Biomedical subjects
Publications and source records attributed to E Tassonyi.
Peritoneal insufflation with CO2 has been associated with profound cardiorespiratory disturbances, which may modify cerebral blood flow (CBF), particularly in hypertensive patients in whom CBF autoregulation is altered. We report a case of bilateral mydriasis during laparoscopic gastrectomy in a patient with chronic hypertension followed by a coma lasting several hours and we shortly discuss the possible mechanisms involved.
We have conducted a prospective, randomized study to evaluate the characteristics of induction of anaesthesia in children with 2% propofol. Children were allocated to receive propofol 3 mg kg-1 (group A), 4 mg kg-1 (group B) or 5 mg kg-1 (group C) of the 2% formulation. We observed a high incidence of spontaneous movements (90%) in group A and an incidence of coughing of 70% in group C. Induction in group B was characterized by a short induction time, low incidence of spontaneous movements (20%), pain on injection (10%) and excellent conditions for manual ventilation.
We describe a case in which jugular venous bulb oxygen saturation (SjvO2) monitoring proved useful during the surgical resection of an intracranial arteriovenous malformation (AVM). Surgical resection of large intracranial AVMs may be followed by normal perfusion pressure breakthrough with brain swelling, hyperemia, and subsequent problems in achieving hemostasis. SjvO2 monitoring during AVM embolization by interventional radiology has been shown to help in deciding whether embolization is sufficient to avoid such postresection hyperemia, but its use during surgical resection has not been described. In the case discussed, SjvO2 monitoring enabled assessment of the risk of postresection hyperemia preoperatively and permitted the degree and completeness of surgical AVM resection to be followed intraoperatively. During the normal perfusion pressure breakthrough bleeding which followed complete AVM resection, SjvO2 monitoring helped with safe management of the controlled hypotension that finally permitted hemostasis to be achieved.
Increasing evidence suggests a neuroprotective potential of magnesium sulfate (MgSO4). Only limited information about the passage of MgSO4 to the cerebrospinal fluid (CSF) is available in neurosurgical patients. However, with regard to the clinical relevance of magnesium's neuroprotective properties, quantitative data about its CSF passage are needed. The present study aims to assess the amount and the time course of magnesium's CSF passage in neurosurgical patients. To this end, 20 patients undergoing general anesthesia for neurosurgery and needing CSF drainage were included. Patients received an i.v. bolus of 60 mg/kg MgSO4. The increase in plasma and CSF magnesium concentration were measured 30, 90, and 240 min after the end of the MgSO4 infusion. These values were compared with the baseline levels taken before the start of the MgSO4 infusion. Thus, each patient served as his or her own control. Values are expressed as means +/- SD. The plasma magnesium levels were measured as follows: baseline, 0.74 +/- 0.12 mM; at 30 min, 1.24 +/- 0.1 mM (p < 0.01); at 90 min, 0.95 +/- 0.15 mM (p < 0.01), and at 240 min, 0.82 +/- 0.14 mM (p < 0.05). The CSF magnesium levels were measured as follows: baseline, 0.95 +/- 0.11 mM; at 30 min, 1.00 +/- 0.15 mM (NS); at 90 min, 1.10 +/- 0.17 mM (p < 0.01); and at 240 min, 1.13 +/- 0.19 mM (p < 0.001). We concluded that a bolus of 60 mg/kg of MgSO4 leads at least after 90 min to a significant increase in the CSF magnesium concentration. Moreover, the increase in plasma and CSF magnesium concentration is not parallel. Thus, plasma magnesium concentration cannot be used to predict the changes in CSF concentrations.
Magnesium sulphate (MgSO4) is currently used for haemodynamic control during anaesthesia and the early postoperative period. We have investigated the effect of this treatment on residual neuromuscular block after administration of vecuronium. Twenty adult patients were allocated randomly to one of two groups to receive MgSO4 60 mg kg-1 either at recovery from vecuronium block to a train-of-four (TOF) ratio of 0.7, or 1 h after recovery to a TOF ratio of 0.7. Neuromuscular transmission was monitored using electromyography and TOF stimulation. MgSO4 caused rapid and profound recurarization in all 20 patients. MgSO4 decreased the amount of acetylcholine released at the motor nerve terminal and thus may lead to recurarization in patients previously exposed to neuromuscular blocking agents.
Nociception can produce segmental spinal sensitization or descending supraspinal antinociception. We assessed both types of sensory change after surgery during isoflurane-nitrous oxide anaesthesia with or without fentanyl before nociception. Patients undergoing back surgery received fentanyl 3 micrograms kg-1 (n = 15) or placebo (n = 15) before anaesthesia in a prospective, randomized, blinded study. Sensation, pain detection and tolerance thresholds to electrical stimulation were measured before operation at the arm, incision and herniated disc dermatomes (HDD) and 1, 2, 4, 6, 24 h and 5 days after operation, together with pain scores and patient-controlled morphine consumption (duration 24 h). For segmental effects, thresholds were normalized to the thresholds at a distant dermatome (arm). Raw pain thresholds were increased after operation (fentanyl > placebo) and were maximal at 4 h (pain tolerance in HDD: fentanyl +5.2 mA (+62.7%), placebo, +3.8 mA (+44.2%); P < 0.05 vs baseline for both). Normalized sensation thresholds decreased for placebo only (HDD/4 h: placebo, -1.8 (-44.8%), P < 0.05; fentanyl, +0.1 (+5.5%) ns). All changes returned to baseline by 24 h except for the placebo group normalized HDD sensation (d5: placebo, -2.4 (-59.7)%, P < 0.05; fentanyl -0.1 (-5.5%) ns). Pain scores and morphine consumption were similar. The study demonstrated both supraspinal analgesia and spinal sensitization after surgery. Fentanyl administration before operation augmented the former while decreasing the latter, and hence sensitization, especially if neuropathic, may particularly benefit from pre-emptive analgesia.
We have investigated the potential of rocuronium 0.6 mg kg-1 (2xED95) and 0.9 mg kg-1 (3xED95) for rapid sequence induction in 100 children, aged 3-7 yr. Intubating conditions with the two different doses of rocuronium were assessed in 70 children (n = 35 in each group) undergoing elective surgery. Intubation was carried out by mimicking rapid sequence induction, and intubation conditions were evaluated according to a standard score. Intubating conditions were good to excellent in all 70 patients investigated (2xED95: excellent 29, good 6; 3xED95: excellent 33, good 2). In another 30 children (n = 15 in each group), we examined the times of rocuronium-induced neuromuscular block using electromyography. Lag time and recovery index did not differ significantly between the two groups (lag time: 37 (SD 12) vs 33 (14) s; recovery index: 9 (3) vs 10 (4) min). Three times the ED95 induced deeper neuromuscular block, 1 min after injection compared with 2xED95 (twitch height: 42 (24) vs 25 (19)%, respectively; P < 0.05). The same was true for onset time (193 (47) vs 118 (23) s; P < 0.01), clinical duration (21 (4) vs 34 (11) min; P < 0.01) and duration to 75% recovery (30 (6) vs 44 (4) min; P < 0.01). By mimicking rapid sequence induction, both doses of rocuronium offered clinically acceptable (good or excellent) intubating conditions.
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The interaction between doxacurium and halothane, isoflurane or alfentanil has not been studied in children. Using the cumulative dose-response technique and electromyography, we determined ED50 and ED90 of doxacurium during halothane (n = 9), isoflurane (n = 12) or alfentanil (n = 9) based anaesthesia in children aged 2-10 years. Both isoflurane and halothane potentiated the effects of doxacurium compared to alfentanil. The ED50 for doxacurium/halothane was 23.9 micrograms.kg-1 compared to 32.7 micrograms.kg-1 for doxacurium/alfentanil. The ED90 for doxacurium/isoflurane was 32.7 micrograms.kg-1 compared to 48.2 micrograms.kg-1 doxacurium/alfentanil (p < 0.05). There were no significant time course differences between the groups. When equipotent doses of doxacurium were used to provide muscle relaxation the duration of the neuromuscular block was similar in children who received aflentanil, halothane or isoflurane supplementation of N2O/O2 anaesthesia.
We have investigated the interaction between magnesium sulphate 40 mg kg-1 i.v. and vecuronium. First, we determined the effect of pretreatment with magnesium on the potency of vecuronium using a single bolus dose-response technique. In addition, we compared the time course of vecuronium-induced neuromuscular block (vecuronium 100 micrograms kg-1) with and without magnesium pretreatment. For both parts, neuromuscular block was assessed by electromyography. In addition, the effect of magnesium pretreatment on vecuronium-induced neuromuscular block was investigated in the context of rapid sequence induction of anaesthesia. We found that the neuromuscular potency of vecuronium was increased by pretreatment with magnesium sulphate. The ED50 and ED90 of vecuronium with MgSO4 were 25% lower than without MgSO4 (ED50: 21.3 vs 26.9 micrograms kg-1; ED90: 34.2 vs 45.7 micrograms kg-1; P < 0.05 for both). Mean onset time was 147.3 (SD 22.2) s in the MgSO4-vecuronium group vs 297.3 (122) s for controls (P < 0.05). Clinical duration was prolonged (MgSO4-vecuronium 43.3 (9) min vs 25.2 (5.1) min for controls; P < 0.05). This was also true for the recovery index (20.1 (6.6) min vs 10.6 (3.4) min; P < 0.05) and duration to 75% recovery (63.4 (9.9) min vs 35.8 (6.9) min; P < 0.05). In the context of rapid sequence induction, pretreatment with MgSO4 improved the intubating score of vecuronium compared with vecuronium without MgSO4, reaching the same quality as that with suxamethonium 1 mg kg-1. We conclude that magnesium pretreatment increased the neuromuscular potency of vecuronium, in addition to modifying the time course of its neuromuscular block.
We studied EEG arousal after laryngoscopy and intubation with standardized bolus induction of anaesthesia. Twenty patients were prospectively allocated randomly to induction with propofol 3 mg kg-1 (n = 10) or thiopentone (6 mg kg-1 (n = 10) and 50% nitrous oxide in oxygen. Neuromuscular block was produced with vecuronium 0.2 mg kg-1 given 30 s after induction. Three minutes after induction, laryngoscopy was performed for 60 s, with intubation at 3 min 30 s, and study end at 5 min. Nociception to laryngoscopy and intubation was followed by loss of low (relative delta activity change: thiopentone -30%, propofol -7%; P < 0.05) and a shift to higher frequency EEG activity (beta activity change: thiopentone +647%, propofol +61%; P < 0.05). This EEG arousal was greater in the thiopentone group, despite the fact that EEG depression was similar to that produced by propofol before laryngoscopy and intubation. Propofol and thiopentone in combination with nitrous oxide had similar cortical depressant effects, but propofol appeared to depress subcortical nociceptive processing more than thiopentone. While the degree of cortical EEG depression seems less useful for predicting reaction to subsequent nociception, EEG arousal reactions may prove suitable for monitoring intra-anaesthetic nociception and its modulation.
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Pipecuronium bromide, a new neuromuscular relaxant with steroidal structure, is devoid of effects on the autonomic nervous system and may be useful in patients where haemodynamic stability is mandatory. However, tracheal intubation may alter this haemodynamic profile. Therefore, we carried out a prospective double-blind study in 30 patients undergoing coronary artery bypass surgery with the purpose (1) of determining if intubation influenced the haemodynamic stability in patients paralyzed with pipecuronium and (2) of comparing plasma catecholamine concentrations after pipecuronium with those after pancuronium. Thirty patients were randomized into two groups receiving either pipecuronium 100 micrograms.kg-1 or pancuronium 150 micrograms.kg-1 after induction of anaesthesia with midazolam and fentanyl. Haemodynamic variables and plasma catecholamines were measured before and after induction, after the muscle relaxant three times and twice after intubation. After anaesthesia induction decreases in heart rate (HR), mean arterial pressure (MAP) and cardiac index (CI) were observed in both groups. These haemodynamic variables were unchanged after pipecuronium whereas after pancuronium HR increased from 53 +/- 11 b.min-1 to 64 +/- 9 b.min-1 after induction (P < 0.05) and CI from 2.5 +/- 0.5 L.min-1 to 3.0 +/- 0.8 L.min-1 (P < 0.05). Furthermore ECG signs of myocardial ischaemia appeared in four patients after pancuronium and the decay of plasma norepinephrine concentration was slower than with pipecuronium. We conclude that pipecuronium given after induction of anaesthesia is free of sympathomimetic or vagolytic activity and does not influence haemodynamic variables for up to ten minutes after tracheal intubation.
BACKGROUND: Rapid assessment of hepatic function early after reperfusion of the liver graft is of great importance, because it may allow for prompt detection of incipient hepatic graft failure. The current study was undertaken to determine whether the continuous recording of neuromuscular transmission could be used as an on-line assessment of hepatic function during liver transplantation when a muscle relaxant with high hepatic uptake is used. METHODS: We quantified and compared the effect of liver exclusion and graft reperfusion on the level of vecuronium-induced neuromuscular blockade in nine pigs studied twice within 3 days. During the 1st day (control session), an intravenous infusion of vecuronium was administered to maintain a constant 90-95% twitch depression during 180 min. The twitch response was then allowed to recover spontaneously to 75% of its prerelaxant value. Neuromuscular transmission was continuously measured on the right anterior leg using an acceleration transducer. During the same time period, the metabolic rate of 14C-labeled aminopyrine (a well-established quantitative test of the liver microsomal function) was determined by measuring the excretion of 14CO2 in expired air after administration of an intravenous bolus of 14C-labeled aminopyrine. Two days later, the pigs underwent a hepatic autotransplantation, during which vecuronium was administered to maintain a constant 90-95% twitch depression. After reperfusion of the liver graft, the vecuronium infusion rate was maintained at its anhepatic level, and the recovery index of the neuromuscular blockade (the time from 25% to 75% recovery of twitch height) was calculated. The aminopyrine breath test was performed during the last 30 min of the anhepatic phase, and during 3 h after reperfusion of the liver graft. RESULTS: During control studies, the mean infusion rate of vecuronium was 1.30 +/- 0.33 mg.kg-1.h-1 and the recovery index was 3.4 +/- 0.5 min. During liver dissection, the infusion rate of vecuronium was similar to the control value (1.18 +/- 0.16 mg.kg-1.h-1), then considerably decreased to 0.05 +/- 0.03 mg.kg-1.h-1 during the anhepatic phase. After reperfusion of the liver graft, the recovery index was markedly prolonged to 35.5 +/- 15.8 min, indicating a prolongation of the recovery of neuromuscular blockade by a factor of 10.4. Excretion of 14CO2 was equal to zero during the anhepatic phase and then increased to 0.19 +/- 0.11% during the 1st h after reperfusion of the liver graft, an excretion rate corresponding to 11.2% of control conditions. The relationship between individual changes in the recovery index of the neuromuscular blockade and 14CO2 excretion in expired air after reperfusion of the liver graft showed a strong significant correlation (r2 = 0.71). CONCLUSIONS: These results indicate that, compared with the control studies, there is a similar decrease in the recovery rate of vecuronium-induced neuromuscular blockade and in the metabolic rate of 14C-labeled aminopyrine during the progressive recovery of hepatic function immediately after unclamping of the liver vessels. Metabolism of 14C-labeled aminopyrine increased progressively during the reperfusion phase. Therefore, recording of neuromuscular transmission during liver transplantation could serve as a continuous and easy to perform assessment of liver graft function provided that a muscle relaxant with a high hepatic uptake is used for neuromuscular blockade.
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End-tidal anaesthetic concentrations at first eye opening in response to a verbal command during recovery from anaesthesia (MAC-awake), were measured for isoflurane (n = 16), enflurane (n = 16) and halothane (n = 14). MAC-awake was measured during either slow or fast alveolar washout. Slow washout was obtained by decreasing anaesthetic concentrations in predetermined steps of 15 min, assuming equilibration between brain and alveolar partial pressures. Fast alveolar washout was obtained by discontinuation of the inhalation anaesthetic, which had been maintained at 1 MAC for at least 15 min. Mean MAC-awake obtained with slow alveolar washout was similar for isoflurane (0.25 (SD 0.03) MAC), and enflurane (0.27 (0.04) MAC) and significantly greater than values obtained by fast alveolar washout (isoflurane: 0.19 (0.03) MAC; enflurane: 0.20 (0.03) MAC). The MAC-awake of isoflurane and enflurane was significantly less than that of halothane, which was 0.59 (0.10) MAC as evaluated by the slow and 0.50 (0.05) MAC as evaluated by the fast alveolar washout method. Recovery time from anaesthesia with fast alveolar washout was 8.8 (4.0) min for halothane, which was not different from isoflurane (15 (2.5) min), but significantly shorter than for enflurane (22 (10) min), reflecting differences in the anaesthetic concentration gradient between MAC and MAC-awake values. These data do not support the hypothesis of a uniform ratio between MAC and MAC-awake values.
The sympathetic response to rigid bronchoscopy, laryngoscopy and esophagoscopy, performed under general anesthesia with isoflurane, was examined in patients who either received 5 ml of 2% lidocaine (n = 7) or 5 ml of saline (n = 7), sprayed on larynx and upper trachea under direct laryngoscopy, 2 min before the introduction of the rigid bronchoscope. Blood pressure, heart rate and plasma catecholamine and lidocaine levels were measured at specific time points of the study. Topical lidocaine led to a rapid and prolonged increase in plasma lidocaine levels. Patients treated with lidocaine showed a small but significant decrease in plasma epinephrine levels from baseline following endotracheal intubation and extubation, as compared to the saline control group. Blood pressure and heart rate response during rigid panendoscopy, isoflurane requirements and time interval from termination of panendoscopy to extubation were not different between the two groups. However, in contrast to the control group, patients who had received lidocaine had no significant rise in blood pressure and heart rate from baseline following the introduction of the rigid bronchoscope. The benefit of this moderate hemodynamic stabilizing effect of lidocaine has to be weighted against the risk of decreased protective airway reflexes due to topical laryngeal lidocaine during recovery from anesthesia.