The epinephrine test dose in obstetrics: note the limitations.
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Biomedical subjects
Publications and source records attributed to B Glosten.
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BACKGROUND: Clinical reports associate the use of epidural anesthesia with an increase in core temperature in women in labor. We tested the hypothesis that epidural anesthesia alters thermoregulatory responses to hyperthermia in human volunteers. METHODS: Each of four volunteers were studied on two days: Control and Anesthesia. On the Control day, the subject was warmed via the skin, and the core (esophageal) temperature threshold for sweating (detected on the forehead) was determined. The subject was then cooled until sweating stopped. The subject was warmed again, and a second sweating threshold was determined. The difference between the first and second sweating thresholds was noted. On the Anesthesia day, two sequential sweating threshold measurements were obtained in a similar fashion; however, a mid-thoracic level of epidural anesthesia was established before the second sweating threshold measurement. The first and second sweating threshold differences were compared between the two study days. The presence or absence of sweating on the thigh was noted during all four warming periods. RESULTS: Average skin temperatures were similar (about 37 degrees C) during all four sweating threshold measurements. On the Control day, the second sweating threshold value was always slightly less than the first (average difference (mean+/-SD): -0.18+/-0.14 degrees C). In contrast, on the Anesthesia day, the second sweating threshold value (determined with an epidural block) was always greater than the first (average difference: +0.37+/-0.16 degrees C). Epidural anesthesia, therefore, increased the sweating threshold by 0.55+/-0.27 degrees C. Epidural anesthesia blocked sweating in the thigh in two of the subjects. CONCLUSIONS: An epidural block alters the thermoregulatory responses to warming by increasing the threshold for thermoregulatory sweating and, in some cases, preventing leg sweating.
UNLABELLED: Among nursing parturients after cesarean delivery, intravenous patient-controlled analgesia (PCA) with meperidine is associated with significantly more neonatal neurobehavioral depression than PCA with morphine. A single dose of epidural morphine (4 mg) decreases postcesarean opioid analgesic requirements and may reduce or prevent neonatal neurobehavioral depression associated with PCA meperidine. Prospectively, 102 term parturients underwent cesarean delivery with epidural anesthesia, 2% lidocaine and epinephrine 1:200,000. After umbilical cord clamping, each patient received epidural morphine 4 mg and was randomly allocated to receive either PCA meperidine or PCA morphine. Initial neonatal characteristics, included gestational age, Apgar scores, weight, and umbilical cord gas partial pressures. Brazelton Neonatal Behavioral Assessment Scale (NBAS) examinations were performed on each of the first 4 days of life. Nursing infants (n = 47) were grouped according to maternal PCA opioid in breast milk (meperidine [n = 24] or morphine [n = 23]); bottle-fed infants (n = 56) served as the control group. The three infant groups were equivalent with respect to initial characteristics and NBAS scores on the first 2 days of life. On the third day of life, infants in the morphine group were significantly more alert and oriented to animate human cues compared with infants in the meperidine or control group. On the fourth day of life, infants in the morphine group remained significantly more alert and oriented to animate human auditory cues than infants in the meperidine group. Average PCA opioid consumption through 48 h postpartum was equivalent (0.54 mg/kg morphine and 4.7 mg/kg meperidine); however, even with these small doses, meperidine was associated with significantly poorer neonatal alertness and orientation than morphine. Morphine is the PCA opioid of choice for postcesarean analgesia among nursing parturients. IMPLICATIONS: Among nursing parturients after cesarean delivery, intravenous patient-controlled analgesia with meperidine is associated with more neonatal neurobehavioral depression than patient-controlled analgesia with morphine. In this study, we found that nursing infants exposed to morphine were more alert and oriented to animate human cues than those exposed to meperidine.
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We developed a continuous quality improvement (CQI) program for anesthesia services based on self-reporting of critical incidents and negative outcomes through a dichotomous (yes/no) response on the anesthesia record. Immediate case investigation provides data for systematic peer review of anesthesia management. Trend analysis of the database of critical incidents and negative outcomes identifies opportunities for improvement. The CQI program resulted in the reporting of nearly twice as many problems related to anesthesia management (5% of all anesthetics) as did the checklist it replaced (2.7%). Escalation of patient care (3.2%) and operational inefficiencies (2.2%) were more common than patient injury (1.5% of all anesthetics). Among the 537 cases with anesthesia management problems were 119 human errors and equipment problems (22%). Regional nerve blocks and airway management represented the most common problem areas. Improvement in anesthesia services was made through prompt implementation of strategies for problem prevention devised by the practitioners themselves through peer review, literature review, and clinical investigations.
Meperidine is a mu opiate agonist that is frequently used to treat pain. We examined in healthy volunteers (N = 10) the effects of intravenous meperidine (0, 0.25, 0.5, and 1.0 mg/kg) on mood and psychomotor performance. A randomized, placebo-controlled, crossover design was used in which subjects were injected with meperidine or saline in a double-blind fashion. Subjects completed several subjective effects questionnaires commonly used in abuse liability testing studies before drug injection and at periodic intervals for up to 5 h after drug injection. Subjects also completed several psychomotor tests. Meperidine produced a constellation of subjective effects in a dose-related fashion, including increases in ratings of "sedated," "coasting or spaced out" and "feel drug effect" ratings. Many of the drug's subjective effects persisted up to 4 or 5 h after administration of the 1.0 mg/kg dose. Drug liking ratings assessed on a visual analog scale were increased after meperidine injection in about half of the subjects (P = 0.09). Eye-hand coordination was affected slightly by meperidine but other indices of psychomotor functioning were unaffected. Miosis increased in a dose-related fashion. Other physiological parameters, such as vital signs, were not affected by meperidine. We conclude that meperidine in healthy volunteers has robust and long-lasting effects on mood, but may have weaker effects on psychomotor performance.
Redistribution of heat from the core to the cool peripheral compartments of the body causes hypothermia during epidural anesthesia. Diminishing the temperature gradient between the core and peripheral tissues by warming the body via the skin before anesthesia should prevent this hypothermia. We measured core temperature, skin temperatures, and cutaneous heat loss in seven volunteers who received two lidocaine epidural injections during a single study day. One epidural injection was given after the volunteer had rested in a cool room (approximately 22 degrees C) ("no prewarming") for 2 h, and one injection was given after the volunteer had been covered with a forced air warming mattress (approximately 38 degrees C) ("prewarming") for 2 h. Skin temperatures were higher after prewarming. The decrease in core temperature during epidural anesthesia was smaller after prewarming [mean within patient difference (prewarming-no prewarming): 0.41; P = 0.003]. However, heat loss was greater after prewarming (mean within patient difference: 26.4; P = 0.02). Shivering was less after prewarming. We conclude that prewarming decreases redistribution hypothermia caused by epidural block. These results support the hypothesis that redistribution of heat within the body, not heat loss, is the most important etiology of hypothermia from epidural anesthesia.
This prospective, randomized, controlled investigation compared the effects of three prophylactic mu-opioid antagonists, epidural butorphanol (BU) 3 mg, epidural nalbuphine (NB) 10 mg, and oral naltrexone (NX) 6 mg, on postcesarean epidural morphine analgesia. After randomization, 102 term parturients underwent cesarean delivery with epidural anesthesia, 2% lidocaine and epinephrine 1:200,000. When the umbilical cord was clamped, each patient received one epidural solution (containing morphine 4 mg plus either saline or treatment drug), and one oral capsule (containing either placebo or treatment drug) in a double-blind manner. Maternal outcomes included pain and satisfaction [assessed with 100-mm visual analog scales (VAS)], and the incidence and severity of respiratory depression, somnolence, pruritus, nausea, and emesis. Through the first 12 h postpartum, the BU group achieved significantly greater analgesia than the morphine sulfate (control) (MS), NB, and NX groups, a significantly lower incidence of severe pruritus than the MS group, and significantly greater satisfaction than MS and NX groups. Epidural morphine and BU promoted better analgesia and satisfaction than any previously documented postcesarean regimen.
Propofol is increasingly being used in medical and surgical procedures in which conscious sedation of the patient is desired. The mood-altering and psychomotor effects of subanesthetic concentrations of propofol have not been well characterized. Therefore, we examined the effects of intravenous infusions of different subanesthetic doses of propofol on mood and psychomotor/cognitive performance in healthy volunteers (n = 10). A prospective, randomized, placebo-controlled, double-blind, crossover design was used in which subjects first were administered an intravenous loading dose of propofol or placebo (Intralipid) and then were infused over a 20-min period with a given dose of propofol or placebo. Each subject received placebo (Intralipid loading dose and infusion), low-dose propofol (0.08 mg/kg loading dose and 0.5 mg.kg-1.h-1 infusion), moderate-dose propofol (0.16 mg/kg loading dose and 1.0 mg.kg-1.h-1 infusion), and high-dose propofol (0.32 mg/kg loading dose and 2.0 mg.kg-1.h-1 infusion) in four sessions spaced approximately 1 week apart. Propofol induced changes in mood in a dose-related fashion. Some of these mood-altering effects lingered for as long as 30 min after termination of the infusion, but, in general mood had returned to baseline levels 1 h after termination of the infusion. Intralipid induced no changes in mood during the infusion period. Psychomotor functioning was impaired during, and anterograde amnesia was present after, the high-dose propofol infusion. These results suggest that propofol as a sedative has a spectrum of effects that are well-suited for ambulatory surgery (e.g., sedation, amnesia, and rapid and complete recovery).
Hypothermia and shivering are common during epidural anesthesia for cesarean delivery but are not always accompanied by a sensation of coldness. To test the hypothesis that central temperature changes are not perceived during epidural anesthesia, we measured central and skin temperatures and thermal perception in 30 patients undergoing cesarean delivery with epidural anesthesia. Central temperature decreased 1.0 +/- 0.6 degrees C from control values during anesthesia and surgery, but thermal perception scores did not reflect central temperatures (P = 0.56) or changes in central temperature (P = 0.63). A feeling of warmth was significantly correlated with increased mean skin temperature (P = 0.02) and increased upper body skin temperature (P = 0.03). We conclude that central temperature is poorly perceived and is less important than skin temperature in determining thermal perception during high levels of epidural anesthesia.
Five healthy, nonpregnant volunteers were studied before and after induction of lumbar epidural anesthesia to determine the cause of central hypothermia during epidural anesthesia. Cutaneous heat loss was measured from 10 area-weighted sites using thermal flux transducers. Oxygen consumption was measured and converted to heat production in watts (W). After a 2-h control period at approximately 20 degrees C, epidural anesthesia was induced by injection of 30-50 ml 3% chloroprocaine. Additional boluses were given to extend the sensory blockade to at least the T5 dermatome. Tremor during epidural anesthesia was compared with normal shivering induced by rapid central venous infusion of approximately 4 l iced saline in six unanesthetized volunteers. Average skin temperature and cutaneous heat loss decreased during the control period, while tympanic membrane temperature remained stable. During the 1st h of epidural blockade, tympanic membrane temperature decreased 1.1 +/- 0.3 degrees C, and average skin temperature increased 0.9 +/- 0.5 degrees C. Cutaneous heat loss increased 16 +/- 6% (15 +/- 5 W), but metabolic heat production increased even more (and was associated with a shivering-like tremor). Tremor during epidural anesthesia and shivering induced by iced saline infusion had similar synchronous waxing-and-waning patterns. No abnormal EMG patterns were detected during epidural anesthesia. We conclude that central hypothermia during the 1st h of epidural anesthesia does not result from heat loss to the environment in excess of metabolic heat production, but results primarily from redistribution of body heat from central to peripheral tissues. Analysis of the tremor patterns suggests that oscillations recorded during epidural anesthesia in nonpregnant individuals is normal thermoregulatory shivering. Shivering occurred sooner and was more intense during iced saline infusion than during epidural anesthesia, despite comparable central hypothermia. The low intensity of shivering during epidural anesthesia, and in some individuals the delay in onset, may result from blockade of afferent cutaneous cold signals.
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To determine the extent to which thermoregulatory vasoconstriction decreases heat loss to the environment, we measured regional heat flux, average skin temperature, and tympanic membrane temperature before and after thermoregulatory vasoconstriction in five minimally clothed volunteers maintained in a 30.8 +/- 0.1 degrees C environment. Thermoregulatory vasoconstriction was induced by central venous infusion of cooled fluid. Peripheral cutaneous blood flow was evaluated with venous-occlusion volume plethysmography and skin-surface temperature gradients. Laser Doppler flowmetry was used to measure vasoconstriction in centrally located skin. This model mimics the common clinical situation in which patients in a warm environment are centrally cooled by administration of cold intravenous fluids or by lavage of internal cavities with cold fluids. Tympanic membrane temperature decreased 1.5 +/- 0.3 degrees C in the first 15 min after the cold fluid infusion was started and remained approximately 1 degrees C below control values during the rest of the study. Average skin-surface temperature decreased slowly to approximately 0.7 degrees C below control. Flow in capillaries of centrally distributed skin, determined with laser Doppler flowmetry, decreased only approximately 40%. Total heat flux, and flux from the arms and legs decreased approximately 25% (15.5 +/- 0.3 W). Heat loss from the trunk and head decreased only 17%, whereas, loss from the hands and feet (10.5% of the body surface area) decreased approximately 50%. All measured values decreased significantly following vasoconstriction (P less than 0.01). Therefore, thermoregulatory vasoconstriction in a thermoneutral environment appears to decrease cutaneous loss of metabolic heat approximately 25%.
The hypothesis that the lipid emulsion of the emulsion formulation of propofol is responsible for the low frequency of nausea, retching, and vomiting after propofol anesthesia was tested. A randomized, prospective, and comparative study was performed to evaluate the antiemetic effect of 10% lipid solution in 60 women, ASA physical status I and II, scheduled for ambulatory laparoscopic procedures. Two groups of patients were studied. Induction of anesthesia (thiopental) and maintenance of anesthesia (enflurane, nitrous oxide) were similar in both groups. At induction the study group received 10% Intralipid (3 mL/min for 20 min). The control group received 5% dextrose in lactated Ringer's solution at the same rate. Other drugs administered during or after anesthesia were similar among the groups. The groups were similar with respect to duration of anesthesia, characteristics of early and intermediate recovery, as well as pain scores in the postanesthesia care unit. There were no differences in the amount of antiemetic medications administered or postoperative nausea, retching, or vomiting when the patients were evaluated objectively by a blinded observer or subjectively by patient self-evaluation. It is concluded that 10% Intralipid, the lipid in the emulsion formulation of propofol, does not possess significant antiemetic effects.