Transient paraplegia during posterior cervical osteotomy.
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Biomedical subjects
Publications and source records attributed to T J Sanford.
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Pulse oximeter arterial hemoglobin oxygen saturation (SpO2) and finger arterial pressure (FINAP) were continuously monitored before, during, and after cardiopulmonary bypass in 15 male patients. SpO2 was monitored simultaneously with two pulse oximeters, a Nellcor N-100 and an Ohmeda Biox III. The readings obtained from the two pulse oximeters were compared with arterial blood measurements obtained using a CO-oximeter. FINAP was monitored by a prototype device (Finapres) based on the Penaz volume-clamp method. FINAP was correlated with intraarterial pressure (IAP). Both pulse oximeters functioned well before cardiopulmonary bypass. The correlations with CO-oximeter values were 0.927 for the N-100 and 0.921 for the Biox III. Immediately after the onset of cardiopulmonary bypass, the N-100 pulse oximeter stopped displaying values. The Biox III pulse oximeter continued to display values during the cardiopulmonary bypass period; the correlation with CO-oximeter values was 0.813. After cardiopulmonary bypass, the N-100 began displaying values in 2 to 10 minutes. After cardiopulmonary bypass the correlation with CO-oximeter values was 0.792 for the N-100 and 0.828 for the Biox III pulse oximeter. The Finapres finger blood pressure device functioned well in 13 of 15 patients before cardiopulmonary bypass. The mean bias +/- precision of FINAP-IAP for mean pressure was 8.3 +/- 10.2 mm Hg (SD) and the correlation coefficient was 0.814. During cardiopulmonary bypass, the Finapres device functioned well in 10 of 15 patients. The mean bias precision of FINAP-IAP, for mean pressure in these 10 patients was 6.6 +/- 8.7 mm Hg and the correlation coefficient was 0.902.(ABSTRACT TRUNCATED AT 250 WORDS)
We studied the pharmacokinetic disposition of alfentanil in 20 volunteers and in 15 surgical patients 20-72 years old. Pharmacokinetic disposition was first order and was well described by a two-compartment open model. Central-compartment volume of distribution was 0.131 +/- 0.087 L.kg-1 (mean +/- SD) in young healthy volunteers and decreased modestly with increasing age (r = -0.32, P less than 0.05). However, apparent volume of distribution at steady-state, 0.404 +/- 0.205 L.kg-1 for the whole study cohort, was not age-related. Plasma clearance of alfentanil in young healthy subjects, 9.3 +/- 6.3 ml.kg-1.min-1, also showed an inverse relationship with age (r = -0.54, P less than 0.001), and was not affected by surgical stress in subjects older than 60 years. Cigarette smoking and sex of the subjects did not contribute to interindividual differences in the kinetic disposition of this drug. Our finding that interindividual differences in disposition of alfentanil were the least in older subjects suggests that its pharmacological effects related to pharmacokinetic disposition should be most predictable in the elderly.
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The tape recorded EEGs of 127 patients anesthetized with large doses of opioids were retrospectively analyzed for evidence of opioid-induced seizures, and in particular, correlated with movements that occurred during induction and could be clinically interpreted as seizures. Bilateral EEG leads in patients receiving fentanyl (20), sufentanil (20), or alfentanil (87) were recorded. Forty-six of these patients from all opioid groups manifested intense rigidity, as assessed both clinically and by EMGs recorded from eight muscles in 69 of the patients receiving alfentanil. This intense rigidity often resembled seizures, in that the phenomenon entailed severe stiffness of both limbs and trunk, with an explosive onset of myoclonic limb movements, and associated vertical nystagmus. Electroencephalographic observations were extensive, entailing 69 h of paper recordings played back from the tapes, at paper speeds of 30 or 60 mm/s, with detailed annotations from the voice track. These paper recordings were examined in detail independently by three of the investigators, who were unaware of the clinical phenomena that had occurred. The only observed EEG activity that could have been interpreted as epileptiform consisted of small sharp waves related to muscle activity or other artifact. The EEG never indicated seizure activity during these drug-induced movements and rigidity. Reports of opioid-induced seizures are reviewed and a set of criteria is offered to help achieve future consistency and credibility in evaluating this phenomenon. The available evidence does not support the existence of opioid-induced seizures in the clinical setting.
Cardiovascular responses and the need for intervention with vasoactive agents were measured prospectively in a randomized study of 50 adult patients receiving sufentanil (n = 20), fentanyl (n = 20), or morphine (n = 10) anesthesia for cardiac surgery. Measurements were recorded and compared during induction and prebypass at intervals during which airway or surgically induced stress responses were likely to be greatest. Randomized, double-blinded doses of opioids were administered slowly and titrated according to clinical responses (hemodynamics) and the electroencephalogram. Mean doses were as follows: from induction until time of incision, sufentanil, 9.1 microg/kg; fentanyl, 58 microg/kg; and morphine, 2.5 mg/kg; and total dose for surgery; sufentanil, 18.9 microg/kg; fentanyl, 95.4 microg/kg; and morphine, 4.4 mg/kg. Equi-anesthetic depth in patients receiving sufentanil or fentanyl was confirmed by continuous electroencephalographic monitoring. Patients anesthetized with sufentanil and fentanyl showed marked cardiovascular stability and rarely responded to stimuli. Systolic arterial pressure, mean arterial pressure, heart rate, cardiac index, systemic vascular resistance index, pulmonary vascular resistance index, stroke volume index, and stroke work index values were similar in the two groups. Patients receiving morphine experienced large changes in several variables. Pharmacologic intervention was made when systolic arterial pressure deviated more than 30% from pre-event values and was uncontrolled by additional opioids. Interventions were necessary more often in patients receiving morphine (nine of ten) or fentanyl (12 of 20) than in patients receiving sufentanil (six of 20), P < 0.05. Results from this study suggest that morphine is a relatively unsatisfactory anesthetic, while sufentanil and fentanyl, at equi-anesthetic depths, provide stable and satisfactory hemodynamics.
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Using aperiodic analysis, we examined the impact on the electroencephalogram (EEG) of muscle activity from opiate-induced rigidity with alfentanil. We compared two groups of patients, one receiving alfentanil with neuromuscular blocking agents and the other group receiving no relaxants. The alfentanil-induced muscle rigidity exerted a noticeable effect on the EEG, with a moderate effect on total power at 1 Hz; a marked effect on the total number of waves, cumulative percent power at 3 Hz, and average power at 17 to 19 Hz; and a striking effect on F90, the frequency below which 90% of the power resides. The presence of electromyographic (EMG) noise in the EEG consistently altered the variables derived from the EEG, so that anesthetic depth appeared less than it actually was. This was true in spite of the fact that we gave slightly more alfentanil in the group not receiving a relaxant. Although the observed muscle activity was greater than that usually seen clinically, and may have differed qualitatively, the results do serve as a warning that muscle noise can interfere with the EEG. Currently, there is no computerized technique that will reject or account for this noise, and we must depend on observation to recognize the EMG patterns within the EEG, either with the raw recording or with a detailed analysis (such as aperiodic analysis), and to compensate for this noise if possible. Techniques that average the EEG or that present a single number have difficulty providing this information. These results do not detract from the usefulness of the EMG contained in EEG recordings as a supplementary or complementary indicator of anesthetic lightness.
The authors investigated the hemodynamic, metabolic, electroencephalographic (EEG), and electromyographic (EMG) characteristics of narcotic-induced rigidity during induction of anesthesia with alfentanil (175 micrograms/kg) in 10 patients. Thiopental (4 mg/kg) was administered to a ten-patient control group. Rigidity was quantified in eight muscle groups (sternocleidomastoid, deltoid, biceps, forearm flexors, intercostal, rectus abdominus, vastus medialis/lateralis, and gastrocnemius). Marked rigidity was observed in all muscle groups in all patients receiving alfentanil and in none receiving thiopental. Central venous pressure increased with onset of rigidity, while mean arterial pressure and cardiac index remained unchanged. Manual ventilation was extremely difficult during alfentanil-induced rigidity. Arterial oxygen tension decreased more rapidly during rigidity than during the same time interval in the control group, while patients experiencing rigidity were more acidotic, as reflected by greater increases in base deficit. The EEG demonstrated an anesthetic state without seizure activity. The immediate increase in central venous pressure with the onset of rigidity, along with occasional simultaneous parallel variations in central venous pressure and the EMG, strongly suggest a mechanical mechanism for the change in central venous pressure. The metabolic changes during rigidity may be partly related to the absence of the normal cardiovascular reflexes that are reported to occur during voluntary isometric muscle contractions. A neurochemical mechanism of narcotic-induced rigidity is briefly reviewed.
We compared anesthetic doses of three popular opiates, morphine (n = 10), fentanyl (n = 9), and sufentanil (n = 9) in patients undergoing cardiac surgery. Opiate administration after induction was based upon EEG and cardiovascular signs of the depth of anesthesia. Total doses were morphine, 4.4 +/- 0.71 mg/kg, fentanyl, 95.4 +/- 9.9 micrograms/kg, and sufentanil, 18.9 +/- 2.2 micrograms/kg. Comparisons among opiates included times for induction of anesthesia, return of consciousness, return of spontaneous ventilation, return of adequate cardiovascular status, and extubation. The following times (mean and SEM) were significantly (P less than 0.05) shorter for sufentanil than for fentanyl or morphine: induction (15 +/- 2.3 min, 5.9 +/- 0.7 min, and 3.0 +/- 0.2 min for morphine, fentanyl, and sufentanil, respectively); return of consciousness (morphine 109.7 +/- 34.4 min, fentanyl 62.3 +/- 17.9 min, sufentanil 17 +/- 8.7 min); return of acceptable and stable cardiovascular status (morphine 587.3 +/- 139.3 min, fentanyl 537.9 +/- 144.8 min, sufentanil 173.7 +/- 56.8 min); and extubation (morphine 1121.3 +/- 61.8 min, fentanyl 1005.7 +/- 77.7 min, sufentanil 533.3 +/- 67.8 min). We conclude that sufentanil administered in the dosage range of 19 micrograms/kg allows more rapid induction, earlier emergence from anesthesia, and faster extubation of patients than either morphine or fentanyl.
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Using aperiodic analysis, we compared the EEG produced by alfentanil with the EEGs produced by two other opiates--fentanyl and sufentanil--on the one hand and with the EEG produced by a barbiturate--thiopental--on the other hand. Alfentanil and thiopental were injected over 1 minute; fentanyl and sufentanil were injected over 10 to 15 minutes. From the aperiodic analysis we derived up to seven single-number variables computed over 30- or 60-second epochs. All the opiates induced EEGs that were qualitatively similar to each other, although the maximum or minimum values tended to be greater and the time course more rapid with alfentanil than with the other two opiates. This finding may have been related to the fact that we injected relatively more alfentanil and administered it more rapidly. The EEGs produced by alfentanil and thiopental differed markedly, both qualitatively and quantitatively. The total power at 1 Hz and cumulative power at 3 Hz went to higher peak values with alfentanil, the latter tending to decrease with thiopental. The total number of waves per epoch went to lower peak values with alfentanil; there was little change with thiopental. The frequency below which 90% of the power resides went to considerably lower peak values with alfentanil than with thiopental. Finally, total power at 10 to 12 Hz (alpha waves) and average power at 17 to 19 Hz (beta waves) went to very high peak values with thiopental, but decreased with alfentanil.(ABSTRACT TRUNCATED AT 250 WORDS)
In 49 patients undergoing open-heart surgery we compared the electroencephalographic (EEG) effects of high-dose morphine, fentanyl, or sufentanil with O2, using two computerized analysis and display techniques: a period analysis (the Klein method) and an aperiodic analysis (the Neurometrics monitor). During fentanyl or sufentanil anesthesia, both techniques revealed a general decrease in frequency, shown by the aperiodic analysis primarily as a marked increase in the very low frequency range: an increase in the 1-Hz bin (TP1, in muv2) from 2.80 X 10(4) +/- 3.20 X 10(4) (SD) to 45.1 X 10(4) +/- 27.2 X 10(4) for fentanyl and from 3.11 X 10(4) +/- 2.83 X 10(4) to 52.8 X 10(4) for sufentanil. The cumulative percent power at 3 Hz (CP3) increased from 27.2 +/- 6.8 to 83.0 +/- 11.0 for fentanyl and from 22.7 +/- 5.2 to 85.1 +/- 10.4 for sufentanil, while the frequency at 90% cumulative percent power (F90, in Hz) decreased from 17.8 +/- 2.9 to 7.9 +/- 2.8 for fentanyl and 16.4 +/- 5.2 to 5.6 +/- 4.3 for sufentanil. The changes with morphine were less obvious, with some attenuation of high-frequency power shown by the Klein method, and an increase from 24.1 +/- 8.6 to 59.3 +/- 20.7 with CP3, but no change in TP1. Low-frequency power with the period analysis and TP1 with the aperiodic analysis decreased between laryngoscopy and the incisions with fentanyl and sufentanil.(ABSTRACT TRUNCATED AT 250 WORDS)
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