Susan L. Sipes

Risk factors for cordocentesis and fetal intravascular transfusion

There is little information on the impact of technical aspects or patient characteristics on the risks of accessing the fetal circulation. We performed 594 diagnostic cordocenteses and 156 intravascular transfusions over 6 years. Pancuronium was administered during 52% of procedures. The number of needle punctures per successful procedure was unrelated to the placental location. However, the number of punctures required was lower if the placental cord origin rather than a midsegment was targeted (p less than 0.0001). Bleeding from either the uterine or umbilical cord puncture site was not believed to be clinically significant, although the duration of bleeding was greater after arterial puncture than after venous puncture (p = 0.01) and after intravascular transfusion than after diagnostic cordocentesis (p less than 0.0001). Amnionitis (suspected plus verified) complicated 0.5% of procedures. Preterm premature rupture of membranes (with or without amnionitis) followed 0.4% of procedures. Fetal bradycardia occurred in 6.6% (6.6 +/- 0.8 minutes; range, 0.1 to 35 minutes). There were five perinatal losses after a diagnostic procedure, yielding an uncorrected loss rate of 0.8% (5/594). Each was associated with a prolonged bradycardia; each fetus was ultimately demonstrated to have been unsalvageable. Two independent risk factors for bradycardia were identified--arterial puncture and severe, early onset intrauterine growth retardation. The administration of pancuronium reduced the incidence of bradycardia in appropriately grown fetuses (6% to 1.5%; p less than 0.05), but did not alter the incidence in growth-retarded fetuses. We conclude that cordocentesis performed with a needle guide is a safe procedure but that its risk varies with both the indication and the vessel punctured.

Magnesium sulfate decreases maternal blood pressure but not uterine blood flow during epidural anesthesia in gravid ewes.

The purpose of this study was to determine whether administration of magnesium sulfate decreased maternal blood pressure during epidural anesthesia in gravid ewes. Twenty-two experiments were performed in 11 chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included: 1) T = 0: magnesium sulfate 4 g intravenously over 5 min followed by an infusion of magnesium sulfate at 4 g/h, or normal saline iv followed by an infusion of normal saline alone; 2) T = 135 min: 500 ml normal saline intravenously over 12 min; and 3) T = 150 min: epidural administration of 2% lidocaine. The initial bolus of magnesium sulfate slightly decreased maternal mean arterial pressure (MAP) but increased uterine artery blood flow (UBF). The increase in UBF was accompanied by an increase in fetal PaO2 at 145 min in the magnesium sulfate group but not in the control group. At 165 min (i.e., 15 min after the epidural injection of lidocaine), epidural lidocaine resulted in a median sensory level of T-10 in the magnesium sulfate group and T-11 in the control group. During epidural anesthesia, maternal MAP was lower (P = 0.001) in the magnesium sulfate group than in the control group. At 165 min, maternal MAP was 18 +/- 3% below baseline (P = 0.0001) in the magnesium sulfate group but did not differ significantly from baseline in the control group. Maternal cardiac output and UBF did not differ from baseline after epidural injection of lidocaine in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Does Magnesium Sulfate Alter the Maternal Cardiovascular Response to Vasopressor Agents in Gravid Ewes

Magnesium sulfate (MgSO4) attenuates the maternal compensatory response to hemorrhage in gravid ewes, perhaps by decreasing the response to endogenous vasopressors. The purpose of this study was to determine whether MgSO4 alters the cardiovascular response of gravid ewes to vasopressor agents. Sixteen gravid ewes underwent a series of experiments consisting of administration of two exogenous and two endogenous vasopressors, each with and without a concurrent MgSO4 infusion. Dose-response curves were constructed for phenylephrine (an alpha 1-adrenergic agonist), ST-91 (an alpha 2-adrenergic agonist), angiotensin II, and arginine vasopressin (AVP). MgSO4 significantly attenuated the increase in maternal mean arterial pressure and systemic vascular resistance and the decrease in cardiac output during ST-91 infusion but not during phenylephrine, angiotensin II, or AVP infusions. MgSO4 significantly attenuated the increase in uterine vascular resistance during phenylephrine, ST-91, and angiotensin II infusions and the decrease in uterine blood flow during phenylephrine and angiotensin II infusions. MgSO4 also appeared to attenuate the decrease in uterine blood flow during ST-91 infusion (P = 0.067). The present study suggests that MgSO4 antagonizes the effects of alpha 1-adrenergic agonists, alpha 2-adrenergic agonists, and angiotensin II on the uterine vasculature, thus providing a level of protection for the fetus in situations of maternal stress.

Prediction of pregnancy outcome with single versus serial maternal serum a-fetoprotein tests

OBJECTIVE The purpose of our study was to determine whether the trend of three maternal serum alpha-fetoprotein samples was more predictive of pregnancy outcome than the initial sample in the evaluation of patients with unexplained alpha-fetoprotein elevations. STUDY DESIGN A total of 432 patients with unexplained elevation of their first two maternal serum alpha-fetoprotein samples had a third sample drawn. Pregnancy outcomes were determined. Patients were grouped for analysis according to the level of the initial sample, the final sample, and the trend of three samples. Statistical analysis was by chi 2 and logistic regression, with p < 0.05 considered significant. RESULTS The initial maternal serum alpha-fetoprotein was most predictive of preterm delivery (p < 0.001), size small for gestational age (p < 0.001), and intrauterine fetal death (p = 0.009). Neither the final value nor the trend of three values was as prognostic. CONCLUSION The first maternal serum alpha-fetoprotein is the best predictor of pregnancy outcome. Obtaining a second sample to confirm the elevation is appropriate, but additional samples provide minimal information.

Epidural Anesthesia Worsens Uterine Blood Flow and Fetal Oxygenation during Hemorrhage in Gravid Ewes

Recent studies suggest that epidural anesthesia initiated before hemorrhage may improve survival and acid-base status in laboratory animals. However, studies of hemorrhagic shock in nonpregnant animals may not be applicable to less severe hemorrhage in pregnant animals. The purpose of this study was to determine whether epidural anesthesia alters maternal and fetal hemodynamic and acid-base responses to hemorrhage in gravid ewes. Twenty-four experiments were performed in twelve chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included: 1) T = 0 min: normal saline 500 ml intravenously; 2) T = 15 min: epidural administration of 0.5% bupivacaine (epidural group) or normal saline (control group); 3) T = 30 min: epidural administration of additional 0.5% bupivacaine (epidural group only) if the sensory level of anesthesia was below T10; 4) T = 45 min: maternal hemorrhage 20 ml/kg over 55 min; and 5) T = 110 min: transfusion of collected maternal blood over 55 min. At 45 min (i.e., 30 min after the epidural injection of bupivacaine), epidural bupivacaine resulted in a median sensory level of T9 in the epidural group. At that time, maternal mean arterial pressure was less (P less than 0.05) in the epidural group than in the control group (14 +/- 2% below baseline versus 4 +/- 1% above baseline, respectively). Maternal mean arterial pressure, heart rate, cardiac output, and uterine blood flow, and fetal PO2 and pH all were significantly less during hemorrhage (P less than 0.05) in the epidural group than in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

The Plasma Renin-Angiotensin System in Preeclampsia: Effects of Magnesium Sulfate

Two groups of women were studied in a prospective longitudinal fashion to determine the effects of a 2.5-hour infusion of magnesium sulfate upon the renin-angiotensin system. Serum magnesium concentration, angiotensin-converting enzyme concentration, and plasma renin activity were measured at uniform intervals in women with either preeclampsia or preterm labor. Plasma renin activity was significantly lower (3.9 +/- 2.2 versus 6.1 +/- 1.8 ng/mL/minute; P = .004) and angiotensin-converting enzyme significantly higher (47.1 +/- 14 versus 34.0 +/- 10 U/mL; P = .008) in women with preeclampsia than in those with preterm labor. Magnesium infusion was associated with a sustained decline in plasma renin activity in preeclamptic women (P = .003). A transient decline in angiotensin-converting enzyme (P = .009) was observed in women with preeclampsia, but not with preterm labor. In contrast to the sustained change in plasma renin activity, angiotensin-converting enzyme concentration returned to baseline activity levels by 2.5 hours. A nonsignificant negative relationship (P = .06) was noted between angiotensin-converting enzyme and gestational age in subjects with preeclampsia. We conclude that a short-term infusion of magnesium sulfate leads to a sustained decline in plasma renin activity in preeclamptic women, but exerts no sustained effect on angiotensin-converting enzyme in women with either preeclampsia or preterm labor.

Does calcium chloride help restore maternal blood pressure and uterine blood flow during hemorrhagic hypotension in hypermagnesemic gravid ewes

Magnesium sulfate worsens maternal hypotension and fetal oxygenation during hemorrhage in gravid ewes. The purpose of this study was to determine whether calcium chloride administration is a useful adjunct to blood transfusion during hemorrhagic hypotension in hypermagnesemic gravid ewes. Sixteen experiments were performed in eight chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included (a) T = 0: magnesium sulfate 4 g IV; (b) T = 5: infusion of magnesium sulfate 4 g/h IV; (c) T = 90: maternal hemorrhage 20 mL/kg over 55 min; (d) T = 147: calcium chloride 10 mg/kg or normal saline (NS-control) 0.1 mL/kg IV; (e) T = 160: transfusion of collected maternal blood over 55 min. Magnesium sulfate alone slightly decreased maternal mean arterial pressure (P = 0.002) and increased uterine blood flow (P = 0.0001) in both groups before hemorrhage. During hemorrhage, maternal mean arterial pressure, cardiac output, and uterine blood flow, and fetal PO2 and pH all decreased sharply (P = 0.0001). Cardiac output increased (P = 0.0005) modestly just after the intravenous bolus of calcium chloride. Maternal mean arterial pressure was significantly higher (P = 0.03) during transfusion in the calcium chloride group than in the NS-control group, but only after mean arterial pressure was near baseline measurements. Maternal uterine blood flow and fetal PO2 and pH responses over time were similar in the two groups. We conclude that intravenous administration of calcium chloride (10 mg/kg) transiently increased cardiac output during hemorrhagic hypotension and slightly increased mean arterial pressure during transfusion in hypermagnesemic gravid ewes.(ABSTRACT TRUNCATED AT 250 WORDS)

The Fetus as a Patient

A 19-WEEK PARTURIENT presented with a fetus with a lung mass. Magnetic resonance imaging (panel A) demonstrated a congenital cystic adenomatous malformation (CCAM) occupying the right chest causing mediastinal shift, cardiac compression (H heart), and displacement of the hemidiaphragm (arrow). Both lungs were compressed. Hydrops fetalis was present (A fetal ascites; B bowel; L liver). Echocardiography revealed a compressed but structurally normal heart. The hydrops improved after aspiration, but the macrocyst recurred and the solid component continued to enlarge. A thoracoamniotic shunt was placed for continuous drainage. Imaging at 36 weeks (panel B) demonstrates the right hemidiaphragm in the correct position and resolution of the fetal ascites. Lung hypoplasia and mediastinal shift necessitated mass resection during ex utero intrapartum therapy. A maternal laparotomy was performed, followed by hysterotomy allowing delivery of the fetal head, chest, and arm. High-dose volatile anesthetic (2 minimum alveolar concentration of desflurane) provided uterine relaxation and fetal anesthesia. Maternal blood pressure was maintained with phenylephrine. Intramuscular fetal injections included fentanyl (20 g/kg), vecuronium (200 g/kg), and atropine (20 g/kg). The fetus was intubated (not ventilated), and pulse oximeter and peripheral venous access were established. After pulmonary lobectomy, the fetus was ventilated and delivery and newborn resuscitation were completed. Congenital cystic adenomatous malformation results from overgrowth of terminal bronchial epithelium. Mass effect results in pulmonary hypoplasia. Cardiac compression with impaired venous return leads to lethal cardiac failure (hydrops). Maternal health is threatened, asa state similar topreeclampsia (maternalmirror syndrome)mayensue. Exutero intrapartumtherapyprocedure isa feasibleandpotentially a life-saving treatment for congenital cystic adenomatous malformation. It provides time on uteroplacental gas exchange for controlled resection of the large fetal lung mass. The anesthetic goals for ex utero intrapartum therapy procedure include achieving uterine hypotonia, usingdeepgeneralanesthesiaornitroglycerin, tomaintainuteroplacentalcirculation;avoidingpostpartumhemorrhage;maintainingnormal maternal blood pressure often requiring -adrenergic agonist support; and achieving surgical anesthesia for the fetus to avoid first breathing while avoiding fetal cardiac depression.