Differentiation of brain stem anesthesia from high spinal anesthesia using auditory brain stem response

A 67-year old woman having intractable chronic postherpetic neuralgia at the neck to forearm for two years was treated with subarachnoid block. Initially, bolus of 1% lidocaine 8 ml, with methylprednisolone acetate 20 mg was injected intrathecally at 6th cervical intervertebral space. The auditory brain stem response (ABR) during high spinal block with intact consciousness was not depressed in its wave height. ABR recorded showed prolongation of latency of 3 and 5 waves and prolongation of 1-3 phase to phase interval without prolongation of 3-5 phase to phase interval. Intrathecal nerve block was then performed with 1% lidocaine 15 ml and methylprednisolone acetate 20 mg, because she complained awareness and shocking sensation with controlled respiration during the first block. She assured that she felt nothing during the second block. The ABR recorded during the second block showed near complete suppression in its height of all waves and prolongation of all wave latencies. During recovery period, 1-3 and 3-5 phase to phase interval prolongation was recorded. One can differentiate brain stem anesthesia from other state that induces unconsciousness after block which is capable of inducing accidental brain stem anesthesia. These two blocks improved activity of daily living of the patient and severity of her pain decreased to 1/5 to 1/10.     

Monitoring of intraoperative auditory brain stem responses

We believe that our initial experience establishes the fact that ABRs can be routinely and reliably performed in an operating room environment. There was no added risk to the patient, and operative delays were minimal. We did note transient fluctuation in latency values up to 1.5 msec. These changes would revert to baseline levels within five to ten minutes. Changes noted during drilling were probably related to the random noise produced. Case 3 was worrisome in that hearing was lost after maintenance of the ABRs during the surgical procedure. Evidently the vestibule was damaged, and a labyrinthitis caused the hearing loss. We feel that this procedure will be most useful in those situations in which the cochlear nerve and blood vessels are at risk. Such procedures as acoustic tumor removal with attempts to preserve hearing, vestibular nerve sections, and facial nerve problems in the IAC should be routinely monitored. Further experience will, of course, be most helpful in explaining and recognizing these changes.     

Reversal of high-dose fentanyl anesthesia by naloxone

The EEG, respiratory and hemodynamic responses to postoperative reversal by naloxone of high-dose fentanyl anesthesia were studied in 20 patients (17 cardiac and 3 non-cardiac surgeries). In power spectrum analysis of EEG, power of delta band markedly decreased after naloxone drip infusion. Respiratory and hemodynamic responses were minimum, but increase in HR by 6.4 +/- 9.2 bpm, increase in diastolic BP by 5.3 +/- 9.6 mmHg, and decrease in CVP by 1.9 +/- 2.9 mmHg were statistically significant. Emergence of pain was also minimum and severe side effect was not observed. Reversal of high-dose fentanyl anesthesia by naloxone can reduce the incidence of postoperative respiratory depression and enables early extubation.     

Serial observations of brain stem function by auditory brain stem responses in central transtentorial herniation

Changes in auditory brain stem responses were serially investigated in a patient with downward transtentorial herniation due to acute obstructive hydrocephalus to correlate the neurological signs with the results of computerized tomography. Neurological deterioration correlated highly with disruption of auditory brain stem responses, especially with that of the components of waves V to VII. A noninvasive technique, the measurement of auditory brain stem responses is thought to be useful in detecting the severity of downward transtentorial herniation and in estimating the recovery of brain stem function after surgical treatment of intracranial hypertension.     

Effects of high-dose fentanyl on intraductal pressure in the choledochoduodenal junction in dogs]

Changes in intraductal pressure in choledochoduodenal junction were studied following intravenous administration of fentanyl in dogs. The intraductal pressure was measured with constant-rate infusion method. A statistically significant increase in the intraductal pressure was demonstrated after the intravenous administration of fentanyl 5 micrograms.kg-1 and 75 micrograms.kg-1. The increase in intraductal pressure following fentanyl administration at a dose of 75 micrograms.kg-1 persisted for more than 5 hours. We conclude that in case of intravenous high-dose fentanyl administration special attention should be paid to spasm of choledochoduodenal sphincter.     

Hemodynamic responses to pancuronium and vecuronium during high-dose fentanyl anesthesia for coronary artery bypass grafting.

The hemodynamic and electrocardiographic (ECG) effects of pancuronium and vecuronium were compared during high-dose fentanyl anesthesia for coronary artery bypass grafting (CABG) surgery. Forty-eight morphine-scopolamine premedicated patients scheduled for elective CABG were anesthetized with fentanyl (100 micrograms/kg) in divided doses, and either of two muscle relaxants, pancuronium (n = 26; 0.10 mg/kg) or vecuronium (n = 22; 0.09 mg/kg). Hemodynamic data, blood gas samples, and ECG tracings were obtained at the following intervals: (1) control; (2) prior to intubation; (3) 1 minute after intubation; (4) prior to sternotomy; and (5) 1 minute after sternotomy. In the pancuronium group, heart rate (HR), cardiac index (CI), and rate-pressure product (RPP) were increased after induction of anesthesia and following intubation. Eleven patients (42.3%) displayed ischemic ST segment changes. Four patients in this group developed tachycardia and hypertension to an extent requiring pharmacological intervention. Vecuronium-treated patients displayed no increases in HR, MAP, and RPP, and a decrease in CI. Only one patient (5.6%) developed evidence of ischemic ECG changes. Four patients in the vecuronium group, all receiving preoperative beta-blocker therapy, became hypotensive and bradycardic after the induction of anesthesia. The present investigation confirms the increased incidence of myocardial ischemia during high-dose fentanyl-pancuronium anesthesia. Although vecuronium was associated with fewer myocardial ischemic changes, the occurrence of bradycardia and hypotension in some patients receiving preoperative beta-adrenergic blocking drugs remains a concern.     

Cardiovascular effects of pancuronium and vecuronium during high-dose fentanyl anesthesia

To define the role of muscle relaxants in hemodynamic responses to high-dose (75 micrograms/kg) fentanyl anesthesia, we compared the circulatory effects of pancuronium (Pc) with those of vecuronium (Vc) in patients about to undergo coronary artery bypass surgery. The first measurements were made while the patients were awake. Thereafter the patients were anesthetized with fentanyl, intubated under succinylcholine relaxation and mechanically ventilated with a mixture of oxygen in air (FIO2 0.50). Ten minutes after completion of the fentanyl injection, the second set of measurements was made. Immediately thereafter, 0.1 mg/kg of either Pc (n = 10) or Vc (n = 10) was given, and no relaxant was administered to 10 control patients. Heart rate (HR) and cardiac index (CI), which had decreased significantly after fentanyl induction, decreased further after Vc, the latter decreases being significantly greater than the decreases in HR and CI observed in control patients. After Pc, HR and CI increased to control awake levels; rate-pressure product also increased and stroke index decreased. Five of ten patients receiving Vc had a HR below 45 beats/min; HRs this low were not seen in patients given Pc. Neither Pc nor Vc affected systemic vascular resistance, but filling pressures of the heart decreased abruptly after both relaxants. We conclude that if maintenance of preanesthetic hemodynamic status is the objective of anesthetic management of patients having coronary artery bypass surgery, Pc helps to achieve this objective during high-dose fentanyl anesthesia. On the other hand, many patients with limited coronary vascular reserve may well benefit from the negative chronotropic effect of Vc.     

Effects of speed of injection on anesthesia induction with propofol and fentanyl]

We examined the effects of injection rate of propofol on injection pain and postinduction hypotension and bradycardia when fentanyl was administrated before propofol. Fifty-five patients premedicated with midazolam and atropine were randomly allocated to two groups. Three minutes after administration of fentanyl 100 micrograms, propofol 1.5 mg.kg-1 was injected to a forearm vein at a rate of 800 ml.hr-1 in Group FS or 1 ml.s-1 in Group FR. Anesthesia was maintained with 67% nitrous oxide in oxygen and supplemental propofol infusion. The incidence and severity of pain on injection were not influenced with injection speed. The rapid rate of injection significantly shortened the induction time. The decrease in systolic and diastolic blood pressures and heart rate after induction were not affected by injection speed. In conclusion, rapid injection of propofol after fentanyl was effective to shorten the induction time without increasing the postinduction hypotension and bradycardia.     

The effect of high-dose fentanyl on human median nerve somatosensory-evoked responses

Median nerve somatosensory evoked responses (MnSSERs) were recorded in nine neurologically normal adult cardiac patients before and during the administration of high-dose fentanyl. MnSSERs were recorded prior to induction and at t = 20 min and t = 45 min postinduction. Fentanyl was administered as a slow bolus (53.2 +/- 9.1 micrograms X kg-1), followed by a continuous infusion at 10-20 micrograms X kg-1 X hr-1 (total dose 63.6 +/- 10.1 micrograms X kg-1). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. The effect of fentanyl was more pronounced on cortical waveform components, leaving subcortical components largely unaffected. There was a significant increase in the latency of the cortical MnSSER at t = 20 min, e.g., for the initial negative cortical wave, N1, the latency was 21.18 +/- 1.55 ms preinduction versus 22.18 +/- 1.42 ms at t = 20 min. There was also a significant decrease in the amplitude of the cortical response at t = 20 min, i.e., 2.04 +/- 1.30 microV preinduction versus 1.31 +/- 0.74 microV at t = 20 min. However, the degree of change was quite variable (range = 0-65 per cent). No further changes occurred at t = 45 min. The authors conclude that MnSSERs can be consistently and reliably monitored during high-dose fentanyl anaesthesia. However, fentanyl produces modest but significant changes in the MnSSER which should be taken into account lest they be misinterpreted as neurologic injury in evolution.     

Wakefulness during the induction with high-dose fentanyl and oxygen anesthesia

The purpose of this study was to investigate the state of wakefulness during the induction of anesthesia with high-dose fentanyl using the isolated forearm technique. Ten patients scheduled for elective cardiovascular surgery were premedicated with morphine (0.15mg/kg) and scoploamine (0.3–0.4mg) intramuscularly one hour before induction. The induction of anesthesia was performed by intravenous administration of 100µg/kg of fentanyl in 15min or over. The pneumatic tourniquet applied on the left upper arm was inflated to 220–240mmHg after 10µg/kg of fentanyl was given and then pancuronium was administered. Verbal commands were given to the patient after 25, 50, 75 and 100µg/kg of fentanyl was administered. Eight patients out of 10 responded to the verbal commands after administration of 25µg/kg of fentanyl. Six patients also responded after administration of 100µg/kg of fentanyl and diazepam 5mg was given to prevent tachycardia and rigidity during endotracheal intubation. Muscle rigidity and tachycardia were noticed in three and four patients respectively. These complications disappeared by diazepam administration.It was noted that wakefulness frequently occurred during the induction by high-dose fentanyl and oxygen anesthesia. To prevent such wakefulness therefore, it is necessary to use anesthetic supplements which do not cause cardiovascular depression.(Watanabe A, Namiki A, Ujike Y et al.: Wakefulness during the induction with high-dose fentanyl and oxygen anesthesia. J Anesth 2: 165–169, 1988)     

Reversal of high-dose fentanyl anesthesia by naloxone: analysis of factors attenuating respiratory and hemodynamic responses to naloxone

The respiratory and hemodynamic responses to postoperative reversal by naloxone of high-dose fentanyl anesthesia were studied in 101 patients after open heart surgery. Respiratory and hemodynamic changes after drip infusion of naloxone were minimum. Change of systolic blood pressure (BPs), mean blood pressure (BPm), CVP and PO2 were statistically significant. BPs increased for 3.8 +/- 14.0 mmHg, BPm increased for 1.6 +/- 8.2 mmHg. CVP decreased for 0.4 +/- 2.1 mmHg, and PO2 decreased for 8.6 +/- 3.4 mmHg. Severe side effect was not observed. Multi-factorial analysis revealed that the abrupt recovery of consciousness from anesthesia and acidosis were the most important factors that attenuate hemodynamic response to naloxone.     

Effects of sevoflurane anesthesia on norepinephrine metabolism in rat brain]

In spite of many investigations done for many years, the mechanism of general anesthesia remains still unclear. To elucidate the mechanism of general anesthesia, effects of sevoflurane anesthesia on norepinephrine metabolism in rat brain was studied. Sevoflurane 3% was administered for 20 minutes to Wistar male rats weighing 230-270g under spontaneous respiration. The rats were sacrificed by decapitation and the brains were rapidly removed. They were dissected into nine discrete regions, locus coeruleus, pons plus medulla oblongata, hypothalamus, thalamus, basal ganglia, hippocampus, amygdala and cerebral cortex. The contents of norepinephrine (NE) and one of its major metabolites, 3-methoxy-4-hydroxyphenyl-ethylene glycol (MHPG) were measured by high performance liquid chromatography with the dual-cell coulometric detector before anesthesia, 20 minutes after the start of anesthesia and at recovery from anesthesia. Significant increases in NE levels were observed in the pons, thalamus and hippocampus by sevoflurane anesthesia for 20 minutes compared with the control group and also in the pons and midbrain at recovery from anesthesia. MHPG levels were significantly decreased in the pons and cortex by sevoflurane anesthesia, while an appreciable increase in MHPG levels was observed in the thalamus by sevoflurane anesthesia. It is concluded that NE metabolism is significantly suppressed in the pons, thalamus and hippocampus during sevoflurane anesthesia and this change in NE metabolism may be associated with a mechanism of sevoflurane anesthesia.