Variation in caregiver perceptions of teamwork climate in labor and delivery units.

OBJECTIVE: To test the psychometric soundness of a teamwork climate survey in labor and delivery, examine differences in perceptions of teamwork, and provide benchmarking data. DESIGN: Cross-sectional survey of labor and delivery caregivers in 44 hospitals in diverse regions of the US, using the Safety Attitudes Questionnaire teamwork climate scale. RESULTS: The response rate was 72% (3382 of 4700). The teamwork climate scale had good internal reliability (overall alpha = 0.78). Teamwork climate scale factor structure was confirmed using multilevel confirmatory factor analyses (CFI = 0.95, TLI = 0.92, RMSEA = 0.12, SRMR(within) = 0.04, SRMR(between) = 0.09). Aggregation of individual-level responses to the L&D unit-level was supported by ICC (1) = 0.06 (P < 0.001), ICC (2) = 0.83 and mean r (wg(j)) = 0.83. ANOVA demonstrated differences between caregivers F (7, 3013) = 10.30, P < 0.001 and labor and delivery units, F (43, 1022) = 3.49, P < 0.001. Convergent validity of the scale scores was measured by correlations with external teamwork-related items: collaborative decision making (r = 0.780, P < 0.001), use of briefings (r = 0.496, P < 0.001) and perceived adequacy of staffing levels (r = 0.593, P < 0.001). CONCLUSION: We demonstrate a psychometrically sound teamwork climate scale, correlate it to external teamwork-related items, and provide labor and delivery teamwork benchmarks. Further teamwork climate research should explore the links to clinical and operational outcomes.

Extracellular glutamate levels and neuropathology in cerebral white matter following repeated umbilical cord occlusion in the near term fetal sheep.

Umbilical cord occlusion causes fetal hypoxemia which can result in brain injury including damage to cerebral white matter. Excessive glutamate release may be involved in the damage process. This study examined the relation between extracellular glutamate levels in the cerebral white matter of the ovine fetus during and after intermittent umbilical cord occlusion and the degree of resultant fetal brain injury. Fetal sheep underwent surgery for chronic catheterisation and implantation of an intra-cerebral microdialysis probe at 130 days of gestation (term approximately 147 days). Four days after surgery (day 1), seven fetuses were subjected to 5x2 min umbilical cord occlusions, and on the following day (day 2) they were subjected to either 4 or 5x4 min umbilical cord occlusions; seven fetuses served as controls. Microdialysis samples were collected before, during and after the umbilical cord occlusions to determine extracellular glutamate levels in the cerebral white matter. Fetal blood gas status was measured and the fetal electrocorticogram was recorded continuously. During the periods of umbilical cord occlusions on both days 1 and 2, fetal arterial oxygen saturation, arterial partial pressure of oxygen and arterial pH decreased (P<0.05) while arterial partial pressure of carbon dioxide increased (P<0.05). All fetuses showed episodes of isoelectric electrocortical activity during umbilical cord occlusions on both days 1 and 2. In fetuses with patent microdialysis probes there were marked increases of glutamate efflux in the cerebral white matter following umbilical cord occlusion. Fetal brains were removed at autopsy on day 5 and subjected to histological assessment. Brain damage was observed in all fetuses exposed to cord occlusion, particularly in the periventricular white matter, with the most extensive damage occurring in the fetuses with the greatest increases in glutamate levels. We conclude that, in the unanesthetised fetus in utero, glutamatergic processes are associated with umbilical cord occlusion-induced brain damage in the cerebral white matter.

Anesthesia for Cesarean section in a patient with paraplegia resulting from tumour metastases to spinal cord.

PURPOSE: Spinal cord injured patients present multiple unique challenges to the anesthesiologist. These include choice of muscle relaxant and management of autonomic hyperreflexia. We report the anesthetic management for Cesarean delivery in a patient who was paraplegic due to spinal canal metastases. Preeclampsia and fever complicated this case. CLINICAL FEATURES: The patient presented at 29 wk gestation with progressive paraplegia at the T10 level due to metastatic osteosarcoma. She had a decompressive laminectomy without improvement in her paralysis. She subsequently developed preeclampsia at 31 wk gestation, and underwent Cesarean delivery for breech presentation under general anesthesia. Anatomical concerns left us unsure of the efficacy or safety of neuraxial anesthesia. CONCLUSIONS: Preeclampsia and autonomic hyperreflexia are generally indications for regional anesthesia for Cesarean section. Tumour in her spinal canal and laboratory abnormalities including thrombocytopenia and a potential urosepsis dissuaded us from this option. Additionally, rapid sequence induction and intubation were not preferred due to paraplegia, leading us to secure the airway fibreoptically.

A preliminary investigation of remifentanil as a labor analgesic.

IMPLICATIONS: In this preliminary investigation, we evaluated the safety and analgesic efficacy of IV remifentanil for labor pain. Four women were studied, and then the trial was terminated because administration of this novel synthetic opioid produced significant maternal side effects in the absence of effective pain control.

Subarachnoid meperidine (Pethidine) causes significant nausea and vomiting during labor. The Duke Women's Anesthesia Research Group.

BACKGROUND: The combined spinal-epidural (CSE) technique using bupivicaine-fentanyl has become an established method of pain control during parturition. One limitation is the relatively short duration of effective analgesia produced by bupivicaine-fentanyl. In contrast, subarachnoid meperidine has been shown to provide a long duration of anesthesia in nonobstetric patients. Therefore, the authors tested the hypothesis that subarachnoid meperidine produces a significant increase in the duration of analgesia compared with bupivicaine-fentanyl. METHODS: Based on a power analysis of preliminary data, the authors intended to recruit 90 patients for the study, randomized to three groups: 2.5 mg bupivicaine-25 microg fentanyl, 15 mg meperidine, or 25 mg meperidine. However, after enrolling 34 patients, the study was discontinued because of a significant increase in nausea or vomiting in the study patients. RESULTS: Nausea or vomiting was substantially increased in both meperidine groups compared with the bupivicaine-fentanyl group: 16 with nausea or vomiting in the meperidine groups (n = 21), compared with 1 in the bupivicaine-fentanyl group (n = 11), P = 0.0011. The mean duration of analgesia provided by 25 mg meperidine was 126 +/- 51 min, compared with 98 +/- 29 min for bupivicaine-fentanyl and 90 +/- 67 min for 15 mg meperidine. These data were not significant (P = 0.27). CONCLUSIONS: Although intrathecal meperidine could potentially prolong subarachnoid analgesia during labor, its use was associated with a significant incidence of nausea or vomiting. These data do not support the use of subarachnoid meperidine in doses of 15 or 25 mg for labor analgesia.

Acute cord occlusion increases blood ionized magnesium concentration in preterm fetal sheep during maternal magnesium sulfate exposure.

This study tested the hypothesis that a pathophysiologic insult to the fetus that decreases pH (umbilical cord occlusion) produces an increase in physiologically active (i.e., ionized) magnesium concentration. Preterm pregnant sheep (n = 7) were instrumented with maternal and fetal catheters and an inflatable vascular occluder was placed around the umbilical cord. After a 2-day recovery period, each ewe received a 4-g loading dose, followed by continuous intravenous infusion of 1 g magnesium sulfate/h. After 48 h, an episode of acute fetal distress was produced by inflation of the umbilical occluder for 10 min. Maternal and fetal arterial blood samples were collected at regular intervals to quantitate ionized magnesium concentration and monitor physiologic status. Magnesium sulfate infusion increased maternal and fetal blood ionized magnesium concentration. In vitro blood analysis demonstrated that there was a linear inverse correlation (r2 = 0.99) between fetal sheep blood pH and ionized magnesium concentration. In vivo, 10 min of umbilical cord occlusion produced an increase in fetal blood ionized magnesium concentration in all animals (P = 0.02) that was temporally related to the decrease in fetal blood pH. Whether this increase in physiologically active magnesium concentration is beneficial (via neuroprotection) or deleterious (via suppression of stress response) to the distressed fetus remains to be determined.

How much labor is in a labor epidural? Manpower cost and reimbursement for an obstetric analgesia service in a teaching institution.

BACKGROUND: Some anesthesiologists avoid provision of obstetric analgesia services (OAS) because of low reimbursement rates for the work involved. This study defines the manpower costs of operating an OAS in a tertiary referral center and examines reimbursement for this cost. METHODS: The time spent providing OAS in a total of 55 parturients was studied prospectively using a modification of classic time and motion studies. RESULTS: Mean duration of OAS in our population was 412 +/- 313 min. Mean bedside anesthesia staff time was 90 +/- 40 min, and mean number of visits to each patient's bedside was 6.3 +/- 2.0 visits. Assuming staffing on demand for service (intermittent staffing), a minimum of 2.5 full-time equivalent (FTE) attending anesthesiologists was required to meet demand. With intermittent staffing, labor cost was $325 per patient. Actual practice at Duke University Medical Center is around-the-clock (dedicated) staffing, which requires 4.4 FTEs at a cost of $728 per patient. Neither average indemnity reimbursement ($299) nor Medicaid reimbursement ($204) covered the cost per OAS patient. Breaking even is possible under indemnity reimbursement because operating room reimbursement subsidizes OAS costs. Breaking even cannot occur with Medicaid reimbursement under any circumstances. CONCLUSIONS: Obstetric analgesia services requires a minimum of 2.5 FTE attending anesthesiologists at Duke University Medical Center. With the current payer mix, positive-margin operating room activities associated with the obstetric service are not sufficient to compensate for the losses incurred by an OAS. Around-the-clock dedicated obstetric staffing (4.4 FTEs) cannot operate profitably under any reasonable circumstances at our institution.

Bolus maternal cocaine administration does not produce a large increase in fetal sheep cerebral cortical glutamate concentration.

Human cocaine use during pregnancy may result in postnatal neurologic dysfunction and abnormal behavior. L-Glutamate, the major excitatory neurotransmitter in the brain, plays an important role in cerebral cortical development. An optimal level of glutamate is required for normal neuronal development. We tested whether acute cocaine exposure produces large increases in glutamate release in the intact cerebral cortex of the near-term fetal sheep. Cocaine 3.0 mg kg(-1) IV bolus produced the expected increase in maternal and fetal mean arterial pressure, increase in fetal heart rate, decrease in uterine blood flow, and decrease in fetal arterial blood pO2 (N = 5). The percentage increases in extracellular glutamate concentration in the fetal cerebral cortex measured by in utero microdialysis were 7%, 15%, 17%, 17%, and 43% in each fetus (upper 95% confidence bound for the median = 43%). We conclude that if cocaine increases glutamate concentration in the developing cerebral cortex, the increase in magnitude is small relative to the changes produced by other interventions such as ethanol or umbilical cord occlusion. Mechanisms other than increases in cerebral cortical glutamate concentration probably contribute to the neurologic injury associated with prenatal cocaine exposure.

Epidural analgesia in parturients with previous spinal irradiation.

PURPOSE: To present two successful cases of labour analgesia in patients who had been treated with radiation to the lumbar spine for neuroblastomas and to discuss the considerations when planning the anaesthetic management of these patients. CLINICAL FEATURES: We recently encountered two primigravidas requesting labour analgesia, both of whom were noted to have very thin backs with prominent spinous processes and obvious scoliosis. In both patients, the epidural space was easily identified and very shallow. Successful labour analgesia was achieved in both patients, one with a combined spinal epidural technique and the other with an epidural catheter. CONCLUSION: Craniospinal irradiation is known to have long-term effects on exposed nervous tissue, bone, and blood vessels. While a larger experience is necessary to demonstrate safety of regional anaesthesia in parturients following previous spinal irradiation, we provide reports of two successful cases.

Nitrate and nitrite anion concentration in the intact cerebral cortex of preterm and nearterm fetal sheep: indirect index of in vivo nitric oxide formation.

Pregnant sheep with a microdialysis probe implanted in the fetal cerebral cortex were used to determine if nitrate and nitrite anions (nitrate/nitrite) could be quantitated in the microdialysate as an indirect index of in vivo nitric oxide formation. Pregnant ewes (term, about 147 days) were surgically instrumented at gestational day (GD) 90 (n = 3; preterm) and GD 121 (n = 3; nearterm). Three days later, following an overnight probe equilibration period, five dialysate samples were collected continuously on ice at 1-h intervals (infusion rate of 1 (microl/min). The nitrate/nitrite concentration was determined by reducing a 10-microl aliquot of each dialysate fraction with hot acidic vanadium followed by chemiluminescence quantitation of the nitric oxide product. The lower limit of quantitative sensitivity of the method is 25 picomoles. Nitrate/nitrite concentration was 16.6+/-7.3 microM for the preterm fetus and 19.7+/-1.9 microM for the nearterm fetus. The data demonstrate that nitrate/nitrite, as an index of in vivo nitric oxide formation, can be quantitated in microdialysate samples collected from the intact fetal sheep cerebral cortex.

Chronic hypoxemia causes extracellular glutamate concentration to increase in the cerebral cortex of the near-term fetal sheep.

Fetal hypoxia is an important cause of neurologic morbidity and mortality. Hypoxia-induced increase in extracellular glutamate concentration can lead to excitotoxic neuronal death in adults. The objective of this study was to test whether chronic fetal hypoxemia increases extracellular glutamate concentration in the unanesthetized intact cerebral cortex of the near-term fetal sheep. Microdialysis probes were implanted into the parasagittal parietal cortex and periventricular white matter of near-term fetal sheep. At 124 +/- 1 days of gestation, extracellular glutamate concentration was determined before and during 24 h of fetal hypoxemia. Chronic hypoxemia was produced by tightening a vascular occluder placed around the maternal common iliac artery. Larger decreases in fetal arterial oxygen content were associated with larger increases in extracellular glutamate concentration in the parietal cortex (Kendall's tau = 0.81, N = 7, p = 0.005). No such relationship was detected in the periventricular white matter. Chronic hypoxemia increases extracellular glutamate concentration in the intact cerebral cortex of the unanesthetized near-term fetal sheep.

Use of an automated anesthesia information system to determine reference limits for vital signs during cesarean section.

INTRODUCTION: We evaluated whether automated anesthesia information systems can be used to calculate reference limits (population-based "normal values") for vital signs. We considered four populations of women undergoing cesarean section: healthy under spinal anesthesia, healthy under general anesthesia, pre-eclamptic/eclamptic under spinal anesthesia, and pre-eclamptic/eclamptic under general anesthesia. METHODS: Reference limits were calculated for each of the study populations by determination of percentiles for: minimum heart rate, maximum heart rate, minimum arterial oxyhemoglobin saturation (SaO2), minimum mean arterial pressure (MAP), maximum MAP, decrease in MAP, and increase in MAP. RESULTS: There was one adverse anesthetic outcome among the 1,300 women in the study; the woman sustained a post-dural puncture headache. The 5th percentiles of SaO2 were at least 95% saturation under spinal versus 90% under general. Under spinal anesthesia, 95th percentiles for decreases in MAP from baseline were 63 mmHg for healthy and 75 mmHg for pre-eclamptic/eclamptic women. Under general anesthesia, the 95th percentiles for maximum MAP were 161 and 177 mmHg, respectively. Two women of the 1,300 patients experienced simultaneously a minimum SaO2 < 92% and minimum MAP < 50 mmHg. DISCUSSION: Automated anesthesia information systems can be used to determine reference limits for vital signs during anesthesia. Reference limits may play a role in malpractice cases when an expert claims that care by an anesthesiologist was sub-standard as shown by vital signs that were not maintained within the normal range during the critical portions of an anesthetic. Automated anesthesia information systems may enhance expert witnesses' clinical judgment.

Management of a parturient with an uncorrected atrioventricular canal defect.

A 24-year-old woman at 37 weeks gestation, with an uncorrected atrioventricular canal defect and incipient congestive heart failure is presented. This rare defect is part of the larger group of endocardial cushion defects. The peripartum anesthetic management of this condition has not been described. Our patient had a large atrial septal defect, a common regurgitant atrioventricular valve, a large left-to-right shunt and a small ventricular septal defect. Her pregnancy was maintained until she developed symptoms of congestive heart failure. We discuss her peripartum management, monitoring and anesthetic choices.

Ethanol-induced changes in prostaglandin E concentration in the intact cerebral cortex of preterm and near-term fetal sheep.

Ethanol-induced changes in fetal prostaglandin E (PGE) concentration may play a role in the toxic effects of prenatal ethanol exposure. Using the novel technique of in utero microdialysis, the present study tested the hypothesis that acute ethanol exposure changes PGE concentration in the intact cerebral cortex of preterm (93 +/- 1 days of gestation) and near-term (124 +/- 1 days of gestation; term, approximately 147 days) fetal sheep. Fetal sheep were surgically instrumented with a microdialysis probe placed in the parasagittal parietal cortex. Three days later, the effects of maternal infusion of 1 g of ethanol/kg maternal body weight on preterm (n = 6) and near-term (n = 7) fetal cerebral cortical and plasma PGE concentrations were determined. In the preterm fetal cerebral cortex, PGE concentration was increased after ethanol infusion in all six animals studied. The median peak increase was 160% with a 95% confidence interval of 115 to 784%. There was considerable variation in the time of occurrence, magnitude, and duration of this increase. In the near-term fetal cerebral cortex, an increase in PGE concentration was observed after ethanol infusion in 5 of the 7 animals studied, whereas a decrease in PGE concentration was observed in the other two animals. Overall, ethanol did not increase significantly near-term fetal cerebral cortical PGE concentration. For both age groups, ethanol infusion had no effect on fetal plasma PGE concentration. These data indicate that ethanol can affect PGE production in the fetal cerebral cortex and that this effect seems to be gestational-age-dependent.

Flumazenil does not affect the increase in rat hippocampal extracellular glutamate concentration produced during thioacetamide-induced hepatic encephalopathy.

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that often occurs as a consequence of acute or chronic liver failure. Previous reports have suggested that alterations in amino acid neurotransmission, particularly glutamate, may play an important role in the pathogenesis of HE. The objectives of the present study were to test the hypothesis that extracellular glutamate concentration is increased during HE, and to determine if flumazenil, a benzodiazepine antagonist, alters the extracellular concentration of glutamate during HE. The experimental approach involved using microdialysis probes to measure rat hippocampal extracellular glutamate concentration. HE was brought about as a result of thioacetamide-induced liver failure. Thioacetamide produced behavioral and metabolic effects, such as somnolence, hyperventilation and hyperammonemia, consistent with stage three HE. Comparison with saline-treated rats demonstrated that HE was associated with a significant increase (p = 0.010) in extracellular hippocampal glutamate concentration. Administration of flumazenil caused a transient increase in arousal level, but did not affect the increase in glutamate concentration (p = 0.93). These results corroborate the theory that glutamate neurotransmission is altered during HE and suggest that the flumazenil arousal of HE rats is not mediated by a change in extracellular glutamate concentration.

Magnesium sulfate adversely affects fetal lamb survival and blocks fetal cerebral blood flow response during maternal hemorrhage.

Magnesium sulfate is commonly used in high-risk pregnancies, even though its actions in the fetus during maternal/fetal stress are not completely understood. The present study tested the hypothesis that magnesium sulfate alters the fetal cerebral blood flow response to hypoxemia produced during maternal hemorrhage. It was conducted in instrumented near-term fetal lambs at 123 days of gestation. Experimental treatment involved four periods of maternal hemorrhage over a 60-min period during fetal infusion of 0.25 g (n = 5) or 0.30 g (n = 6) magnesium sulfate, or normal saline (n = 11). The level of fetal cerx500l blood flow was determined using radiolabeled microspheres. For all three treatment groups, maternal hemorrhage produced fetal hypoxemia and some fetal demise. During fetal infusion of saline, 1 of 11 (9%) of the fetuses died; with the 0.25-g magnesium sulfate regimen, 1 of 5 (20%) died; and with the 0.30-g magnesium sulfate regimen, 3 of 6 (50%) of the fetuses died. Magnesium sulfate caused an increase in the proportion of fetal death produced by maternal hemorrhage (P < 0.05). Among surviving fetuses, hemorrhage-induced hypoxemia increased fetal cerebral blood flow during saline infusion. In contrast, infusion of magnesium sulfate had an inhibitory effect on this compensatory increase in fetal cerebral blood flow (P = 0.003). These data indicate that, in the sheep, magnesium sulfate increases fetal mortality and inhibits the compensatory increase in fetal cerebral blood flow during maternal hemorrhage-induced fetal hypoxemia.