule-1 (S-ELAM-1), interleukin8 and 6 (IL-8, 6) were measured using ELISA kits.

Results

Serum S-ICAM-1 concentration in Group I increased from the preoperative value of 297 ± 27 ng · kg^?1 to 418 ± 106 ng · kg^?1 at 60 min after declamping of the aorta (P < 0.01) but did not change in Group II. Serum S-ELAM-1 concentration did not change in either group. Serum concentration of IL-8 and IL-6 in Group I (37 ± 44 pg · kg^?1, and 59 ± 59 pg · kg^?1, preoperatively) increased to 169 ± 86 pg · kg^?1 and 436 ± 143 pg · kg^?1 at 60 min after declamping of the aorta (P < 0.001, P < 0.001). The increases were greater than those from 25 ± 6 pg · kg^?1 and 30 ± 26 pg · kg^?1 to 56 ± 36 pg · kg^?1 and 132 ± 78 pg · kg^?1 in Group II (P < 0.001, P < 0.001). The levels of S-ICAM-1 correlated with those of IL-8 (r = 0.5, P < 0.001).

Conclusion

These results suggest that ulinastatin may suppress the increase in IL-8 production and the expression of ICAM-1 during cardiac surgery.     

Rocuronium prevents succinylcholine-induced fasciculations

Purpose

The aim of this study was to assess the effect of rocuronium pretreatment at 3 and 1.5 min before succinylcholine administration on fasciculations, neuromuscular blockade and intubating conditions.

Methods

Sixty ASA I or II adults scheduled for elective surgery were anaesthetised with midazolam, fentanyl, propofol, N₂O and isoflurane. They were randomised in a double blind manner into three groups: group ROC-3 min (n = 22) received 0.05 mg·kg^?1 rocuronium, 3 min before 2 mg·kg^?1 succinylcholine; group ROC-1.5 min (n = 20) received 0.05 mg·kg^?1 rocuronium 1.5 min before 2 mg·kg^?1 succinylcholine; and group NO ROC (n = 18) had no rocuronium before injection of 2 mg·kg^?1 succinylcholine. Fasciculations and intubating conditions were evaluated by the same physician who was unaware of the randomisation. Neuromuscular block was measured at the adductor pollicis with an accelerometer.

Results

The incidence of fasciculations was lower in the ROC-3 min (9%) and ROC-1.5 mm (30%) groups than in the NO ROC group (83%;P < 0.001 ). The intensity of fasciculations was also less in both pretreatment groups. No statistical difference was noted between pretreatment at 3 and 1.5 min. Intubating conditions, onset time and duration of succinylcholine blockade were comparable in all three groups.

Conclusion

The incidence and severity of succinylcholine fasciculations can be reduced by giving 0.05 mg·kg^?1 rocuronium either 1.5 min or 3 min before succinylcholine. The effects of 2 mg·kg^?1 succinylcholine with rocuronium pretreatment, and 1 mg·kg^?1 succinylcholine, without pretreatment, are similar with respect to intubating conditions, onset of paralysis and duration of blockade.     

Conscious sedation for interventional neuroradiology: a comparison of midazolam and propofol infusion

Purpose

The aim of this study was to compare two conscious sedation techniques, midazolam (M) and propofol (P), for interventional neuroradiology by assessment of the incidence of complications and satisfaction scores.

Methods

Forty patients were randomized to receive 0.75 μg · kg^?1 fentanyl and a M or P bolus followed by an infusion; (M I5 μg · kg^?1 + 0.5 μg · kg^?1 · min^?1: P 0.5 mg · kg^?1 + 25 μg · kg^?1 min^?1). The incidences of complications and untoward events requinng intervention were documented. These included respiratory depression, excessive pain, inappropriate movements and the inability to examine the patient. The satisfaction of the anaesthetic technique from the perspective of both the neuroradiologist and the patient was scored.

Results

The incidence and types of complications were not different between the two groups. Pain occurred in 12 patients (6M, 6P), inappropriate movements in 17 (7M, 10P) and respiratory changes in 10 patients (2M, 8P).

Conclusions

Both techniques were satisfactory and the incidence of complications was similar for both groups.     

Intubating conditions and neuromuscular block after divided dose mivacurium or single dose rocuronium

Purpose

To evaluate the tracheal intubating conditions and neuromuscular blocking charactenstics of divided dose mivacurium or single dose rocuronium.

Methods

Thirty-two patients undergoing elective surgery were studied. Anaesthesia was with propofol 2 mg · kg^?1, followed by an infusion of l50 μg · kg^?1 · min^?1. Patients were randomized to receive either mivacurium-0.15 mg · kg^?1 followed 30 sec later by 0.1 mg · kg^?1, or rocuronium-0.9 mg · kg^?1, followed 30 sec later by placebo. Tracheal intubating conditions were assessed 90 sec after the initial dose of relaxant by an anaesthetist who was unaware of patient group. The electromyographic (EMG) response of the first dorsal interosseus muscle to ulnar nerve train-of-four was measured.

Results

Successful tracheal intubation was performed in all patients after both mivacurium and rocuronium. Intubating conditions (jaw relaxation, open visible vocal cords) were judged to be good-excellent in all but one patient before insertion of the tracheal tube. However, patients receiving mivacunum were more likely to experience coughing and bucking after tracheal tube insertion (10/16 patients) than those receiving rocuronium (3/16 patients, P < 0.05). No patient in the rocuronium group experienced moderately vigorous coughing and bucking after insertion of the tracheal tube vs six patients in the mivacurium group (P < 0.05). Time to 10 and 25% recovery of neuromuscular function was faster (P < 0.05) after divided dose mivacunum (20 ± 1 and 23 ± 1 min, respectively) than after rocuronium (45 ± 5 and 57 ± 8 min, respectively).

Conclusion

The results suggest that, during conditions of the study, divided dose mivacurium is not recommended for a 90-sec tracheal intubation in patients where moderate coughing and bucking is deemed unacceptable.     

Midazolam reverses histamine-induced bronchoconstriction in dogs

Purpose

Midazolam has been used clinically as a sedative and as an anaesthetic induction agent. However, the bronchodilating effects of midazolam have not been comprehensively evaluated. We sought to determine relaxant effects of midazolam on the airway.

Methods

After our Animal Care Committee approved the study, eight mongrel dogs were anaesthetized with 30 mg · kg^?1 pentobarbitoneiv, and were paralysed with 200 μg · kg^?1 · hr^?1 pancuronium. The trachea was intubated with an endotracheal tube (ID 7 mm) that had a second lumen for insertion of a superfine fibreoptic bronchoscope (OD 2.2 mm) to measure the bronchial cross-sectional area (BCA) continuously. The tip of the bronchoscope was placed at the level of the second or third bronchial bifurcation of the nght bronchus. A videopnnter printed the BCA which was then measured with a NIH Image program. Bronchoconstnction was produced with histamine (H) 10 μg · kg^?1 followed by 500 μg · kg^?1 · hr^?1. Thirty minutes later, 0 [saline], 0.01, 0.1 and 1.0 mg · kg^?1 midazolam and 25 μg · kg^?1 flumazenil were given. The BCA was assessed before (basal area) and 30 min after the start of H infusion, and was also measured five minutes after each midazolam and flumazeniliv. At the same time, arterial blood was sampled for plasma catecholamine measurement.

Results

Histamine infusion decreased BCA to 49.7 ± 17.3% of basal BCA More than 0.1 mg · kg^?1 midazolam increased BCA up to 71.7 ± 15.3% of the basal (1.0 mg · kg^?1) (P < 0.01). Plasma adrenaline concentration was decreased from 6.9 ± 3.8 to 3.7 ± 1.9 ng · ml^?1 by 1.0 mg · kg^?1 midazolam (P < 0.05). Flumazenil did not antagonize the relaxant effect of midazolam but reversed the inhibitory effect of midazolam on histamine-induced adrenaline release.

Conclusion

Midazolam has a spasmolytic effect on constricted airways but this bronchodilatation was not reversed by flumazenil.     

Sevoflurane and isoflurane impair edrophonium reversal of vecuronium-induced neuromuscular block

Purpose

A dose-response relationship study for edrophonium to examine the modification of volatile anaesthetics on reversal of vecuronium block.

Methods

One hundred and twenty ASA (I–II) patients were anaesthetized with sevoflurane, isoflurane (I minimum alveolar anaesthetic concentration [MAC] end-tidal concentration), or fentanyl-diazepam anaesthesia, in combination with 66% nitrous oxide (n = 40 for each group). The evoked electromyogram (EMG) response of the abductor digiti minimi was monitored at 20 sec intervals following train-of-four (TOF) stimulation of the ulnar nerve. The initial neuromuscular block was produced by vecuronium 100 μg · kg^?1. When the amplitude of the first response (T₁) had spontaneously recovered to 10% of the control, edrophonium (0, 125, 400, 700 or 1000 μg · kg^?1; eight patients each) was randomly administered, and the ratio of the fourth TOF to the first response (TOFR ) was monitored at one minute intervals for 10 min.

Results

Sevoflurane and isoflurane impaired the edrophonium-assisted TOFR recovery in an edrophonium dose and time dependent manner. The dose-response curves at 10 min exhibited a greater shift to the right in the sevoflurane and isoflurane groups than in the fentanyl-diazepam-nitrous oxide group (P < 0.05). Higher ED₅₀ values (the edrophonium dose required to obtain TOFR value of 50%) in the sevoflurane (> 1000 μg · kg^?1) and isoflurane groups (851 · μg · kg^?1) were observed than in the fentanyl-diazepam-nitrous oxide group (339 μg · kg^?1) (P < 0.05).

Conclusion

One MAC sevoflurane and isoflurane anaesthesia impair edrophonium reversal of vecuronium block to a similar degree.     

Antinociceptive effects of epidural and intravenous ketamine to somatic and visceral stimuli in rats

Purpose

To evaluate the antinociceptive effect of epidural and intravenous ketamine on somatic and visceral stimuli and to address the emergency reaction.

Methods

Rats were randomly allocated into nine groups (n = 6); five groups with chronically implanted epidural catheters received saline or 0.5, 1, 2 and 4 mg · kg^?1 ketamine epidurally, four groups received saline, or 1, 5 and 10 mg · kg^?1 ketamine iv. To assess somatic and visceral antinociceptive effects, tail flick (TF) test and colorectal distension (CD) test were carried out, respectively. Emergence reactions were graded. Maximal possible effects (% MPE) were calculated.

Results

Epidural ketamine increased % MPE in both tests in a dose-dependent fashion for 30 min (vs saline group, P < 0.05). Epidural ketamine 0.5 mg · kg^?1 produced an increase in % MPE in the CD test (P < 0.05) but failed in the TF test. Intravenous ketamine, 10 mg · kg^?1, produced 100 ± 0 (mean ± SE) % MPE in the CD test but 36 ± 15 % MPE in the TF test. Dose response curves indicated greater visceral antinociception than somatic. All rats showed emergence reactions following intravenous ketamine 10 and 5 mg · kg^?1.

Conclusion

Both epidural and intravenous ketamine produce greater antinociceptive effects to visceral than to somatic stimulation, and that epidural ketamine has a low incidence of emergence reactions.     

Topical lidocaine improves conditions for laryngeal mask airway insertion

Purpose

We hypothesized that optimal laryngeal mask airway (LMA?) insertion conditions might be achieved with topical lidocaine and a smaller dose of propofol. In this study, insertion conditions after topical lidocaine 40 mg followed by propofol 2 mg·kg^?1 were compared with propofol 2 mg·kg^?1 or propofol 3 mg·kg^?1 alone.

Methods

Ninety patients were recruited for this randomized prospective double-blind study. One group received four sprays of topical lidocaine (40 mg) over the posterior pharyngeal wall followed by propofol 2 mg·kg^?1 (Group 2PL; n = 30). The other two groups received four sprays of 0.9% normal saline followed by propofol 2 mg·kg^?1 (Group 2P; n = 30) or by propofol 3 mg·kg^?1 (Group 3P; n = 30). The frequency of optimal insertion conditions (successful insertion at the first attempt without adverse responses) and side effects were recorded.

Results

The frequency of optimal insertion conditions was greater in Group 2PL (20/30, 67%) and Group 3P (22/30, 73%) than in Group 2P (11/20, 37%) (P = 0.009). In Group 3P, the mean blood pressure was lower than in the other groups prior to LMA-Classic? insertion (P = 0.003) but was similar after insertion. The incidence of apnea was greater in Group 3P patients (17/30, 57%) than in Group 2P (2/30, 7%) or Group 2PL patients (1/30, 3%) (P < 0.001).

Conclusion

Topical lidocaine 40 mg followed by propofol 2 mg·kg^?1 can provide optimal insertion conditions of the LMA-Classic comparable to those of propofol 3 mg·kg^?1, with fewer hemodynamic changes and a lower incidence of apnea.     

Epidural and intravenous bolus morphine for postoperative analgesia in infants

Purpose

To compare two doses of bolus epidural morphine with bolus iv morphine for postoperative pain after abdominal or genitourinary surgery in infants.

Methods

Eighteen infants were randomly assigned to bolus epidural morphine (0.025 mg · kg^?1 or 0.050 mg · kg^?1) or bolus iv morphine (0.050–0.150 mg · kg^?1). Postoperative pain was assessed and analgesia provided, using a modified infant pain scale. Monitoring included continuous ECG, pulse oximetry, impedance and nasal thermistor pneumography. The CO₂ response curves and serum morphine concentrations were measured postoperatively.

Results

Postoperative analgesia was provided within five minutes by all treatment methods. Epidural groups required fewer morphine doses (3.8 ± 0.8 for low dose [LE], 3.5 ± 0.8 for high dose epidural [HE] vs. 6.7 ± 1.6 for iv, P < 0.05) and less total morphine (0.11 ± 0.04 mg · kg^?1 for LE, 0.16 ± 0.04 for HE vs 0.67 ± 0.34 for iv, P < 0.05) on POD1 Dose changes were necessary in all groups for satisfactory pain scores. Pruritus, apnoea, and haemoglobin desaturation occurred in all groups. CO₂ response curve slopes, similar preoperatively (range 36–41 ml · min^?1 · mmHg ETco ₂ ^?1 · kg^?1) were generally depressed (range, 16–27 ml · min^?1 · mmHg ETco ₂ ^?1 · kg^?1) on POD1. Serum morphine concentrations, negligible in LE (<2 ng · ml^?1), were similar in the HE and iv groups (peak 8.5 ± 12.5 and 8.6 ± 2.4 ng · ml^?1, respectively).

Conclusion

Epidural and iv morphine provide infants effective postoperative analgesia, although side effects are common. Epidural morphine gives satisfactory analgesia with fewer doses (less total morphine); epidural morphine 0.025 mg · kg^?1 is appropriate initially. Infants receiving epidural or iv morphine analgesia postoperatively need close observation in hospital with continuous pulse oximetry.     

Heart rate changes in cardiac transplant patients and in the denervated cat heart after edrophonium

Purpose

The effect of edrophonium on heart rate in cardiac transplant patients and in an animal model of acute cardiac denervation were studied, to evaluate the functional state of the peripheral parasympathetic pathway fol lowing cardiac denervation.

Methods

Edrophonium was studied in patients with normally innervated hearts (controls) and m cardiac trans plants. Edrophonium was also studied in vagotomized. beta-blocked cats. In Group I animals, the vagus nerve was not stimulated. In Groups 2 & 3 the right vagus nerve was electrically stimulated to produce approximately 20% and 40% reductions in baseline heart rate, respectively.

Results

Maximum heart rate reduction in transplants (7.3 ± 0.8 beats·min^?1 with 0.6 ± 0.08 mg·kg^?1) was less than in controls (13.3 ± 1.6 beatsmm with 0.4 + 0.05 mg·kg^?1, P < 0.01). In Group I animals heart rate decreased maximally by 20.9 ± 2.5 beats·min^?1 with 9.0 ± 1.9 mg·kg^?1. In Groups 2 and 3, with doses < 15 mg·kg^?1, reduc tions m heart rate were greater than in Group I and maximual reductions were obtained with lower doses (Group 2: maximum reduction by 20.3 ± 2.8 beats·min^?1 with 1.3 ± 0.1 mg·kg^?1: Group 3: 22.6 ± 4.0 beats·min^?1 with 0.8±0.2 mg·kg^?1, P < 0.001) Doses > 1.5 mg·kg^?1 in Groups 2 and 3 produced increases in heart rate.

Conclusion

Edrophonium produced bradycardia in cardiac transplants suggesting spontaneous release of acetylcholinee from parasympathetic postganglionic neurons m the transplanted heart. The magnitude of the brady cardia was less in transplant than in control patients. Findings from animal studies suggest that the reduction in transplants can be attributed to diminution or absence of tonic cardiac parasympathetic drive. At high doses, edrophonium may interfere with parasympathetic neuron activation.     

Optimal dose of thiamylal in combination with midazolam for induction of anaesthesia

Purpose

The optimal dose range of thiamylal, combined with midazolam, in the induction of anaesthesia was evaluated using haemodynamic variables.

Methods

The 200 patients, aged 30 to 70 yr, were randomly divided into five groups by midazolam dosage. Anaesthesia was induced with midazolam 0.05, 0.075, 0.10, 0.15, or 0.20 mg · kg^?1. Two minutes later, 50 mg thiamylal was administered followed by 25 mg increments until verbal response and eyelash reflex disappeared and blood pressure decreased to a level less than that of preinduction. Tracheal intubation was performed with 0.15 mg · kg^?1 vecuronium. Blood pressure and heart rate were monitored during induction. Optimal induction was defined as a systolic blood pressure one minute after intubation within ±20% of that before induction.

Results

There were 164 patients whose systolic blood pressure were within these criteria. Blood pressure decreased two minutes after induction and 3 to 15 min after intubation in all groups. Heart rate increased one minute after intubation in 0.05 mg · kg^?1, 0.075 mg · kg^?1 and 0.10 mg · kg^?1 midazolam groups. The optimal range of thiamylal was 4.0 ± 1.1 (mean + SD), 3.1 ± 1.2, 2.8 ± 1.1, 2.3 ± 1.2, and 1.7 ± 1.0 mg · kg^?1 in combination with midazolam 0.05, 0.075, 0.10, 0.15, and 0.20 mg · kg^?1, respectively.

Conclusion

The optimal dose range, to maintain haemodynamic stability, for thiamylal induction of anaesthesia in combination with midazolam, 0.05-0.2 mg · kg^?1 was found to range from 4.0 to 1.7 mg · kg^?1.     

Cerebrovascular autoregulation in critically ill patients during continuous hemodialysis

Purpose

In chronic renal failure, intermittent hemodialysis decreases cerebral blood flow velocity (CBFV); however, in critically ill patients with acute renal failure, the effect of continuous venovenous hemodialysis (CVVHD) on CBFV and cerebrovascular autoregulation (AR) is unknown. Therefore, a study was undertaken to investigate the potential effect of CVVHD on CBFV and AR in patients with acute renal failure.

Methods

This cohort study investigated 20 patients with acute renal failure who required CVVHD. In these patients, the CBFV and index of AR (Mx) were measured using transcranial Doppler before and during CVVHD.

Results

The median Mx values at baseline were 0.33 [interquartile range (IQR): 0.02-0.55], and during CVVHD, they were 0.20 [0.07-0.40]. The differences in Mx (CVVHD – baseline) was (median [IQR]) ?0.015 [?0.19-0.05], 95% confidence interval (CI) ?0.16 to 0.05. The Mx was > 0.3 in 11/20 patients at baseline measurement. Six of these patients recovered to Mx < 0.3 during CVVHD. The CBFV was (median [IQR]) 47 [36-59] cm·sec^?1 at baseline and 49 [36-66] cm·sec^?1 during CVVHD. The difference of CBFV was 0.0 [?4 - 2.7], 95% CI ?2.5 to 4.2.

Conclusion

Compared with patients with intermittent hemodialysis, CVVHD did not influence CBFV and AR in critically ill patients with acute renal failure, possibly due to lower extracorporeal blood flow, slower change of plasma osmolarity, and a lower fluid extraction rate. In a subgroup of patients with sepsis, the AR was impaired at baseline in more than half of the patients, and this was reversed during CVVHD. The trial was registered at ClinicalTrials.gov ID: NCT01376531.     

Cerebral oxygénation during prostaglandin E1 induced hypotension

Purpose

To evaluate the cerebral oxygenation effects of hypotension induced by prostaglandin E₁(PGE₁) during fentanyl-oxygen anaesthesia.

Methods

Ten patients who underwent elective cardiac surgery received infusion of PGE₁. After measuring the baseline arterial, mixed venous and internal jugular vein blood gases, systemic haemodynamics, and regional cerebral oxygen saturation (rSO₂) estimated by INVOS 3l00^R, PGE₁ was continuously infused at 0.25-0.65 μg·kg^?1·min^?1 (mean dosage: 410 ± 41.4 mg·kg^?1·min^?1) intravenously. Ten, 20 and 30 minutes after the start of drug infusions, blood gases described above were obtained simultaneously with the measurement of systemic haemodynamics and rSO₂. Thirty minutes from the start of drug infusions, administration of PGE₁ was stopped. The same parameters were measured again 10, 30 minutes after the stop of drug infusion.

Results

PGE₁ decreased mean arterial pressure (MAP) to approximately 70% of the baseline value (P < 0.05). PGE₁ increased mixed venous saturation, but in contrast did not effect internal jugular pressure, internal jugular oxygen saturation and rSO₂.

Conclusions

These results suggest that PGE₁ is a suitable drug for induced hypotension because flow/metabolism coupling of brain and regional cerebral oxygenation were well maintained during hypotension.     

Heparin and protamine titration do not improve haemostasis in cardiac surgical patients

Purpose

Weight-based heparin and protamine dosing strategies for cardiopulmonary bypass (CPB) do not take into account interpatient variability in drug sensitivity and may result in bleeding complications. We compared the Hemochron® RxDx heparin and protamine titration system with standard weight based management with regard to heparin dose, protamine dose, and perioperative bleeding.

Methods

One hundred and thirty-five cardiac surgical patients were randomised into four groups. Group I received standard heparin and protamine management: Group 2 received heparin and protamine byin vitro titration. Group 3 had the heparin dose titrated, and group 4 had the protamine dose titrated. Coagulation tests, bleeding, and transfusion requirements were measured.

Results

The initial heparin bolus predicted by the titration was < 300 U· kg^?1 in all patients. Group 2 received a lower heparin bolus for the initiation of bypass but total heparin doses were not different among groups (group 1 = 365 ± 43, group 2= 348 ± 73 U · kg^?1, group 3= 394 ± 86 U · kg^?1, group 4= 376 ± 60; P = 0.06). Groups 2 and 4 received a lower initial and a lower total protamine dose (total dose group 1 = 4.03 ± 0.65 mg · kg^?1, group 2 = 3.56 ±1.11 mg · kg^?1, group 3= 4.22 ± 0.90 mg · kg^?1, group 4= 3.38 ± 0.98 mg· kg^?1,P = 0.001). The incidences of incomplete heparin neutralisation (P = 0.14) and heparin rebound (P = 0.1) were not different among groups. Postoperative bleeding and transfusion requirements did not differ.

Conclusion

In cardiac surgical patients, heparin and protamine titration did predict a lower protamine dose but did not result in a measurable improvement in haemostasis during the perioperative period.     

40 Hz Auditory steady-state response and EEG spectral edge frequency during sufentanil anaesthesia

Purpose

The auditory steady-state evoked response (ASSR) is an evoked potential which provides a sensitive measure of the effects of general anaesthetics on the brain. We used pharmacokinetic-pharmacodynamic (PK-PD) modelling to compare the effects of sufentanil on the amplitude of the ASSR with its effect on spectral edge frequency (SEF) of the electroencephalogram.

Methods

Nine patients scheduled for elective cardiac surgery participated. Midazolam (70 μg·kg^?1 im) was given 60 min before entering the operating room. Anaesthesia was induced with 5 μg·kg^?1 sufentanil at a rate of 0.83 μg·kg^?1·min^?1. The ASSR, SEF and plasma sufentanil concentrations were measured for 30 min ater induction of anaesthesia before surgery. The half-life between the central and effect site compartments (t_1/2K_eo), the 50% inhibitory concentration (IC₅₀) and the slope factor (gamma) were computed.

Results

The amplitude of the ASSR increased during the first three minutes of infusion of sufentanil by up to 40%. This was followed by a rapid decrease between the fourth and fifth minutes to 16% of baseline. The SEF decreased progressively during the first five minutes of infusion to 18% of baseline. Both measures subsequently showed modest recovery. The parameters gamma, IC₅₀ and t_1/2K_eofor ASSR were (mean ±SD) 6,0 ±3.7, 2.1 ±1,2 ng·ml^?1 and 7.3 ±2.4 min. For SEF the values were 5.9 ±5.2, 1.4 ±0.7 ng·ml^?1 (P < 0.05 compared with ASSR) and 6.8 ±2,4 min.

Conclusion

The sensitivity of ASSR to sufentanil is less than that of the SEF.     

RETRACTED ARTICLE: Diltiazem-lidocaine combination for the attenuation of cardiovascular responses to tracheal intubation in hypertensive patients

Purpose

Hypertensive patients are prone to haemodynamic changes after laryngoscopy and tracheal intubation. This study was undertaken to compare the efficacy of a combination of diltiazem and lidocaine with that of each drug alone for suppressing the cardiovascular responses to trachéal intubation.

Methods

Sixty hypertensive patients (ASA II), defined as systolic blood pressure > 160 mmHg and/or diastolic blood pressure > 95 mmHg (World Health Organization), undergoing elective surgery received, in a randomized, double-blind manner, 0.3 mg·kg^?1 diltiazem, 1.5 mg·kg^?1 lidocaine, or 0.3 mg·kg^?1 diltiazem plus 1.5 mg·kg^?1 lidocaineiv (n = 20 of each) before the initiation of laryngoscopy. Anaesthesia was induced with 5 mg·kg^?1 thiopentoneiv, and tracheal intubation was facilitated with 2 mg·kg^?1 succinylcholineiv after precurarization with 0.02 mg·kg^?1 vecuroniumiv. Changes in heart rate (HR), mean arterial pressure (MAP) and rate-pressure product (RPP) were measured before and at immediate, 1, 2, 3, 5 and 10 min after tracheal intubation.

Results

The inhibitory effects of diltiazem-lidocaine combination on cardiovascular responses to tracheal intubation was greater than those of diltiazem or lidocaine as a sole medicine (RPP; 10602 ± 1448 (combination)vs 11787 ± 1345 (diltiazem), 15428 ± 1756 (lidocaine), mean ± SD,P < 0.05).

Conclusion

Prophylactic therapy with diltiazem-lidocaine combination is more effective than diltiazem or lidocaine alone for attenuating the cardiovascular changes associated with tracheal intubation in hypertensive patients.     

Preoperative ketorolac increases bleeding after tonsillectomy in children

Purpose

To compare the incidence of vomiting following codeine or ketorolac for tonsillectomy in children.

Methods

We had planned to enrol 240 patients, aged 2–12 yr undergoing elective tonsillectomy into a randomized, single-blind study in University Children’s Hospital. The study was terminated, after 64 patients because interim analysis of the data by a blinded non-study scientist concluded that the patients were at undue risk of excessive perioperative bleeding. After induction of anaesthesia by inhalation with N₂O/halothane or with propofol 2.5?3.5 mg· kg^?1 iv, the children were administered 150 μg· kg^?1 ondansetron and 50 μg · kg^?1 midazolam. Maintenance of anaesthesia was with N₂O and halothane in O₂. Subjects were administered either 1.5 mg · kg^?1 codeine im or 1 mg· kg^?1 ketorolac iv before the commencement of surgery. Intraoperative blood loss was measured with a Baxter Medi-Vac® Universal Critical Measurement Unit. Postoperative management of vomiting and pain was standardized. Vomiting was recorded for 24 hr after anaesthesia. Data were compared with ANOVA, Chi-Square analysis and Fisher Exact Test.

Results

Thirty-five subjects received ketorolac. Demographic data were similar. The incidence of vomiting during the postoperative period was 31% in the codeine-group and 40% in the ketorolac-group. Intraoperative blood losses was 1.3 ± 0.8 ml · kg^?1 after codeine and 2.2 ± 1.9 ml · kg^?1 after ketorolac (mean ± SD) P < 0.05. Five ketorolac-treated patients had bleeding which led to unscheduled admission to hospital, P < 0.05, Exact Test.

Conclusion

Preoperative ketorolac increases perioperative bleeding among children undergoing tonsillectomy without beneficial effects.     

Comparative effects of three doses of intravenous ketorolac or morphine on emesis and analgesia for restorative dental surgery in children

Purpose

The optimal dose of intravenous ketorolac tromethamine (ketorolac), a nonsteroidal antiinflammatory drug has not been determined in children. There are only limited published data on the use of intravenous ketorolac for paediatric analgesia. This study compares the analgesic and emetic effect of three different doses of ketorolac with morphine in paediatric dental surgical outpatients.

Methods

Following institutional approval and parental consent, 120 ASA I or II children, age 2– 10 yr were randomized to four groups and received ketorolac 0.75, 1.0, and 1.5 mg · kg^{? 1} or morphine 0.1 mg · kg^{? 1} iv at induction of a standardized anaesthetic. At 15 and 30 min after arrival in the recovery room a blinded observer assessed pain using the Objective Pain Score (OPS). Twentyfour hours after surgery a telephone interview was carried out with a parent at home.

Results

There were no differences in demographic data, anaesthesia time, recovery and daycare unit time, OPS and postoperative analgesic requirements in the four groups. Postoperative vomiting in the first 24 hr occurred more frequently in the morphine group than in the other groups (P <0.0166). No patient had excessive surgical bleeding.

Conclusions

Ketorolac, in all doses studied (0.75, 1.0 and 1.5 mg · kg^{? 1}) was as effective an analgesic as morphine 0.1 mg · kg^{? 1} given intravenously at induction to children having restorative dental surgery. Its use was associated with a significant reduction in the incidence of postoperative vomiting.     

Neuromuscular blocking effects of rocuronium during desflurane, isoflurane, and sevoflurane anaesthesia

Purpose

To determine the magnitude of the potentiation of rocuronium by desflurane, isoflurane and sevoflurane 1.5 MAC anaesthesia.

Methods

In a prospective, randomised, study in 80 patients, the cumulative dose-effect curves for rocuronium were determined during anaesthesia with desflurane, sevoflurane and isoflurane (with N₂O 70%, 15 min steady state) or total intravenous anaesthesia (TIVA) using propofol/fentanyl. Neuromuscular block was assessed by acceleromyography (TOF-Guard®) after train-of-four (TOF) stimulation of the ulnar nerve (2Hz every 12sec, 200 μsec duration), Rocuronium was administered in increments of 100 μg·kg^?1 until first twitch (T₁) depression > 95%.

Results

Rocuronium led to more pronounced T₁ depression with desflurane or sevoflurane anaesthesia than with TIVA. The ED₅₀ and ED₉₅ were lower during desflurane (95 ± 25 and 190 ± 80 μg·kg^?1) and sevoflurane (120 ±30 and 210 ± 40 μg·kg^?1) than with TIVA (150 ± 40 and 310 ± 90 μg·kg^?1) (P < .01), while the difference was not significant for isoflurane (130 ± 40 and 250 ± 90 μg·kg^?1). Following equi-effective dosing (T₁ > 95%) the duration to 25% T₁ recovery, recovery index (25/75), and TOF_0.70 was: 13.2 ± 1.8, 12.7 ± 3.4, and 26.9 ± 5.7 min during anaesthesia with desflurane; 15.5 ± 5.0, 11.4 ± 3.8, and 31.0 ± 6.0 min with sevoflurane; 13.9 ± 4.7, 10.7 ± 3.3, and 26.3 ± 8.9 min with isoflurane; and 13.9 ± 3.9, 11.3 ± 5.7, and 27.5 ± 8,2 min with TIVA anaesthesia (P: NS).

Conclusion

Interaction of rocuronium and volatile anaesthetics resulted in augmentation of the intensity of neuromuscular block but did not result in significant effects on duration of or recovery from the block.     

Antagonism of atracurium-induced block in obese patients

Purpose

To investigate the relationship between total body weight (TBW) or body mass index (BMI) and atracurium reversal time.

Methods

The study population comprised 25 patients with TBW < 80 kg and 25 patients with TBW ≥80 kg anaesthetised with midazolam, thiopentone, fentanyl, nitrous oxide and halothane. Neuromuscular block was induced with 0.5 mg· kg^?1 atracurium and maintained with doses of 0.15 mg· kg^?1. Neuromuscular transmission was recorded using train-of-four (TOF) nerve stimulation and mechanomyography. Neostigmine, 0.07 mg· kg^?1, was administered when the first twitch in TOF had recovered to 10% of control. Reversal time was defined as: time from administration of neostigmine until TOF ratio recovered to 0.70.

Results

There was no difference in reversal time between patients with TBW < 80 kg (7.2 ± 2.6 min, mean ± SD), and patients with TBW ≥80 kg (6.9 ± 3.6 min). When patients were grouped according to BMI there was no difference in reversal time between groups with low BMI (6.9 ± 2.6 min) or high BMI (7.1 ± 3.6 min). There was, furthermore, no difference in reversal time between the 15 patients in the study population with the smallest TBW or BMI and the 15 patients with the greatest TBW or BMI. There was no correlation between TBW or BMI and reversal time.

Conclusion

When atracurium-induced neuromuscular block is antagonised with 0.07 mg· kg^?1 neostigmine, TBW or BMI have no influence on reversal time.